Rigor mortis in skeletal muscle begins approximately 1–3 hours after death at room temperature (23°C) and is fully established (in-sensu complete) by approximately 6–12 hours. The biochemical mechanism driving rigor is:
- A Progressive ATP depletion preventing myosin head detachment from actin (crossbridge lock) ✓
- B Accumulation of lactic acid causing pH-dependent actomyosin irreversible binding
- C Calcium leakage from mitochondria activating calpain proteases
- D Autolytic breakdown of the sarcoplasmic reticulum releasing calcium
Explanation
Rigor mortis results from progressive depletion of ATP. In the living state, ATP is required for the power-stroke cycle of myosin cross-bridges to detach from actin after each contraction. As oxidative phosphorylation ceases at death, ATP falls and cross-bridges cannot complete the detachment phase — myosin heads remain locked to actin, causing the muscles to stiffen. Resolution of rigor (24–48 hours later) is due to autolytic protease activity that degrades the actomyosin complex. Lactic acid accumulation reduces pH and slightly accelerates ATP depletion but is not the direct mechanism. Calpain activation and sarcoplasmic reticulum breakdown contribute to secondary processes.
Reference: The Essentials of Forensic Medicine and Toxicology (Narayan Reddy), 34th ed.
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Written and medically reviewed by the StethoPrep medical team.