--- module: 032-01 language: en chapter: 32 title: "Skeletal Muscle, Bone, Joint, and Connective Tissue Physiology" module_title: "Foundations" source_sha256: eab19f101b93674e8b3da2fa8c48b8f46de3f7564f9123c230dff969b2ed78a3 --- # Musculoskeletal foundations ## Orientation ### Converts chemical energy into transmitted force ### Supports organs, stores mineral, houses marrow ### Disease from contractile, matrix, mineral, nerve failure ## Skeletal-muscle organisation ### Muscle, fascicle, fibre, myofibril, sarcomere ### Thin filaments: actin, tropomyosin, troponin ### Titin centres thick filaments, passive elasticity ### Actin slides past myosin; filaments keep length #### Adenosine triphosphate binding releases, hydrolysis recocks #### Without adenosine triphosphate, cross-bridges stay attached ### Force depends on filament overlap ### Parallel fibres: excursion and speed ### Pennate fibres: more material, greater force #### Physiological cross-sectional area predicts force ### Tendon compliance stores elastic energy ## Excitation-contraction coupling ### Acetylcholine at the neuromuscular junction ### Action potential along sarcolemma and T tubules #### Ryanodine receptors release calcium #### Calcium binds troponin C, moves tropomyosin ### Calcium pumps permit relaxation ### Repeated stimuli summate force #### Rapid stimulation produces tetanus ### Recruitment and firing rate set whole-muscle force ## Fibre types and metabolism ### Slow oxidative: economical, fatigue resistant ### Fast oxidative-glycolytic: power, moderate endurance ### Fast glycolytic: high power, rapid fatigue ### Phosphocreatine rapidly buffers adenosine triphosphate ### Oxidative phosphorylation powers sustained work ### Lactate is fuel and gluconeogenic substrate ### Fatigue: metabolic, neural, central, thermal causes ### Delayed soreness is microinjury, not lactate ## Mechanical actions and adaptation ### Concentric, eccentric, isometric contraction ### Moment arm and angle change joint torque ### Resistance: neural first, then hypertrophy ### Endurance: mitochondria, enzymes, capillaries ### Recovery needs sleep, energy, protein, time ### Disuse rapidly weakens muscle, tendon, bone #### Early progressive loading when safe ### Ageing loses motor units, training still works ## Bone composition and architecture ### Collagen gives toughness, mineral stiffness ### Cortical shells, trabecular load-aligned network ### Osteocytes sense strain via canaliculi ### Osteoclasts resorb, coupled to formation ### Hormones, signals, and load regulate turnover ### Strength beyond mass: geometry, quality, falls ## Growth and fracture healing ### Endochondral ossification at growth plates ### Sex steroids accelerate growth, close plates ### Haematoma, soft callus, hard callus, remodelling ### Stability and blood supply are essential #### Motion, infection, smoking impair union ### Primary healing with little callus ## Cartilage and synovial joints ### Collagen resists shear, proteoglycans compression ### Loading expresses fluid, unloading recovers ### Avascular cartilage has limited repair ### Synoviocytes make hyaluronan, clear debris ### Menisci and labra distribute load ### Stability from shape, ligaments, muscle, proprioception #### Laxity invites injury, stiffness concentrates load ### Movement nourishes cartilage ## Tendon, ligament, and matrix ### Tendons transmit force, ligaments constrain ### Toe region, linear region, then failure ### Matrix adapts more slowly than muscle ### Tendinopathy: disordered matrix and load response #### Rest without reloading fails ### Fibroblasts: fibrosis or fragility ### Type one in bone, type two in cartilage ### Flexibility alone is not a syndrome ## Integrated movement and reserve ### Many failures feel like weakness #### Separate force loss from pain, stiffness, instability ### Power declines faster than strength with age #### Critical for falls and rising from a chair ### Load is injury risk and adaptive signal