Experimental studies examining the effects of regular exercise on cardiac responses to ischemia and reperfusion (I/R) are limited. Therefore, these experiments examined the effects of endurance exercise training on myocardial biochemical and physiological responses during in vivo I/R. Female Sprague-Dawley rats (4 mo old) were randomly assigned to either a sedentary control group or to an exercise training group. After a 10-wk endurance exercise training program, animals were anesthetized and mechanically ventilated, and the chest was opened by thoracotomy. Coronary occlusion was achieved by a ligature around the left coronary artery; occlusion was maintained for 20 min, followed by a 10-min period of reperfusion. Compared with untrained, exercise-trained animals maintained higher ( P < 0.05) peak systolic blood pressure throughout I/R. Training resulted in a significant ( P < 0.05) increase in ventricular nonprotein thiols, heat shock protein (HSP) 72, and the activities of superoxide dismutase (SOD), phosphofructokinase (PFK), and lactate dehydrogenase. Furthermore, compared with untrained controls, left ventricles from trained animals exhibited lower levels ( P < 0.05) of lipid peroxidation after I/R. These data demonstrate that endurance exercise training improves myocardial contractile performance and reduces lipid peroxidation during I/R in the rat in vivo. It appears likely that the improvement in the myocardial responses to I/R was related to training-induced increases in nonprotein thiols, HSP72, and the activities of SOD and PFK in the myocardium.

Background: Aerobic capacity has been shown to be inversely proportionate to cardiovascular mortality and morbidity and there is growing evidence that high-intensity interval training (HIIT) appears to be more effective than moderate-intensity continuous training (MICT) in improving cardiorespiratory fitness within the cardiac population. Previously published systematic reviews in cardiovascular disease have neither investigated the effect that the number of weeks of intervention has on cardiorespiratory fitness changes, nor have adverse events been collated. Objective: We aimed to undertake a systematic review and meta-analysis of randomized controlled trials (RCTs) within the cardiac population that investigated cardiorespiratory fitness changes resulting from HIIT versus MICT and to collate adverse events. Methods: A critical narrative synthesis and meta-analysis was conducted after systematically searching relevant databases up to July 2017. We searched for RCTs that compared cardiorespiratory fitness changes resulting from HIIT versus MICT interventions within the cardiac population. Results: Seventeen studies, involving 953 participants (465 for HIIT and 488 for MICT) were included in the analysis. HIIT was significantly superior to MICT in improving cardiorespiratory fitness overall (SMD 0.34 mL/kg/min; 95% confidence interval [CI; 0.2-0.48]; p<0.00001; I 2 =28%). There were no deaths or cardiac events requiring hospitalization reported in any study during training. Overall, there were more adverse events reported as a result of the MICT (n=14) intervention than the HIIT intervention (n=9). However, some adverse events (n=5) were not classified by intervention group. Conclusion: HIIT is superior to MICT in improving cardiorespiratory fitness in participants of cardiac rehabilitation (CR). Improvements in cardiorespiratory fitness are significant for CR programs of >6-week duration. Programs of 7-12 weeks' duration resulted in the largest improvements in cardiorespiratory fitness for patients with coronary artery disease. HIIT appears to be as safe as MICT for CR participants.

The present study has shown that when HIT incorporates P(max) as the interval intensity and 60% of T(max) as the interval duration, already highly trained cyclists can significantly improve their 40-km time trial performance. Moreover, the present data confirm prior research, in that repeated supramaximal HIT can significantly improve 40-km time trial performance.

These experiments examined the independent effects of short-term exercise and heat stress on myocardial responses during in vivo ischemia-reperfusion (I/R). Female Sprague-Dawley rats (4 mo old) were randomly assigned to one of four experimental groups: 1) control, 2) 3 consecutive days of treadmill exercise [60 min/day at 60-70% maximal O2 uptake (VO2 max)], 3) 5 consecutive days of treadmill exercise (60 min/day at 60-70% VO2 max), and 4) whole body heat stress (15 min at 42 degrees C). Twenty-four hours after heat stress or exercise, animals were anesthetized and mechanically ventilated, and the chest was opened by thoracotomy. Coronary occlusion was maintained for 30-min followed by a 30-min period of reperfusion. Compared with control, both heat-stressed animals and exercised animals (3 and 5 days) maintained higher (P < 0.05) left ventricular developed pressure (LVDP), maximum rate of left ventricular pressure development (+dP/dt), and maximum rate of left ventricular pressure decline (-dP/dt) at all measurement periods during both ischemia and reperfusion. No differences existed between heat-stressed and exercise groups in LVDP, +dP/dt, and -dP/dt at any time during ischemia or reperfusion. Both heat stress and exercise resulted in an increase (P < 0.05) in the relative levels of left ventricular heat shock protein 72 (HSP72). Furthermore, exercise (3 and 5 days) increased (P < 0.05) myocardial glutathione levels and manganese superoxide dismutase activity. These data indicate that 3-5 consecutive days of exercise improves myocardial contractile performance during in vivo I/R and that this exercise-induced myocardial protection is associated with an increase in both myocardial HSP72 and cardiac antioxidant defenses.