This study compared strategies to equalize the volume of aerobic exercise performed with different intensities by Wistar rats, based on the distance covered during exercise bouts and energy expenditure (EE, isocaloric sessions) obtained from oxygen uptake (V̇O2) or respiratory exchange ratio (RER). Thirty-three male rats (270.5±12.8 g) underwent maximal exercise tests to determine V̇O2 reserve (V̇O2R), being randomly assigned to three groups: moderate-intensity continuous exercise at speed corresponding to 50% V̇O2R (MIC; n=11); high-intensity continuous exercise at 80% V̇O2R (HIC; n=11); and high-intensity intermittent exercise (HII; n=11) at 60% V̇O2R (3 min) and 80% V̇O2R (4 min). Exercise duration was calculated individually to elicit EE of 5 kcal in each session. No difference between groups was found for total running distance (MIC: 801±46, HIC: 734±42, HII: 885±64 m; P=0.13). Total EE measured by RER was systematically underestimated compared to values obtained from V̇O2 (HII: 4.5% and MIC: 6.2%, P<0.05). Total EE (calculated from V̇O2), and duration of HIC bouts (2.8 kcal and 30.8±2.2 min) were lower (P<0.0001) than in MIC (4.9 kcal and 64.7±1.8 min) and HII (4.7 kcal and 46.9±2.2 min). Predicted and actual values of total V̇O2, total EE, and duration of isocaloric sessions were similar in MIC and HII (P>0.05), which were both higher than in HIC (P<0.0001). In conclusion, the time to achieve a given EE in exercise bouts with different intensities did not correspond to the total distance. Therefore, the volume of aerobic exercise in protocols involving Wistar rats should be equalized using EE rather than total covered distance.
Systemic and central cardiovascular adaptations may vary in response to chronic exercise performed with different intensities and volumes. This study compared the effects of aerobic training with different intensities but equivalent volume upon microvascular reactivity in cremaster muscle and myocardial biomarkers of oxidative stress in Wistar rats. After peak oxygen uptake (VO2peak) assessment, rats (n=24) were assigned into three groups: moderate-intensity exercise training (MI); high-intensity exercise training (HI); sedentary control (SC). Treadmill training occurred during 4 weeks, with exercise bouts matched by the energy expenditure (3.0-3.5 Kcal). Microvascular reactivity was assessed in vivo by intravital microscopy in cremaster muscle arterioles, while biomarkers of oxidative stress and eNOS expression were quantified at left ventricle and at aorta, respectively. Similar increasing vs. sedentary control group (SC) occurred in moderate intensity training group (MI) and high-intensity training group (HI) for endothelium-dependent vasodilation (10−4M: MI: 168.7%, HI: 164.6% vs. SC: 146.6%, P=0.0004). Superoxide dismutase (SOD) (HI: 0.13 U/mg vs. MI: 0.09 U/mg and SC: 0.06 U/mg; P=0.02), glutathione peroxidase (GPX) (HI: 0.00038 U/mg vs. MI: 0.00034 U/mg and SC: 0.00024 U/mg; P=0.04), and carbonyl protein content (HI: 0.04 U/mg vs. MI: 0.03 U/mg and SC: 0.01 U/mg; P=0.003) increased only in HI. No difference across groups was detected for catalase (CAT) (P=0.12), Thiobarbituric acid reactive substances (TBARS) (P = 0.38) or eNOS expression in aorta (P=0.44). In conclusion, higher exercise intensity induced greater improvements in myocardium antioxidant defenses, while gains in microvascular reactivity appeared to rely more on exercise volume than intensity.
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