Human A&PBIO 304 · American River College
BIO 304 · Human Anatomy & Physiology · Week 4 · Study Guide
Muscle Physiology
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Sequence
- Motor neuron fires an action potential to the axon terminal
- ACh is released across the neuromuscular junction and binds the motor end plate
- An end-plate potential triggers an action potential along the sarcolemma
- The signal travels down the T-tubules
- DHP and ryanodine receptors open and the SR releases calcium
Key events
- ACh: vesicles in the axon terminal release acetylcholine into the synaptic cleft
- Receptors: ACh binds nicotinic receptors on the motor end plate
- Depolarization: Na+ enters and the sarcolemma reaches threshold (end-plate potential)
- Always excitatory: the neuromuscular junction never inhibits, it always triggers contraction
One job
- Acetylcholinesterase: an enzyme in the synaptic cleft that breaks down ACh
- This clears the signal so the muscle can relax between impulses
- If it is blocked, ACh builds up and the muscle cannot relax
Sequence
- Action potential travels down the T-tubules
- DHP receptors pull open the ryanodine receptors on the SR
- The SR releases calcium into the cytosol
- Calcium binds troponin
- Tropomyosin shifts and uncovers the myosin-binding sites on actin
Function
- Calcium binds troponin, changing its shape
- Troponin pulls tropomyosin off the actin binding sites
- This exposes the myosin-binding sites so cross-bridges can form
- Calcium is the on-switch for contraction
Sequence
- Formation: the energized myosin head binds actin
- Power stroke: the head pivots and pulls the thin filament toward the M line; ADP and Pi are released
- Detachment: a new ATP binds myosin and it releases actin
- Re-cocking: ATP splits to ADP and Pi, re-energizing the head to bind again
Steps
- The motor neuron stops firing and acetylcholinesterase clears the ACh
- SERCA pumps calcium back into the SR (this needs ATP)
- With calcium gone, tropomyosin re-covers the actin sites
- Cross-bridges can no longer form, and the fiber lengthens
Why it happens
- After death there is no ATP
- Without ATP, myosin cannot detach from actin
- Cross-bridges lock and the muscles stay rigid
- It resolves as enzymes break the proteins down
Definitions
- Motor unit: one motor neuron plus every fiber it innervates
- Size principle: small units recruit first; larger ones join as more force is needed
- All-or-none: a single fiber contracts fully or not at all; the muscle grades force by recruiting more units and firing faster
Fiber types
- Type I, slow oxidative: red, aerobic, fatigue-resistant, for posture and endurance
- Type IIa, fast oxidative: intermediate, uses both aerobic and glycolytic fuel
- Type IIx, fast glycolytic: white, anaerobic, powerful but fatigues quickly
Definitions
- Twitch: the response to one action potential
- Wave summation: a second stimulus arrives before relaxation and adds force
- Unfused tetanus: rapid stimulation with partial relaxation
- Fused tetanus: stimulation so rapid there is no relaxation, giving smooth maximal force
Contraction types
- Isotonic: the muscle changes length under a constant load (lifting)
- Isometric: force is produced with no length change (holding a plank)
- Concentric: isotonic shortening (curling a weight up)
- Eccentric: isotonic lengthening under load (lowering it); causes most soreness
Why length matters
- Force depends on how much the thick and thin filaments overlap
- Optimal length: maximum overlap gives maximum force
- Too short: thick filaments collide with the Z discs, force drops
- Too long: too little overlap to form bridges, force drops
Energy systems
- Stored ATP: about 2 seconds
- Creatine phosphate: fast ATP regeneration for about 10 to 15 seconds
- Anaerobic glycolysis: about 30 to 60 seconds, produces lactate
- Aerobic respiration: minutes to hours, needs oxygen, makes the most ATP
Fatigue
- Fatigue: a drop in force from ion imbalances, low energy stores, and reduced calcium release (not lactate alone)
- Oxygen debt: the extra oxygen used after exercise to rebuild ATP and creatine phosphate and clear metabolites
Clinical reasoning
- Myasthenia gravis: antibodies destroy ACh receptors, so the signal weakens with use
- Organophosphates: block acetylcholinesterase, so ACh builds up and muscle cannot relax
- Botulinum toxin: blocks ACh release, relaxing the muscle