ABSTRACT
UNLABELLED: It is well established that both short-term (1-5 days) and long-term (weeks to months) high intensity exercise (i.e. 70-75%VO2max) provides cardioprotection against ischaemia-reperfusion injury. However, it is unclear if moderate intensity exercise will also provide cardioprotection. AIM: Therefore, these experiments compared the protective effects of moderate vs. high intensity exercise in providing defense against ischaemia-reperfusion injury. METHODS: Male Sprague-Dawley rats were randomly assigned to one of three-experimental groups: (1) sedentary (control); (2) moderate intensity treadmill exercise (60 min day(-1) at approximately 55%VO2max); or (3) high intensity treadmill exercise (60 min day(-1) at approximately 75%VO2max). Hearts were exposed to 20 min of global ischaemia followed by 30 min reperfusion in an isolated working heart preparation. RESULTS: Compared with sedentary rats, both moderate and high intensity exercised rats maintained a higher (P < 0.05) percentage of pre-ischaemia cardiac output and cardiac work (cardiac output x systolic blood pressure) during reperfusion. No differences in the percent recovery of cardiac output and heart work existed (P > 0.05) between the two exercise groups. CONCLUSIONS: These data reveal that both moderate and high intensity exercise training provide equivalent protection against ischaemia-reperfusion injury.
Subject(s)
Myocardial Ischemia/physiopathology , Myocardial Reperfusion Injury/prevention & control , Physical Conditioning, Animal/physiology , Animals , Antioxidants/analysis , Blood Pressure/physiology , Cardiac Output/physiology , HSP72 Heat-Shock Proteins , Heart/physiopathology , Heat-Shock Proteins , L-Lactate Dehydrogenase/metabolism , Male , Myocardium/metabolism , RNA, Messenger/analysis , Rats , Rats, Sprague-Dawley , Superoxide Dismutase/analysis , Ventricular Dysfunction, Left/physiopathologyABSTRACT
Muscular exercise results in an increased production of radicals and other forms of reactive oxygen species (ROS). Recent evidence suggests that radicals and other ROS are an underlying aetiology in exercise-induced disturbances in muscle redox status. These exercise-induced redox disturbances in skeletal muscle are postulated to contribute to both muscle fatigue and/or exercise-induced muscle injury. To defend against ROS, muscle cells contain complex cellular defence mechanisms to reduce the risk of oxidative injury. Two major classes (enzymic and non-enzymic) of endogenous protective mechanisms work together to reduce the harmful effects of oxidants in the cell. Primary antioxidant enzymes include superoxide dismutase (EC 1.15.1.1; SOD), GSH peroxidase (EC 1.11.1.9; GPX), and catalase (EC 1.11.1.6); these enzymes are responsible for removing superoxide radicals, H2O2 and organic hydroperoxides, and H2O2 respectively. Important non-enzymic antioxidants include vitamins E and C, beta-carotene, GSH and ubiquinones. Vitamin E, beta-carotene and ubiquinone are located in lipid regions of the cell, whereas GSH and vitamin C are in aqueous compartments of the cell. Regular endurance training promotes an increase in both total SOD and GPX activity in actively-recruited skeletal muscles. High-intensity exercise training has been shown to be generally superior to low-intensity exercise in the upregulation of muscle SOD and GPX activities. Also, training-induced upregulation of antioxidant enzymes is limited to highly-oxidative skeletal muscles. The effects of endurance training on non-enzymic antioxidants remain a relatively uninvestigated area.
