Final answer:
Calcium ions (Ca²+) are released from the sarcoplasmic reticulum into the sarcoplasm to initiate skeletal muscle contraction. This process involves the binding of the neurotransmitter acetylcholine (ACh) to receptors on the muscle fiber and the subsequent release of calcium ions, which trigger the sliding of actin and myosin filaments. Muscle contraction is sustained by ATP.
Step-by-step explanation:
The substance released from the sarcoplasmic reticulum into the sarcoplasm to initiate skeletal muscle contraction is calcium ions (Ca²+).
When a motor neuron releases the neurotransmitter acetylcholine (ACh) at the neuromuscular junction, it triggers an action potential that travels down the T-tubules of the muscle fiber. This depolarization of the membrane causes the release of calcium ions from storage in the sarcoplasmic reticulum (SR). The calcium ions then bind to actin, shifting the position of the tropomyosin and exposing the myosin binding sites on actin, which initiates muscle contraction.
The process of muscle contraction is sustained by adenosine triphosphate (ATP) and involves the cross-bridging of myosin heads with actin filaments, resulting in the sliding of the thin filaments by thick filaments. Ultimately, the sarcomeres, myofibrils, and muscle fibers shorten to produce movement.
The substance released from the sarcoplasmic reticulum into the sarcoplasm to initiate skeletal muscle contraction is calcium ions (Ca2+). Here's a brief overview of the process:
Acetylcholine released from the axon terminal binds to receptors on the sarcolemma.
An action potential is generated and travels down the T tubule.
Ca2+ is released from the sarcoplasmic reticulum in response to the change in voltage.
When the calcium ions are released, they bind to troponin, causing a conformational change that shifts tropomyosin away from myosin binding sites on the actin filaments. This action exposes the binding sites, allowing for the interaction between actin and myosin that results in muscle contraction, powered by ATP.