Final answer:
The true statement about cardiac muscle contraction is that calcium influx through L-type channels is necessary for opening RyR on the SR membrane, which in turn releases more calcium that binds to troponin to facilitate contraction. ATP binds to myosin, not actin, during muscle contraction.
Step-by-step explanation:
The statement that is true regarding cardiac muscle contraction is that the influx of calcium through L-type calcium channels is required to open RyR on the SR membrane. The contraction of cardiac muscle involves a complex interaction of ions and molecules. As an action potential travels through the heart muscle, it triggers the opening of L-type calcium channels.
The influx of calcium through these channels then prompts the release of more calcium from the sarcoplasmic reticulum (SR) via ryanodine receptors (RyRs). These calcium ions then bind to the regulatory protein troponin, enabling the contraction of the muscle. Moreover, it is crucial to note that ATP is required for muscle contraction; ATP binds to myosin, not actin, and allows myosin to detach from actin after the power stroke.
Furthermore, the influx of calcium ions is responsible for the characteristic plateau phase of the cardiac action potential, which is critical for preventing tetanus (a sustained contraction) in cardiac muscle tissue. This plateau phase is due to the prolonged opening of slow L-type calcium channels, allowing the Ca2+ to enter the cell, which sustains the depolarization.