Load and length regulation of cardiac energetics is a fundamental adaptive mechanism of the heart mediated partly by troponin C calcium sensitivity.
Crossbridge cycling and consequent energy utilization during contraction are subject to physiologic regulation by load and length; the length effect on the sensitivity of troponin C to a given Ca2+i is an important, newly defined mechanism for this length regulation in cardiac muscle. Further, energy utilization persists throughout the cardiac contraction, demonstrably for isometric contractions initiated at optimal length, and is continuously modulated by length changes during variably loaded twitch contractions. The extent, rate, and time of load-induced length changes during myocardial contraction appear to be the primary variables affecting crossbridge activity and energetics. Load and length regulation of the properties of the heart represents a remarkably simple and direct biological response to the physiologic input and role in this organ. This mechanism is utilized by the heart in response to its dynamic loading environment both for long-term adaptation of cardiac mass to chronic load alterations, as discussed here recently (23), and for short-term adaptation of cardiac mechanics and energetics to instantaneous load alterations, as discussed above. It is probably no coincidence, given their central physiologic importance, that both of these most basic adaptive responses of the heart are simultaneously coming to be understood at the molecular level.
George Cooper (Mon,) studied this question.