Module 3 Study Guide

Whole muscle (epimysium) → fascicle (perimysium) → muscle fiber (the cell, wrapped in sarcolemma) → myofibril → sarcomere → thick and thin filaments → proteins (myosin, titin, actin, nebulin, tropomyosin, troponin). (M3 slides 3–6)

The A band (full width of the thick filaments, dark) alternates with the I band (thin filaments only, light). Repeating sarcomeres line those bands up across the cell. (M3 slide 6)

Ca²⁺ entering at the surface would have to diffuse 50 µm to the core, and diffusion time grows with distance squared. T tubules carry the action potential deep into the cell so the SR can release Ca²⁺ right beside every myofibril, making contraction fast and uniform. (M3 slides 4, 17)

One T tubule flanked by two patches of SR. The DHPR in the T tubule is physically connected to the RyR on the SR; that contact lets a voltage change mechanically open the Ca²⁺ release channel. (M3 slides 4, 17)

Troponin I binds actin, troponin T binds tropomyosin, troponin C binds Ca²⁺. When Ca²⁺ binds troponin C the complex changes shape and pulls tropomyosin off actin’s binding site, letting myosin bind. (M3 slides 6, 16)

AP reaches the terminal → voltage-gated Ca²⁺ channels open → Ca²⁺ in → ACh exocytosis → ACh binds nicotinic receptors (ligand-gated) on the motor end plate → Na⁺ in → EPSP → at the edge of the end plate, voltage-gated Na⁺ channels open → muscle AP spreads in all directions. (M3 slide 11)

The end plate has ligand-gated channels, not voltage-gated Na⁺ channels, so it can only make graded potentials. The action potential begins where the end plate meets regular sarcolemma, which has voltage-gated Na⁺ channels. (M3 slide 11)

Same: shape, steep Na⁺-driven depolarization through voltage-gated Na⁺ channels, steep K⁺-driven repolarization. Different: the muscle AP lasts about 2 ms against 1 ms, and on the slide it starts from about −80 mV. (M3 slide 12)

Tetrodotoxin: voltage-gated Na⁺ channels in nerve and muscle, instant lethal paralysis. Dendrotoxin: neural voltage-gated K⁺ channels, prolonged depolarization, ACh over-release, cramps and convulsions. Botulinum toxin: blocks ACh release, paralysis including breathing muscles. (M3 slide 13)

Myasthenia gravis: ACh-gated channels on the motor end plate, progressive weakness. Neuromyotonia: neural voltage-gated K⁺ channels, poor repolarization of the neuron. Lambert-Eaton: presynaptic voltage-gated Ca²⁺ channels, too little ACh release. (M3 slide 13)

Sarcolemmal AP → down the T tubule → DHPR changes conformation → pulls open the RyR on the SR → Ca²⁺ flows down its gradient into the sarcoplasm. (M3 slide 17)

ATP binds at the first arrow, detaching the head. It is hydrolyzed by myosin ATPase at the second, recocking the head. P_i release strengthens binding, then the power stroke, then ADP release. (M3 slide 18)

The AP only triggers Ca²⁺ release. Force lasts as long as Ca²⁺ stays bound to troponin C and cross-bridges cycle, then decays only as SERCA pumps Ca²⁺ back. Those chemical and mechanical steps take far longer than the electrical one. (M3 slide 22)

At rest free and bound Ca²⁺ balance at low levels. In contraction the RyR floods free Ca²⁺; the reaction shifts right, loading troponin C to a new high equilibrium. In relaxation SERCA drains free Ca²⁺; the reaction shifts left, unloading troponin C back to the low equilibrium. (M3 slide 21)

Speed: creatine phosphate > glycolysis > oxidative (glucose) > oxidative (fatty acids). Yield: the reverse, 1, 2, 34, 90–140 ATP. More steps extract more energy but take longer, so a pathway can be fast or efficient, not both. (M3 slides 28–29)

At high intensity oxygen runs short, pyruvate becomes lactic acid, and muscle pH drops until contractile proteins stop working. The body has plenty of glucose, so byproduct buildup, not supply, ends it. (M3 slide 28)

M3 slide 30

Color tracks myoglobin, plus capillaries and mitochondria. Type I fibers, built for oxidative metabolism, are packed with myoglobin and look dark red. Type IIx rely on glycolysis, have little myoglobin, and look pale. (M3 slides 30–31)

A bell curve of active force against resting sarcomere length, peaking around 2.0–2.3 µm. Too long: little filament overlap, few cross-bridges. Too short: thin filaments hit the M line and thick filaments crash into the Z disc, wrecking the arrangement. (M3 slide 35)

Passive tension comes from stretch alone and rises with length. Total tension is the force measured during contraction. Active tension is total minus passive, the bell curve. (M3 slide 35)

5 Hz: separate twitches with full relaxation. 10 Hz: summation, each twitch starts before the last relaxes. 25 Hz: unfused tetanus, high tension with ripples. 50 Hz: fused tetanus, smooth and maximal. (M3 slide 36)

A motor unit is one somatic motor neuron and every fiber it innervates. Precision muscles (like the eye) have small innervation ratios, few fibers per neuron, for fine steps of force. Power muscles have large ratios, many fibers per neuron. (M3 slide 37)

I = CV. V, the voltage change needed to depolarize, is the same for every cell. C varies with membrane area: small cells have small capacitance and need less current. So the smallest motor units, with Type I fibers, are recruited first and the largest last. (M3 slide 38)

Concentric: force > load, shortens, accelerates. Eccentric: force < load, lengthens, decelerates. Isometric: force = load (or less than an immovable load), no length change, fixation and stability. (M3 slides 41–43)

The backpack: longer isometric phase before shortening starts, much less shortening, shorter total duration, and lower shortening velocity. The phone: the reverse on every count. (M3 slide 44)

Above the zero-velocity line: concentric. At the crossing: isometric. Below it: eccentric. Fast-twitch fibers have higher myosin ATPase activity and cycle cross-bridges faster, so they shorten faster at every load and their curve sits higher. (M3 slide 45)

Power peaks at about one third of maximum force. (M3 slide 46)