Controversy abounds in the cardiac muscle literature over the rate-limiting steps of cardiac muscle contraction and relaxation. However, the idea of a single biochemical mechanism being the all-inclusive rate-limiting step for cardiac muscle contraction and relaxation may be oversimplified. There is ample evidence that Ca2+ concentration and dynamics, intrinsic cross-bridge properties, and even troponin C (TnC) Ca2+ binding and dissociation can all modulate the mechanical events of cardiac muscle contraction and relaxation. However, TnC has generally been thought to play no role in influencing cardiac muscle dynamics due to the idea that Ca2+ exchange with TnC is very rapid. This definitely is the case for isolated TnC, but not for the more sophisticated biochemical systems of reconstituted thin filaments and myofibrils. This review will discuss the biochemical influences on Ca2+ exchange with TnC and their physiological implications.

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