Muscular Adaptations to Exercise Chapter 14

Meetings 2 nd year Health & PE 3 rd years who will be out on prac mid session quiz followup

Muscle contraction

Receptors Chemoreceptors- carry messages about O2 and Co2 concentrations, muscle pH, potassium Sensory feedback –Golgi tendon organs- give CNS feedback about tension developed in the muscle –Muscle spindles give feedback about length of the muscle

Muscle spindles- length detector

Types of muscle contraction Isotonic= muscle changes length –Concentric = shortening/ contraction –Eccentric= lengthening/ extension Isometric= muscle stays the same length

Overload Placing increased demand on the muscle –Increased load –Increased reps –Increased speed Usually 60-70% of 1RM for strength training Muscle responds to the intensity rather than the form of overload

Adaptations Muscle fiber hypertrophy- increase in size Muscle fiber hyperplasia- increase in number

Hypertrophy 2 main types –Sarcoplasmic hypertrophy- sarcoplasmic fluid in the muscle cell increases no increase in contractile strength >12 reps of submax resistance –Myofibrillar hypertrophy- increase in myofibrals increase in strength & size 2-8 reps of 80-90% of 1RM.

Myofibrillar Hypertrophy Increased size/amounts of –Contractile proteins- Actin & Myosin –Myofibrals per muscle fibre –Connective tissue- ligaments etc –Enzymes & stored nutrients –mitochondria

Physiology of Hypertrophy Satellite cells –Located on outer surface of muscle fibre –Usually dormant, until… –Muscle damage/ trauma –Then satellite cells multiply and fuse to site of injury –Donate their nucleus to repair the muscle fibre –Therefore increasing the number of contractile proteins (actin & myosin) in that muscle fibre

What would happen…

Role of testosterone Acute increases after maximal exercise Anabolic effect Induces hypertrophy No relationship between total hypertrophy and testosterone

And the ladies? Similar strength gains, but without hypertrophic response 10 x less testosterone Men have larger initial muscle mass

Atrophy Muscle degeneration from disuse –Not synthesising new proteins –May be used as fuel Begins after 3 days disuse More apparent with complete inactivity (bed rest) Effects are reversible

Age related changes Sarcopenia –Slow phase- 10% loss from –Rapid phase- Extra 40% loss years –Therefore by 80, 50% muscle lost Predominant loss of fast fibres  slow ones

Variability in adaptation Individual training responsiveness

Genetics Myostatin- gene that inhibits muscle growth Therefore when this gene is inactive- extraordinary muscle growth occurs Some babies born with 1/ both myostatin genes inactive

Belgian Blue cattle

Muscle soreness Acute –Lactic acid build-up –Acidosis caused by low pH –sually returns to pre exercise levels 1 or 2 hours

Delayed Onset Muscle soreness

Treatment of DOMS More exercise –Lower intensity, continuous, aerobic Massage Stretching –Thought to relieve muscle spasms Ice baths –‘remove tired blood’ –Decreased tissue temp swelling Inflammation oedema

Summary Understand muscle physiology Principle of overload Adaptation to overload –Hypertrophy Sarcoplasmic Myofibrillar DOMS Genetics

Meetings 2 nd year Health & PE 3 rd years who will be out on prac mid session quiz followup

Meeting 3 rd years Clashes with Prac/ teaching rounds Miss 2 labs –8/10- Ergogenic aids –Repeat of fitness testing