Muscle Physiology

Muscle anatomy

each myofiber is composed of a syncytium of multiple cells. (muscle cell = myofiber)

each myofiber is innervated by a nerve terminal

T-tubules are invaginations of the sarcolemmic membrane that are associated with the SR that have DHPr channels.

The Sarcoplasmic membrane has Ryanodine receptors that release Ca²⁺ as well as Ca²⁺ ATPase to sequester Ca²⁺.

Each Sarcomere is comprised of THIN filaments (actin with tropomyosin and troponin) and THICK filaments (myosin).

Nebulin determines the length of the thin filament, Titin anchors the thick filament to the Z-line.

	Type one	Type two A	Type two B
Myosin ATPase	Slow	Fast	Fast
SR Ca²⁺ ATPase	Slow	Fast	Fast
Diameter	Small	Small	Large
Oxidative capacity	High	High	Low
Glycolytic capacity	Mod	High	High

Motor Units

Each motor unit is comprised of only one type of fiber. Large motor units are mainly type II, fast, relatively unexcitable, and mainly recruited when force is needed. Small motor units are relatively excitable, type I, slow, and recruited first.

The CNS can modulate overall muscle function by activating varying degrees of small and large motor units.

Contraction Sequence

When the sarcolemma is depolarized the depolarization travels through the T-tubules triggering the DHPr channels. By an as-of-yet unknown mechanism a signal is sent from the T-tubule to the SR causing the release of Ca²⁺ stored in the SR. The Ca²⁺ binds troponin, which pulls tropomyosin out of the way so that actin and myosin can bind.
Force Ca²⁺ relationship – as [Ca²⁺] increases, so does Force.
Force Velocity relationship – the smaller the velocity the greater the force that can be generated
Power = Force / Velocity – peek power for all muscle is between 30-40% of maximal force.

Regulation of Force Development

Ways to modulate force:

(1) Change muscle length, maximum force is generated at maximum overlap without interference

(2) Change stimulation frequency, how fast the neuron is firing (Ý frequency = Ý force because not all Ca²⁺gets sequestered)

(3) Change Ca²⁺ sensitivity, Ý sensitivity would result in more force per unit calcium. (In fatigue muscle is less sensitive)

(4) Change motor unit recruitment, recruit motor units with extra fibers.

Muscle Metabolism

There are 2 ways for a muscle to get energy. Glycolysis is used for short, heavy work, OxPhos for endurance activity.

The level of ATP stays constant in a muscle cell. This is accomplished in part by Creatine phosphate, which acts like a buffer to store potential ATP’s for later use: Cr-P + ADP Þ Cr + ATP

Exercise

Response depends on the type of activity (which fibers are recruited) and the energy source (OxPhos or Glycolysis)

Oxygen debt – exercise precedes oxygen movt into mito for OxPhos . O₂ consumption lags at the start of exercise but Ý O₂ consumption continues after exercise has stopped.

Anaerobic threshold – the intensity of exercise where serum lactate starts to rise signaling a transition from OxPhos to glycolysis. This can be used to follow a patient because with training it should rise.

Training Strength = big fibers, fatigable (e.g. weight lifters)

Endurance = low force, Ý mito content, Ý OxPhos utilization, shift to smaller, fatigue resistant fibers and increased capillary density of muscle. (e.g. marathoners)

Muscle Fatigue

Definition: "Reversible decrease in force or velocity as a result of activity" (has to be reversible and due to activity)

Origin: Central "General" – perception of effort "I’m tired"
Neuromuscular – failure of impulses to reach the muscle, loss of neurotransmitter, receptors not as sensitive
Muscular "Cellular" – changes due to activity take place within the muscle itself.

2 theories for Muscular fatigue

(1) accumulation of metabolites: ions, K⁺ outside, lactate, H⁺, inorganic phosphate. (H⁺ and PO₄ cause a shift of the Calcium Force curve to the right / make muscle less calcium sensitive)
(2) Depletion of metabolic substrates: ran out of CrP, glycogen, glucose [ ATP] remains constant. However recovery of fatigue does not correlate with restoration of normal glycogen levels.

Damage: how much fatigue is due to physical damage to muscle fibers following an exercise event is unknown.