Short-term exercise provides left ventricular myocardial protection against intermittent hypoxia-induced apoptosis in rats

We investigated whether exercise provides beneficial effects to attenuate intermittent hypoxia (IH)-induced myocardial apoptosis. Male Sprague-Dawley rats were randomly assigned to four groups: control (CON), IH, exercise (EXE) or IH interspersed with EXE (IHEXE). IH rats were exposed to repetitive hypoxia–reoxygenation cycles (30 s of 5% O₂; 45 s of 21% O₂, 6 h day⁻¹) during the light phase (1000–1600 h) for 12 consecutive days. EXE rats were habituated to treadmill running for 5 days, permitted 2 days of rest, followed by 5 exercise bouts (30 m min⁻¹ for 60 min on a 2% grade) on consecutive days during the dark phase (2000–2200 h). IHEXE rats were exposed to IH during the light phase interspersed with exercise programs during the dark phase on the same day. Apoptosis levels, cytochrome c (Cyt-c), cleaved caspase-3, oxidative stress and antioxidant capacity were determined in the left ventricular (LV) myocardium. IH rats showed higher myocardial levels of the apoptotic index, mitochondria-released Cyt-c, cleaved caspase-3 and oxidative stress and lower catalase activity levels than CON rats (p < 0.05, for all). These changes were not observed in EXE rats (p > 0.05, for all) except that catalase activity increased (p < 0.05). IHEXE rats showed lower myocardial levels of apoptotic index, mitochondria-released Cyt-c, cleaved caspase-3 and oxidative stress and higher catalase activity levels (p < 0.05, for all) than IH rats. We conclude that short-term exercise provides potent cardioprotective effects by attenuating IH-induced myocardial apoptosis.