Which adaptation represents a response to increased functional demand rather than cell injury, and is the underlying mechanism for physiological cardiac hypertrophy in athletes?

• A Hyperplasia of cardiomyocytes driven by stem cell activation
• B Metaplasia of cardiac fibroblasts into contractile myocytes
• C Dysplasia of cardiomyocytes with increased nuclear:cytoplasmic ratio
• D Hypertrophy mediated by IGF-1/PI3K/Akt/mTOR pathway (concentric and eccentric patterns) ✓

Explanation

Physiological cardiac hypertrophy in athletes is driven by the IGF-1/PI3K/Akt/mTOR signaling axis, leading to balanced increases in sarcomere proteins and organelles without fibrosis. Endurance training causes eccentric hypertrophy (increased cavity volume + wall thickness) while strength training causes concentric hypertrophy (increased wall thickness, normal or reduced cavity). Cardiomyocytes are terminally differentiated and cannot undergo true hyperplasia. Physiological hypertrophy is reversible (detraining), unlike pathological hypertrophy driven by pressure overload (calcineurin-NFAT, MAPK pathways), which is irreversible and associated with fibrosis.

Reference: Robbins & Cotran Pathologic Basis of Disease, 10th ed.

High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP

Written and medically reviewed by the StethoPrep medical team.