Endurance training does not affect intrinsic calcium current characteristics in rat myocardium.

Authors:
  • XWXinrui Wang
    Xinrui Wang
  • RFRobert H. Fitts
    Robert H. Fitts
  • EKEinat Kodesh
    Einat Kodesh
  • NNNir Nesher
    Nir Nesher
  • ASAssi Simaan
    Assi Simaan
  • BHBenny Hochner
    Benny Hochner
  • RBRonen Beeri
    Ronen Beeri
  • DGDan Gilon
    Dan Gilon
  • MSMichael D. Stern
    Michael D. Stern
  • GGGary Gerstenblith
    Gary Gerstenblith
  • MHMichal Horowitz
    Michal Horowitz
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Abstract
The voltage-dependent Ca2+ channel (L-type channel) controls an inward Ca2+ current (ICa) that is centrally involved in the regulation of myocardial excitation-contraction (EC) coupling. A significant body of evidence exists to support the idea that exercise training elicits alterations in myocardial Ca2+ regulation, and the L-type channel has been implicated as a possible site of adaptation. The purpose of this study was to determine whether training elicits adaptations at the level of the L-type Ca2+ channel, as reflected by alterations in whole cell ICa characteristics in single myocytes isolated from rat left ventricle (LV). Female rats were treadmill trained at a moderately high intensity for a minimum of 20 wk. Body weight was unaffected by the training protocol, whereas there was a trend (P = 0.06) for a modest increase in LV weight (approximately 8%). Training produced significant (P < 0.05) increases in mean myocyte capacitance (approximately 9%) and myocyte length (approximately 6%), thus providing electrophysiological and morphological evidence that training elicited LV cardiocyte hypertrophy. Whole cell ICa vs. voltage and ICa density vs. voltage relationships as well as ICa inactivation and recovery characteristics were unaffected by our training paradigm. These findings do not support the hypothesis that training elicits adaptations in L-type Ca2+ channel number or intrinsic function in a model exhibiting classical exercise training-induced myocardial hypertrophy. Our results do not, however, preclude the possibility that training-induced adaptations at sites other than the L-type Ca2+ channel could affect ICa and myocardial EC coupling.