The correct answer is b. Ca2+.

Here's the step by step explanation:

1. An action potential arrives at the axon terminal of a motor neuron, which triggers the release of acetylcholine (ACh) into the synaptic cleft.

2. ACh binds to receptors on the sarcolemma (the cell membrane of a muscle cell), causing an influx of Na+ ions into the muscle cell and generating an action potential that spreads across the entire sarcolemma and along the T-tubules (transverse tubules).

3. The action potential traveling along the T-tubules triggers the release of Ca2+ ions from the sarcoplasmic reticulum, a specialized type of endoplasmic reticulum in muscle cells.

4. The released Ca2+ ions bind to troponin, a protein found on actin filaments in muscle cells. This binding causes a conformational change in the troponin-tropomyosin complex, exposing the myosin-binding sites on actin.

5. Myosin heads bind to these exposed sites on actin, forming cross-bridges. The myosin heads then undergo a power stroke, pulling the actin filaments towards the center of the sarcomere and causing muscle contraction.

6. After the power stroke, ATP binds to the myosin head, causing it to detach from actin. The ATP is then hydrolyzed, and the energy released is used to re-cock the myosin head, ready for another power stroke.

7. This process continues as long as Ca2+ ions are present. When the action potential ends, Ca2+ ions are pumped back into the sarcoplasmic reticulum, and the muscle relaxes.

So, in response to action potentials arriving along the transverse tubules, the sarcoplasmic reticulum releases Ca2+ ions.

Question

The correct answer is b. Ca2+.

Here's the step by step explanation:

1. An action potential arrives at the axon terminal of a motor neuron, which triggers the release of acetylcholine (ACh) into the synaptic cleft.

2. ACh binds to receptors on the sarcolemma (the cell membrane of a muscle cell), causing an influx of Na+ ions into the muscle cell and generating an action potential that spreads across the entire sarcolemma and along the T-tubules (transverse tubules).

3. The action potential traveling along the T-tubules triggers the release of Ca2+ ions from the sarcoplasmic reticulum, a specialized type of endoplasmic reticulum in muscle cells.

4. The released Ca2+ ions bind to troponin, a protein found on actin filaments in muscle cells. This binding causes a conformational change in the troponin-tropomyosin complex, exposing the myosin-binding sites on actin.

5. Myosin heads bind to these exposed sites on actin, forming cross-bridges. The myosin heads then undergo a power stroke, pulling the actin filaments towards the center of the sarcomere and causing muscle contraction.

6. After the power stroke, ATP binds to the myosin head, causing it to detach from actin. The ATP is then hydrolyzed, and the energy released is used to re-cock the myosin head, ready for another power stroke.

7. This process continues as long as Ca2+ ions are present. When the action potential ends, Ca2+ ions are pumped back into the sarcoplasmic reticulum, and the muscle relaxes.

So, in response to action potentials arriving along the transverse tubules, the sarcoplasmic reticulum releases Ca2+ ions.

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