Exercise mediates an excessive free radical production leading to oxidative stress (OS). The body has natural antioxidant systems that help decrease OS, and these systems may be enhanced with exercise training. However, only a few studies have investigated the differences in resting OS and antioxidant capacity (AOC) between aerobically trained athletes (ET), anaerobically trained athletes (RT), and untrained individuals (UT). Therefore, this study sought to investigate the resting and postexercise OS and AOC in ET, RT, and UT. Sixty healthy young males (26.6±0.8 yr) participated in this study. Subjects were divided into three groups, ET, RT, and UT by distinct training background. Resting plasma malondialdehyde (MDA) and protein carbonyls (PC) were not significantly different in ET, RT, and UT. However, MDA and PC were significantly increased following a graded exercise test (GXT) in UT but not in ET and RT. Resting total antioxidant capacity (TAC) levels and TAC were not different in ET, RT, and UT. Interestingly, TAC levels significantly decreased after the GXT in all groups. Additionally, UT showed lower post-exercise TAC levels compared to ET and RT. These results showed that ET, RT, and UT have similar OS and AOC at rest. However, both ET and RT have greater AOC against exercise mediated OS compared to UT. These findings may explain, at least in part, why both aerobic and anaerobic types of exercise training improve redox balance. However, it appears there is no specific exercise type effect in terms of redox balance.

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ObjectivesCentral adiposity, in particular the accumulation of intra‐abdominal visceral fat, has been linked to adipose tissue dysfunction and obesity‐related diseases including hypertension and atherosclerosis, however regulatory mechanisms are poorly understood. We hypothesized that increased micro‐vascular tone specifically in visceral fat may contribute to abnormal peripheral vascular resistance.MethodsIn 30 obese subjects(age 42±10 yr, BMI 42±3 kg/m2) undergoing elective bariatric surgery, we characterized vaso‐contractile responses of isolated subcutaneous (SC) and visceral (VIS) adipose tissue arterioles using videomicroscopy, and examined relevant depot‐specific gene expression using qPCR.ResultsVisceral arterioles exhibited significantly greater angiotensin II‐mediated vasoconstriction by 20% in obese hypertensives (OH, SBP 146±8 mmHg) compared to obese normotensives (O, SBP 118±5 mmHg) (p<0.05). Additionally, VIS arterioles showed greater vasoconstriction in response to angiotensin II compared to SC in OH (by 25%, p<0.05) but not in O. Angiotensin converting enzyme (ACE) mRNA expression was significantly increased in VIS compared to SC (2‐fold, p<0.05) in OH but not O. In contrast, vasopressor responses to other agonists including endothelin‐1 and phenylephrine were not different between fat depots or subjects with or without hypertension.ConclusionThe findings demonstrate differential activation of the renin‐angiotensin system (RAS) in the visceral adipose tissue microvasculature that may contribute to mechanisms of systemic hypertension in obesity. RAS targeting, in particular, may provide incremental clinical benefit in treating obesity‐related hypertension.Support or Funding InformationNIH grants P01HL081587 and RO1 HL1145675