Sarcology II

Weak synaptic transmission reduces acetylcholine release at the neuromuscular junction, limiting action potential propagation in muscle fibers. This prevents sufficient calcium release needed for actin-myosin cross-bridge formation, weakening muscle contractions.

Isometric exercises can lead to muscle hypertrophy by increasing the cross-sectional area of muscle fibers, particularly in response to the constant tension applied, which results in an increase in muscle size and strength.

Myosin ATPase is responsible for breaking down ATP to enable myosin heads to “reset” after each contraction. Reduced ATPase activity would slow down this process, leading to slower muscle contraction and relaxation cycles, impacting movement speed and response.

ATP is essential for muscle contraction and relaxation cycles. During high-intensity exercise, rapid ATP usage can outpace ATP production, leading to immediate fatigue as muscles lack energy for sustained contraction.

Calcium ions are crucial for muscle contraction, as they bind to troponin to shift tropomyosin and allow myosin-actin interactions. A deficiency hinders calcium release, impairing muscle contraction and potentially causing muscle weakness or cramps.

Tropomyosin covers the binding sites on actin filaments, preventing myosin binding in a relaxed muscle. Upon calcium binding, troponin shifts tropomyosin to expose these sites for contraction.

Myofibrils are thread-like structures within muscle cells that contain repeating units of sarcomeres, responsible for muscle contraction.

Type I slow-twitch fibers are fatigue-resistant and suited for endurance activities due to their high aerobic capacity.

A motor unit consists of a motor neuron and all the muscle fibers it innervates, allowing coordinated contraction of the fibers