## Biochemical Mechanism of Rigor Mortis ### Primary Cause: ATP Depletion **Key Point:** Rigor mortis occurs because **ATP is depleted after death**, preventing the detachment of myosin heads from actin filaments. This locks the muscle in a state of permanent contraction. ### Step-by-Step Mechanism 1. **Normal muscle physiology (living state):** - Myosin heads bind to actin (power stroke) - ATP binds to myosin head → causes detachment - ATP hydrolysis provides energy for next cycle 2. **After death:** - Aerobic respiration stops → no new ATP synthesis - Existing ATP is rapidly consumed - Myosin heads cannot detach from actin (ATP required for detachment) - Cross-bridges remain locked → muscle stiffness ### Why Other Options Are Wrong | Option | Why It's Incorrect | |--------|-------------------| | Lactic acid accumulation | Contributes to muscle acidosis but is NOT the primary mechanism; rigor occurs even without significant lactate buildup | | Potassium loss | Occurs postmortem but is secondary; not the direct cause of cross-bridge locking | | Protein denaturation | Requires higher temperatures; not the primary mechanism in normal PMI | **High-Yield:** The **ATP-myosin-actin cross-bridge model** is the gold-standard explanation for rigor mortis in all forensic medicine textbooks. This is frequently tested in NEET PG. **Mnemonic:** **ATP = Allows Temporary Parting** (of myosin from actin). Without ATP, myosin stays glued to actin → rigor. **Clinical Pearl:** Rigor mortis is essentially a "frozen" version of muscle contraction—the muscle is locked in the state it was in at the moment ATP ran out.
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