The Anatomy of Exercise

The Anatomy of Exercise
SunCoast Seminars Presents: The Anatomy of Exercise Educator: Willem Stegeman, DPT, MTC, CEAS Jorit Wijnmaalen, DPT, MBA, MTC, CEAS

Why do we need to know and understand the anatomy of muscle?
SunCoast Seminars Why do we need to know and understand the anatomy of muscle? This will allow the clinician to specify their exercise program geared towards the function of the muscle. Different muscles have different functions and these functions are in part defined by the anatomy of the muscle. There are approximately 639 skeletal muscles in the human body. There are different types of muscles, each with their distinct anatomy. Understanding the anatomy of the muscle will also help the clinician understand how different (intrinsic and extrinsic) factors can impact muscles and exercising. We are looked upon as the experts when it comes to exercise therapy. Understanding the anatomy of muscles is an important part of being an exercise expert.

SunCoast Seminars Program Objectives:
Reviewing muscular anatomy and physiology This will include a review of tissue healing Discuss how extrinsic factors such as medication, progression, exercise objectives etc. may affect the exercise therapy program Discuss how intrinsic factors including disease processes age, vital signs etc. may affect muscles and exercise programs. Discuss the basics of exercise therapy Discuss common exercise principles Open chain vs. closed chain Eccentricisometricconcentric

SunCoast Seminars A few rules:
We are in a hospital and should be aware of any codes that might be called. Bathrooms are right outside of this room We will break for lunch are around noon Please turn off all cell phones. I would like to make this lecture as interactive as possible. Please feel free to ask questions, share your experiences, opinions etc. with the rest of the group.

SunCoast Seminars About the educators: Background Education
Work experience Hobbies

About SunCoast Seminars
4 educators Dr Brian Healy Johan Sloots Dr. Willem Stegeman Dr Jorit Wijnmaalen

About SunCoast Seminars
More courses: Orthopedic Joint Replacement course: 10.5 CEU Comprehensive Management of back & neck pain: 10 CEU Joint Replacement, online: 7 CEU Thoracic Outlet Syndrome: 6 CEU, Online HIV/Medical Errors/Abuse: 4 CEU The anatomy of exercise: 7.5 CEU

Muscular anatomy and physiology
SunCoast Seminars Muscular anatomy and physiology Muscle Types: Smooth muscles Cardiac muscles Skeletal muscles

SunCoast Seminars Smooth muscles
These muscles are very important in physiological regulation. Help to regulate the flow of blood. Help control BP They control the movement of food through the digestive system. Control of the uterus during labor Contraction of a smooth muscle cell is generated by a sliding mechanism of the myofilaments. Contraction is involuntary and may be initiated by Nerve impulse Hormones (i.e. cardiac function) Mechanical change to the muscle

SunCoast Seminars Smooth Muscles
Crucial difference with skeletal muscles: nervous control is absolutely required for skeletal muscles, smooth muscles can, to a degree, work with out nervous stimulation! Lastly, these muscles are not striated (the myofilaments are arranged into light and dark bands as in striated muscles). Striations are formed by alternating segments of thick and thin protein filaments, which are anchored by segments called T-lines

SunCoast Seminars Cardiac Muscles
This muscle may look like a skeletal muscles (especially the contraction of it since they are striated as well) but it acts much like smooth muscle (it does not require nervous system input to function) The attachment site between cells is called an intercalated disc, which is present only in cardiac muscle cells and allows forces to be transmitted from one cell to the next.

SunCoast Seminars Skeletal Muscles:
Striated (banded) type. This distinctive banding pattern of striated muscle is an effect that comes from the alignment of sarcomeres in register across the myofibrils Skeletal muscles are under voluntary control; no skeletal muscle works without “orders” from the nervous system Skeletal muscles have elongated muscle cells (fibers) with multiple nuclei lying along the periphery of the cell. The sarcoplasm of each cell is contained by a sacrolemma (plasma membrane) and an external lamina. Each muscle contains many myofibrils and each myofibril contains thin actine and thick myosin myofilaments. These muscles normally make up the largest portion of a person's lean body mass

SunCoast Seminars Skeletal Muscles
These are the muscles that are responsible for all voluntary movements (movements controlled by the central nervous system and which typically are directed at some sort of interaction with the environment) These muscles only contract in response to instructions from the central nervous system (few exceptions) Shivering is a response to the cold. Human have a stable body temperature - the average temperature of the human body is 36.9[degrees]C (98.6[degrees]F). In order to remain healthy humans must keep their body temperature within the narrow range of 36[degrees].-38[degrees]C. The hypothalamus, which acts as a thermostat. It responds if the skin cools down and as nerve endings signal danger. in cold conditions, the skin's thermal receptors send messages to the hypothalamus, which directs blood away from the skin to minimize heat exchange with the air.

SunCoast Seminars As the skin cools, shivering sets in with the muscles contracting and releasing in bursts, to exert some "muscle exercise" in order to increase heat production and warm the body Shivering is an early warning sign of cold stress and a signal to get out of the cold or put on extra clothing. Shivering usually starts in the head and neck, then spreads down through the back and to the muscles in the lower body Some muscles shiver more efficiently than others - such as the mouth muscles that make the "teeth chatter." With more body cooling, shivering becomes more violent, with maximum shivering at a cooling to 34[degrees]-35[degrees]C. Moderate hypothermia (core body cooling) sets in around 33[degrees]-30[degrees]C with cessation of shivering as people lose core heat. Below 30[degrees]C, hypothermia becomes severe and life-threatening.

SunCoast Seminars A drop in core body temperature of only 2[degrees]C can produce confusion, light-headedness, stumbling and slowed movements. With increasing cooling of the core temperature, severe hypothermia sets in with coma and eventually death. When shivering stops, it is a danger signal. But if the sense of cold is impaired or if the shivering response is less efficient, people are at increased risk of hypothermia and cold injuries, such as frostbite. Some people have a reduced ability to respond to cold, for example the elderly, who cannot shiver as readily as younger people. They may therefore not respond to cold and are especially prone to hypothermia. Not recognizing the early symptoms of hypothermia, the sluggish behavior can be taken for slowed reflexes or signs of other disorders and not receive proper medical attention. Babies younger than a year old also cannot shiver.

In short, these skeletal muscles have the following functions: provide joints with the forces necessary to produce movement to control movement to stabilize and protect joints when loads are applied to them. Skeletal muscles are a striated type of muscle with a rich blood supply, extensive afferent and efferent innervation and an extremely high metabolic capacity. Skeletal muscles have a tremendous adaptive capacity that allows then to hypertrophy, atrophy, increase in physiological length, decrease in physiological length and change metabolic capacities.

Out of the three muscle types discussed, the skeletal muscle are the muscles that we will be most concerned within this course.

SunCoast Seminars Muscular anatomy and physiology Let’s review!

SunCoast Seminars The Anatomy review of a skeletal muscle
Each muscle cell is surrounded by a basal lamina and connective tissue. They are bound to each other and to surrounding tissues by connective tissue to form a gross "muscle". Skeletal muscle fibers are NOT joined by cell junctions. The endomysium consists of the basal lamina and thin connective tissue that surrounds individual muscle cells. The perimysium consists of sheets of connective tissue which separate the fibers into groups known as fascicles. The epimysium surrounds the groups of fasicles that comprise the “muscle”.

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SunCoast Seminars Quick anatomic review of a skeletal muscle
Connective tissue transmits the mechanical force of muscle. Tendons connect muscle to bone. The myotendinous junction occurs at the end of the muscle cell where the terminal actin filaments connect to the plasma membrane Skeletal muscle fibers are multi-nucleate cells that arise by fusion of mono-nucleate myoblasts. The many nuclei are located at the periphery of the cell. Mono-nucleate satellite cells, associate with the muscle fiber and reside within the muscle basal lamina. They promote limited regeneration of muscle in the adult.

The muscle-tendon junction
SunCoast Seminars The Yellow line is corresponding to the tendon. How do we classify this Connective tissue? Dense Regular. The yellow arrows are pointing the nuclei of the fibroblasts making the collagen. The blue line is showing where the Striated Muscle is beginning The muscle-tendon junction

SunCoast Seminars Innervation of a Skeletal Muscle
Skeletal muscle is innervated and highly vascularized, due to its high energy requirements. It is penetrated of blood vessels into the epimysium with branches into the peri- and endomysium.

Motor end plates (neuromuscular junctions) are specialized sites at which a nerve contacts a muscle cell. The terminal branches of motor axons lie in the surface of the muscle cell, where the plasma membrane is highly folded. Muscle action begins at the motor end plate (or neuromuscular junction), which is analogous to a synapse Acetylcholine(ACh) binds to receptors localized in the muscle membrane at the motor end plate, resulting in local depolarization at the end plate. When this depolarization exceeds the threshold, it will result in an action potential

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SunCoast Seminars Neuromuscular Junction or Motor End Plate
axon of Motor (Efferent) Neuron White arrow - Skeletal Muscle Fiber

Additional proprioceptor endings (Golgi tendon organs) are located at the point where muscle fibers attach to tendon These Golgi tendon organs (GTO) respond to tension (force) exerted by the muscle; activity in these axons inhibits muscle contraction (they are for instance stretched when a joint is swollen).

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SunCoast Seminars Nerve Conduction
Both nerve cells and muscle cells are excitable Their cell membrane can produce electrochemical impulses and conduct them along the membrane. In muscle cells, this electric phenomenon is also associated with the contraction of the cell The origin of the membrane voltage is the same in nerve cells as in muscle cells. In both cell types, the membrane generates an impulse as a consequence of excitation. The long nerve fiber, the axon, transfers the signal from the cell body to another nerve or to a muscle cell The axon may be covered with an insulating layer called the myelin sheath, which is formed by Schwann cells

This myelin sheath is not continuous but divided into sections, separated at regular intervals by the nodes of Ranvier The junction between an axon and the next cell with which it communicates is called the synapse. Information proceeds from the cell body uni-directionally over the synapse, first along the axon and then across the synapse to the next nerve or muscle cell (think about peripheral leasion) The part of the synapse that is on the side of the axon is called the pre-synaptic terminal The part on the side of the adjacent cell is called the postsynaptic terminal. Between these terminals, there exists a gap. A chemical neurotransmitter, released from the pre-synaptic cell, is responsible for the impulse to transfer across the synapse.

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This transmitter, when released, activates the postsynaptic terminal. The synapse between a motor nerve and the muscle it innervates is called the neuromuscular junction

If a nerve cell is stimulated, the trans-membrane voltage necessarily changes. The stimulation may be excitatory (i.e., depolarizing; characterized by a decrease in the normally negative resting voltage) or inhibitory (i.e., hyperpolarizing, characterized by an increase in the magnitude of the membrane voltage). After stimulation the membrane voltage returns to its original resting value If the excitatory stimulus is strong enough, the trans-membrane potential reaches the threshold, and the membrane produces a characteristic electric impulse, the nerve impulse. Remember the Na+/K+ pump?

Many factors may affect nerve conductivity but discussion of those factors would be outside the scope of this lecture. Temperature Properties of the membrane Sodium levels Calcium levels Age Anatomical changes because of disease (ALS)

A myelinated axon (surrounded by the myelin sheath) can produce a nerve impulse only at the nodes of Ranvier In these axons the nerve impulse propagates from one node to another The myelin sheath increases the conduction velocity The conduction velocity of the myelinated axon is directly proportional to the diameter of the axon

SunCoast Seminars Nerve Conduction

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SunCoast Seminars Types of Skeletal muscles
Not all skeletal muscle is the same. Some cells are thicker than others Some shorten faster Some produce more tension Some fatigue more rapidly Looking at these different features, there appear to be three major types of skeletal muscles:

SunCoast Seminars Types of Skeletal muscles Slow Twitch
Fast Fatigue Resistant Fast Twitch Fatigable

SunCoast Seminars Slow Twitch
These muscles produce the least amount of force. They actually produce less than half the force produced by fast twitch fatigue resistant fibers and are most resistant to fatigue. Slow twitch muscles use oxygen for power and have a predominance of aerobic enzymes. Slow twitch muscles are red, because they contain lots of blood vessels. These muscle fibers are "hit", or engorged with nitrogen-rich blood, during higher rep training, specifically in sets of 12 to 20 reps. Slow twitch muscles are used for holding posture

SunCoast Seminars Fast Twitch (Type II)
Fast Twitch fibers use anaerobic metabolism to create fuel and so they are much better at generating short bursts of strength or speed than slow muscles. These types of muscles are best trained during sets of 2-5 repetitions. They fatigue more quickly. Fast twitch fibers generally produce the same amount of force per contraction as slow muscles, but they get their name because they are able to fire more rapidly. Having more fast twitch fibers can be an asset to a sprinter since she needs to quickly generate a lot of force (genetically determined, 50/50 on average; some research suggests that some fibers might be able to convert).

SunCoast Seminars Two Types: Type IIa Fibers / Fast Fatigue Resistant
These fast twitch muscle fibers are also known as intermediate fast-twitch fibers. They can use both aerobic and anaerobic metabolism almost equally to create energy. In this way, they are a combination of Type I and Type II muscle fibers. Produce forces greater than slow twitch fibers but less than fast twitch fatigable fiber. These fibers are more resistant to fatigue than fast fatigable but less fatigue resistant than slow twitch fibers.

SunCoast Seminars Type IIb Fibers
These fast twitch fibers use anaerobic metabolism to create energy and are the "classic" fast twitch muscle fibers that excel at producing quick, powerful bursts of speed. This muscle fiber has the highest rate of contraction (rapid firing) of all the muscle fiber types, but it also has a much faster rate of fatigue and can't last as long before it needs rest. Produce the greatest amount of force Are least resistant to fatigue Force produced is typically 2-3 times greater than fast twitch fatigue resistant fibers

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SunCoast Seminars Conclusion
So the lesson here is quite simple. As we are exercising our patients, we must keep in mind the main objective of our exercise program. In order to recruit the largest possible number of muscle fibers of both types during the exercise program, we must vary the repetition ranges . Keeping in mind that on average, there is a 50/50 split of these fibers so… Any therapist, who puts a patient on an exercise program that doesn't include a variation of repetition ranges might significantly limit the success of the exercise program.

SunCoast Seminars Skeletal Muscle Fiber Arrangement
It is important to realize that there are different alignments of muscle fibers in the various skeletal muscles. These different fiber arrangements will have an effect on the length, mechanical properties and the number of muscle fibers of a muscle. Muscle fibers can be arranged in parallel or at angles to the tendon. Parallel fibered muscles are muscle composed of parallel aligned fibers. These muscles have long muscle fibers that can produce a large excursion on the tendon. Fusiform Triangular Spiral Pinnated fibers muscles are muscles composed of angled fibers Unipinnate Bipinnate Multipinnate

SunCoast Seminars Parallel Fusiform Bipennate Spiral Unipennate
Triangular

SunCoast Seminars Structure & Function of a Skeletal muscle

SunCoast Seminars The cell comprises a series of striped or striated, thread-like myofibrils. Within each myofibril there are protein filaments that are anchored by dark Z line. The fiber is one long continuous thread-like structure. The smallest cross section of skeletal muscle is called a sarcomere which is the functional unit within the cell. It extends from one Z line to the next attached Z line. The individual sarcomere has alternating thick myosin and thin actin protein filaments. Myosin forms the center or middle of eache M line. Thinner actin filaments form a zig zag pattern along the anchor points or Z line.

SunCoast Seminars Muscle Contraction
Upon stimulation by an action potential, skeletal muscles perform a coordinated contraction by shortening each sarcomere. The best proposed model for understanding contraction is the sliding filament model of muscle contraction. Actin and myosin fibers overlap in a contractile motion towards each other. ATP binds to the cross bridges between myosin heads and actin filaments. The release of energy powers the swiveling of the myosin head Myosin filaments have club-shaped heads that project toward the actin filaments. Larger structures along the myosin filament called myosin heads are used to provide attachment points on binding sites for the actin filaments.

SunCoast Seminars Muscle Contraction (cont.)
The myosin heads move in a coordinated style, they swivel toward the center of the sarcomere, detach and then reattach to the nearest active site of the actin filament. This is called a rachet type drive system. This process consumes large amounts of adenosine triphosphate (ATP). Calcium ions are required for each cycle of the sarcomere. Calcium is released from the sarcoplasmic reticulum into the sarcomere when a muscle is stimulated to contract. This calcium uncovers the actin binding sites. When the muscle no longer needs to contract, the calcium ions are pumped from the sarcomere and back into storage in the sarcoplasmic reticulum

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SunCoast Seminars Images from Purves et al., Life: The Science of Biology, 4th Edition, by Sinauer Associates ( and WH Freeman (

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SunCoast Seminars Muscle contraction (cont.)
ATP is the main source of energy for all muscle contraction. There are several chemical reactions that take place to produce ATP. When a muscle is used, a chemical reaction breaks down ATP to produce energy: ATP + Actin + Myosin Actomyosin + Phosphate + ADP + Energy This is the chemical reaction that produces energy, however, there is only enough ATP stored in the muscle cell for two or three slow twitch contractions, or one burst of power from a fast twitch contraction. More ATP must be created. There are three enzyme systems that can create more ATP. The enzyme system that is used depends on whether the type of muscle is fast twitch or slow twitch, and whether the muscle is used for strength, burst power, or endurance.

SunCoast Seminars Muscle Contraction (Cont.)
The Strength Enzyme System When muscle strength is required, ATP is created quickly from the following chemical reaction. The enzyme creatine kinase mediates ATP production from the high energy molecule creatine phosphate by an anaerobic reaction: CP + ADP ATP + Creatine The CP (Creatine Phosphate) is depleted in just a few seconds. This is the reason your maximum power can be maintained for only a few seconds. To continue producing high strength power, the speed enzyme system kicks in.

The Burst Power Enzyme System The enzymes required for this reaction are depleted in less than two minutes. This reaction is called Anaerobic Glycolysis because it uses glucose without oxygen. Glucose 2ATP + 2 Lactate To continue muscle usage requires the aerobic system to kick in. The aerobic system uses oxygen and sugar for fuel. The ability to perform well after about two minutes of maximum exertion depends on the aerobic conditioning of the body.

The Endurance Enzyme System This system consists of three processes: Carbohydrate Metabolism: Carbohydrates metabolize most efficiently and are therefore used first Fat Metabolism: If no carbohydrates are available, the body metabolizes fat. Amino Acid Protein Metabolism: If no fat is available, the body metabolizes Amino Acids. The body stores glucose and fatty acids for these reactions. In addition, the cardiovascular system provides a continuous supply of oxygen.

Cardiac muscle is adapted to be highly resistant to fatigue: it has a large number of mitochondria, enabling continuous aerobic respiration. The heart is so tuned to aerobic metabolism that it is unable to pump sufficiently in ischaemic conditions. (It has no back up system). At basal metabolic rates, about 1% of energy is derived from anaerobic metabolism. This can increase to 10% under moderately hypoxic conditions, but, under more severe hypoxic conditions, not enough energy can be liberated by lactate production to sustain ventricular contractions. Under basal aerobic conditions, 60% of energy comes from fat (free fatty acids and triglycerides), 35% from carbohydrates, and 5% from amino acids. However, these proportions vary widely according to nutritional state. For example, during starvation, lactate can be recycled by the heart

Glycogen is stored in the muscles and liver in sufficient quantities for about two hours of strenuous exercise. This timeframe can be extended by aerobic physical conditioning and high carbohydrate diet. After the glycogen stores are used up, the body obtains its energy from fatty acid metabolism and amino acid protein metabolism. These reactions are not efficient, which consequently causes your strength and endurance to drop drastically (hitting a brick wall or man with the hammer).

SunCoast Seminars EXERCISING AND BUILDING MUSCLES
Muscles change and develop with regular exercise but the effects differ, depending on whether you engage in strength, speed, or endurance training. Strength and burst training causes the muscle fibers to enlarge. Individual muscle fibers increase in diameter as a result of an increase in intracellular protein fibrils. Endurance training causes more blood vessel formation than does speed or strength training, which produces an increased capacity for aerobic metabolism within the muscle cell. This change is seen after a few weeks of training and is maximized in about three months. The aerobic enzymes that metabolize carbohydrates, fats, and proteins, double. It is important to develop your strength and speed systems, but if you want to continue past about two minutes of high intensity workouts, you need to have your aerobic systems developed

SunCoast Seminars Motor Units within a muscle
A motor unit is defined as all of the muscle fibers supplied by a single motoneuron, and therefore, by a single axon and its branches Skeletal muscles are organized into hundreds of motor units, each of which involves a motor neuron, attached by a series of thin finger-like structures called axon terminals. These attach to and control discrete bundles of muscle fibers. A coordinated and fine tuned response to a specific circumstance will involve controlling the precise number of motor units used. While individual muscle units contract as a unit, the entire muscle can contract on a predetermined basis due to the structure of the motor unit. Motor unit coordination, balance, and control frequently come under the direction of the cerebellum of the brain. This allows for complex muscular coordination with little conscious effort, such as when one drives a car without thinking about the process.

SunCoast Seminars Motor Units within a muscle
Muscles responsible for fine coordination have small motor units. Muscles responsible for gross movements have large motor units. The smaller motor units are more excitable than the larger ones, and are stimulated first when a weak signal is sent by the CNS to contract a muscle As the strength of the signal increases, more motor units are excited in addition to larger ones, with the largest motor units having as much as 50 times the contractile strength as the smaller ones As more and larger motor units are activated, the force of muscle contraction becomes progressively stronger. This concept is know as “the size principle”.

SunCoast Seminars Motor Units within a muscle: Conclusion
At low exercise intensities, like walking or slow running, slow twitch fibers are selectively utilized because they have the lowest threshold for recruitment. If suddenly the pace is increased to a sprint, the larger fast units will be recruited. In general, as the intensity of exercise increases in any muscle, the contribution of the fast fibers will increase. For the muscle, intensity translates to force per contraction and contraction frequency/minute. Motor unit recruitment is regulated by required force. In the unfatigued muscle, a sufficient number of motor units will be recruited to supply the desired force (wave contraction).

SunCoast Seminars Motor Units within a muscle: Conclusion
Initially desired force may be accomplished with little or no involvement of fast motor units. However, as slow units become fatigued and fail to produce force, fast units will be recruited as the brain attempts to maintain desired force production by recruiting more motor units. Consequently, the same force production in fatigued muscle will require a greater number of motor units. This additional recruitment brings in fast, fatigable motor units. As a result, fatigue will be accelerated toward the end of long or severe bouts due to the increased lactate produced by the late recruitment of fast units. (Again, the man with the hammer)

SunCoast Seminars Contraction Strength
For skeletal muscles, the force exerted by the muscle is controlled by varying the frequency at which action potentials are sent to muscle fibers. Action potentials do not arrive at muscles synchronously, and during a contraction some fraction of the fibers in the muscle will be firing at any given time. Typically when a human is exerting a muscle as hard as they are consciously able, roughly one-third of the fibers in that muscle will be firing at once, but various physiological and psychological factors (including Golgi tendon organs and Renshaw cells) can affect that. This 'low' level of contraction is a protective mechanism to prevent avulsion of the tendon - the force generated by a 95% contraction of all fibers is sufficient to damage the body.

The repetitive firing of a motor unit creates a train of impulses known as the motor unit action potential train (MUAPT). To sustain muscle contraction, the motor units must be repeatedly activated . As the firing rates of motor units active in a contraction increase, the twitches associated with each firing will eventually fuse to yield large forces The firing rates of earlier recruited motor units are greater than those of later recruited motor units at any given force value The control to the muscle is not designed to generate constant-force contractions.

SunCoast Seminars Maximal Voluntary Contraction (MVC)

So concluding, the strength of a muscular contraction can be influenced 2 factors: By increasing the number and size of contractile units simultaneously, called multiple fiber summation. By increasing the frequency at which action potentials are sent to muscle fibers, called frequency summation.

SunCoast Seminars Types of Muscle Contraction
Concentric muscle contraction Eccentric muscle contraction Isometric muscle contraction Isotonic muscle contraction

SunCoast Seminars Concentric muscle contraction
Muscle contraction in which the muscles shorten while generating force. The insertion and origin of the muscle are moving toward eachother. During a concentric contraction muscle fibers slide across each other pulling the Z-lines together During a concentric contraction, a muscle is stimulated to contract according to the sliding filament mechanism. This occurs throughout the length of the muscle, generating force at the musculo-tendinous junction, causing the muscle to shorten and changing the angle of the joint. In relation to the elbow, a concentric contraction of the biceps would cause the arm to bend at the elbow. A concentric contraction of the triceps would change the angle of the joint in the opposite direction, straightening the arm.

SunCoast Seminars Eccentric Muscle Contraction
During an eccentric contraction, the muscle elongates while under tension. The origin and the insertion of the muscle are moving away from eachother. The muscle acts to decelerate the joint at the end of a movement or otherwise control the repositioning of a load. This can occur involuntarily (when attempting to move a weight too heavy for the muscle to lift) or voluntarily (when the muscle is 'smoothing out' a movement). Over the short-term, strength training involving both eccentric and concentric contractions appear to increase muscular strength more than training with concentric contractions alone. During an eccentric contraction of the biceps muscle, the elbow starts the movement while bent and then straightens as the hand moves away from the shoulder. During an eccentric contraction of the triceps muscle, the elbow starts the movement straight and then bends as the hand moves towards the shoulder.

Muscles are approximately 10% stronger during eccentric contractions than during concentric contractions Eccentric contractions are being researched for their ability to speed rehab of weak or injured tendons. Achilles tendinitis has been shown to benefit from high load eccentric contractions. During virtually any routine movement, eccentric contractions assist in keeping motions smooth. Muscles undergoing heavy eccentric loading suffer greater damage when overloaded (such as during muscle building or strength training exercise) as compared to concentric loading. During an eccentric contraction, the filaments slide past each other the opposite way, though the actual movement of the myosin heads during an eccentric contraction is not known.

Exercise featuring a heavy eccentric load can actually result in greater muscular damage and delayed onset muscle soreness one to two days after training. Exercise that incorporates both eccentric and concentric muscular contractions (i.e. involving a strong contraction and a controlled lowering of the weight) can produce greater gains in strength than concentric contractions alone. While unaccustomed heavy eccentric contractions can easily lead to overtraining, moderate training may confer protection against injury.

SunCoast Seminars Isometric Muscle Contraction.
An isometric contraction of a muscle generates force without changing length. An example can be found in the muscles of the hand and forearm grip an object; the joints of the hand do not move but muscles generate sufficient force to prevent the object from being dropped. Isometrics are done in static positions, rather than being dynamic through a range of motion. The joint and muscle are either worked against an immovable force (overcoming isometric) or are held in a static position while opposed by resistance (yielding isometric).

SunCoast Seminars Isotonic Muscle Concentration
Isotonic contractions occur when tension in the muscle remains constant despite a change in muscle length. This can occur only when a muscle's maximal force of contraction exceeds the total load on the muscle.

SunCoast Seminars A: Concentric/eccentric B: Isometric

SunCoast Seminars Other Types of Muscle Contraction Spasm Hypnic jerk
Dystonia Myoclonus Cramp

SunCoast Seminars Spasm
is a sudden, involuntary contraction of a muscle, a group of muscles usually harmless and ceases after a few minutes In very severe cases, the spasm can induce muscular contractions that are more forceful than the sufferer could generate under normal circumstances. This can lead to torn tendons and ligaments.

SunCoast Seminars Hypnic jerk
A hypnic or hypnagogic jerk is an involuntary muscle twitch (commonly known as a myoclonic twitch) which occurs during the transition into hypnagogia. It is often described as an electric shock or falling sensation, and can cause movement of the body in bed. Hypnic jerks are experienced by most people, especially when exhausted or sleeping uncomfortably Hypnic jerks may be felt once or twice per night This normally happens to subjects who have deprived themselves of sleep for longer than 24 hours, or to those who have recently awakened after insufficient sleep

SunCoast Seminars Dystonia
Dystonia is a neurological movement disorder in which sustained muscle contractions cause twisting and repetitive movements or abnormal postures. The disorder may be inherited or caused by other factors such as birth-related or other physical trauma, infection, poisoning (eg. lead poisoning) or reaction to drugs. Torticollis

SunCoast Seminars Myoclonus
Myoclonus is a brief, involuntary twitching of a muscle or a group of muscles. The myoclonic twitches or jerks are usually caused by sudden muscle contractions; they also can result from brief lapses of contraction. Contractions are called positive myoclonus; relaxations are called negative myoclonus. The most common time for people to encounter them is while falling asleep (hypnic jerk). Myoclonic jerks can also be a sign of a number of neurological disorders. Hiccups are also a kind of myoclonic jerk specifically affecting the diaphragm. Myoclonic jerks may occur alone or in sequence, in a pattern or without pattern. They may occur infrequently or many times each minute. Most often, myoclonus is one of several signs in a wide variety of nervous system disorders such as multiple sclerosis, Parkinson's disease, Alzheimer's disease, and Creutzfeldt-Jakob disease (CJD) and some forms of epilepsy.

SunCoast Seminars Cramp
Cramps are sometimes called Charley horses, are unpleasant, often painful, sensations caused by contraction or over shortening of muscles. Cramps can be caused by cold, overexertion or low calcium level in blood (especially for adolescents where they need calcium for both blood and bone maturing). Illness or poisoning can also cause cramps, particularly in the stomach, which is referred to as colic if it fits particular characteristics

SunCoast Seminars Cramp: Causes. Hyperflexion Inadequate oxygenation
Exposure to large changes in temperature Dehydration Low blood salt Low blood calcium Muscle cramps may also be a symptom/complication of pregnancy, kidney disease, thyroid disease, hypokalemia or hypocalcemia (as conditions), restless legs syndrome, varicose veins[1], and multiple sclerosis.[2]

SunCoast Seminars Electrolyte disturbance may cause cramping and tetany of muscles, particularly hypokalaemia (a low level of potassium) and hypocalcaemia (a low level of calcium). This disturbance arises as the body loses large amounts of interstitial fluid through sweat. This interstitial fluid is composed mostly of water and table salt (NaCl). The loss of osmotically active particles outside muscle cells(NaCl) leads to a disturbance of the osmotic balance and swelling of muscle cells as these contain more osmotically active particles. This causes the calcium pump between the muscle lumen and sarcoplasmic reticulum to short circuit and the calcium ions remain bound to the troponin and the muscle contraction is continued. This may occur when the lactic acid is high in the cells.

SunCoast Seminars Practical Isometric Eccentric Concentric

SunCoast Seminars Muscle Functions
Muscle tissue has four main properties: Excitability or the ability to respond to stimuli Contractibility or the ability to contract Extensibility or the ability of a muscle to be stretched without tearing Elasticity or the ability to return to its normal shape Through contraction, the muscular system performs three important functions: Motion - walking, running etc. Heat production - maintain normal body temperature Maintenance of posture - standing, sitting etc.

SunCoast Seminars Muscle Functions Muscles have two states Relaxed
Contracted.

SunCoast Seminars Motion: Understanding Muscle Levers
There are different types of levers dependent upon the position of fulcrum, effort and resistive force. First Class lever: Muscle force and resistive force is on different sides of the fulcrum e.g. the head resting on the vertebral column. As the head is raised, the facial portion of the skull is the resistance, the fulcrum is between the atlas and occipital bone, and the effort is the contraction of the muscles of the back. Second Class lever: Muscle force and resistive force act on the same side of the fulcrum, with the muscle force acting through the level longer than that through which the resistive force acts - e.g. raising the body up onto the toes. The body is the resistance, the ball of the foot is the fulcrum, and the effort is the contraction of the calf muscle.

SunCoast Seminars Third Class lever:
Muscle force and resistive force act on the same side of the fulcrum, with the muscle force acting through the lever shorter than that through which the resistive force acts - e.g. adduction of the thigh. The weight of the thigh is the resistance, the hip joint is the fulcrum, and the contraction of the adductor muscle is the effort. Most of the limbs of the human body are articulated by third class levers.

SunCoast Seminars Motion: Understanding Muscle levers

SunCoast Seminars Muscle Function: Heat production
Muscle contractions produce heat and as much as 70% of body heat is produced by energy produced in muscle tissue. Blood is an essential element in temperature control during exercise, taking heat from the body core and working muscles and redirecting it to the skin when the body is overheating. When the internal heat of the body reaches too low a level thermo-receptors in the skin relay a message to the hypothalamus in the brain. In response to this signal, the skeletal muscles contract and relax in an involuntary manner (shivering) increasing muscle activity to generate heat. In turn, muscles are also responsive to exterior heat - cold air increases muscle tone, and hot conditions have a relaxing effect on muscles.

SunCoast Seminars Maintenance of posture
As well as enabling movement, muscles also maintain posture and body position. Sensory receptors in the muscles monitor the tension and length of the muscles and provide the nervous system with crucial information about the position of the body parts, therefore enabling posture to be maintained. Muscles are never completely at rest, nor do they actually have to shorten in length when they contract. The tension or tone produced as a result of these contractions between various opposing groups of muscle helps us remain in a static position, even when we are asleep.

Break!

Connective Tissue Connective tissue is a form of fibrous tissue.
It is one of the four types of tissue in traditional classifications (the others being epithelial, muscle and nervous tissue. Understanding the microscopic and macroscopic structure of connective tissue along with the biomechanical characteristics is important as a foundation for every therapist using exercise therapy to improve a patients function.

Knowledge of tissue histology and biomechanics will improve a therapists’ understanding of the influence of implications of trauma, immobilization and remobilization of this tissue. Connective tissue accounts for 16% of a persons bodyweight, and stores 23% of a body’s total water content. Collagen is the main protein of connective tissue, making up about 25% of the total protein content.

Connective tissue proper includes the following five types:
Blood, cartilage and bone are usually considered connective tissue, but, because they differ so substantially from the other tissues in this class, the phrase "connective tissue proper" is commonly used to exclude those three. Connective tissue proper includes the following five types: loose connective (organ walls and it fills space) dense connective (Collagen type I, tendons, liggs) Elastic (can be stretched 1.5 x original length), skin, lungs, arteries, veins etc. Reticular: The fibers form a soft skeleton to support the lymphoid organs (lymph nodes, red bone marrow, and spleen). Adipose

Components of connective structures:
Water Type I collagen fibers Ground substance Elastin fibers Fibroblasts The fibers and ground substance, which exist outside the cells, are collectively called the extra-cellular matrix. Function: Separates and protects cells, bearing weight, tension offering defense.

Defense Connective tissue contains cells and metabolites important in immune function, such as inflammation, and in tissue repair after injury. Nutrition and transport of molecules Blood vessels, which are also considered a connective tissue, transport substances throughout the body. Components in connective tissue regulate movement of nutrients between cells.

In ordinary connective tissue the majority of the cells are fibroblast
In ordinary connective tissue the majority of the cells are fibroblast. These are involved in the production of fibrous elements and the non- fibrous ground substance. They are particularly active during wound repair, migrating along strands of fibrin by amoeboid movements and distributing themselves through the healing area to start repair. Fibroblast activity is influenced by various factors as partial pressure of Oxygen (V.A.C. ), steroid hormone levels and nutrition. Macrophages, mast cells, plasma cells and pigment cells are the other cell types characteristic of connective tissue. Lymphocytes and leukocytes are more variable but may increase considerably in pathological conditions.

Connective tissue forms the following:
base of the skin muscle sheaths nerve sheaths tendons ligaments joint capsules fascia periosteum blood vessel walls

bed and framework of the internal organs
bone adipose tissue cartilage intervertebral discs aponeuroses lens capsules kidney glomeruli granulation tissue

Traditional classification of connective tissue structures:
Loose connective tissue Areolar (space filling) Adipose Reticular Dense Connective tissue Regular Irregular (for support of organs etc.) Elastic Cartilage Hyaline Fibrocartilage Other Bone Blood Lymphatics

Unlike other connective tissues, cartilage does not contain blood vessels.
The chondrocytes are fed by diffusion, helped by the pumping action generated by compression of the articular cartilage or flexion of the elastic cartilage. Thus, compared to other connective tissues, cartilage grows and repairs more slowly. The same is true for the intervertebral disk, which is made out of fibrocartilage)

Except for cartilage, connective tissue is innervated (has a nerve supply).
Vascularity (blood supply) in tendons and ligaments is sparse, whereas cartilage is avascular (has no blood supply). FIBERS Collagen Elastic Reticular fibers

Fiber types Collagenous fibers: Collagen is the main protein of connective tissue making up about 25% to 35% of the whole-body protein content. Tough bundles of collagen called collagen fibers are a major component of the extracellular matrix that supports most tissues and gives cells structure from the outside, but collagen is also found inside certain cells. Collagen has great tensile strength, and is the main component of fascia, cartilage, ligaments, tendons, bone and skin. Along with soft keratin, it is responsible for skin strength and elasticity, and its degradation leads to wrinkles that accompany aging. It strengthens blood vessels and plays a role in tissue development.

Degradation of collagen?

Elastic fibers: Elastic fibers (or yellow fibers) are bundles of proteins (elastin) found in extracellular matrix of connective tissue and produced by fibrobasts and smooth muscle cells in arteries. These fibers can stretch up to 1.5 times their length, and snap back to their original length when relaxed (if not stretched past their physiological length)..

Reticular fibers: Reticular fibers or reticulin is a histological term used to describe a type of fiber in connective tissue composed of type III collagen. Reticular fibers crosslink to form a fine meshwork (reticulum). This network acts as a supporting mesh in soft tissues such as liver, bone marrow, and the tissues and organs of the lymphatic system.

Collagen Fibers, types:
Collagen One - skin, tendon, vascular, ligamenture, organs, meniscus, annulus, bone (main component of bone) Great circulation with great tensile strength Collagen Two - cartilage (main component of cartilage), nucleus pulposus. Poor Circulation, compression tension strength Collagen Three - reticulate (main component of reticular fibers), skin, blood vessels, granulation tissue, commonly found alongside type I. Collagen Four - forms bases of cell basement membrane

Characteristics of collagen based structures
Tensile strength Extensibility Type I - found principally in structures exposed to tension Mostly found in skin, tendon, ligament, capsule, annulus, muscle, menisci and bone Type II - found principally in structures exposed to pressure Mostly found in nucleus pulposus and articular cartilage

Bone Components: minerals, water, type I collagen, proteoglycans Mineral gives the bone its hardness and ability to withstand compression loads. Tolerance of tensile loads is due to both mineral and matrix components combined. Determinants of the mechanical properties of bone: Size and density of bone Mechanical properties of the bone substance Geometrical characteristics of the bone specimen Loading mode applied (compression, tension, etc) Rate of loading Frequency of loading

Cortical bone: Very high ultimate strength in compression and tension High stiffness Compression strength 15000PSI Tension strength 12000PSI Shear strength 4000PSI Stiffness and ultimate load increase with increasing speed of loading

Trabecular bone Moderate to low ultimate strength Moderate to low stiffness Strength – lower than for cortical bone, but depends on porosity Stiffness and ultimate load increase with increasing speed of loading

Cortical bone (a.k.a. compact bone) 5-30% porous
External shell of all bones, also forms diaphysis (shaft of the bone). Lamellar build up. Trabecular bone 30-90% porous. Also named cancellous or spongy bone. Fills the ends of long bones and is inside of flat and irregular bones (e.g. vertebrae). Bone is 65% mineral, 30% collagen, 5% proteoglycan by dry weight. Fresh bone is 25% water by weight

SunCoast Seminars Shoulder Arthritis

SunCoast Seminars Non WB. Guess which site…

Tendons, ligaments and joint capsules
The density and regularity of these structures are determined by the strength required and the uniformity of direction of loads they are exposed to. Components: water, type I collagen, ground substance, elastin fibers, fibroblasts Dense regular: tendons, ligaments Dense irregular: capsule, fascia Determinants of the mechanical properties of these types of connective tissue:

Tendons, ligaments and joint capsules
Size and density of the structures Properties of the collagen and elastic fibers contained in the structure Proportion of collagen and elastic fibers in the structure Orientation of fibers in the tissue Genetics

Dense regular connective tissue Dense irregular connective tissue r

Mechanical properties of tendons, ligaments and joint capsules
Tensile strength up to PSI Fail at strains as low as 9% with structures with little or no elastic fiber content (extremity tendons), and at strains of up to 70% for structures with a high elastic fiber content (ligamentum flavum) Ultimate load increase with increasing speed of loading, stiffness does not increase

Clinical notes Aging affects connective tissues in that there is a general loss of collagen. They do however acquire an increased number of cross links with age, resulting in greater tensile strength. During pregnancy the hormone relaxin is released during the last trimester causing a general loss of stiffness and strength in connective tissue. NSAID’s can cause increased tensile strength in connective tissues (increase of collagen content and proportion of non-soluble collagen).

Clinical notes Connective tissue structures are subject to fatigue type failures from exposure to loads that are too large, too numerous or too frequent (overuse or repetitive strain injuries)

Cartilage: Components of cartilage structure: (in descending order of relative amounts) Water Type II collagen (mostly in ligaments and tendons) = compressive cartilage Type I collagen ( mostly in fibro cartilage) Elastin (mostly in elastic cartilage) Proteoglycans

Micro structure of cartilage~ see next slide for seeweed comparison with aging.

Articular cartilage is 60-87% water, 10-30% type II collagen, and 3-10% proteoglycans by weight.
About 30% of the water is bound within the matrix with the remainder being in cells or free to move in the interstices. Proteoglycans compression results in release of synovial fluid, decreased compression leads to absorption of synovium (sponge effect) Synovial fluid: lubrication of joints, adhesion of joint surfaces (glass plates) and nutrition for cartilage (which is aneural, avascular and alymphatic) Talk about cavitation

Sensory receptors Type: location: Fired by: Type I postural capsule oscillations Type II dynamic capsule oscillations Type III inhibitive capsule/ stretch or sustained ligament pressure Type IV nociceptive most tissues injury and inflammation

Type 1 receptors (Merkel’s disk receptors):
Sensory Receptors Type 1 receptors (Merkel’s disk receptors): Present in the superficial layers of the fibrous joint capsule. They respond to stretch and pressure within the capsule (inhibitive) and are slow-adapting receptors with a low threshold. They signal joint position and movement.

Type 2 receptors: (Ruffini endings)
Present in the deep layers of the fibrous capsule. They respond to rapid movement, pressure change and vibration but adapt quickly. They have a low threshold and are inactive when the joint is at rest.

Sensory Receptors Type 3 receptors are present in ligaments. (Pacini) These receptors inform the central nervous system of ligamentous tension, so preventing excessive stresses. The threshold is high and they adapt slowly. They are not active in rest.

Sensory Receptors Type 4 : Free unencapsulated terminals, also called nocisensors These sensors ramify within the fibrous capsule, adjacent fatpads and around bloodvessels. They are thought to signal excessive joint movements and also to signal pain; they have a high threshold and are slow-adapting. The synovial membrane is relatively sensitive to pain due to the absence of these nerve endings.

All these receptors influence muscle tone via the spinal reflex arcs which are formed by the same nerves that supply the muscles acting on the joint. Parts of the joint capsule supplied by a given nerve correspond with the antagonist muscles. Tension given on this part of the capsule produces reflex contraction of these muscles and prevents overstretching of the capsule.

In consequence, all receptors have an important function in stabilizing and protecting the joint.
After rupture of joint capsule and ligament, perception is considerably disturbed due to disruption of afferent information. For example a sprained ankle shows loss of control off locomotion. Even months after repair of ligamentous and capsular tissues has taken place, perception might still be distorted. Increased likelihood to re-injury in the acute healing phase.

Neural Arch supplying agonist and antagonist

Toe region Elastic region Elastic limit Plastic region (talk about biological memory following manipulation) Maximum stress Necking Failure point If you stretch in the elastic only, you won’t achieve anything. In fact, studies suggest that this actually may shorten the muscle

Effects of immobilization on connective tissue
Before we discuss theses effects, let’s discuss the three stages of tissue healing Inflammation Cell proliferation Remodeling

Effects of immobilization on connective tissue Inflammation
During the initial inflammatory stage, which lasts 3-5days, prostaglandins initiate multiple tasks: stimulate the immune system build up platelets around the lesion attract white blood cells that protect against infection clean up the damaged tissue. Specialized cells called fibroblasts produce disorganized fibrous (scar) tissue.

Stages of inflammation
Mechanical trauma to soft connective tissue leads to a generalized inflammatory reaction. This reaction has several mostly functional effects that prompt the subject to restrict activities while it initiates the reparative process (e.g. pain) Stages of inflammation Vasoconstriction stage of the arterioles. This decreases the blood flow to reduce bleeding. followed by vasodilatation and increased capillary permeability. This phase usually starts within 5 – 10 min and may last up to 1 – 3 days. Function of pain with definition(an unpleasant awareness of a noxious stimulus or bodily harm) or (“an unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms of such damage“ IASP)

Stages of inflammation (Continued)
Exudation stage: Starts within a few hours. Physical signs: local warmth, swelling and pain. During this phase plasma, cells and protein flow into the damaged area. This dilutes potential noxious substances and products of cell destruction. . The cellular part of the exudate consist of multiple cells influencing phagocytosis. Another important product of plasma is fibrinogen which forms extensive networks for the fibroblast which migrates along strands of fibrin by amoebic movements and distribute themselves through the healing area. In the presence of an inflammatory reaction there is a significant stimulus for abnormal production of non neoplastic fibrous tissue which can interfere with granulation and repair.

Granulation phase (within 48 hours to 6 weeks) vascular infiltration and fibroblast proliferation. Fibroblast and capillaries grow along the fibrin network. This usually starts within 48 hours and by day 5 after the injury the amount of collagen formed is significant and it increases for up to 6 weeks. Normally the initial arrangement of these fibers is disorganized. Capillaries at the edge of the injured tissue infiltrate via forming arches capable of maintaining circulation. This ensures supply of oxygen and nutrition into a relatively anoxic region and at the same time enables removal of metabolic waste products. These regenerating capillaries are still very fragile and therefore stay within the support of the newly synthesized collagen.

Repair (begins at the end of the third week and may continue for 1 to 3 years) At the end of the third week maturation begin. From this time vascularization decreases and many of the new vessels atrophy and disappear as the bloodsupply becomes appropriately adjusted to the needs of the tissue. Also the amount form and strength of scar collagen tissue changes. Tension by gentle movements in functional directions reorients the collagen and breaks weak, unnecessary intermolecular cross links that may have formed.

Mechanical stress thus has its greatest influence on the remodeling process at this time. Non- functional collagen is while this is taking place removed by phagocytosis. Tensile strength in the functional directions slowly increases due to the continuing process of crosslinking and the formation of bundles oriented with their longitudinal axis in the direction of the greatest stress. Remodeling may be due to Turn over of collagen Fiber linkage Increased intermolecular bondage.

Self perpetuating inflammation.
The reaction of tissues to harmful stimuli frequently is an excessive prolongation of the normal response. Excessive edema formation, muscle spasms and other defense mechanisms can, when not managed appropriately may lead to chronic disability by impeding movement that is crucial in the early stages of the lesion. Cyriax described the chronic inflammation of soft tissues as a self perpetuating inflammation.

Such may be a result from a trauma though can continue long after the cause had ceased.
This is particularly prone to happening after minor injury to a tendon or a ligament. Cyriax describes the cause as lack of movement during the period of tissue repair causing adhesive scar formation. He suggests local steroid infiltration to interrupt the inflammatory process. An even better result may be reached by deep transverse friction massages to get rid of the chaotically formed scar tissue eventually followed by manipulation.

The Cell proliferation phase.
During the second phase, the cell proliferation phase, which lasts 4-6 weeks, cells proliferate to replace the damaged cells and scar tissue becomes organized. Physical activity eliminates unnecessary scar tissue that has inadvertently adhered to neighboring tissue(!!)

The Remodeling Phase. During the remodeling stage, lasting about six months or more, the repaired tissue remodels itself. Interestingly forensic anthropologists and archeologists observe changes in bone structure, for example, to determine the types of work a person performed based on the fact that remodeling is an automatic process accompanying use. During the third stage of healing this process can restore damaged tissue so it is stronger than it was before the injury. If remodeling doesn’t occur, it leads to weakened tissue prone to reinjury.

So keeping these characteristics in mind, consider the following:
Injuries are an opportunity to become stronger. When the three stages proceed normally, tissue becomes stronger and less prone to injury. This principle is used by performance athletes. Likewise, pain is rare if the damage heals quickly and thoroughly, without abnormal adhesions.

The effect of immobilization has been well documented and studied:
Loss of GAG (Glycosaminoglycans) in connective tissues. Increase in crosslink formation in connective tissues. Poor orientation of newly deposited collagen fibers. Fatty fibrous infiltration of edematous areas. Pannus formation inside of joints. Ulcerated cartilage found in immobilized non traumatic dog knees after 6 weeks of immobilization via casting and exostosis with deep ulceration after 8 weeks. General atrophy of all tissue types.

Effects of immobilization
A study by Noyes et al. (1974) using the ACL in monkeys, that did not have a trauma or surgery, showed that after 8 weeks of immobilization using a lower limb cast, there was significant loss of ligament tensile strength which took 9 months to recover from. The predominant mode of failure in these experiments was ligament failure as opposed to avulsion fracture failure. Another important study is that of Amiel et al from 1985 done on rabbits. This showed a decrease in collagen mass of a the MCL of a rabbit by 30% and sign. decrease in tensile strength. Tipton et al. reported similar findings in decreased number and size of collagen bundles when examining ACL’s in dogs through a light microscope.

Gerber et al published a study in Sweiz Z Sportmed. in 1980, that claims they found 20% loss of maximum muscle-strength after 2 weeks of immobilization in a plaster cast. They also found slow muscle fibers more susceptible to immobilization atrophy and felt this was due to their greater dependence on oxidative metabolism.

Erickson et al described findings of laxity, destruction of ligament insertion sites and failure at a lower load after 3 months of immobilization, in Medicine science and Sports in 1976. Appell described significant disturbances in neuromuscular coordination of muscle groups after immobilization in Sports Med. in 1990.

Benefits of Flexibility and Range of motion.
A decrease in musculoskeletal flexibility has been associated with both the aethiology as well as the consequences of musculoskeletal injuries (Nicholas 1970, Glick 1980). Furthermore it has been documented that flexibility training, effectively increases range of motion in human subjects ( de Vries1962, Henrickson et al 1984) However it is crucial that health professionals prior to prescribing flexibility training evaluate a subject and keep in mind the established guidelines for flexibility of joints and muscles ( Janda 1983, Kendall & Mc Greary 1983).

Benefits of Flexibility and Range of motion.
When range of motion testing reveals values that exceed the normal flexibility training might be considered contra- indicated. Instead stability-training, posture training and strengthening should be considered.

Effects of mobilization on tissue healing and repair.
With this basic biological knowledge there is now rationale for the use of early controlled mobilization of patients with ligament trauma. The use of a limited motion cast with adjustable double-action hinge for the knee joint is now accepted in clinical practice and enhances more rapid repair and remodeling as well as preserving quadriceps strength and bulk. Now patients are usually mobilized early in a limited motion cast for a minimum of 3 weeks with range of motion from 20-60degrees.

Analysis of transverse session cuts through the ACL’s of the exercised rats showed a 29% increase in fibrils with a significant increase in fibril diameter. In the exercised PCL the amount of collagen found per microgram of DNA was almost double that of the control group, suggesting that the PCL was more loaded with this exercise regimen than the ACL. Similar structural observations have been made for collagen fibers of exercised mice flexor tendons (Michna 1984) Amiel et al (1987) have shown that maximal collagen deposition and turn over occurs during the first 3-6 weeks post injury in the rabbit.

Frank et al (1991) have further shown that collagen remodeling of the repairing rabbit MCL appears to be encouraged by early immobilization but after 3 weeks of collagen alignment and remodeling appears to be favored by mobilization.

The benefits of early mobilization in most of the soft tissue lesions already was advocated by Hippocrates more than 2400 years ago. He described the increase in circulation, aiding nutrition and eliminating cartilage damage. Numerous studies since have found significantly improvement in strength of ligaments, tendons and capsule with exercise training.

Oakes did a study in 1988 where 5 rats were placed on a progressive 4 week exercise program of alternate days of swimming and treadmill running. At the conclusion the rats were running min on a 10% incline and on alternate days swimming for 60 min with 3% body weight attached to their tails. Five caged rats of similar age and bodyweight were controls.

Definitions: Flexibility: The range of motion that is available in a joint or group of joints that is influenced by muscles, tendons and bones ( Anderson & Burke 1991) Flexibility has also been described as the degree to which muscle length permits movement over that which it has an influence (Toppenburg and Bullock 1986) Flexibility in the musculotendinous unit is directly related to tension in that musculotendinous unit. There are two components to tension. An active component which lies in the reflex activity of the muscle a passive component which lies in the viscous and elastic properties of the connective tissue.

Benefits of flexibility training
Decreased risk for injury: Musculotendinous units that posses greater flexibility are less likely to be overstretched. Flexible joints can withstand greater amount of stress before injury occurs. Decreased muscle soreness: Stretching has been advocated as a method to decrease muscle soreness. Improved athletic performance: It has been suggested ( Broms 1984) that reduced ROM can reduce workefficiency. Musculotendinous unit flexibility is needed to move a limb through its ROM.

Also stretching will reduce stiffness and enhance “rebound performance”. Mechanical work is absorbed by the series elastic component of the musculotendinous unit during eccentric contraction and is stored as potential energy. This energy is then available for use during the subsequent concentric contraction.( Bosco & Komi 1979)

Muscle relaxation (De Vries 1962) Avoidance of skeletal dysfunction, which was defined by Mc Kenzie as the syndrome that is the result of prolonged incorrect biomechanical usage of the joints. Prevention of scar tissue formation in the musculotendinous units shortened position (Reilly 1992) Prevention of imbalance at the joints, which is the result of one muculotendinous unit at a joint being either significantly weaker or significantly less flexible than the other musculotendinous units at that joint (Kendall and Mc Greary).

Flexibility training is essential to restore loss of range of motion in soft tissue following injury or surgery. There are multiple factors responsible for loss of ROM in soft tissue following injury or surgery: Increased fibrosis in the scar. Scarformation is normally self-limiting though is frequently excessive in wounds. Woundcontraction, inward movement of woundedges by myofibroblast as part of the repair process. Immobilization or prolonged usage in limited ROM.

Benefits of flexibility training (continued)
Nerve root tension Decreased tissue temperature Increased age Obesity

If not adequately managed this could lead to contractures, pain, dysfunction and even disability.
Loss of ROM is one of the main reasons for failed orthopedic surgeries including Total Knee Arthroplasties, Rotator Cuff repairs and even post arthroscopic shoulder decompression and athroscopic menisectomies and frequently can simply be prevented by adequate Rehabilitation. It is also the number one reason for frustration by orthopedic surgeons upon follow up visits and loss of referrals.

Physiology of stretching:
Stretching implies that a force applied to the tissue elongates the tissue. Elongation is being accomplished by a combination of neural effects and plastic/ elastic effects of the tissue. A force that is applied to a tissue and held will decrease activity of the stretch reflex , with decrease in neural excitability. The non contractile element within the musculotendinous unit, fascial sheats, connective tissue, is mainly responsible for the plastic elongation of the unit..

Methods of stretching PNF:
a) Contract-relax; a therapist stretches a muscle to the point where a limitation in ROM is felt. The therapist holds the muscle in this or a sub maximum position and lets the patient actively contract against the resistance of the therapist. The muscle is then relaxed and moved passively to the new lengthened position. The rationale behind this is that increased stress through contraction of the musculotendinous unit will result in autogenic inhibition in the musculotendinous unit. The Golgi Tendon Organ activity will decrease tension and cause relaxation by resetting the musculotendinous unit length.

Methods of stretching PNF:
b)Contract-relax agonist- contract; with this form of stretching the muscle is stretched as with the contract-relax. However in addition to this the therapist facilitates contraction of the antagonist, to obtain reciprocal inhibition of the unit being stretched.

Ballistic stretching:
During Ballistic stretching the limb is moved to the end of its ROM where the stretch sensation is felt, either by the clinician or the subjects themselves. Once this stretched position is achieved, repetitive bouncing or jerking movements are added. Use of ballistic stretching appears to increase risk of injury due to sudden increases in musculotendinous unit ROM. It’s effectivity in research has also been questioned by Voss 1985, Matthews 1993, who felt that lengthening of the musculotendinous unit can not be achieved without relaxation of the stretch reflex.

Static stretching: The most common method of stretching that is used by athletes, coaches and therapist is the static stretch. Static stretching is characterized by the limb being moved slowly and gently to the end of its available ROM, in order to obtain a stretch sensation in the tissues.

To ensure optimal effectiveness of flexibility training it is essential that the stretches are being executed in a proper position, with the right amount of force and that the subject warms up before stretching. A study by Gerson from 1955 showed significantly greater increase in ROM of the m. triceps surea after static stretching when continuous ultrasound application for 7 min was added.

Williford et al studied the effect of active warm up prior to stretching.In this study the flexibility of the shoulder hamstrings trunk and ankles were measured. The subjects were divided into 2 groups. Group 1 performed a stretch that was held for 30 sec. followed by another stretch of 30 sec. The second group was instructed to jog lightly but progressively for 5min. and than perform the same stretching routine. Results indicated that the stretching only group gained 11% in ROM. The group that did a warm up prior to stretching however gained 25%.

Voss researched the effect of position on the efficacy of stretch procedures. He felt that increased ROM in a musculoskeletal unit cannot be achieved when the unit is contracting. In this study normal subjects underwent 3 types of stretching procedures to the Hamstrings.1. Standing and stretching 2.standing but stretching a non weight-bearing hamstring muscle 3.lying supine and stretching a non weight bearing hamstring muscle. The ROM was measured after 3 repetitions of 30 sec. hold. The standing and weight bearing group gained 4deg. the standing and NWB group gained 5 deg. The group that stretched in supine gained an avg. of 10 deg.

Conclusion and practical guidelines:
Injury or surgery can result in decreased joint ROM / flexibility, mainly due to fibrosis and wound contraction. Flexibility training is an important component of rehabilitation in order to minimize the loss of ROM. Flexibility training should begin in the first week following injury or surgery to prevent decrease in ROM. Static stretching is the most commonly used form of stretching. It is Safe and effective. PNF is more effective than static stretching but it requires some training to master the technique and in some instances an assistant.

Conclusion and practical guidelines:
Ballistic stretching may be effective but it has been postulated to increase the risk of injury Two to three static stretch sessions should be performed per day for maximum benefit. An optimum static stretch session should consist of 3 stretches lasting 30 sec each. A warm-up has additive effect if it precedes a static stretch session. A static stretch should be performed in a NWB position with the muscle relaxed for max. gain in ROM.

SunCoast Seminars Common Medications and their effect on Exercise
Aspirin: Watch the side effects. Do not take with NSAID’s (will negate the blood thinning effect) Muscle relaxors Flexeril: Look at half life Skelaxin Sinemet/dopamine (increases heart function with low BP) Stimulates beta 1 receptors in heart, causing more complete and forceful contractions Cardiac function controlling medication BP controlling medication HR controlling medication Kidney function controlling medication Pulmonary function controlling medication

SunCoast Seminars The importance of a thorough evaluation
The concept is very simple here; without a complete and detailed evaluation, you cannot develop an appropriate exercise program. This evaluation is ongoing and does not stop after the “ initial evaluation” (there is a reason for that name…) Understanding the true dysfunction and understanding why that dysfunction exists will put the clinician in the position to address the dysfunction effectively and permanently.

SunCoast Seminars Different types of exercises with different objectives Objectives/Goals of exercise: Strength Muscular Atrophy Coordination Firing Patterns Endurance ROM PROM vs. AROM Endfeel? PROM of the Joint Muscle length (Muscle energy) Muscle tone Decrease of muscle tone Increase of muscle tone Pain control

SunCoast Seminars Components of an effective Exercise Program:
Starts with a thorough and complete evaluation (evaluate the complete chain. Have clear outcome objectives. What are you looking to exercise Why are you exercising that What outcome do you expect Depends on patient/age/function/other intrinsic and extrinsic factors Measure and document these objectives ongoing Don’t over exercise. Exercise to improve function not too complete a number of reps. When you feel or see the correct movement, continue to the next level.

SunCoast Seminars Components of an effective Exercise program:
Get the buy-in from the patient Detailed documentation Quality of the movement Speed Cues given/needed Strength Shaky/Tremorous Coordination Sensation Intensity Activity it is related to improve

SunCoast Seminars Progression/Regression of exercise
Establish base point or midline Method of observation Points of contact: Progress from larger base of support to smaller base of support Open chain vs. Closed chain # of repetitions or sets Speed of the reps Alignment/change angles Cues: tactile& Verbal Level of resistance Point of reference eccentric Isometric  concentric Stabilize vs. destabilize Weightshifting/weightbearing Sequence: Instruct correct movementrepeatchallenge add complexityput into a functional activity

SunCoast Seminars Exercise Therapy
We will now discuss and practice several patient scenarios. We’ll present several patients with different conditions and develop an appropriate and effective exercise strategy for them. These patients will fall into the following categories: Neurological conditions Orthopedic conditions Surgical Non-surgical Geriatrics Sports injuries Spine conditions

SunCoast Seminars Neurological conditions Includes conditions such as
CVA ALS MS Parkinson’s Muscular Dystrophy

SunCoast Seminars CVA Inhibition
Assess movements occurring and compare it to normal. Then only allow for normal movements to occur Facilitation Facilitate normal movement and keep a close eye on the result of your facilitation Three focus areas: Postural control Transitional movement Function in Postures

SunCoast Seminars CVA Framework for normal movement:
Trunk mobility and control Midline orientation Movement of the base of support (weight shift) Head control Limb function Treatment sequence: Ask for the movement Facilitate the movement where needed Take the patient through the movement Stretch/mobilize/increase ROM Repeat/challenge/add complexity/put into function

SunCoast Seminars CVA Guidelines for facilitation utilizing physical cues Know the movement Determine your points of contact Determine the direction of your pressure Determine how much pressure: Initial contact/additional pressure Facilitate in functional activities/provide a purpose where appropriate

SunCoast Seminars CVA Activity training
Activities selected are preferable related to the environment the patient is currently living in or returning to. Pt’s interest. What does the patient want to work on? Activities selected must provide the opportunity to demonstrate the component being tested. Pt’s level of function to the activity. Find the right activity (it needs to be a bit of a challenge but you do not want to discourage the patient. Also try higher level activity to help improve lower level activity) When assessing the performance, break down the activity observed into movements etc. that can then be separately addressed or that can be addressed more successfully in a different activity,

SunCoast Seminars CVA PRACTICAL
Find the impairment limiting the activity Write a comprehensive management plan/treatment plan that addresses both the impairments and the activities that are restricted or limited. PRACTICAL Midline training in sitting Sit to stand to chair (and chair to chair) Stepping forward from standing Arm function in sitting (with hand and with use of walker) going into standing Midline in standing using corner principle (also for amputees)

SunCoast Seminars CVA: Do’s and don’ts when working on the flaccid arm. Do’s Get the attention of the patient Wear a face that tells the patient he/she can do it Scapula/humerus have to move in all directions Align before you move Ask the patient to push straight down Only use this to initiate movement, don’t repeat this if the patient is doing it incorrectly Pay attention to the slightest movement, focus on this! You're programming the brain! When you feel the correct movement, continue with the correct sequence, go to the next level. If you see no movement, alternate this with the stool/walker exercise.

SunCoast Seminars CVA: Do’s and don’ts when working on the flaccid arm. Don’ts Ignore normal alignment Provide too much resistance Let go too suddenly Wait too long Move fast Let them push forward Let the weight go over the fingers Flex the wrist Let elbow pop out (rotation of the shoulder) Repeat for no reason if the patient is doing it, move to the next level

SunCoast Seminars ALS A-myo-trophic means “No muscle nourishment." When a muscle has no nourishment, it "atrophies" or wastes away. "Lateral" identifies the areas in a person's spinal cord where portions of the nerve cells that signal and control the muscles are located. As motor neurons degenerate, they can no longer send impulses to the muscle fibers that normally result in muscle movement.

SunCoast Seminars ALS In short, the supply of motor neurons that control a particular muscle has degenerated, and these cannot be regenerated by exercise or anything else In the early stages of ALS exercise may be helpful in reducing stress and preventing muscle atrophy. In the later stages exercise may help to avoid some of the discomfort that accompanies muscle weakness and tightness. Keep in mind that exercise should never create discomfort. Particularly in the earlier stages of ALS, many people have found both physiological and psychological boosts from various types of exercise. Along with helping to combat stress, providing a brief escape and being a welcome way to relax, proper exercise is important for preventing atrophy of muscles from disuse — a key to remaining mobile for as long as possible — and, as long as the pt is able to exercise comfortably, for keeping their cardiovascular system strong.

SunCoast Seminars ALS The key to gaining these benefits is finding the most appropriate exercise for your patient. While the medical literature has firmly established the importance of exercise for people without serious medical conditions, very little research has been done on the subject of exercise and its role in ALS. In fact, it isn’t known whether exercises are beneficial for increasing muscle strength for people with ALS. As the disease advances, the patient will continue to benefit from doing range-of-motion and stretching exercises. It is important to realize that exercise will not strengthen muscles that have been weakened by ALS

SunCoast Seminars ALS So, in review the purpose of exercise for people with ALS include: to maintain or improve the flexibility of muscles not affected by ALS; to maintain the flexibility of muscles that have been affected; to maintain the flexibility of joints in the neck, trunk and limbs. Please keep in mind: It is important that all exercise be performed in moderation. Fatigue will only increase your patient’s weakness and rob them of energy that they need for theirr daily routines and activities.

SunCoast Seminars Multiple Sclerosis
Multiple sclerosis is an autoimmune condition in which the immune system attacks the central nervous system (CNS), leading to demyelination. Disease onset usually occurs in young adults, is more common in women, and has a prevalence that ranges between 2 and 150 per 100,000 depending on the country or specific population

MS affects the areas of the brain and spinal cord known as the white matter. Different types with different progressions White matter cells carry signals between the grey matter areas, where the processing is done, and the rest of the body When the myelin is lost, the neurons can no longer effectively conduct their electrical signals. The name multiple sclerosis refers to the scars (scleroses - better known as plaques or lesions) in the white matter Although much is known about the mechanisms involved in the disease process, the cause remains elusive: the most widely-held theory being that the condition results from attacks to the nervous system by the body's own immune system.

This disease does not have a cure, but several therapies have proven helpful Treatments attempt to return function after an attack, prevent new attacks, and prevent disability and also reduce the inflammatory damage effects of active leasions. The prognosis, or expected course of the disease, depends on the subtype of the disease, the individual patient's disease characteristics, the initial symptoms, and the degree of disability the person experiences as time advances. Life expectancy of patients, however, is nearly the same as that of the unaffected population, and in some cases a near-normal life is possible.

SunCoast Seminars Multiple Scleroris
T1-weighted MRI scans (post-contrast) of same brain slice at monthly intervals. Bright spots indicate active lesions.

SunCoast Seminars Multiple Sclerosis: Relapses
Multiple sclerosis relapses are often unpredictable and can occur without warning with no obvious inciting factors. Some attacks, however, are preceded by common triggers. In general, relapses occur more frequently during spring and summer than during autumn and winter. Infections, such as the common cold, influenza, and gastroenteritis, increase the risk for a relapse. Emotional and physical stress may also trigger an attack, as can severe illness of any kind

SunCoast Seminars Multiple Sclerosis: Treatment
During symptomatic attacks administration of high doses of intravenous corticosteroids has become a routine treatment routine. Stops the attack and limits the damage Does not affect the long term prognosis May cause osteoporosis Effect is typically short term When the initial disease course is the relapsing-remitting subtype, the average time until such equipment is needed is twenty years

SunCoast Seminars MS

SunCoast Seminars MS Recent research suggests that multiple sclerosis is triggered when the immune system goes awry and attacks the protein sheath of nerve cells. This led scientists to test beta interferon, a substance which inhibits certain white blood cells, to treat the disease. Studies showed beta interferon can reduce the number and severity of multiple sclerosis attacks and brain abnormalities in patients. It was recently approved for widespread use by patients with one form of MS

SunCoast Seminars MS

SunCoast Seminars MS Most studies have shown that persons with MS will not respond to an acute bout of exercise, as would the average, age- and gender-matched, non-disabled, adult without MS. Furthermore, variability in the type and magnitude of symptoms seen with this disease often results in a wide range of responses to acute exercise. In spite of the variability, one common effect of acute exercise in individuals with MS is an overwhelming sense of fatigue during the recovery period following exercise. Some research has shown that in the presence of an upper motor neuron lesion, antagonist muscles are also activated during concentric contraction of an agonist. Maximal muscle force during sustained dynamic exercise has also been shown consistently lower for persons with MS

SunCoast Seminars MS A supervised program of aerobic exercise for as little as 15 weeks can improve aerobic fitness level (i.e., VO2max) in some persons with MS. Improvement in aerobic fitness has been reported as to be as little as 22% and as great as 48% . Less dramatic changes are often seen in more severely impaired persons (+7%). This raises an important issue regarding the development of realistic expectations based upon the baseline impairment level of the individual.

SunCoast Seminars MS When evaluating fitness in the person with MS, it is important to consider special needs related to the specific symptoms experienced by the client: Flexibility: Because many MS patients experience lower extremity spasticity, flexibility may be restricted in the hip, knee and ankle joints. Hip flexor, hamstring, and gastroc-soleus tightness is particularly problematic and should be evaluated in the sitting position (e.g., Sit-and-Reach Test). Use of this test will serve to eliminate any problem with balance during testing. Lateral trunk flexibility should also be evaluated from a sitting position or, if standing, the clinician may place his/her hands on the client's waist to prevent loss of balance.

SunCoast Seminars MS Balance:
To truly appreciate how balance deficits might affect the MS patient's ability to perform exercise safely, balance should be evaluated under both static and dynamic conditions. A fairly short and easy battery of tests can be found using the Berg Balance Scale. This test is valid for neurological conditions such as MS and takes approximately 15 minutes to administer. The results of this test will provide a better understanding of the client's ability to exercise safely using standard equipment.

SunCoast Seminars MS Aerobic Fitness:
As previously noted, many persons with MS experience problems with balance. In addition, foot drop associated with dorsiflexor weakness can be present prior to exercise or it may be easily initiated shortly after the onset of weight bearing exercise. Therefore, for safety purposes, aerobic fitness is best evaluated using a bicycle ergometer. Even so, this mode of exercise testing can also present challenges. Ankle clonus (i.e., spasmodic alternation of contraction and relaxation of muscles), and sensory abnormalities (e.g., numbness, tingling, and deficits in joint proprioception) can make it difficult for the client to keep their feet on the pedals. The use of standard toe clips and Velcro-secured heel straps can reduce or eliminate this problem.

SunCoast Seminars Parkinson’s
Parkinson's disease is a degenerative disorder of the central nervous system that often impairs the sufferer's motor skills and speech, as well as other functions It is characterized by muscle rigidity, tremor, a slowing of physical movement (bradykinesia) and, in extreme cases, a loss of physical movement (akinesia). The primary symptoms are the results of decreased stimulation of the motor cortex by the basal ganglia, normally caused by the insufficient formation and action of dopamine, which is produced in the dopaminergic neurons of the brain. Secondary symptoms may include high level cognitive dysfunction and subtle language problems. PD is both chronic and progressive

SunCoast Seminars Parkinson’s Pathology
Dopaminergic pathways of the human brain in normal condition (left) and Parkinson's disease (right). Red Arrows indicate suppression of the target, blue arrows indicate stimulation of target structure

The direct pathway facilitates movement and the indirect pathway inhibits movement, thus the loss of these cells leads to a hypokinetic movement disorder. The lack of dopamine results in increased inhibition of the ventral anterior nucleus of the thalamus, which sends excitatory projections to the motor cortex, thus leading to hypokinesia. Latest research on pathogenesis of disease has shown that the death of dopaminergic neurons by alpha-synuclein is due to a defect in the machinery that transports proteins between two major cellular organelles — the endoplasmic reticulum (ER) and the Golgi apparatus.

The symptoms of Parkinson's disease result from the loss of pigmented dopamine-secreting (dopaminergic) cells in the pars compacta region of the substantia nigra (literally "black substance"). These neurons project to the striatum and their loss leads to alterations in the activity of the neural circuits within the basal ganglia that regulate movement, in essence an inhibition of the direct pathway and excitation of the indirect pathway. Most people with Parkinson's disease are described as having idiopathic Parkinson's Someone who has Parkinson's disease is more likely to have relatives that also have Parkinson's disease. However, this does not mean that the disorder has been passed on genetically

SunCoast Seminars Parkinson’s Treatment
Parkinson's disease is a chronic disorder that requires broad-based management including patient and family education, support group services, general wellness maintenance, physical therapy, exercise, and nutrition At present, there is no cure for PD, but medications or surgery can provide relief from the symptoms The most widely used form of treatment is L-dopa in various forms. L-dopa is transformed into dopamine in the dopaminergic neurons. However, only 1-5% of L-DOPA enters the dopaminergic neurons. The remaining L-DOPA is often metabolized to dopamine elsewhere, causing a wide variety of side effects. Due to feedback inhibition L-dopa eventually becomes counterproductive

SunCoast Seminars Parkinson’s Treatment
MAO-B inhibitors. Selegiline and rasagiline reduce the symptoms by inhibiting Monoamine Oxidase-B (MAO-B) inhibitors, inhibit the breakdown of dopamine secreted by the dopaminergic neurons. This might result in side effects such as insomnia. Sinemet: A form of Levodopa. Levodopa is used as a prodrug to increase dopamine levels for the treatment of Parkinson's disease, since it is able to cross the blood-brain barrier, whereas dopamine itself cannot. Once levodopa has entered the central nervous system (CNS), it is metabolized to dopamine. Half life is minutes. (The biological half-life of a substance is the time it takes for a substance (drug)to lose half of its pharmacologic activity).

SunCoast Seminars Parkinson’s
Because Parkinson's disease affects the ability to move, exercise helps to keep muscles strong and improve flexibility and mobility. Exercise will not stop Parkinson’s disease from progressing; but, it will improve the patient’s balance and it can prevent joint stiffening. Evidence suggests that regular exercise can improve some of the typical Parkinson’s symptoms, including tremor, rigidity, slowness and impaired movement and therefore enhance the quality of life. See handout for sample exercise program

SunCoast Seminars Orthopedic conditions Surgical Total Hip Replacement
Total Knee Replacement Total shoulder replacement Rotator Cuff repair Non-surgical Joint sprains/strains

SunCoast Seminars Geriatrics
Most of your geriatric patients will require a different exercise approach because of age related changes to their exercise physiology. In addition, many of these patients will suffer from conditions that may affect their exercise tolerance including (Eighty-four percent of individuals aged 65 and over have at least one chronic illness): CHF HTN Hyperlipidemia DM PVD Alzheimer’s As we know, these diseases bring other symptoms (cognitive impairment, falls, incontinence, low body mass index, dizziness, vision impairment, hearing impairment) and dependency in activities of daily living (bathing, dressing, eating, transferring, toileting).

SunCoast Seminars Congestive Heart Failure
Left-sided heart failure causes fluid to back up and accumulate in the lungs. This leads to the patient symptoms of shortness of breath, inability to sleep on only one pillow, waking up in the middle of the night gasping for breath, inability to exercise without shortness of breath, inability to catch your breath while at rest, and for severe cases coughing and gurgling with frothy sputum. Right-sided heart failure causes the blood entering the heart from the body to back up in the veins causing swelling of the legs, feet , and stomach. Usually, because the chambers of the heart are interconnected and work off a pressure system, congestive heart failure is a combination of left and right sided heart failure Scientific evidence has demonstrated significant improvement in cardiopulmonary function, functional status, and psychosocial status of individuals with heart failure It also has been documented that patients with CHF have abnormal hemodynamic responses to exercise making it difficult for physical therapists to develop exercise programs for these individuals.

SunCoast Seminars Exercise objectives for patients with CHF.
Beta Blockers ACE inhibitors Diuretics increase exercise tolerance decrease dyspnea and fatigue reduce the risk of arrhythmias Improve the quality of life Initial stress testing is important to create a baseline Patients may need to begin aerobic exercise with interval training and progress slowly. Strength exercise is also useful. Exercise used along with the customarily prescribed CHF medications improves symptoms more than either modality alone.

SunCoast Seminars Things to consider:
The heart's impaired pumping efficiency results in decreased blood flow to the muscles Pulmonary congestion interferes with alveolar gas transport, causing dyspnea and reducing the oxygen available for delivery to the muscles Hormonally, CHF is associated with elevated levels of catecholamines, which increases vascular resistance and further reduce muscle oxygenation Muscle atrophy often occurs early in the disease probably as a result of decreased activity and reduced blood flow. There is an increased proportion of type 2 (fast-twitch) muscle fibers, which produce more lactate at lower workloads and thus fatigue more easily than type 1 fibers

SunCoast Seminars Other benefits of exercises for CHF patients
Studies documenting the benefits of exercise for CHF patients are fewer than those demonstrating its benefits for coronary artery disease patients Increased Exercise tolerance,-defined as time to exhaustion at sub-maximal intensity—increases in the range of 26% to 37%. Individuals report less fatigue, more energy, and more endurance after training programs. This effect doubles when the patient is also taking ACE inhibitors. Quality of life. Research (3,5-9) has also shown that exercise can produce significant and lasting changes in patients' quality of life. One investigator (5) found that 50% of patients returned to work after exercise training. Three years after the study, 92% were still physically active, 31% were asymptomatic during activity, and 46% reported minimal impairment in daily life

SunCoast Seminars Other benefits of exercises for CHF patients
Functional improvements. Improvements in walking speed became apparent by the fourth week of the trial and rose to a mean of 18% over baseline by the end of the trial. Peak oxygen uptake, resting heart rate, peak power output, and ventilatory threshold also improved significantly, while fatigue decreased significantly. Patients in a control group showed virtually no changes in these variables Cellular changes. A number of investigators have observed a reversal of the decline in mitochondria and peripheral oxidative capacity associated with CHF. For example, in a 6-month study of patients who exercised 40 minutes daily, volume density of cytochrome c oxidase-positive mitochondria increased by 41%, and the change was significantly associated with oxygen uptake at the ventilatory threshold and with peak oxygen uptake.

SunCoast Seminars Exercise protocol for CHF
Although most studies have used aerobic programs in which patients aimed at achieving 50% to 75% of maximum heart rate with exercise, less demanding protocols are beneficial as well. In one controlled trial, 27 patients who had mild, chronic CHF were randomly assigned to 8 weeks of low-intensity aerobic training (performed at 40% of peak oxygen uptake, 3 times per week) or no training. Significant increases in peak oxygen uptake, volume density of mitochondria, lactic acidosis threshold, and peak workload occurred in the training group but not in controls. Another trial (7) tested the effects of graded resistance training on CHF patients. By using a protocol that works one muscle group at a time, researchers hoped to achieve positive results while putting less demand on the cardiovascular system, relative to other methods of strength training. After 90 days, the patients' scores on a multidimensional quality-of-life survey increased 63%, and 80% wanted to continue the program.

SunCoast Seminars In addition to its positive impact on the disease itself, regular exercise is beneficial for a host of other medical and non-medical problems to which CHF patients are prone. Seventy percent of CHF cases are related to coronary heart disease and hypertension, and exercise has a documented value for both. Exercise also improves lipid profiles and reduces the risk of diabetes. Most CHF patients are over 65, and exercise has been shown to help prevent and ameliorate osteoporosis and the decreased mobility of aging. Research has shown that the greatest aerobic gains occur when CHF patients exercise at 60% to 80% of their maximum heart rate. (symptom free max HR)

SunCoast Seminars To calculate a safe, maximally effective target heart rate for the patient's exercise prescription, subtract the resting heart rate from the maximum heart rate on the test, multiply by 0.6 to 0.8, and add back the resting pulse. A gradual approach. Long warm-ups are important to promote vasodilatation before the demands of exertion. A protocol of at least 10 minutes of stretching, slow walking, or other exercise can increase blood flow to muscles without raising the pulse above 40% to 50% of maximum heart rate Ideally, patients should exercise—walk or ride a stationary bicycle—at their prescribed heart rate for 20 to 40 minutes three to five times a week. Patients should generally start interval training with 2 to 4 minutes of exercise followed by a minute of rest, until they can do 10 to 15 minutes of exercise. They should then work up to 5 minutes of exercise followed by 2 minutes of rest for a total of 20 to 40 minutes of exercise per session. Patients should progress gradually until they can sustain continuous exercise for the entire session.

SunCoast Seminars Strength training. While aerobic training is the cornerstone of the exercise program, exercises to strengthen ventilatory muscles of the diaphragm and abdomen have been shown to reduce dyspnea, improve quality of life, and boost exercise tolerance Resistance training using dumbbells and ankle weights or strength training machines can be added to redress the muscle fatigue that often limits activity in CHF. Using low weight and high repetitions prevents straining and breath holding, which place greater demands on the heart. The focus should be on the major muscles of the upper and lower body and torso. One to two sets with 12 to 15 repetitions per set provides an adequate training stimulus.

SunCoast Seminars Cautions for patients.
Patients must be taught the signs of decompensation—angina, worsening breathlessness, weight gain, or leg swelling—and counseled to discontinue exercise and seek medical attention if they occur. Exacerbations are common in CHF and are usually unrelated to exercise, but patients should refrain from activity until the condition has been controlled Patients—especially those with impaired renal function—should avoid excessive water consumption. Sodium restriction (a maximum of 2 g per day) is usually part of the strategy to minimize edema. Given the considerable benefits of exercise, its limited risks, and its compatibility with other modes of treatment, a systematic training program should be part of the management of CHF for almost all patients.

SunCoast Seminars Hypertension
Having high blood pressure and not getting enough exercise are closely related Regular physical activity makes your heart stronger. A stronger heart can pump more blood with less effort. If your heart can work less to pump, the force on your arteries decreases, lowering your blood pressure. Becoming more active can lower the systolic blood pressure — the top number in a blood pressure reading — by an average of 5 to 10 millimeters of mercury (mm Hg). That's as good as some blood pressure medications. For some people, getting some exercise is enough to reduce the need for blood pressure medication.

SunCoast Seminars Hypertension
It takes about one to three months for regular exercise to have an impact on blood pressure. These benefits last only as long as you continue to exercise Flexibility and strengthening exercises such as lifting weights are an important part of an overall fitness plan, but it takes aerobic activity to control high blood pressure. Any physical activity that increases heart and breathing rates is considered aerobic. Mowing the lawn, raking leaves or scrubbing the floor counts — as long as it takes effort. Other common forms of aerobic activity include climbing stairs, walking, jogging, bicycling and swimming. Aim for at least 30 minutes of aerobic activity most days of the week. Taking the stairs instead of the elevator or taking a walk during your lunch break.

SunCoast Seminars Hyperlipidemia
The term hyperlipidemia means high lipid levels. Lipid is the scientific term for fats in the blood. At proper levels, lipids perform important functions in the body, but can cause health problems if they are present in excess. Typically associated with high cholesterol and high triglyceride levels. High lipid levels can speed up a process called atherosclerosis, or hardening of the arteries. Plaque is made of lipids and other materials circulating in your blood. As more plaque builds up, your arteries can narrow and stiffen. Atherosclerosis increases your risk of heart disease, stroke, and other vascular diseases. Fortunately, you may be able to reduce high lipid levels and, therefore, prevent or slow the progression of atherosclerosis.

SunCoast Seminars

SunCoast Seminars Hyperlipidemia
Exercise makes is an important component of the management of hyperlipidemia. Physician often will recommend an exercise program, such as walking briskly for 20 to 30 minutes most days of the week. Exercise can help lose or maintain weight, relieve stress, raise HDL, and lower triglycerides and LDL. Make sure to talk with your physician before starting any exercise program and gradually increase how long and how often you exercise.

SunCoast Seminars Diabetes Mellitus
Exercise can help control weight and lower blood sugar levels. It also lowers the risk of heart disease, a condition that is common in people who have diabetes. Exercise can also help you feel better about yourself and increase your overall health. Focus should be on aerobic exercises Exercise changes the way the body reacts to insulin. Regular exercise makes the body more sensitive to insulin, and the blood sugar level may get too low (called hypoglycemia) after exercising. Symptoms include: feel a change in your heartbeat, suddenly sweat more, feel shaky or anxious, or feel hungry. Shoes and footcare are very important because of peripheral neuropathy that might be present.

SunCoast Seminars So before you exercise a patient with DM, you should do the following: Get a complete medical history. Check patient’s blood sugar level before and after exercising. Have the patient check their feet for blisters or sores before and after exercising. Make sure the patient wears the proper shoes and socks. Make sure the patient drinks plenty of fluid before, during and after exercising. Warm up before exercising and cool down afterward. Have a snack handy in case your blood sugar level drops too low. Know when your patient is taking insulin (and how often, how much)

SunCoast Seminars PVD

SunCoast Seminars Peripheral Vascular Disease (PVD)
Pathophysiology of PVD Atherosclerosis is the initiating event which limits oxygen delivery to skeletal muscle during exercise. This leads to skeletal muscle ischemia, which leads in turn to muscle dysfunction. Finally, continuance of this process leads to muscle injury manifested by denervation, mitochondrial DNA injury, abnormal oxidative metabolism, and muscle atrophy. Exercise therapy is the cornerstone of treatment for PVD but must be done in a rigorous fashion. It is important to objectively assess the severity of claudication using a treadmill exercise test. Patients are instructed to exercise until moderate claudication occurs and then rest. Exercise followed by rest cycles should be repeated in 30- to 40-minute sessions 3 to 4 times weekly. Exercise is not recommended for people with severe rest pain.

SunCoast Seminars Peripheral Vascular Disease
Randomized trials of exercise for patients with intermittent claudication have shown significant increases in exercise duration and quality of life. Patients assigned to an exercise program were able to increase their exercise time until developing pain by 180%, compared with a 40% increase for patients receiving usual care.This translates into an extra 2 blocks of walking time. Other studies have suggested that patients who exercise in a supervised program do better than those who exercise unsupervised. The best predictors of a response to exercise therapy are: 1) program involves walking exercise rather than biking or swimming; 2) patients push to moderate pain; 3) sessions continue for longer than 6 months; and 4) sessions are supervised.

SunCoast Seminars Alzheimer’s
Moderate exercise helps many people with Alzheimer's disease feel better — both physically and emotionally. As little as 20 minutes of walking three times a week can boost mood, decrease risk of falls, reduce wandering and delay nursing home placement in people with Alzheimer's. Research has shown that exercising reduces the tendency of an Alzheimer patient to become depressed (typically, 70% becomes depressed) In a sample of people with Alzheimer's, a moderate exercise program totaling at least 60 minutes a week for three months reduced rates of depression.

SunCoast Seminars Improving sleep Fall Prevention Reduce wandering
Sleep disturbances are common in people with Alzheimer's disease. Some become agitated at bedtime, wander at night or sleep fitfully. Caregivers become exhausted when they can obtain only a few hours of sleep at a time, night after night. Regular physical activity is a natural sleep-enhancer. A daily walk or exercise class can help a person with Alzheimer's sleep more soundly at night. Fall Prevention Moderate exercise improves strength and coordination, which can reduce the risk of falls and injury. Reduce wandering Studies have shown that giving an Alzheimer patient functional activities as an exercise, reduces wandering. Tie the exercises to an activity, such as walking the dog, getting the mail, sweeping, folding the laundry and other things and make it a daily routine for the patient.

SunCoast Seminars Case Discussions CASE 1 85 year old male.
Condition: Day 1 s.p Right THA ( non cemented 50% WB) Factors to consider: Has been confused, is aneamic. Lives alone in a mobile home Function to be restored: Walking. How would you start this patient day one and progress him. With what frequency would you treat. And are there other factors you would consider.

SunCoast Seminars Spine Disorders Spinal Stenosis vs. Claudication
How do we differentiate? How do we exercise? Pelvic tilts vs. aerobic exercise Lumbar instability: Iliopsoas Poor posture, forward head posture. Cervical neck exam and basic exercises/stretching S/P surgery: Laminectomy (new endoscopic approach) ACD

SunCoast Seminars Case Discussions CASE 1 85 year old male.
Condition: Day 1 s.p Right THA ( non cemented 50% WB) Factors to consider: Has been confused, is aneamic. Lives alone in a mobile home Function to be restored: Walking. How would you start this patient day one and progress him. With what frequency would you treat. And are there other factors you would consider.

SunCoast Seminars Case 2 85 year old male
Condition: Day 3 s.p. Right THA Factors to consider: Feels great wants to get up is 50% WB Is scheduled to go to SNF tomorrow. How would you treat this patient today.

SunCoast Seminars Case 3
85 year old male. Day 8 s.p. R THA. Has been in SNF for 4 days. Desperately wants to go home. He hates old people, appears depressed, did not eat all day yesterday. Patient lives in a mobile home. Reportedly can’t wash his face due to receiving IV- Fluids. How would you treat this patient today ? How would you progress? What are your goals for today?

85 year old male. 12 days s.p. right THA (50% WB) Patient came home last night from SNF. Both sons carried him up 3 steps into his mobile home. You walk into his home and find him in his favorite spot. A 20 year old couch with broken springs in the bottom. He is thrilled to be home. How would you treat this patient today? Where would you start and how would you progress

85 year old male, 4 weeks s.p. right THA. Lives in mobile home. Reports he saw his dr. today who wanted him to get rid of the walker and start walking with a quad cane. How would you treat this patient today? And how would you progress?

85 year old male 6 weeks s.p right THA( FWB) Presents to you in outpatient clinic. Wants to get back to playing golf. His mobile home sit on the 18th hole. Problem is he can’t stand the pain in his groin when walking. He has been having to use his walker a lot. You notice the pt walks in an abducted gait pattern with grossly 30 deg. abduction throughout stance phase. How would you treat this patient today? Name 3 dysfunctions that could contribute to this gait pattern. How would you progress?

Your patient is a 17 year old female volleyball player who is 3 days s.p. ACL-repair of the R knee. She presents with extensive swelling in her complete R leg. Severe pain in R thigh and knee. Wearing a ROM brace set at 0-90deg. The orders are for therex, gt training FWB as per protocol. What would you do today? How would you progress? What are your 2 priority short term goals, and how do you intent to meet them?

Your patient is a 17 year old high school student who presents 3 days after repair of a torn ACL and a repaired torn medial meniscus. Before the surgery she was immobilized for 4 weeks with a brace locked in 30 deg flexion. Today she is wearing a ROM-brace set at 0-90deg. and she is avoiding WB on her Sx.-leg. She complains to you about extreme pain 10/10 on VAS. She has been unable to sleep. Appears pale The prescription requests therex as per protocol (no rom resticktions) and gt-training 50%WB. How would you preceed? how would you progress? What are your first 3 priorities?

Your patient is a 60 year old male. Dx. Torn Rotator cuff R shoulder. He reports he tore his RTC while stepping on the back of a garbage truck while working. He presents 5 days post open RTC repair wearing an immobilizer. Which he states he has to wear for 6 weeks. The pain is rated 9/10 with inability to get comfortable. I take “catnaps” all day and night. Pt. has been unable to take of his immobilizer. The prescription for PT. Requests PROM/ AAROM with weight of arm supported. No erot. ext. beyond neutral. How would you start treating this patient and how would you progress.

Your patient is the same sanitation worker but he is 8weeks sp RTC repair and cleared to start weight and resistive training. How would you start this phase? And how would you progress?

Questions or suggestions?
SunCoast Seminars Questions or suggestions?

SunCoast Seminars References:
(MOVIE)

SunCoast Seminars References:
Berne RM, Levy MN (1993): Physiology, 3rd ed., 1091 pp. C. V. Mosby, St. Louis. Bullock TH (1959): Neuron doctrine and electrophysiology. Science 129:(3355) Davis LJ, Lorente de Nó R (1947): Contributions to the mathematical theory of the electrotonus. Stud. Rockefeller Inst. Med. Res. 131: Elsberg CA (1931): The Edwin Smith surgical papyrus. Ann. Med. Hist. 3: Ganong WF (1991): Review of Medical Physiology, 15th ed., Appleton & Lange, Norwalk, Conn. Guyton AC (1992): Human Physiology and Mechanisms of Disease, 5th ed., 690 pp. Saunders, Philadelphia. Hermann L (1872): Grundriss der Physiologie, 4th ed., (Quoted in L Hermann (1899): Zur Theorie der Erregungsleitung und der elektrischen Erregung. Pflüger Arch. ges. Physiol. 75: ) Hermann L (1905): Lehrbuch der Physiologie, 13th ed., 762 pp. August Hirschwald, Berlin. Kandel ER, Schwartz JH (1985): Principles of Neural Science, Elsevier Publishing, New York. Lorente de Nó R (1947): A Study of Nerve Physiology, 293 pp. Rockefeller Institute for Medical Research, New York. Muler AL, Markin VS (1978): Electrical properties of anisotropic nerve-muscle syncytia - II. Spread of flat front of excitation. Biophys. 22: Nunez PL (1981): Electric Fields of the Brain: The Neurophysics of EEG, 484 pp. Oxford University Press, New York. Patton HD, Fuchs AF, Hille B, Scher AM, Steiner R (eds.) (1989): Textbook of Physiology, 21st ed., 1596 pp. W. B. Saunders, Philadelphia. Ruch TC, Patton HD (eds.) (1982): Physiology and Biophysics, 20th ed., 1242 pp. W. B. Saunders, Philadelphia. Schadé JP, Ford DH (1973): Basic Neurology, 2nd ed., 269 pp. Elsevier Scientific Publishing, Amsterdam. Thompson CF (1985): The Brain - An Introduction to Neuroscience, 363 pp. W. H. Freeman, New York.

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The Anatomy of Exercise

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The Anatomy of Exercise

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