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

Abstract

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% O(2); 45 s of 21% O(2), 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.

Zinc Is Indispensable in Exercise-Induced Cardioprotection against Intermittent Hypoxia-Induced Left Ventricular Function Impairment in Rats

“…Short-term exercise has been shown to increase myocardial levels of catalase activity and attenuate the myocardial oxidative damage induced by IH [33]. Additionally, in line with previous studies [33, 68], our results showed that exercise training can increase myocardial levels of catalase activity and that this effect was abolished by TPEN treatment. Thus, our findings suggest that zinc may play a role in exercise that provides antioxidant effects that prevent IH-induced reductions in myocardial antioxidant capacity.…”

“…This may be due to differences in the type, duration, intensity, and period of exercise training, or from differences in the rat strain or organs. Also, compared with ischaemia and reperfusion, IH generates only mild myocardial oxidative stress in rats [33]. Additionally, the exercise intensity in our study was not high enough to generate large amounts of ROS in rat hearts.…”

“…Myocardial tissue preparation was as described previously [33]. Urethane has long been considered a desirable compound for providing anesthesia during physiological experiments [34].…”

“…This protocol was adapted and modified from our previous studies [29, 33]. Total cytosolic fraction extracts were obtained from the LV myocardium using a commercially available isolation kit (Pierce, Rockford, IL, USA), according to the manufacturer’s instructions.…”

High-intensity training reduces intermittent hypoxia-induced ER stress and myocardial infarct size

“…To our knowledge, there is only one study that has reported a protective effect of exercise in the context of IH. The authors reported a beneficial effect of exercise on IH-induced myocardial oxidative stress and apoptosis (10). In the present study, we first tested whether HIT would exert greater effects on performance and mitochondrial adaptations than MIT.…”