Abstract 4886: Hydrogen Peroxide Prevents Impaired Endothelium-dependent Dilation Following Acute Exertion in Chronic Exercising but Not in Sedentary Subjects
Introduction: Exercise-induced hypertension increases reactive oxygen species (ROS) generation and threatens vascular endothelial health. Recent studies indicate conditioned subjects (EX) are protected from endothelial dysfunction observed in sedentary (SED) subjects after acute hypertension induced by weight lifting (WL).
Hypothesis: We hypothesized that:
chronic exercise protects against endothelial dysfunction induced by acute exertion and
the mechanism of maintained dilation after acute hypertension involves hydrogen peroxide (H2O2) in microvessels from exercise trained subjects.
Methods: Healthy, lean SED and EX subjects (runners > 15 miles/week or WL > 3x/week), underwent a single progressive 15 minute leg press WL session. Brachial artery flow- mediated dilation (FMD) and nitroglycerin (NTG; 0.4 mg) dilations were measured with ultrasound. Isolated arterioles (gluteal fad pad biopsies) from the same subjects were cannulated to assess dilation to acetylcholine (ACh; 10−9–10−4 M) pre and post WL. Separately, H2O2 production was assessed with DCF fluorescence.
Results: All subjects were free of hypertension with similar blood pressure responses to WL (max SBP: 183.7±5 mmHg). Brachial artery FMD was maintained after WL in EX (+2.0±0.3%; p<0.001 vs. SED; n=48) but not SED (−3.0±0.2%; n = 28). Dilation to ACh was maintained in EX [Max dilation (MD): 87±3 %; n = 10] but not SED (50±5%; n = 10) post WL. Inhibition of NOS with LNAME eliminated baseline ACh dilation in EX but not post WL (73±6%). Indomethacin and 17-ODYA had no effect on post WL ACh responses. In EX subjects, WL increased hydrogen peroxide (DCF fluorescence ratio: 3.4±0.4; p = 0.001 vs. baseline; n = 9). The H2O2 scavenger PEG-catalase (500 U/ml) reduced DCF fluorescence and ACh dilation post WL (29±7%; p<0.001 vs. pre WL) but had no effect before WL. Endothelium-independent responses to papaverine were similar pre and post WL. In conclusion, these data indicate
chronic exercise protects against microvascular endothelial dysfunction after exertion and
although NOS is responsible for ACh dilation before acute weight lifting in EX, H2O2 maintains endothelium-dependent dilation in microvessels after exposure to exercise-induced hypertension.