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, wrapped in a connective tissue sheath called the epimysium, is 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 merge at the ends of the muscle into the tendon, and the junction between muscle and tendon, the myotendinous junction, is where many strains occur.

A muscle fibre is a single, long, multinucleated cell packed with myofibrils, and each myofibril is a chain of sarcomeres, the basic contractile unit. Within a sarcomere, thin filaments of actin and thick filaments of myosin overlap in a regular pattern that gives skeletal muscle its striped appearance. The sarcomere runs between two Z-discs, which anchor the actin, with the myosin held at the central M-line, and a giant elastic protein, titin, provides passive tension and stability. Contraction follows the sliding filament model: myosin heads form cross-bridges with actin and, powered by adenosine triphosphate (ATP), pull the actin filaments towards the centre, shortening the sarcomere without the filaments themselves changing length.

Contraction is triggered by the nervous system. A motor nerve meets the fibre at the neuromuscular junction (NMJ), where acetylcholine sets off an electrical impulse that travels along the membrane and into the fibre through T-tubules, releasing calcium from the sarcoplasmic reticulum. Calcium binds troponin, moving tropomyosin off the actin binding sites so the cross-bridges can form. A motor neuron and the fibres it supplies form a motor unit, and units are recruited from small to large as more force is needed. Fibres differ in type: type I fibres are slow, fatigue-resistant and suited to endurance, while type II fibres are faster and more powerful 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; eccentric work generates high force and is central to both muscle strains and rehabilitation. Muscle adapts to how it is used, hypertrophying with resistance training mainly through increased muscle protein synthesis, with satellite cells, the resident stem cells, contributing to repair and some of this growth, and wasting with disuse.

Muscle problems reach the SEM clinic in familiar ways. A muscle strain, a tear of fibres often at the myotendinous junction, typically follows a sudden forceful or eccentric effort, giving sharp pain, loss of power and sometimes bruising, most often in the hamstrings, calf or quadriceps. Delayed onset muscle soreness (DOMS), the stiffness and tenderness a day or two after unaccustomed, particularly eccentric, exercise, reflects transient exercise-induced muscle damage rather than a structural strain, and settles on its own. Cramp, atrophy from disuse, and weakness from a neurological cause also present. The history, the mechanism and the pattern of weakness point to the underlying problem.

Muscle is assessed mainly clinically, by testing strength, power and range and by the pattern of any weakness. Ultrasound and magnetic resonance imaging (MRI) are used selectively, to show the site and extent of a muscle tear when this will change management or return-to-sport decisions; MRI defines the anatomy and extent, but the imaging grade alone should not dictate prognosis or return to sport. A raised blood creatine kinase reflects muscle damage and is markedly high in rhabdomyolysis; suspected rhabdomyolysis, which can occur without dark urine, needs urgent assessment with creatine kinase, renal function, electrolytes and urine testing, alongside attention to fluid balance. Where weakness suggests a nerve or muscle disease rather than a simple injury, nerve conduction studies and electromyography help localise the problem. Imaging is not needed for straightforward low-grade strains or for delayed onset muscle soreness.

Managing muscle rests on load. An acute strain is settled with a short period of relative rest and protection, then early, progressive loading, since prolonged rest weakens muscle and delays recovery. Pain-guided movement and strengthening are reintroduced as symptoms allow, building towards the eccentric and high-speed demands of the sport. Strength and conditioning underpins both recovery and prevention, with progressive resistance work to build muscle and eccentric strengthening to protect against strains. Adequate protein and overall energy support muscle repair and growth. A high-grade or complete tear, or a strain that fails to progress, warrants specialist assessment, and rhabdomyolysis is managed acutely in its own right.

Rehabilitation rebuilds muscle capacity in stages. Loading starts gently and progresses through range, then adds resistance, speed and eccentric work, matching the demands the muscle will face on return. Eccentric strengthening is a mainstay for muscles prone to strain, the hamstrings in particular; programmes including the Nordic hamstring exercise reduce hamstring injury and may increase fascicle length and eccentric strength. Progress is guided by pain, strength and function rather than time alone, and return to sport follows restored strength, full range and the ability to tolerate sport-specific, high-speed loading.

• •Programmes including the Nordic hamstring exercise reduce hamstring injury incidence and may increase fascicle length and eccentric strength.
• •Progressive resistance training builds muscle size and strength and is the basis of both rehabilitation and conditioning.
• •Early, progressive loading after a muscle strain gives better outcomes than prolonged rest.
• •Muscle regenerates through satellite cells, so structured loading supports repair as well as adaptation.
• •Markedly raised creatine kinase with dark urine after extreme exertion points to rhabdomyolysis, which needs urgent care.

• •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.