Can heart muscles cramp in the way calf muscles do? If not, why not?
鈥� In cramp, the muscle filaments known as within the muscle are stuck in full or hyper contraction, in a state of energy depletion that may be exacerbated by electrolyte disturbance. The normal rhythmic contraction of the heart muscle 鈥� a phase called systole 鈥� pumps blood out of the left ventricle to the body. A systolic spasm or cramp would kill you very quickly. However, the heart is more likely to suffer serious disturbance to its rhythm rather than cramp, such as ventricular fibrillation, or asystole 鈥� when cardiac electrical activity stops.
But spasm of the smooth muscle of the coronary arteries can occur and cause a heart attack.
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In Queensland we have the world鈥檚 most venomous animal, , a box jellyfish that lives along the coast and in the estuaries of Queensland. One of its toxic effects is to cause the heart to spasm in systole 鈥� it can kill you in minutes, and possibly in as little as 20 seconds. There is an antivenom but the chances of it working against a fatal dose are slim because you die before it can be injected. Immediate CPR should be attempted and I have seen it work in a marginal case.
Vinegar inhibits further release of the toxin, and prudent bathers in 鈥渟tinger鈥� territory carry vinegar both to sprinkle on their fish and chips and, if necessary, to flush sticky tentacles from their skin.
Bob McCrossin, Cooroy, Queensland, Australia
鈥� Can the heart cramp like a calf muscle? Yes, if sustained muscle shortening is included in our definition of cramp. Such a contracture happens in severe metabolic inhibition, as in a heart attack. My group and I have shown this contracture depletes cells of their energy currency, .
鈥淭he heart can cramp, if we include any sustained muscle shortening in our definition of cramp鈥�
We found this out by injecting a single heart-muscle cell with , which releases light in the presence of ATP, while simultaneously watching the cell shorten 鈥� or cramp 鈥� in infrared laser light. (Thanks to the Biochemical Society, our paper is free at ).
During the contracture, myosin converts the ATP to which then spreads to the next cell. ADP initiates the cell shortening so the injury process propagates from cell to cell. We can speculate that preventing ADP from passing through the pores in the junctions between cells could prevent the spread of injury. To do this, I would suggest applying cytoplasmic to the pores. This enzyme rapidly converts ADP to ATP. The question is how to do it. Like all science, one question begets more.
Peter Cobbold, Emeritus professor of human anatomy and cell biology
Corwen, Denbighshire, UK