Muscle Structure and Function

There are three muscle types, skeletal, cardiac and smooth, and this page concerns skeletal muscle, the voluntary muscle attached to the skeleton. It is built in a clear hierarchy. A whole muscle is wrapped in a connective tissue sheath called the epimysium and divided into bundles of fibres called fascicles, each wrapped in perimysium, and within each fascicle every individual muscle fibre is surrounded by endomysium. These sheaths carry the vessels and nerves and merge at the ends of the muscle into the tendon, and the junction between muscle and tendon, the myotendinous junction, together with the myoaponeurotic junctions within the muscle, is a common interface for strain injury.

A muscle fibre is a single, long, multinucleated cell, bounded by a membrane called the sarcolemma and packed with rod-like myofibrils. The membrane dips into the fibre as a network of transverse (T) tubules, which run close to the sarcoplasmic reticulum, the internal store of calcium. Each myofibril is a chain of sarcomeres, the basic contractile unit, and it is the regular overlap of filaments within them that gives skeletal muscle its striped, or striated, appearance. Within a sarcomere, thin filaments of actin and thick filaments of myosin interdigitate: the sarcomere runs between two Z-discs that anchor the actin, the myosin is held at the central M-line, and a giant elastic protein, titin, runs from the Z-disc to the M-line to provide passive tension and keep the filaments aligned.

A contraction is generated by the filaments sliding past one another. In the sliding filament model, myosin heads form cross-bridges with actin and, powered by adenosine triphosphate (ATP), swivel to pull the actin filaments towards the centre of the sarcomere, shortening it without the filaments themselves changing length. Each cross-bridge attaches, pulls, detaches and re-cocks in a repeating cycle, and the force produced depends on how many cross-bridges are active and on the degree of filament overlap, which is why muscle has an optimal length for generating force.

Contraction is switched on by the nervous system. A motor nerve meets the fibre at the neuromuscular junction (NMJ), where acetylcholine triggers an electrical impulse that sweeps along the sarcolemma and down the T-tubules, releasing calcium from the sarcoplasmic reticulum. The calcium binds troponin, which moves tropomyosin off the binding sites on actin so the cross-bridges can form; when the signal stops, calcium is pumped back and the muscle relaxes. A motor neuron together with all the fibres it supplies forms a motor unit, and force is graded both by recruiting units from small to large and by firing them faster. Fibres differ in type: type I fibres are slow, fatigue-resistant and suited to endurance, while the faster, more powerful type II fibres generate more force but tire sooner. Contractions are concentric when the muscle shortens, isometric when its length is held, and eccentric when it lengthens under load, as in controlling a descent, with eccentric contractions generating the highest forces.

Muscle is highly adaptable, remodelling to match the demands placed on it. Resistance training makes muscle hypertrophy, chiefly through an increase in muscle protein synthesis that enlarges the existing fibres, supported by satellite cells, the resident stem cells that also drive repair after injury. Some of the early gains in strength come from the nervous system learning to recruit and coordinate motor units more effectively, before much change in size occurs. Eccentric loading is a particularly strong stimulus for adaptation, but unaccustomed eccentric exercise also produces the transient microscopic damage felt as delayed onset muscle soreness a day or two later, which settles on its own. Endurance training shifts muscle towards a more fatigue-resistant, aerobic profile, with more mitochondria and capillaries, whereas disuse has the opposite effect, causing muscle to waste and weaken. The balance of fibre types is partly inherited but is also influenced by training, so sustained endurance work and heavy power work nudge a muscle in different directions over time.

This physiology runs through everyday sports medicine. Because the myotendinous junction and the myoaponeurotic junctions within the muscle are common injury interfaces, muscle strains tend to occur at or near them, typically during a forceful eccentric effort, and most often in the hamstrings, calf or quadriceps. The transient damage of unaccustomed eccentric exercise underlies delayed onset muscle soreness, which is distinct from a structural tear, while very intense or crushing exertion can rarely cause rhabdomyolysis, a breakdown of muscle that needs urgent care. Because muscle adapts to load, individualised progressive loading, including eccentric and high-speed work where appropriate, is central to rehabilitating these injuries and reducing their risk, with the strongest prevention evidence for hamstring programmes; structured loading rather than prolonged rest is what rebuilds the muscle.

• •Skeletal muscle hierarchy: muscle, fascicle, fibre, myofibril, sarcomere.
• •The sarcomere runs between Z-discs; contraction shortens it by sliding actin over myosin.
• •Contraction needs calcium, which moves tropomyosin off actin, and adenosine triphosphate to power the cross-bridges.
• •Type I fibres are slow and fatigue-resistant; type II fibres are fast and powerful.
• •Eccentric contraction is lengthening under load and generates high force.
• •Strains occur most often at the myotendinous junction, commonly in the hamstrings.