Animal & Human Physiology: Chapter 2 — Nerve and muscle at the physiological level

2.1 From the nerve to the fibre #

2.1.1 The action potential, restated once #

A resting nerve or skeletal-muscle membrane is polarised, inside negative by about 70–90 mV, because potassium is high inside, sodium is high outside, and the resting membrane is more permeable to potassium. The sodium–potassium pump built the gradients. Cell Biology and Neurobiology own the pump and the channel kinetics.

A sufficient depolarisation opens voltage-gated sodium channels. Sodium entry flips the membrane toward the sodium equilibrium potential: the Hodgkin cycle of Chapter 1. The channels then inactivate, potassium channels open, and the membrane repolarises. For a millisecond or two it cannot fire again. The refractory period sets a maximum rate and stops the impulse echoing backwards. The impulse travels because local current depolarises the next patch. In a myelinated axon the current jumps between nodes. Conduction is all-or-none. Strength is not the size of one action potential. It is which axons fire, and how often.

A skeletal-muscle action potential lasts only a few milliseconds and is conducted into the T-tubules. A ventricular cardiac action potential lasts about 200–300 ms because of a calcium plateau. That difference is why a heart cannot tetanise.

2.1.2 The neuromuscular junction #

Each skeletal fibre has one neuromuscular junction. The motor terminal releases acetylcholine when calcium enters, and acetylcholine binds nicotinic receptors, which are ligand-gated cation channels. The endplate potential is normally far above threshold, so every nerve impulse produces a muscle impulse. Acetylcholinesterase in the cleft ends the signal, and the choline is recovered. This synapse is a reliable relay, not a site of delicate summation. Summation in skeletal muscle is summation of twitches inside the fibre. Autonomic junctions, in Chapter 3, are different: transmitter diffuses from varicosities onto receptors spread over a wider area, and the effect can be slow and graded.

2.2 Skeletal muscle as an organ #

2.2.1 The motor unit and the size principle #

A motor unit is one motor neuron and every fibre it innervates. A fibre receives only one motor neuron. The neuron may supply a few fibres, as in an extraocular muscle, or hundreds to more than a thousand, as in a large limb muscle. Force is graded by recruitment of more units and by rate coding, raising the firing rate of units already active so that twitches summate.

For most movements, recruitment follows Henneman’s size principle. Small motor neurons have lower thresholds and fire first. They innervate slow oxidative fibres. Larger motor neurons, innervating fast glycolytic fibres, are recruited as force rises. The order follows from neuronal electrical properties: a given synaptic current depolarises a small cell more. Everyday force therefore uses fatigue-resistant fibres. Powerful, fatigable fibres are kept for high force.

2.2.2 Twitch, summation, and tetanus #

A single action potential releases a pulse of calcium and produces a twitch, outlasting the electrical event because the cross-bridge cycle and calcium reuptake take tens of milliseconds. A second impulse before relaxation adds force. At a low rate the sum is an unfused tetanus, with ripple. At a higher rate the ripple disappears into a fused tetanus. Slow units fuse at lower rates than fast units, often at a few tens of impulses per second, because their twitches last longer. Tendon elasticity smooths the ripple further, so force at the bone is steadier than force in one fibre. Cardiac muscle cannot do this: its refractory period outlasts the moment at which a second twitch would have to start.

2.2.3 Length–tension and force–velocity #

Active isometric force is greatest near the sarcomere length where actin and myosin overlap well, about 2.0–2.2 µm, and falls if the sarcomere is longer (fewer bridges) or very short (filaments collide). The geometry is the sliding-filament account in the Cell Biology notes. Skeletal muscle in the body sits near that plateau, because bones and tendons set the range. Cardiac muscle at ordinary filling sits on the ascending limb, shorter than the optimum. Extra filling lengthens sarcomeres toward the optimum and active force rises. That is the structural basis of the Frank–Starling law. The pericardium normally prevents the heart from being stretched onto the descending limb.

The force–velocity relation, formalised by A. V. Hill, describes shortening. With no load, velocity is maximal and depends largely on the myosin isoform. As load rises, velocity falls. At isometric force, velocity is zero. Power, force times velocity, is zero at both ends and greatest at an intermediate load, roughly a third of isometric force. Fast glycolytic fibres have a higher maximum velocity than slow oxidative fibres. Recruitment sets how much force is available. Fibre type sets the velocity at which that force can still be delivered.

2.2.4 Fibre types #

Small mammals also have a faster IIb fibre that is scarce in human muscle. Training shifts metabolic capacity, especially between IIa and IIx, more readily than it turns a type I fibre into a type IIx fibre. A quiet standing posture may use almost only type I units. A maximal jump recruits all three.

2.3 Coupling, smooth muscle, and cardiac muscle #

The study of Coupling, smooth muscle, and cardiac muscle provides fundamental principles governing cellular architecture, molecular interactions, and physiological regulation.

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2.3.1 Excitation–contraction coupling, briefly #

In skeletal muscle the T-tubule voltage sensor (the dihydropyridine receptor, CaV1.1) is mechanically linked to the ryanodine receptor of the sarcoplasmic reticulum. Depolarisation releases stored calcium. Calcium binds troponin C, tropomyosin moves, and the cross-bridge cycle runs. ATP both powers that cycle and is required for a bridge to detach; the structural steps are in the Cell Biology notes. Without ATP the bridges lock, which is the rigidity of muscle after death, not a living contraction. Relaxation is calcium removal by the sarcoplasmic reticulum calcium ATPase. A twitch is one calcium pulse. A tetanus is a train that keeps cytosolic calcium high.

2.3.2 Smooth muscle #

Smooth muscle has no troponin and no sarcomeres in register. Actin is anchored at dense bodies. Calcium binds calmodulin, and the complex activates myosin light-chain kinase, which phosphorylates myosin. Only then can bridges work. Relaxation needs a fall in calcium and dephosphorylation by myosin light-chain phosphatase. In the latch state, dephosphorylated bridges stay attached, so a vessel can hold force with very little ATP turnover. Contraction is slow, often seconds, and can be started by voltage, stretch, or a ligand without a nerve impulse at every cell. Innervation is by autonomic varicosities, not by an endplate.

Many muscles sit between the two. Gut muscle shows the single-unit pattern plus a second control. Interstitial cells of Cajal generate slow waves, about three a minute in the stomach and about twelve a minute in the duodenum. A wave that crosses threshold opens calcium channels and causes contraction. Hormones and autonomic transmitters change that chance. They do not invent the rhythm.

2.3.3 Cardiac muscle as a bridge #

Cardiac muscle is striated and uses troponin, so the intracellular switch resembles skeletal muscle. The tissue resembles single-unit smooth muscle. Intercalated discs join cells mechanically (fascia adherens and desmosomes) and electrically (gap junctions). An impulse from the sinoatrial node spreads through the myocardium. Force is graded by fibre length and by contractility, not by recruiting silent motor units.

The ventricular action potential has a plateau, carried largely by L-type calcium current, lasting about as long as the twitch. Sodium channels stay inactivated, so a second impulse cannot start until relaxation has begun. Tetanus is impossible. A fused contraction would lock the ventricle and stop filling. The long refractory period is what makes a pump that must alternate ejection and filling able to do so. Chapter 4 is the anatomy of this same impulse.

2.4 Fuels #

2.4.1 What contraction spends #

The immediate fuel is ATP, and the store would last only a second or two of hard work. Phosphocreatine buffers it: creatine kinase refills ATP for a few more seconds of maximal effort. Beyond that, anaerobic glycolysis supports tens of seconds, and oxidative phosphorylation supports minutes to hours, using glucose and fatty acids and requiring blood flow and mitochondria. The pathways are Biochemistry. Three physiological limits matter. Oxygen delivery and mitochondrial capacity set the sustainable rate. Glycogen inside the fibre sets a local ceiling. The hormones of Chapter 9 decide whether the blood is offering glucose, fatty acids, or both.

After work stops, oxygen consumption stays high for a while. The old phrase “oxygen debt” suggested a single repayment of lactate. The elevation covers several restorations at once: phosphocreatine, oxygen stores, recycling of lactate, and the cost of a still-raised temperature and circulating catecholamines. It is not a one-to-one oxygen account of glycolysis.

2.5 Key terms, summary, and self-check #

Key terms. Motor unit; size principle; twitch; tetanus; length–tension; force–velocity; type I, IIa, IIx; troponin; calmodulin; myosin light-chain kinase; latch; single-unit; multi-unit; intercalated disc; phosphocreatine.

Summary. An action potential is all-or-none. Skeletal force is graded by recruiting motor units in size order and by raising firing rate until twitches fuse. Length sets filament overlap, and velocity falls as load rises, so power peaks at an intermediate load. Calcium binds troponin C in skeletal and cardiac muscle, but calmodulin in smooth muscle, which can hold force cheaply in the latch state. Cardiac muscle pairs a troponin switch with gap junctions and a long refractory period, so it contracts as a whole and cannot tetanise. ATP is buffered by phosphocreatine and then supplied by pathways left to Biochemistry.

Self-check.

1. Why does the size principle bring slow oxidative units in before fast glycolytic units?

2. Why can a skeletal fibre tetanise, and why would a tetanised ventricle be unable to pump?

3. Where on the length–tension curve does cardiac muscle normally operate, and why does that matter for Starling’s law?

4. What does calcium bind in skeletal muscle, and what does it bind in smooth muscle?

5. As load rises from zero to the isometric maximum, what happens to shortening velocity, and where is power greatest?

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