OPBS Musculoskeletal Biomechanics
Parallel fibred muscles are commonest. They shorten a long way but produce little force.
Pennation raises cross-sectional area and force but reduces excursion. Bipennate is stronger than unipennate.
Muscle fibres are multinucleated, with nuclei at the periphery under the sarcolemma.
Transverse tubules carry the action potential inward. Sarcoplasmic reticulum stores and releases calcium.
Skeletal muscle arises from mesodermal somites. Myoblasts fuse into multinucleated myotubes.
Growth in length adds sarcomeres in series near the myotendinous junction. Sarcomere length stays constant. More on gross structure Fascia lets the muscle slide on neighbouring tissue. A myofibre can run the full length of the muscle and measure many centimetres. The endomysium includes basement membrane, a reticular layer and extracellular matrix around the sarcolemma. Element Made of Anchor Thick filament (A band) Myosin, plus C protein, M protein, titin, creatine kinase M line Thin filament Actin, troponin, tropomyosin Z line Z line proteins Desmin, α-actinin, filamin Not applicable
Troponin subunit Binds or does Troponin C Binds calcium Troponin T Binds tropomyosin Troponin I Inhibits actin myosin interaction
Myosin heads (cross-bridges) bind actin and hydrolyse ATP to slide the filaments.
Tropomyosin blocks myosin binding until calcium binds troponin C. Motor neuron releases acetylcholine. Postsynaptic receptors raise sodium permeability and depolarise the sarcolemma.
Depolarisation runs down T tubules and triggers calcium release from sarcoplasmic reticulum.
Relaxation follows acetylcholine breakdown, repolarisation and calcium pumping back into the reticulum.
A motor unit is one axon and all the fibres it supplies, 10 to 1000 fibres.
Fine control muscles have few fibres per motor unit.
The contractile mechanism has no refractory period, so rapid stimuli summate into tetanus . Contraction Muscle force versus load Length Concentric Greater Shortens Isometric Equal Unchanged Eccentric Smaller Lengthens
Peak tension occurs at resting length, where actin and myosin overlap most.
Force falls away as the fibre shortens or lengthens from resting length.
Hill force velocity curve. Heavier load, slower shortening.
Eccentric contraction makes more force at the same velocity and costs less energy.
Quadriceps work eccentrically at heel strike and concentrically in knee extension. Type Name Size and speed Force Fatigue I Slow oxidative Small, slow Low Resistant IIA Fast oxidative glycolytic Intermediate Intermediate Intermediate IIB Fast glycolytic Large, fastest Highest Most fatigable
Myosin ATPase isoform sets shortening speed.
Smallest motor units (type I) are recruited first, larger type II units for intense effort.
Endurance training raises type I oxidative capacity through mitochondrial density. Resistance training enlarges type II fibres.
Motor learning works mainly through nervous system adaptation. System Duration Detail Creatine phosphate 10 to 20 seconds Creatine kinase regenerates ATP from ADP. Sprinting Anaerobic glycolysis From about 30 seconds Glycogen to lactate, 2 ATP per glucose Aerobic oxidation Beyond about 1 minute Glucose and fatty acids, 32 ATP per glucose
Anaerobic threshold is reached at plasma lactate of about 4 mmol/L, then fatigue comes fast. More on endurance limits The endurance limit, about 370 W in elite athletes, is set by oxygen delivery and aerobic oxidation. Lactate and hydrogen ions lower pH and inhibit the contractile reactions. Muscle held stretched adds sarcomeres over weeks, restoring resting sarcomere length at the new muscle length.
A lengthened muscle peaks at greater length and gives less passive force on stretch.
A muscle kept shortened gives more passive force for the same stretch.
Immobilisation without tension causes more atrophy and force loss than immobilisation under stretch.
Disuse atrophy combines lower protein synthesis with higher protein breakdown.
Sarcopenia affects about 25 percent at 65 to 70 years and 40 percent over 80. Stage Events Degeneration and inflammation Haematoma. Neutrophils first, monocytes from day 1, maturing into macrophages Regeneration 1 to 4 weeks. Satellite cells form myoblasts that fuse with injured fibres Fibrosis Fibrin and fibronectin granulation tissue, then type III, then type I collagen Revascularisation and reinnervation Capillaries for aerobic metabolism, nerve regrowth to stop new fibre atrophy
Strains rupture near the musculotendinous junction. Contusions and lacerations damage tissue at the impact site.
Contraction bands confine necrosis along the fibre. The membrane defect seals within hours.
Satellite cells sit beneath the basal lamina. Mature myofibres are terminally differentiated.
FGF, IGF-1 and hepatocyte growth factor stimulate satellite cells.
Late reruptures occur at the scar to myofibre interface.
Early myotubes have few mitochondria and run on anaerobic metabolism. RICE limits bleeding. Brief immobilisation limits retraction, haematoma and scar size.
Immobilisation beyond a few days harms regeneration. Mobilise at about 3 to 5 days.
COX-2 inhibitors delayed regeneration and raised TGF-β1 and fibrosis in mice.
TGF-β1 drives muscle fibrosis. Blockers include decorin, suramin, relaxin, interferon-γ and losartan.
Losartan is an angiotensin II blocker that reduced fibrosis and improved regeneration in mice.
IGF-1 and basic FGF injections improve regeneration in mice but need high repeated doses.
PRP may shorten return to play without long-term benefit. It also carries fibrogenic TGF-β1. More on biological therapies Recombinant growth factors have short half-lives and clear rapidly, explaining the high doses (100 ng per injection in mice). A double blind trial of leukocyte poor PRP found no difference from placebo. Two single blind trials found faster return to sport. Neutralising TGF-β1 within PRP reduced collagen deposition and raised Pax-7 positive satellite cells in animals. Gene therapy targets include MG53, IGF-1 and sonic hedgehog, limited by immune response and cytotoxicity. Muscle-derived stem cells injected at day 4 raised angiogenesis through VEGF and reduced scar in mice. Combinations such as losartan with stem cells or PRP aim at regeneration and fibrosis together. Blood flow restriction training builds strength at low loads, allowing earlier rehabilitation. Twitch duration. About 7.5 ms in fast fibres, 100 ms in slow fibres.Motor unit. 10 to 1000 fibres.ATP yield. 2 anaerobic, 32 aerobic per glucose.Regeneration. 1 to 4 weeks after injury.Troponin C, T, I. Calcium, Tropomyosin, Inhibition.Ten, thirty, sixty. Seconds of phosphocreatine, then glycolysis from 30 seconds, then aerobic after a minute.Type I fibres are small, slow and fatigue resistant, and are recruited first.
Eccentric contraction produces more force with less energy than concentric contraction.
Growth in length adds sarcomeres. Individual sarcomeres do not lengthen permanently.
Neutrophils lead the acute response. Macrophages follow from monocytes.
Type III collagen precedes type I in muscle scar. Related pages. Muscle Tears and Ruptures , Muscles , General Principles of Neuromuscular Disorders
Huard J, Utsunomiya H, Ravuri SK, Philippon MJ. Form and Function of Skeletal Muscle. In. Aaron RK, editor. Orthopaedic Basic Science. Foundations of Clinical Practice. 5th ed. Philadelphia, Wolters Kluwer, 2021.
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Reviewed by Professor Phong Tran , Head of Orthopaedic Surgery, Western Health. Last updated 17 October 2026.
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