The partitioning of altered mechanics in hypertrophied heart muscle between the sarcoplasmic reticulum and the contractile apparatus by means of myothermal measurements.

Cardiac hypertrophy in the rabbit, secondary to pulmonary artery stenosis, results in a decrease in unloaded shortening velocity (Vmax) and maximum rate of isometric force development (dP/dtmax), while the peak isometric twitch tension is unchanged and time to peak tension (TPT) is increased. The principle hypothesis used to explain these results involve 1) slowing of myosin cross bridge movement as reflected in depressed myosin ATPase activity and 2) changes in excitation contraction coupling phenomena resulting in changes in intracellular Ca++ movement. Ca++ and actin activated myosin ATPase from the hypertrophied (H) muscles is depressed by 30%. Total initial heat, tension dependent heat and tension independent heat are depressed in H muscles by 57, 56, and 61% respectively. The rate of tension independent heat production in H preparations is depressed by 66%. From these data it is concluded that 61% of the depression in Vmax could be accounted for by the alteration in myosin with the reminder attributable to changes in EC coupling. Increased TPT can be accounted for by the change in rate of Ca++ flux as indicated by the alterated rate of tension independent heat evolution.