In the Frank-Starling mechanism, the fundamental cellular explanation for increased stroke volume with increased end-diastolic volume is:
- A Activation of additional sarcomeres that were previously inactive
- B Increased intracellular Ca2+ sensitivity of troponin C with greater sarcomere stretch ✓
- C Increased ATP availability from stretch-activated metabolic enzymes
- D Greater myosin cross-bridge cycling rate due to conformational change
Explanation
The cellular basis of the Frank-Starling mechanism involves two main components: (1) Optimal filament overlap — within physiological sarcomere lengths (1.8–2.2 µm), increased stretch improves actin-myosin overlap. (2) Increased Ca2+ sensitivity of troponin C — stretch reduces inter-filament spacing, increasing the probability of Ca2+ binding to TnC and cross-bridge formation for a given [Ca2+]. The dominant mechanism in the heart is the length-dependent increase in myofilament Ca2+ sensitivity, which is the key cellular explanation tested in physiology.
Reference: Guyton & Hall, Textbook of Medical Physiology, 14th ed.
High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP
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