Regular exercise training is recognized as a powerful tool to improve work capacity, endothelial function and the cardiovascular risk profile in obesity, but it is unknown which of high-intensity aerobic exercise, moderate-intensity aerobic exercise or strength training is the optimal mode of exercise. In the present study, a total of 40 subjects were randomized to high-intensity interval aerobic training, continuous moderate-intensity aerobic training or maximal strength training programmes for 12 weeks, three times/week. The high-intensity group performed aerobic interval walking/running at 85-95% of maximal heart rate, whereas the moderate-intensity group exercised continuously at 60-70% of maximal heart rate; protocols were isocaloric. The strength training group performed 'high-intensity' leg press, abdominal and back strength training. Maximal oxygen uptake and endothelial function improved in all groups; the greatest improvement was observed after high-intensity training, and an equal improvement was observed after moderate-intensity aerobic training and strength training. High-intensity aerobic training and strength training were associated with increased PGC-1alpha (peroxisome-proliferator-activated receptor gamma co-activator 1alpha) levels and improved Ca(2+) transport in the skeletal muscle, whereas only strength training improved antioxidant status. Both strength training and moderate-intensity aerobic training decreased oxidized LDL (low-density lipoprotein) levels. Only aerobic training decreased body weight and diastolic blood pressure. In conclusion, high-intensity aerobic interval training was better than moderate-intensity aerobic training in improving aerobic work capacity and endothelial function. An important contribution towards improved aerobic work capacity, endothelial function and cardiovascular health originates from strength training, which may serve as a substitute when whole-body aerobic exercise is contra-indicated or difficult to perform.

Objectives To study the effect of exercise and a high fat meal (HFM) on endothelial function. Background Postprandial lipemia and exercise oppose each other in terms of cardiovascular risk, however the mechanism of their interaction is not well understood. Methods Endothelial function was assessed by brachial artery flow mediated dilation (FMD), in eight healthy men before and after a HFM preceded (16–18 hrs) by rest, a single bout of continuous moderate intensity exercise (CME), and high intensity interval exercise (HIIE). Results Before the HFM, initial brachial artery diameters were similar in all trials (0.43±0.04 cm), but after the HFM basal diameter decreased only in the control (0.39±0.03) and CME (0.38±0.04) trials. Prior to the HFM, FMD/shear was improved by a single bout of CME (+20%, p<0.01) and HIIE (+45%, p<0.01, group differences, p<0.01), with no effect in the control trial. After the HFM (30, 120, and 240 mins), FMD decayed to a lesser extent with CME, but in a similar fashion to the control trial. In contrast FMD in the HIIE trial remained elevated following the exercise despite a clear meal-induced lipemia. Although, there were no correlations between vascular function and food-induced markers of cardiovascular risk, antioxidant status was strongly correlated with FMD (r=0.9, p<0.001). Conclusion These findings reveal a clinically relevant protective effect of acute exercise upon the vasculature that is clearly exercise intensity dependent and tightly related to exercise-induced antioxidant capacity.

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In healthy elderly females, there seems to be an interaction between LV apical rotation, BP and body mass. Peak apical rotation and peak diastolic rotation velocity correlate with indices of LV filling and ejection, indicating that suction, a crucial element for effective early LV filling, may be preserved in healthy elderly subjects. Suction deteriorates with elevations of the arterial BP. An age- and BP-related reduction in LV end-diastolic volume may represent an additional impediment to LV filling. Both features may contribute to the development of LV diastolic dysfunction and to episodes of diastolic heart failure.