Muscle

Part 1 · General anatomy

From whole muscle to sarcomere, fibre types, and the motor unit

Why this chapter is the centre of the subject

Muscle is the only tissue you can instruct directly. You cannot tell a ligament to shorten or a disc to rehydrate, but you can tell a muscle to contract, and by choosing how often, how hard, how fast and through what range, you can change its size, its fibre-type expression, its neural drive, its length, its stiffness and its metabolic capacity. Every exercise prescription is an intervention on the material in this chapter.

Learning outcomes

By the end you should be able to:

• Compare skeletal, cardiac and smooth muscle in structure, control and clinical relevance.
• Describe the connective tissue hierarchy of a muscle and explain its mechanical role.
• Classify muscles by fibre architecture and predict the force–excursion trade-off of each.
• Describe the sarcomere in detail and name every band, line and zone.
• Explain excitation–contraction coupling and the cross-bridge cycle step by step.
• Explain the length–tension and force–velocity relationships and apply them clinically.
• Describe the motor unit, the size principle, rate coding and motor unit territory.
• Compare fibre types and predict their response to training and disuse.
• Describe muscle spindles and Golgi tendon organs, and the reflexes they mediate.
• Describe muscle blood supply, energy systems, and the mechanisms of hypertrophy, atrophy, DOMS and regeneration.

The three muscle tissues

Figure 1 · The three types of muscle

The rest of this chapter concerns skeletal muscle, of which there are over 600 named muscles making up roughly 40–45% of body mass in a healthy adult.

Gross structure and the connective tissue hierarchy

Figure 2 · Levels of skeletal muscle structure

A muscle is a composite of contractile cells and a continuous connective tissue framework. The framework is not packing material: it transmits force, stores elastic energy, carries the vessels and nerves, and determines the muscle’s passive properties.

All three layers converge distally and continue into the tendon (or aponeurosis, its flattened form), which inserts into bone through a fibrous or fibrocartilaginous enthesis, anchored by Sharpey’s fibres.

Clinical relevance. The muscle–tendon junction is the commonest site of strain injury, because it is the stiffness transition where strain concentrates. The classic examples — the long head of biceps femoris, the medial head of gastrocnemius, rectus femoris — are all biarticular, superficial, with a high proportion of type II fibres and a long intramuscular tendon. Those four features together define the muscles you should expect to strain.

Muscle attachments

• Origin (conventionally the proximal, less mobile attachment) and insertion (distal, more mobile). The distinction is functional rather than absolute: in a closed-chain movement the insertion is often fixed and the origin moves. Standing up from a chair, the hamstrings work with the “insertion” (tibia) fixed and the “origin” (ischium) moving.
• Fleshy attachment: muscle fibres attach almost directly to periosteum over a wide area; produces a smooth bone surface.
• Tendinous attachment: concentrates force onto a small area; produces a rough tuberosity or crest — which is what Chapter 1 taught you to read.

Fibre architecture: the force–excursion trade-off

Figure 3 · Fascicular arrangements

The single most useful architectural concept is physiological cross-sectional area (PCSA) — the cross-sectional area measured perpendicular to the fibres, not to the muscle. Force is proportional to PCSA (roughly 20–35 N/cm² of specific tension). Excursion and velocity are proportional to fibre length. A muscle of fixed volume must trade one against the other.

Pennation angle costs force: only the component along the tendon (cos θ) is transmitted, so at 30° pennation about 87% of fibre force reaches the tendon. The gain in PCSA from packing more, shorter fibres into the same volume far outweighs this loss. Pennation angle increases with hypertrophy, which is why ultrasound-measured pennation is used as a training-adaptation marker.

Worked comparison. Sartorius and gluteus maximus have comparable volumes, but sartorius has very long parallel fibres and a small PCSA (large excursion, small force), while gluteus maximus has short fibres and a huge PCSA (small excursion, enormous force). The architecture is a direct statement of function: sartorius positions the limb through range; gluteus maximus extends the hip against body weight.

The muscle fibre and the sarcomere

5.5.1 The fibre

A single multinucleated cell, 10–100 µm in diameter, formed by fusion of myoblasts. Key components:

• Sarcolemma: the plasma membrane, with invaginations forming transverse (T) tubules, which conduct the action potential into the fibre’s depth.
• Sarcoplasmic reticulum (SR): modified smooth endoplasmic reticulum forming a sleeve around each myofibril, with expanded terminal cisternae flanking each T-tubule to form a triad at the A–I junction. Two triads per sarcomere. The SR stores calcium bound to calsequestrin and pumps it back with SERCA.
• Myofibrils: 1–2 µm cylinders of contractile protein running the fibre’s length, made of serially repeating sarcomeres.
• Sarcoplasm: containing glycogen granules, myoglobin (oxygen store, gives red muscle its colour), and mitochondria.
• Peripheral nuclei, each governing a myonuclear domain of surrounding cytoplasm.

5.5.2 The sarcomere

The contractile unit, ~2.0–2.5 µm at resting length, running Z line to Z line.

The single most examined fact: during contraction, the A band length does not change; the I band and H zone shorten. Filaments slide, they do not shorten — the sliding filament theory (Huxley and Huxley, 1954).

5.5.3 The proteins

Excitation–contraction coupling

Learn this as a sequence; it is asked in every examination and it explains several drugs and diseases.

• Action potential arrives at the motor nerve terminal.
• Voltage-gated Ca²⁺ channels open; calcium entry triggers exocytosis of acetylcholine from synaptic vesicles.
• ACh crosses the synaptic cleft and binds nicotinic ACh receptors on the junctional folds of the motor end plate.
• Cation influx produces an end-plate potential, which reaches threshold and generates a fibre action potential. (ACh is then hydrolysed by acetylcholinesterase.)
• The action potential propagates along the sarcolemma and down the T-tubules.
• Dihydropyridine receptors (voltage sensors in the T-tubule) are mechanically coupled to ryanodine receptors in the SR terminal cisternae, which open.
• Ca²⁺ floods into the sarcoplasm and binds troponin C.
• Troponin changes conformation, tropomyosin shifts, and the myosin-binding sites on actin are exposed.
• Cross-bridge cycling begins.
• Relaxation: ACh is degraded, the AP ceases, and SERCA pumps Ca²⁺ back into the SR against a gradient — an ATP-dependent process. Tropomyosin re-covers the binding sites.

The cross-bridge cycle

ATP is therefore required for both contraction and relaxation. Two clinical facts follow immediately: rigor mortis (no ATP → no detachment) and the fact that a muscle in energy crisis becomes stiff, not floppy.

Pathology of the neuromuscular junction

Mechanical properties

5.7.1 Length–tension relationship

Active tension depends on the degree of overlap between thick and thin filaments:

• At optimal length (L₀, ~2.0–2.2 µm sarcomere length), the maximum number of cross-bridges can form → peak active force.
• Shortened: thin filaments overlap each other and collide with the M line; cross-bridge formation is obstructed → force falls (active insufficiency at the whole-muscle level).
• Lengthened: overlap decreases → fewer cross-bridges → force falls, reaching zero at ~3.6 µm.

Passive tension comes from the connective tissue framework and, principally, from titin. It is negligible at short lengths and rises steeply — exponentially — beyond resting length.

Total tension = active + passive. This is why a muscle can generate high total force at long lengths despite low active force, and why eccentric work at long muscle lengths (Nordic curls, Copenhagen adductor exercise) is such a potent stimulus: it loads both the contractile and the elastic elements, and it increases fascicle length by adding sarcomeres in series — an adaptation that shifts the whole curve rightward and is protective against strain injury.

5.7.2 Force–velocity relationship

Hill’s classic relationship:

• Concentric: as shortening velocity increases, force falls hyperbolically (fewer cross-bridges are attached at any instant). Maximum velocity occurs at zero load; maximum force at zero velocity.
• Isometric: force is higher than at any concentric velocity.
• Eccentric: as lengthening velocity increases, force rises, plateauing at roughly 1.2–1.8 × maximum isometric force.

The eccentric plateau is explained by forcible detachment of cross-bridges under strain plus the contribution of titin, which stiffens on calcium binding. It has three clinical consequences:

• eccentric work is the strongest and least metabolically costly mode
• it generates the greatest mechanical stress and hence the most microdamage and DOMS
• and it is the mode most implicated in strain injury (the muscle is decelerating a load beyond its capacity, at length, at speed)

5.7.3 The stretch–shortening cycle

An eccentric contraction immediately followed by a concentric one produces more force than the concentric contraction alone, through: elastic energy storage in tendon and titin, stretch reflex facilitation, and the time available to build active state. It is the basis of walking, running, jumping and every plyometric exercise. The amplification is lost if the coupling time between phases exceeds roughly a second.

The motor unit

Figure 4 · The motor unit

A motor unit = one alpha motor neuron + all the muscle fibres it innervates. It is the smallest functional unit of voluntary movement; every fibre in a unit is of the same type and contracts together, all-or-none.

Innervation ratio

Low innervation ratio = fine control. High innervation ratio = gross power. The motor unit territory is scattered, not clustered: the fibres of a unit are distributed across the muscle cross-section, interdigitating with other units, which produces smooth force rather than lumpy local contraction.

Force gradation

The nervous system increases force by two mechanisms operating together:

• Recruitment, governed by the size principle (Henneman): motor units are recruited in order of increasing motor neuron size — small, slow, fatigue-resistant type I units first, then larger type IIa, then largest type IIx. They de-recruit in reverse order. The principle is highly robust and holds regardless of the task.
• Rate coding: increasing the firing frequency of already-recruited units, producing summation and, at high frequencies, fused tetanus.

Most muscles complete recruitment at ~50–85% of maximum voluntary contraction, above which additional force comes from rate coding alone; the hand muscles complete recruitment much earlier.

Why the size principle governs your exercise prescription

Type II fibres are recruited only at high force or high velocity demands. It follows that:

• Light, slow, low-effort exercise trains type I units almost exclusively
• To train type II units you need either heavy load, or high velocity, or sustained effort to the point where fatigue forces recruitment of the higher-threshold units (which is why sets taken close to failure with lighter loads can produce comparable hypertrophy to heavy loads, and why blood-flow-restriction training works at 20–30% of 1RM)
• In the frail elderly, in whom type II fibres atrophy preferentially, power training (fast concentric intent) is superior to slow strength training for functional outcomes such as chair rise and stair climbing

Neural adaptation

The first 4–6 weeks of a strength programme produce large strength gains with minimal hypertrophy. These are neural: increased motor unit recruitment, increased firing rate, reduced antagonist co-contraction, improved intermuscular coordination, and reduced neural inhibition. This is directly clinically useful — it explains why an early post-operative patient gains strength quickly, and why cross-education (training the uninjured limb produces measurable strength gain in the immobilised contralateral limb, typically 5–15%) is a legitimate intervention when one side cannot be loaded.

Fibre types

Figure 5 · Skeletal muscle fibre types

Human muscle is mixed, in proportions that vary by muscle, by individual and to a limited extent with training. Fibre-type conversion within the type II family (IIx ⇄ IIa) is readily achieved with training; I ⇄ II conversion is limited and requires extreme stimuli such as prolonged electrical stimulation or spinal cord injury.

Disuse and ageing. Both cause preferential type II atrophy. Sarcopenia involves loss of motor units (particularly the large, fast ones), denervation of type II fibres with partial reinnervation by slow motor neurons, fibre-type grouping, and a fall in muscle quality. The consequence is that older adults lose power faster than strength, and strength faster than mass — which is why power, not just mass, should be the training target.

Muscle receptors and reflexes

Gamma motor neurons innervate the contractile poles of intrafusal fibres. Their function is alpha–gamma co-activation: as the muscle shortens under alpha drive, gamma drive keeps the spindle taut so it continues to signal. Without this the spindle would fall slack and go silent during contraction.

The clinical uses of these two receptors

• Stretch reflex — the basis of tendon jerk testing, and of hyperreflexia and clonus in upper motor neuron lesions (loss of descending inhibition).
• Autogenic inhibition — the theoretical basis of contract–relax / hold–relax PNF stretching, though modern evidence attributes most of the acute range gain to increased stretch tolerance rather than to reflex inhibition or true tissue lengthening.
• Reciprocal inhibition — the basis of the agonist-contract stretching technique and of much of PNF.
• Spindle sensitivity is why rapid stretch facilitates and prolonged slow stretch or sustained pressure inhibits — a principle used throughout neurological facilitation and inhibition techniques.

Blood supply, energy and fatigue

Blood supply enters at the neurovascular hilum and forms an extensive capillary bed running longitudinally in the endomysium, with 3–5 capillaries per type I fibre. Muscle blood flow rises 20-fold or more during exercise. Because intramuscular pressure occludes flow during contraction, sustained isometric contraction above roughly 15–20% MVC progressively restricts its own perfusion — which is why isometric holds fatigue disproportionately and why they raise blood pressure through the pressor reflex.

Energy systems, in order of onset:

Fatigue is not lactic acid. Contemporary accounts distinguish:

• Peripheral fatigue: accumulation of inorganic phosphate (impairing cross-bridge force and SR calcium release), reduced SR Ca²⁺ release, glycogen depletion, and altered excitation–contraction coupling. Lactate is a fuel and a signalling molecule, and lactic acidosis is largely exonerated as the cause
• Central fatigue: a decline in voluntary drive from the CNS, influenced by afferent feedback from group III/IV endings, and by perception and motivation

Adaptation, damage and regeneration

Hypertrophy

Mechanical tension is the principal driver, acting through mechanotransduction → mTOR pathway → increased myofibrillar protein synthesis, with metabolic stress and muscle damage as secondary contributors. Adaptation includes increased myofibril number and size, increased pennation angle, and satellite cell donation of new myonuclei to maintain the myonuclear domain.

Myonuclear permanence (“muscle memory”): nuclei acquired during hypertrophy appear to be retained through subsequent atrophy, which provides a cellular explanation for the rapidity with which previously trained muscle regains size. This is a directly usable message for a patient facing a long immobilisation.

Atrophy

Driven by the ubiquitin–proteasome system (atrogin-1/MAFbx and MuRF1) and autophagy. Rates are sobering: quadriceps cross-sectional area falls measurably within a week of immobilisation, and disuse atrophy is greatest when the muscle is immobilised in a shortened position — which also causes loss of sarcomeres in series and true contracture. Immobilising in a lengthened position preserves both length and mass far better, and this should guide splinting and positioning decisions.

Exercise-induced muscle damage and DOMS

Delayed-onset muscle soreness follows unaccustomed, predominantly eccentric work: onset 6–12 h, peak 24–72 h, resolution by 5–7 days. Mechanism: sarcomere strain and popping, Z-line streaming, membrane and excitation–contraction coupling disruption, calcium influx and a secondary inflammatory response sensitising group III/IV afferents. Creatine kinase rises and peaks later; strength deficits and reduced range accompany it.

The repeated-bout effect is the striking protective adaptation: a single bout of eccentric work confers substantial protection against damage from a repeat bout for weeks. It is why load should be introduced gradually and why an early sub-maximal eccentric exposure is a legitimate way to prepare an athlete.

DOMS is not a marker of a good session, nor an injury. Its clinical value is as a warning that load was progressed too fast.

Regeneration and repair

Satellite cells (Pax7-positive), quiescent between basal lamina and sarcolemma, activate after injury, proliferate as myoblasts, and either fuse with damaged fibres, fuse into new myotubes, or return to quiescence to replenish the pool. Regeneration is effective when the basal lamina scaffold survives; where it is destroyed (complete tear, deep laceration, severe contusion), fibrous scar forms instead, with reduced compliance and a predisposition to re-injury.

Muscle strain grading and the practical implication:

Rehabilitation principles: brief protection, then early controlled loading (which orients regenerating fibres and limits scar), progressive eccentric work at long muscle lengths, restoration of fascicle length, and criteria-based rather than time-based return to sport. Prolonged immobilisation produces a larger, denser, more disorganised scar.

Where students consistently go wrong

• Saying the A band shortens. It does not. I band and H zone do.
• Forgetting that ATP is needed for relaxation. Hence rigor mortis.
• Confusing spindle and GTO. Spindle = parallel, length. GTO = series, tension.
• Reversing the size principle. Small, slow units first — always.
• Assuming light exercise trains type II fibres. It does not unless taken near failure.
• Thinking lactic acid causes fatigue or DOMS. Neither is true.
• Confusing muscle cross-sectional area with PCSA. Force follows PCSA, measured perpendicular to the fibres.
• Immobilising a muscle in a shortened position when a lengthened position preserves sarcomere number and mass.
• Treating DOMS as a goal. It is a warning about load progression.
• Attributing all PNF stretch gains to autogenic inhibition. Most acute gain is increased stretch tolerance.

Check yourself

15 questions on this chapter. Tap one to see the answer and the reasoning.

Quick review

Further reading

Chapter 5 of 24 · Human Anatomy · Physiotherapist India Next: Chapter 6 — How Muscles Work Together: agonists and fixators, contraction types, levers, and the two insufficiencies.

Reviewed by the Physiotherapist India Team. · Human Anatomy contents