These results suggest that impaired endothelial vasodilator function may be a mechanism contributing to exercise hypertension and may also be one link between exaggerated exercise BP and worsening hypertension.

Plasma nitrite is a major oxidation product of nitric oxide. It has also recently been suggested to perform an endocrine-like function as a nitric oxide donor in hypoxic tissues, allowing vasodilation. Exercise performance is limited in peripheral arterial disease due to an inadequate blood supply to working tissues. We hypothesized that exercise training in peripheral arterial disease subjects will demonstrate improved "plasma nitrite flux" and endothelial function, to accompany increased exercise performance. Peripheral arterial disease subjects were tested at baseline and following 3 months supervised or home exercise training.Venous blood (arm) was drawn at rest and 10min following a maximal graded treadmill test. Samples were added to heparin, centrifuged and plasma snap frozen for analysis by reductive chemiluminescence. Brachial artery endothelial function was measured in response to a hyperemic stimulus (flow-mediated dilation). At 3 months the peripheral arterial disease-supervised exercise group showed increases in claudication onset pain time (+138sec, p≤0.05) peak walking time (+260sec, p≤0.01), VO 2peak (1.3ml/kg/min, p≤0.05), brachial artery flow-mediated dilation (+2%, p≤0.05) and plasma nitrite flux (+33% p≤0.05). There were no changes in the peripheral arterial disease-home exercise group. The change in plasma nitrite flux predicted the change in claudication onset pain (r2=0.59, p≤0.01).These findings suggest changes in plasma nitrite are related to endothelial function and predict exercise performance in peripheral arterial disease.

BACKGROUND: Increased blood pressure (BP) in type 2 diabetes (T2DM) markedly increases cardiovascular disease morbidity and mortality risk compared to having increased BP alone. OBJECTIVE: To investigate whether exercise reduces suboptimal levels of untreated suboptimal BP or treated hypertension. DESIGN: Prospective, randomized controlled trial for 6 months. SETTING: Single center in Baltimore, MD, USA. PATIENTS: 140 participants with T2DM not requiring insulin and untreated SBP of 120-159 or DBP of 85-99 mmHg, or, if being treated for hypertension, any SBP <159 mmHg or DBP<99 mmHg; 114 completed the study. INTERVENTION: Supervised exercise, 3 times per week for 6 months compared with general advice about physical activity. MEASUREMENTS: Resting SBP and DBP (primary outcome); diabetes status, arterial stiffness assessed as carotid-femoral pulse-wave velocity (PWV), body composition and fitness (secondary outcomes). RESULTS: Overall baseline BP was 126.8±13.5 / 71.7 ± 9.0 mmHg, with no group differences. At 6 months, BP was unchanged from baseline in either group, BP 125.8±13.2 / 70.7±8.8 mmHg in controls; and 126.0 ± 14.2 / 70.3 ± 9.0 mmHg in exercisers, despite attaining a training effects as evidenced by increased aerobic and strength fitness and lean mass and reduced fat mass (all p<0.05), Overall baseline PWV was 959.9±333.1 cm/s, with no group difference. At 6-months, PWV did not change and was not different between group; exercisers, 923.7±319.8 cm/s, 905.5± 344.7, controls. LIMITATIONS: A completion rate of 81 %. CONCLUSIONS: Though exercisers improve fitness and body composition, there were no reductions in BP. The lack of change in arterial stiffness suggests a resistance to exercise-induced BP reduction in persons with T2DM.KEY WORDS: exercise training; diabetes; high blood pressure; randomized trial.

Obstructive sleep apnoea (OSA) is associated with increased cardiovascular disease (CVD) morbidity and mortality. It is accepted that OSA and obesity commonly coexist. The American Academy of Sleep Medicine recommends dietary-induced weight loss and exercise as lifestyle treatment options for OSA. However, most clinical trials upon which this recommendation is based have focused on establishing the effectiveness of calorie-restricted, often low-fat diets for improving OSA severity, whereas less attention has been given to the means through which weight loss is achieved (e.g. altered dietary quality) or whether diet or exercise mediates the associations between reduced weight, improved OSA severity and the CVD substrate. The current evidence suggests that the benefits of a low-carbohydrate or Mediterranean diet in overweight and obese individuals go beyond the recognised benefits of weight reduction. In addition, exercise has an independent protective effect on vascular health, which may counter the increased oxidative stress, inflammation and sympathetic activation that occur in OSA patients. This review aims to expand our understanding of the effects of diet and exercise on OSA and associated CVD complications, and sets the stage for continued research designed to explore optimal lifestyle strategies for reducing the CVD burden in OSA patients.

Purpose To examine the influence of a unilateral exercise training protocol on brachial artery reactivity (BAR) in 12 men (aged 81 ± 5 yr). Methods Brachial artery diameters and blood flow parameters were assessed, in both arms, using high-resolution ultrasonography, before and after 5 min of forearm occlusion, before and at the end of each week of a 4-wk training program. Training consisted of a unilateral handgrip training protocol (nondominant arm) at 60% of maximal voluntary handgrip strength, performed for 4 wk, 4 d·wk −1, 20 min per session, and a cadence of one contraction per 4 s. Results After training, handgrip strength increased 6.2% (baseline = 32.4 ± 7.0 kg vs week 4 = 34.4 ± 6.7 kg) in the trained arm only but failed to reach statistical significance (P = 0.10). No statistical changes were observed for blood pressure or resting HR. In contrast, BAR increased 45% (Pre = 2.9% vs Post = 4.1%, P = 0.05) in the trained arm only. Improvements in BAR were observed after the second week of training, without significant changes in the main vasodilatory trigger, defined as the relevant shear stimulus after forearm occlusion (P > 0.05). Conclusions These data indicate that a localized short-term exercise program results in significant improvements in vascular function in the trained arm of elderly men compared with the control arm. Furthermore, the findings indicate a statistically significant increase in BAR at the end of the second week of training, despite a similar trigger for dilation versus before training.

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These results indicate that the amount of physical activity was generally adequate on CRP days, but failed to reach target levels on non-CRP days. Thus CRP participants, when it is medically appropriate, should be encouraged to incorporate lifestyle physical activity, additional exercise, or both on non-CRP days to supplement their caloric expenditure from CRP exercise sessions.

Objective To investigate the effect of an exercise intervention on flow-mediated dilation (FMD) and circulating endothelial biomarkers in adults with type 2 diabetes (T2DM) Methods Sedentary adults (n=140), aged 40–65, with T2DM and untreated pre- or Stage I hypertension or treated hypertension were randomized to a 6-month, supervised, exercise program (3×week) or a sedentary control. Assessments included BMI, body and visceral fat, blood pressure, lipids, HbA1c, insulin sensitivity (QUICKI), fitness, FMD, E-selectin, P-selectin, intracellular and vascular cellular adhesion molecules (ICAM, VCAM), and tissue plasminogen activator (tPA). Intervention effects were compared by t-tests. Pearson’s correlations were calculated between changes in cardiovascular risk factors and endothelial outcomes. Results Exercisers significantly improved BMI (−0.6 kg/m2), body fat % (−1.4%), HbA1c (−0.5%), and fitness (2.9 mL/kg·min) vs. controls (p<0.05). However, there were no differences between groups in changes in FMD, E-selectin, P-selectin, ICAM, VCAM, or tPA. Among exercisers, changes in cardiovascular risk factors correlated with several biomarkers. Decreased P-selectin correlated with decreased BMI (r=0.29, p=0.04) and increased HDL cholesterol (r=−0.36, p=0.01). Decreased ICAM correlated with decreased triglycerides and HbA1c (r=0.30, p=0.04; r=0.31, p=0.03) and increased QUICKI (r=−0.28, p=0.05). Decreased tPA correlated with decreased total body and visceral fat (r=0.28, p=0.05; r=0.38, p=0.008) and increased QUICKI (r=−0.38, p=0.007). Conclusions While exercise resulted in improved fitness, body composition, and glycemic control, there were no changes in FMD or circulating endothelial biomarkers. The associations of changes in cardiovascular risk factors and endothelial biomarkers suggest that improvement in risk factors could mediate the exercise-induced improvements in endothelial function seen in prior studies.