USA Biology Olympiad (USABO) 2025 – 400 Free Practice Questions to Pass the Exam

Skeletal muscle relaxation after contraction is primarily aided by the breakdown of acetylcholine in the neuromuscular junction by acetylcholinesterase. During muscle contraction, acetylcholine is released from the motor neuron into the synapse, leading to muscle depolarization and subsequent contraction. For the muscle to relax, it is essential to terminate this signal.

The enzyme acetylcholinesterase plays a crucial role by hydrolyzing acetylcholine into acetic acid and choline, thereby reducing the concentration of acetylcholine in the synaptic cleft. This cessation of acetylcholine's action allows the muscle cell membrane to repolarize, ultimately leading to muscle relaxation.

In contrast, the other processes mentioned do not directly contribute to the relaxation phase. While calcium ions must be removed from the cytoplasm to facilitate relaxation, this occurs as a consequence of the action initiated by acetylcholinesterase and not through calcium buildup. Additionally, an increase in acetylcholine synthesis would promote continued muscle contraction rather than relaxation. Lastly, potassium influx is involved in repolarization but does not serve as a primary mechanism for muscle relaxation itself. Thus, the degradation of acetylcholine by acetylcholinesterase is the key factor that promotes relaxation