Answer: Length-dependent activation of cardiac myofilaments: increased stretch exposes more troponin C binding sites and improves actin-myosin overlap.
- A Autonomic neural control of heart rate acting via vagal and sympathetic input to the SA node rather than any change in the intrinsic stretch-tension relationship of cardiac muscle fibres
- B Length-dependent activation of cardiac myofilaments: increased stretch exposes more troponin C binding sites and improves actin-myosin overlap
- C Hormonal modulation produced by circulating epinephrine binding beta-adrenergic receptors alone without any contribution from the length-dependent stretch of cardiac sarcomeres themselves
- D Direct regulation of the rate of ATP synthesis within cardiac mitochondria during stretch independent of any sarcomere length change or troponin C binding site exposure involved
Correct answer: B. Length-dependent activation of cardiac myofilaments: increased stretch exposes more troponin C binding sites and improves actin-myosin overlap
Explanation: Frank-Starling: increased ventricular filling stretches sarcomeres, increasing myofilament sensitivity to Ca<sup>2+</sup> (exposing more troponin C sites) and reducing steric hindrance. More crossbridges form, increasing force.
A single ECG cycle: the P wave marks atrial depolarisation (contraction signal), the large QRS complex marks ventricular depolarisation, and the T wave marks ventricular repolarisation (recovery) before the next cycle begins.
Concept context
Blood, lymph, the heart, the cardiac cycle, blood pressure, and ECG. High NEET weightage.