Musculoskeletal System

Sliding Filament Mechanism

• Sequence: ACh at the neuromuscular junction depolarizes the end plate; the signal runs down T-tubules, DHP receptors mechanically open ryanodine receptors, and SR calcium floods the cytosol. $Ca^{2+}$ binds troponin C, tropomyosin shifts, and myosin heads cycle: bind, power stroke, ATP-dependent detachment, re-cocking.
• Relaxation requires the SERCA pump to return $Ca^{2+}$ to the SR — ATP is spent both to detach myosin and to relax, which is why rigor mortis locks cross-bridges.
• During contraction the A band stays constant while the I band and H zone shrink; force follows the length-tension relationship because overlap sets the number of available cross-bridges.

Muscle and Fiber Types

• Skeletal muscle is striated, voluntary, multinucleate; cardiac muscle uses gap junctions and calcium-induced calcium release (so it needs extracellular $Ca^{2+}$); smooth muscle contracts via calmodulin and MLCK, not troponin. Type I slow-oxidative fibers resist fatigue; type IIx fast-glycolytic fibers sprint and tire.

Bone Remodeling

• Osteoblasts deposit hydroxyapatite; osteoclasts resorb bone; osteocytes sense load. PTH raises blood calcium via RANKL-driven osteoclast activity, calcitonin restrains it, and calcitriol boosts intestinal absorption.

Key Takeaways

• Trace excitation-contraction coupling step by step, including both ATP costs.
• Only the I band and H zone shorten — the A band never does.
• Cardiac contraction depends on extracellular calcium; skeletal does not.
• PTH, calcitonin, and vitamin D form the calcium control triangle.