lihassäätelyn

Lihassäätely refers to the coordinated control of muscle contraction and relaxation in animals, an essential physiological process that enables movement, posture, and various involuntary functions such as breathing and heart pumping. The primary mechanism of lihassäätely is excitation‑contraction coupling, where a neural impulse travels along a motor neuron, reaches the neuromuscular junction, and triggers the release of neurotransmitter acetylcholine. This signal rapidly depolarizes the sarcolemma (muscle cell membrane), opening voltage‑gated L‑type calcium channels (DHPR) in the transverse tubules. The depolarization induces calcium release from the sarcoplasmic reticulum via ryanodine receptors, raising cytosolic calcium concentration.

Calcium binds to troponin C on the thin filament, causing tropomyosin to shift and expose the myosin‑binding sites on actin. Cross‑bridge cycling between myosin heads and actin filaments generates the sliding motion that shortens the sarcomere and produces force. Contraction ends when calcium is actively pumped back into the sarcoplasmic reticulum by SERCA pumps and extruded from the cell via the sodium‑calcium exchanger and plasma membrane Ca²⁺‑ATPase, lowering intracellular calcium and allowing the muscle to relax.

Lihassäätely involves multiple regulatory layers: neural input (motor units, firing frequency), hormonal modulation (epinephrine, thyroid hormones), metabolic status (ATP, lactate), and intrinsic muscular properties (fiber type, myosin heavy‑chain isoforms). Imbalances or mutations affecting any of these components can lead to disorders such as muscular dystrophies, myotonic disorders, or acute conditions like rhabdomyolysis. Current research explores gene therapy, pharmacological modulation of calcium handling, and exercise‑based rehabilitation to restore normal lihassäätely in disease states.