Mechanics of Cardiac Muscle Contraction
Description: Cardiac muscle activation is regulated by the troponin complex, which confers Ca2+ sensitivity to the actomyosin (AM) crossbridge cycle responsible for force production. Under physiological conditions, crossbridge cycling models suggest that cardiac muscle actomyosin may produce force in at least two distinct steps: i) a transition between two post-ATP hydrolysis states, A*M.ADP.Pi — AM*.ADP.Pi and ii) release of Pi from the AM*.ADP.Pi state to yield AM*.ADP. Transient or chronic reduction of blood flow to the myocardium impairs force production regardless of ATP or Ca2+ availability, suggesting that the depression of force associated with the pathophysiology of heart failure is explained, at least in part, by intrinsic changes to the contractile filaments. This area of interest examines the impact of altered myocardial blood flow on the post-translational state of sarcomeric contractile proteins and its consequence on steady-state and transient cardiac muscle mechanics. Non-invasive interventions that aim to minimize the loss of myocardial contractility during altered blood flow are also examined.