Exercise training downregulates the I Ks channel current, contributing to action potential prolongation and a more metabolically efficient heart.
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Animal data suggest exercise remodels ventricular electrophysiology for efficiency; leaves open human translation.
Results demonstrate that exercise training (TRN) downregulates ventricular I Ks channel current and the channel’s responsiveness to β-agonist factors mediated by TRN-induced decline in channel subunits KCNQ1 and KCNE1 and the A-kinase anchoring protein yotiao. The reduced I Ks current helps explain the TRN-induced prolongation of the action potential in basal conditions and, coupled with previously reported upregulation of the K ATP channel, results in a more efficient heart that is better able to respond to beat-by-beat changes in metabolism.
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Wang et al. (2020) studied this question.
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