Rigor Mortis, Vasoconstriction, Vasodilation, and Hemodynamic Physiology

"There is no adequate defense, except stupidity, against the impact of a new idea."--Percy Williams Bridgeman

Conventional physiology attributes blood propulsion and distribution to organs and tissues to opposing muscular forces of cardiac contraction, vasoconstriction, and vasodilation, all of which are ATP dependent. This implies that hemodynamic physiology is inherently inefficient.

Rigor mortis illustrates the ATP dependence of both muscle contraction and muscle relaxation. The sarcoplasmic reticulum releases Ca+ into cytoplasm to initiate muscle contraction. An intracellular calcium pump mechanism returns Ca+ to the sarcoplasmic reticulum to enable muscle relaxation. Cardiorespiratory function is essential to deliver oxygen and glucose to cells to enable ATP generation via the Krebs cycle. The circulatory failure of death disrupts oxygen transport and delivery, causing cellular anoxia that halts ATP generation, so that universal muscle flaccidity ensues in the immediate aftermath of death, including vascular smooth muscle. Anaerobic respiration generates enough ATP to sustain the calcium pump for a few hours after death, but as the failing sarcoplasmic reticulum releases its calcium into the cytoplasm, the muscular “ratcheting mechanism” locks in place for lack of ATP, causing rigor mortis in all types of muscle, including vascular smooth muscle.

The resilience of the calcium pump prevents rigor mortis in life, but intense exercise depletes ATP reserves, causing muscle fatigue. Athletic conditioning induces angiogenesis (capillary proliferation) that reduces flow resistance, enhances tissue oxygenation, increases ATP generation, and improves exercise tolerance.

Vasoconstriction provides a weak explanation of essential hypertension, because sustained muscular contraction depletes ATP, causing obligatory muscle exhaustion and relaxation.

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