Endurance exercise alters the contractile responsiveness of rat heart to extracellular Na+ and Ca2+

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Purpose and Methods:

The isovolumic contractile responsiveness of left ventricular (LV) myocardium to altered extracellular [Ca2+], [Na+], and pacing frequency was examined using perfused hearts (37°C) isolated from sedentary (SED) and treadmill-trained (TR) adult female rats.


The suppressive effect of reducing perfusate free [Ca2+] to 0.7 mM on LV developed pressure (ΔLVP) was greater in the TR hearts compared with SED hearts (P < 0.05). When perfusate [Na+] was reduced to 120 mM ([Ca2+] = 0.7 mM), ΔLVP augmentation was greatest in the TR hearts (P < 0.05). The negative force-frequency relationship observed at physiologic [Ca2+] and [Na+] was progressively altered toward a positive force-frequency relationship with each subsequent change in perfusate [Ca2+] and [Na+] although the effect was greatest in TR hearts (P < 0.05).


Training elicited a small but significant (P < 0.05) prolongation in the pressure development phase of contraction. Under the physiological [Ca2+], [Na+] perfusion condition, training produced an increase in the magnitude of extrasystolic potentiation of LV pressure, whereas the time constant of mechanical restitution was unaffected. Training affected neither the Ca2+-dependence nor the maximal capacity of [3H] ryanodine binding to LV myocardial homogenates. The simplest interpretation of [Na+] and [Ca2+] reduction experiments is that myocardial Ca2+ efflux was augmented by exercise training.

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