Experiments were performed in human working myocardium to investigate the relationship of intracellular calcium handling and availability to alterations in the strength of contraction produced by changes in stimulation rate and pattern. Both control and myopathic muscles exhibited potentiation of peak isometric force during the postextrasystolic contraction which was associated with an increase in the peak intracellular calcium transient. Frequency-related force potentiation was attenuated in myopathic muscles compared to controls. This occurred despite an increase in resting intracellular calcium and in the peak amplitude of the calcium transient as detected with aequorin. Therefore, abnormalities in contractile function of myopathic muscles during frequency-related force potentiation are not due to decreased availability of intracellular calcium, but more likely reflect differences in myofibrillar calcium responsiveness. Sarcolemmal calcium influx may also contribute to frequency-related changes in contractile force in myopathic muscles as suggested by a decrease in action potential duration with increasing stimulation frequency which is associated with fluctuations in peak calcium transient amplitude. (J.

We tested the hypothesis that intracellular Ca++ ([Ca+Jli)

The purpose of this study was to determine whether the cardiac contractile abnormalities induced by hyperthyroidism or hypothyroidism are caused by changes in intracellular Ca T hyroid hormone influences the contractile state of cardiac muscle by altering the rates of contraction and relaxation. 1 However, it has been difficult to identify the steps in excitationcontraction coupling that are modified by changes in the thyroid state. In some species, thyroid hormone influences the distribution of myosin isozymes in ventricular muscle.2 -3 In rabbits, the maximum velocity of papillary muscle shortening directly correlates with the fraction of thyroid hormoneFrom the Charles A.

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