Imagine a genetic mutation that causes troponin to bind to calcium much more strongly than usual,...

Imagine a genetic mutation that causes troponin to bind to calcium much more strongly than usual, i.e., once the troponin binds to calcium, it is very slow to release the calcium again. What effects would this have an effect on muscle contraction? (That is, would contractions be stronger/weaker than normal? Would they last longer than normal, or not as long?) Explain your reasoning.

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Expert Solution

Troponin (Tn) is the sarcomeric Ca2+ regulator for striated (skeletal and cardiac) muscle contraction. On binding Ca2+ Tn transmits information via structural changes throughout the actin-tropomyosin filaments, activating myosin ATPase activity and muscle contraction.
The sarcoplasmic reticulum stores calcium ions, which it releases when a muscle cell is stimulated; the calcium ions then enable the cross-bridge muscle contraction cycle.
The neuromuscular symptoms of hypercalcaemia are caused by a negative bathmotropic effect due to the increased interaction of calcium with sodium channels. Since calcium blocks sodium channels and inhibits depolarization of nerve and muscle fibers, increased calcium raises the threshold for depolarizationThis results in diminished deep tendon reflexes (hyporeflexia), and skeletal muscle weakness.
thus decreasing excitability, which leads to hypotonicity of smooth and striated muscle. This explains the fatigue, muscle weakness, low tone and sluggish reflexes in muscle groups.

Sydney Mullin answered 10 months ago

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