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Muscular System Part B.

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Presentation on theme: "Muscular System Part B."— Presentation transcript:

1 Muscular System Part B

2 Muscular mechanics

3 The minimal or smallest amount of stimulation that causes the muscle to contract is called the threshold stimulus. When a muscle cell receives a threshold stimulus, it contracts to its full extent – an all-or-none response.


5 Give a series of identical stimuli - series of twitch contractions with complete relaxation in between contractions Strength of contractions increases slightly each time – staircase effect or treppe

6 Time


8 Contraction period – 10 – 100 milliseconds
Latent period – Ca++ is released, filament movement takes up slack – 2 milliseconds Contraction period – 10 – 100 milliseconds Relaxation period - 10 – 100 milliseconds Refractory period – time after a contraction until the muscle is able to respond to a second stimulus. Skeletal muscle – 5 msec Cardiac muscle – 300 msec (0.3 sec)

9 When stimuli do not allow muscle to relax completely between contractions, the muscle contraction becomes sustained. If stimulation is great enough, get a sustained contraction called a tetanic contraction or tetanus.

10 Sustained contraction
Tetanic contraction

11 Muscle fiber length

12 Whole muscle myogram A brief, single stimulus results in a twitch contraction. A twitch is a brief contraction of all the muscle fibers in a motor unit.

13 When a motor neuron fires, all of its muscle fibers contract fully.
Some motor units are more easily stimulated than others. If only some of the motor units in a muscle contract, the entire muscle contracts partially. The process of adding more motor units for a greater muscle contraction is called recruitment or multiple motor unit summation.

14 To prevent fatigue, there is asynchronous recruitment of motor units.
Recruitment varies with the type of muscle fibers. Muscles maintain a firmness at rest called muscle tone .

15 Types of muscle contraction
Isotonic contraction (iso = same, tonus = tension) results in movement at a joint Because shortening of the muscle occurs it is called a concentric contraction. When the muscle lengthens it is called an eccentric contraction.


17 Isometric contraction (iso= same, metric = measure) the force of contraction changes, but the muscle length remains the same.


19 Cardiac Muscle – similar to skeletal muscle in:
Striations – caused by organization of myofilaments Contains troponin and tropomyosin – site of activation of cross-bridge activity by Ca++ Clear length-tension relationship Numerous mitochondria and myoglobin (for aerobic respiration) T tubules and moderately well developed sarcoplasmic reticulum (T tubule at Z line)

20 Cardiac Muscle – differs from skeletal muscle in:
Shorter, larger diameter than skeletal muscle Branch, forming 3-D networks Usually only one nucleus Autorythmicity –influenced by nervous system and hormones Sarcoplasm is more abundant with more mitochondria Only one t-tubule per sarcomere




24 Well developed S.R., but less than skeletal muscle; cisternae store less Ca++.
During contraction a lot of Ca++ enters cell from the extracellular fluid in the t-tubule and extracellular fluid around the cell, so extracellular calcium partially controls the strength and length of contraction. Intercalated discs – desmosomes; gap junctions Two networks – atria and ventricles – cells contract together linked by gap junctions - functional syncytium


26 Cardiac muscle physiology
Contraction starts at the pacemaker or sinoatrial node. Autorhythmicity Contraction due in large part to influx of Ca++ from ECF Resting potential of -90 mV Opening of voltage-gated Na+ channels reverses polarity to +30 mV

27 Membrane potential rapidly reverses due to influx of Na+
Plateau phase lasts several hundred milliseconds due to slow influx of Ca++ (and slowing of exit of K+) Repolarization is due to rapid out flow of K+ ions. Remains contracted times longer Long refractory period Allows for filling of heart chambers Prevents tetanic contractions



30 In skeletal muscle the amount of Ca2+ released is sufficient to bind all of the troponin molecules
In cardiac muscle only a portion of troponin has bound Ca2+; allows for changes in contractility In cardiac muscle SR does not release enough Ca2+ to activate muscle contraction. Ca2+ entering cell during plateau phase triggers release of calcium from SR (calcium-induced calcium release)

31 DHP channels: RyR is 1:1 Release of “calcium sparks” sum to trigger release Increased cytosolic calcium


33 Removal of Ca2+ from cytosol
Ca2+ATPase in SR runs continuously and is further activated by high cytoplasmic calcium levels (extracellular Ca++ that entered cell can be stored for next contraction) Also Ca2+ATPase located in sarcolemma Na+/Ca++ exchange proteins (3:1 ; secondary active transport)


35 Effects of extracellular K+ on heart
Changes in K+ in ECF alter the concentration gradient across sarcolemma Leads to ectopic foci and cardiac arrhythmias Decrease in action potential leads to weak contractions and dilation of heart At extremes, heart can stop

36 Effects of extracellular Ca++ on heart
Rise in ECF Ca++ increases strength of contraction by prolonging plateau phase Tends to contract spastically Drugs can influence Ca++ movement across sarcolemma (calcium channel blockers, digitalis e.g.)

37 Inotropy Positive inotropes increase contractility of heart
Sympathetic nervous system stimulation Catecholamine hormones (epinephrine) Digitalis Increased heart rate Negative inotropes decrease contractility Decreased heart rate Coronary artery disease Certain drugs (calcium channel blockers)

38 Starling’s Law Within certain physiological limits, an increase in the stretching of the ventricles causes an increase in the force of contraction of the heart. This allows for instantaneous regulation of contraction for increases in blood entering heart

39 Smooth muscle Nonstriated and involuntary
Cells smaller than skeletal muscle cells Spindle-shaped Single nucleus NO T tubules Different arrangement of myofilaments Thin, thick and intermediate filaments


41 Smooth muscle Thick and thin filaments not arranged in sarcomeres
Thick filaments are longer than in skeletal muscle Thin filaments lack troponin 10-15 thin filaments/ thick (skeletal 2:1) Intermediate fibers act as cytoskeleton Typically less SR than in skeletal muscle Intermediate filaments attach to dense bodies ( act like Z discs)

42 Intermediate fibers connect dense bodies
Thick- and thin-filament contractile units oriented slightly diagonally in a diamond-shaped lattice pattern Contraction causes the lattice to decrease in length and expand from side to side.


44 During contraction, the sliding thick and thin filaments generate tension that is transmitted to the intermediate filaments, which pull on the dense bodies in the sarcoplasm and those attached to the sarcolemma. Isolated smooth muscle cells contract by twisting into a helical shape, but this is prevented in intact tissues due to their attachment to other cells.

45 Gap Junctions Often connect smooth muscle cells
May be temporary, and may be under hormonal control The electrical joining of smooth muscle cells is the basis for classifying smooth muscle into two types: Visceral (single-unit) smooth muscle Many cells acting together Multiunit smooth muscle Cells contract in small groups

46 Single-unit smooth muscle
Multiunit Smooth Muscle

47 Visceral (single-unit) smooth muscle
More common type Wrap-around sheets Fibers form networks that contract together Connected by gap junctions Some cells also have autorhythmicity Largely responsible for peristalsis

48 Multiunit Smooth Muscle
Individual fibers within motor units; few gap junctions In walls of large arteries, large airways, arrector pili, iris muscles and ciliary body in eye. Contracts only after stimulation by motor neuron or hormones

49 Physiology of Smooth Muscle
Contractions start slower and last longer Can shorten and extend to greater extent Resting potential is much lower and can vary over time due to automatic cyclical changes in the rate at which Na+ is pumped across the membrane. “Slow wave”

50 Sodium is not the major carrier of current during an action potential, instead it is Ca2+ which enters through voltage-gated channels Also have receptor-activated or chemically activated Ca2+ channels Repolarization due to outflow of K+ though voltage-gated channels and some channels sensitive to intracellular Ca2+ levels


52 Physiology of Smooth Muscle
Calcium ions come from the small amount of S.R. and from extracellular fluid through DHP channels Instead of troponin, contains calmodulin which regulates contraction Myosin-linked regulation Camodulin binds with Ca++ and activates myosin light chain kinase (MLCK)

53 ATP for actual contraction is separate
MLCK uses ATP to add a phosphate group to the myosin head. Myosin can then bind to actin ATP for actual contraction is separate Enzymes work slowly (100 x slower than skeletal muscle) Calmodulin is sensitive to Ca2+ conc. in ICF At 10-7 M Ca2+ , no calcium is bound At 10-4 M Ca2+ all 4 calmodulin sites are bound and rate of phosphorylation is maximal In between see gradations in contractile force



56 Relaxation of Smooth Muscle
When Ca2+ levels fall, calmodulin is no longer active and phosphorylation of myosin is reversed by the enzyme myosin light-chain phosphotase (MLCP)


58 Ca2+ also leaves the cell slowly, which delays relaxation and provides for smooth muscle tone.
Sustained tone is important, and in some cases smooth muscle can maintain a low level of active tension for long periods of time; a long sustained contraction is called tonus rather than tetanus

59 Regulation of Smooth Muscle contraction
Responds to signals from autonomic nervous system ( responds to ACh and norepinephrine) Some have no nerve supply and depolarize spontaneously or to ligands that bind to G protein linked receptors Many also contract or relax in response to stretching, hormones or local factors (such as changes in pH, oxygen or carbon dioxide levels, temperature or ion concentration). Enhances or inhibits entry of Ca2+

60 Origin and Insertions Origin – the attachment of a muscle to the less movable part (torso, etc.) Insertion – the attachment of a muscle to the more movable part


62 Interactions of muscles
Prime mover – the muscle primarily responsible for a movement Synergist – stabilizes or assists prime mover Antagonist – opposes action of prime mover and must relax for prime mover to contract completely

63 Major muscles will be covered in lab.

64 Life Span Changes Develops from mesoderm cells called myoblasts
Multinucleate skeletal muscle cells form through fusion of myoblasts to form myotubes Fibers are contracting at 7 weeks ACh receptors sprout over surface of myoblast Agrin released by nerve endings stimulates clustering of ACh receptors

65 Remaining receptor sites dispersed
Electrical activity in the motor neurons plays a critical role in maturation of muscle fibers The number of fast and slow fiber types is determined. Myoblasts producing cardiac and smooth muscle fibers do not fuse. Both develop gap junctions early. Cardiac muscle is pumping blood 3 weeks after fertilization.

66 Repair of muscle Skeletal and cardiac muscle cells stop dividing early, but retain ability to lengthen and thicken in a growing child and to hypertrophy in adults. After first year, growth of skeletal muscle is by hypertrophy. Enlarged fibers may split down middle Satellite cells (stem cells)repair injured fibers and may allow a very limited regeneration of fibers. Most repair by fibrosis

67 Repair of cardiac muscle
Cardiac fibers do divide at a modest rate. Injured heart muscle repaired mostly by fibrosis (scar tissue). Fibers can hypertrophy and enlarge heart

68 Repair of Smooth Muscle
Limited to good capacity for division and regeneration throughout life Some increase due to hyperplasia New fibers can arise from pericytes (stem cells) Proliferate in atheroscerolsis

69 Development At birth movements are uncoordinated and reflexive
Develops head-to-toe and proximal-to-distal Through childhood control becomes more sophisticated. Early hand dominance Midadolescence reach peak of natural neural control of muscles

70 Male vs. Female Strength has a biological basis Women 36% muscle
Primarily due to effects of testosterone Strength per unit mass is the same in both sexes

71 Aging changes Connective tissue and fat increase and there is a slow, continuous reduction in the number of muscle fibers and loss of strength. At age 30 sarcopenia begins to occur as proteins degrade faster than they are replaced. (regulatory molecules?) Up to 30% of muscle fibers may be lost by age of 80.

72 Loss of fibers reduces size of motor units
More motor units must be recruited to move a given weight, so requires more effort. Fast-twitch glycolytic fibers atrophy earlier than slow-twitch oxidative fibers. Posture not affected until very late in life. Reduction of ability of muscle to adapt to exercise. Some loss is disuse atrophy

73 Impairment of synthesis of new muscle proteins
Reduction in nerve activity due to changes in nervous system Loss of motor neurons Reduction in synthesis of ACh Contributes to muscle fiber atrophy and efficiency of stimulation

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