Changes that occur within the cardiac cell in response to Beta-adrenergic stimulation result in a dual effect on the mammalian cardiac contraction: a potentiating effect, manifest as an enhancement of twitch force, and a relaxant effect, evidenced by a decrease in the time to peak force and an enhanced rate of relaxation. Since these two manifestations of the relaxant effect occur concomitantly, it is not known whether they are governed by one or more than one mechanism. One approach toward an understanding of this would be to selectively block one of the relaxant effects of Beta-adrenergic stimulation. We have observed in the hyperthyroid heart that the effect of catecholamines to shorten time peak force does not occur, but that the enhancement of the rate of relaxation of the terminal twitch is preserved. Thus these two manifestations of the relaxant effect occur via different mechanisms. It can be hypothesized that the shortening of time to peak force results from enhanced calcium accumulation rate of sarcoplasmic reticulum, which is blunted in the hyperthyroid model, while the effect later in the twitch may be attentuable to catecholamine induced phosphorylation of troponin resulting in less calcium affinity.