Key result
Exercise training increases coronary flow ~33% via nitric oxide pathways in preclinical models.
Why the study?
The role of nitric oxide in myocardial adaptation to increased workload and intracellular calcium during physical training remains unclear.
Endogenous nitric oxide production is required for the myocardial adaptations and extended functional reserves induced by physical training.
Answers are grounded in this paper and cite their sources.
May inform NO modulation of Ca2+ and Frank-Starling responses in vitro; leaves open relevance to in vivo myocardial adaptation.
Intensive constitutive production of nitric oxide (NO) during physical training improves vasodilatation and heart function. However, it remains unclear how NO takes part in myocardial adaptation to workload, which is accompanied by an increased heart inflow and intracellular 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 the 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 stretching of balloon in left ventricle provoked greater contraction in trained comparing to untrained hearts, demonstrating extended functional reserves after swimming course. Mitochondrial membrane potential was significantly increased in hearts of trained rats. Furthermore, training prevented fast increase of the end diastolic pressure during calcium upload. Mitochondrial factor release due to opening of mitochondrial permeability transition pore (MPTP) in trained hearts was detected at higher concentrations of calcium that reveals extended calcium capacity of mitochondria and lesser sensitivity of MPTP to its inductor-calcium. Blockade of NO synthesis with L-NAME application 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 extension of functional reserves in heart are provided by endogenous NO production.
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Tv et al. (2010) studied Healthy (adaptation to physical training). Physical training (swimming) vs. Untrained control was evaluated on Coronary flow (ml/min) (p=<0.05). A 4-week swimming training program in rats improved heart function, increasing myocardial contractile activity by 20% and coronary flow from 12.0 to 16.0 ml/min, effects that were abolished by nitric oxide synthesis blockade.
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