Abstract
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.
Highlights
Aerobic training is widely acknowledged as an effective strategy to maintain health and reduce cardiovascular risk [1]
VO2peak decreased in sedentary control (SC) (P = 0.007), increased in high-intensity exercise training (HI) (P = 0.001) and increased twice in HI than moderateintensity exercise training (MI), this difference lacked of statistical significance (VO2peak Δ = 4.9 vs. 2.2 ml.kg.-1min.-1; P = 0.12)
Despite the differences detected for oxygen uptake (VO2) after training, gains in body mass were similar across groups during all the experimental period (P = 0.59) (Fig 1), as well as the energy intake (SC: 94.9 ± 2.2 kcal/day; MI: 93.3 ± 4.8 kcal/day; HI: 92.9 ± 4.2 kcal/day; P = 0.58)
Summary
Aerobic training is widely acknowledged as an effective strategy to maintain health and reduce cardiovascular risk [1]. Different exercise intensities may elicit dissimilar chronic effects upon systemic and central cardiovascular markers– endothelial function may be jeopardized by high-intensity training [14, 17], myocardium antioxidant protection could be benefited [15]. Given that improvements in endothelial function may rely on the amount of EE during exercise [17, 18], it is feasible to speculate that isocaloric protocols would be able to induce favorable effects regardless of training intensity [19]. This approach would help to avoid bias, since protocols with higher intensities can be related to greater EE. This confounding factor precludes isolating the specific effects of exercise intensity upon endothelial function or myocardium integrity
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