Massage therapy restores peripheral vascular function after exertion.

OBJECTIVE: To determine if lower extremity exercise-induced muscle injury reduces vascular endothelial function of the upper extremity and if massage therapy (MT) improves peripheral vascular function after exertion-induced muscle injury. DESIGN: Randomized, blinded trial with evaluations at 90 minutes, 24 hours, 48 hours, and 72 hours. SETTING: Clinical research center. PARTICIPANTS: Sedentary young adults (N=36) were randomly assigned to 1 of 3 groups: (1) exertion-induced muscle injury and MT (n=15; mean age ± SE, 26.6 ± 0.3); (2) exertion-induced muscle injury only (n=10; mean age ± SE, 23.6 ± 0.4), and (3) MT only (n=11; mean age ± SE, 25.5 ± 0.4). INTERVENTION: Participants were assigned to exertion-induced muscle injury only (a single bout of bilateral, eccentric leg press exercise), MT only (30-min lower extremity massage using Swedish technique), or exertion-induced muscle injury and MT. MAIN OUTCOME MEASURES: Brachial artery flow-mediated dilation (FMD) was determined by ultrasound at each time point. Nitroglycerin (NTG)-induced dilation was also assessed (0.4 mg). RESULTS: Brachial FMD increased from baseline in the exertion-induced muscle injury and MT group and the MT only group (7.38%±.18% to 9.02%±.28%, P<.05 and 7.77%±.25% to 10.2%±.22%, P<.05, respectively) at 90 minutes and remained elevated until 72 hours. In the exertion-induced muscle injury only group, FMD was reduced from baseline at 24 and 48 hours (7.78%±.14% to 6.75%±.11%, P<.05 and 6.53%±.11%, P<.05, respectively) and returned to baseline after 72 hours. Dilations of NTG were similar over time. CONCLUSIONS: Our results suggest that MT attenuates impairment of upper extremity endothelial function resulting from lower extremity exertion-induced muscle injury in sedentary young adults.

Improved arterial flow-mediated dilation after exertion involves hydrogen peroxide in overweight and obese adults following aerobic exercise training.

OBJECTIVE: Acute strenuous physical exertion impairs arterial function in sedentary adults. We investigated the effects of 8 weeks of regular aerobic exercise training on acute physical exertion-induced arterial dysfunction in sedentary, overweight, and obese adults. METHODS: Twenty-five overweight and obese adults (BMI 30.5 ±â€Š7.2 years) were assigned to 8 weeks of aerobic training or to a control group. Brachial artery flow-mediated dilation (FMD) was assessed before and after acute leg press exercise at weeks 0 and 8. Gluteal adipose biopsies were performed at rest and post acute leg press to measure microvessel FMD with and without nitric oxide synthase inhibition via L-nitroarginine methyl ester or hydrogen peroxide (H2O2) scavenging with Catalase. Microvessel nitric oxide and H2O2 production were assessed via fluorescence microscopy. RESULTS: Brachial artery dilation was reduced post acute leg press at week 0 in the aerobic exercise and control groups, but was preserved in the aerobic-exercise group post acute leg press at week 8 (P < 0.05). Post acute leg press microvessel FMD was preserved in the aerobic exercise group but impaired in the control group at week 8 (P < 0.05). Preserved dilation in the aerobic exercise group was more sensitive to H2O2 scavenging than inhibition of nitric oxide, and post acute leg press microvessel H2O2 production was increased compared with at rest (P < 0.05). CONCLUSION: Aerobic exercise prevents acute exertion-induced arterial dysfunction in overweight and obese adults via a phenotypic switch from nitric oxide-mediated dilation at rest to a predominately H2O2-mediated dilation after acute physical exertion.

Circuit resistance training attenuates acute exertion-induced reductions in arterial function but not inflammation in obese women.

BACKGROUND: Cardiovascular disease (CVD) is a leading cause of preventable death among young women in the United States. Habitual resistance exercise training is known to have beneficial effects on endothelial function and CVD risk factors, including obesity; however, previous studies show that acute resistance exercise impairs endothelial function in obese adults who are sedentary, a response that may be linked to inflammation. We sought to determine if circuit-based resistance training (CRT) attenuates acute resistance exercise-induced reductions in endothelial function in a population of young, obese, sedentary women and whether or not inflammation plays a role in this response. METHODS: Eighteen obese [body mass index (BMI) 30.0-40.0 kg · m(-2)] young premenopausal women were randomly assigned to either a CRT group or a no-exercise control group (CON). Conduit artery endothelial function was assessed using brachial artery flow-mediated dilation (FMD) determined by ultrasound before and after a single bout of strenuous weightlifting (SWL). In addition, circulating inflammatory mediators (tumor necrosis factor-α and C-reactive protein), blood pressure, fasting blood lipids, glucose, waist circumference, body composition, and aerobic capacity were assessed. RESULTS: Among participants randomized to the CRT group, 8 weeks of training led to considerable increases in FMD after SWL (P=0.001) compared to the CON group. However, no significant differences between the groups were observed in circulating inflammatory mediators, blood pressure, fasting blood lipids, or other physical and physiological characteristics. CONCLUSIONS: This study shows that CRT alleviates acute exertion-induced reductions in endothelial function among obese sedentary women in the absence of changes in inflammation.