Swimming training can affect intrinsic calcium current characteristics in rat myocardium.

Endurance exercise is widely assumed to improve cardiac function in humans, but the mechanisms involved in such changes are not clearly understood. The purpose of this study is to determine whether training elicits adaptations at the level of the L-type Ca(2+) channel. Sprague-Dawley rats performed swimming training at either moderate intensity (MOD) or high intensity (HIGH) during 8 weeks. The trained rats were studied by echocardiography and the whole-cell L-type Ca(2+) currents (I (Ca,L)) characteristics in a single cell were measured by standard whole-cell patch-clamp recording technique. Echocardiography showed that septal and posterior wall thickness in MOD and HIGH increased with the increased LV mass by 43 and 41%, respectively (P < 0.05). Training (P < 0.05) increased mean myocyte capacitance (approximately 38% in MOD and HIGH) and myocyte length (approximately 20% longer in MOD and 26% longer in HIGH), thus providing electrophysiological and morphological evidence that the training elicited LV cardiocyte hypertrophy. Mean peak I (Ca,L) was not different in three groups. However, whole-cell I (Ca,L) density was decreased in MOD and HIGH versus sedentary (P < 0.05), but there was no significant difference between MOD and HIGH. The present study provides the evidence of a training adaptation in intrinsic I (Ca,L) characteristics in ventricular myocardium, which demonstrates a remarkable adaptive plasticity of L-type channel characteristics in training rat heart.