摘要

Intensive constitutive production of nitric oxide (NO) during physical training improves vasodilatation and heart function. However it reminds unclear how NO takes part in myocardial adaptation to workload, which accompanied with increased heart inflow and intra-cellular calcium content. Using isolated rat heart by Langendorf preparation we studied myocardial response to gradually increased left ventricular volume (Frank-Starling low) and increasing concentration of Ca²⁺ in perfusion solution (from 1.7 mM to 12.5 mM) in trained and untrained rats. It was shown that 4 weeks swimming course improved heart function: heart rate was decreased; contractile activity (dP/dt max) and coronary flow were increased by 20% and 33% respectively. Equal volume of balloon stretching in left ventricle provoked greater contraction in trained comparing to untrained hearts, demonstrating extended functional reserves of myocardium after swimming course. Furthermore, physical training significantly increased mitochondrial membrane potential (−176.5 ± 8.4 mV vs −156 ± 3.5 mV in control), that points to improved efficiency of oxidative phosphorylation. Heart contracture and increase of end diastolic pressure during calcium upload were much prevented in trained rat hearts. Mitochondrial factor release due to opening of mitochondrial permeability transition (MPT) pore in trained heart was detected at higher concentration of calcium that reveals extended calcium capacity of mitochondria and lesser sensitivity of MPTP to its inductor − calcium. Pretreatment with NO synthesis inhibitor − L-NAME − in dose of 10⁻⁴ M for 15 min abolished reaction of trained heart during Frank-Starling and calcium upload. Thus, heart adaptation to physical training and extend of functional reserves of heart are provided by endogenous NO production.