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The mitochondrial KATP channel does not mediate exercise preconditining against long duration ischemia

Exercise attenuates arrhythmias during the early moments of ischemia by mitochondrial ATP sensitive K+ (MKATP) channel activation. The purpose of this investigation was to evaluate whether the MKATP channel activation remains essential to exercise mediated arrhythmia prevention in response to extended duration IR (50min I, 120min R). The role of the sarcolemmal ATP sensitive K+ (SKATP) channel and endogenous antioxidant enzyme activities were also examined. 4 mo old rats were randomly assigned to either sham, sedentary, or exercise treatments (3 d × 60 min, ~70% VO2max). Exercised subgroups received MKATP inhibitor (″EXM″, 5HD, 10mg/kg) or SKATP inhibitor (″EXS″, HMR1098, 10mg/kg). ECGs recorded during surgical IR were examined for ventricular ectopy under blinded conditions. All treatment groups exhibited a similar rise in arrhythmias (SED 9.01±4.18, EX 7.19±4.62, EXM 8.02±2.99, & EXS 7.85±3.24) as compared to sham (0.98±0.97; p ≤ 0.001). In conclusion, these data demonstrate that exercise preconditioning affords a finite amount of arrhythmia protection against IR.