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Aims Treatment of arrhythmias evoked by hypothermia/rewarming remains challenging, and the underlying mechanisms are unclear. This in vitro experimental study assessed cardiac electrophysiology in isolated rabbit hearts at temperatures occurring in therapeutic and accidental hypothermia. Methods and results Detailed ECG, surface electrogram, and panoramic optical mapping were performed in isolated rabbit hearts cooled to moderate (31°C) and severe (17°C) hypothermia. Ventricular activation was unchanged at 31°C while action potential duration (APD) was significantly prolonged (176.9 ± 4.2 ms vs. 241.0 ± 2.9 ms, P < 0.05), as was ventricular repolarization. At 17°C, there were proportionally similar delays in both activation and repolarization. These changes were reflected in the QRS and QT intervals of ECG recordings. Ventricular fibrillation threshold was significantly reduced at 31°C (16.3 ± 3.1 vs. 35 ± 3.5 mA, P < 0.05) but increased at 17°C (64.2 ± 9.9, P < 0.05). At 31°C, transverse conduction was relatively unchanged by cooling compared to longitudinal conduction, but at 17°C both transverse and longitudinal conduction were proportionately reduced to a similar extent. The gap junction uncoupler heptanol had a larger relative effect on transverse than longitudinal conduction and was able to restore the transverse/longitudinal conduction ratio, returning ventricular fibrillation threshold to baseline values (16.3 ± 3.1 vs. 36.3 ± 4.3 mA, P < 0.05) at 31°C. Rewarming to 37°C restored the majority of the electrophysiological parameters. Conclusions Moderate hypothermia does not significantly change ventricular conduction time but prolongs repolarization and is pro-arrhythmic. Further cooling to severe hypothermia causes parallel changes in ventricular activation and repolarization, changes which are anti-arrhythmic. Therefore, relative changes in QRS and QT intervals (QR/QTc) emerge as an ECG-biomarker of pro-arrhythmic activity. Risk for ventricular fibrillation appears to be linked to the relatively low temperature sensitivity of ventricular transmural conduction, a conclusion supported by the anti-arrhythmic effect of heptanol at 31°C.
BACKGROUND: High-intensity interval training (HIIT) with interspersing active recovery is an effective mode of exercise training in cohorts ranging from athletes to patients. Here, we assessed the intensity-dependence of the intervals and active recovery bouts for permitting a sustainable HIIT protocol. METHODS: 14 males completed 4x4-minute HIIT protocols where intensities of intervals ranged 80-100% of maximal oxygen uptake (VO2max) and active recovery ranged 60-100% of lactate (La-) threshold (LT). Blood Lameasurements indicated fatigue, while tolerable duration of intervals indicated sustainability. RESULTS: HIIT at 100% of VO2max allowed 44±10% [30-70%] completion, i.e. fatigue occurred after 7minutes:6seconds of the intended 16 minutes of high intensity, whereas HIIT at 95-80% of VO2max was 100% sustainable (p<0.01). Measured intensity did not differ from intended intensity across the protocols (p>0.05). Blood Laconcentration [La-] increased to 9.3±1.4mM during HIIT at 100% of VO2max, whereas at 80-95% of VO2max stabilised at 2-6mM in an intensity-dependent manner (p<0.01 vs 100% of VO2max and p<0.05 vs baseline). Active recovery at 60-70% of LT during HIIT associated with steady-state blood [La-] peaking at 6-7mM, whereas at 80-100% of LT, blood [La-] accumulated to 10-13mM (p<0.05). After HIIT, active recovery at 80-90% of LT cleared blood [La-] 90% faster than at 60-70% of LT (p<0.05). CONCLUSIONS: To permit highest exercise stress during 4x4-minute HIIT, exercise intensity should be set to 95% of VO2max, whereas active recovery should be set to 60-70% of LT during HIIT and 80-90% of LT after HIIT to most efficiently prevent excess Laand aid recovery.
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