This study showed that aerobic training promotes an increase in the expression of miRNA-126 and that this may be related to exercise-induced cardiac angiogenesis, by indirect regulation of the VEGF pathway and direct regulation of its targets that converged in an increase in angiogenic pathways, such as MAPK and PI3K/Akt/eNOS.

Post-exercise hypotension (PEH), calculated by the difference between post and pre-exercise values, it is greater after exercise performed in the evening than the morning. However, the hypotensive effect of morning exercise may be masked by the morning circadian increase in blood pressure. This study investigated PEH and its hemodynamic and autonomic mechanisms after sessions of aerobic exercise performed in the morning and evening, controlling for responses observed after control sessions performed at the same times of day. Sixteen pre-hypertensive men underwent four sessions (random order): two conducted in the morning (7:30am) and two in the evening (5pm). At each time of day, subjects underwent an exercise (cycling, 45 min, 50%VO2peak) and a control (sitting rest) session. Measurements were taken pre- and post-interventions in all the sessions. The net effects of exercise were calculated for each time of day by [(post-pre exercise)-(post-pre control)] and were compared by paired t-test (P<0.05). Exercise hypotensive net effects (e.g., decreasing systolic, diastolic and mean blood pressure) occurred at both times of day, but systolic blood pressure reductions were greater after morning exercise (-7±3 vs. -3±4 mmHg, P<0.05). Exercise decreased cardiac output only in the morning (-460±771 ml/min, P<0.05), while it decreased stroke volume similarly at both times of day and increased heart rate less in the morning than in the evening (+7±5 vs. +10±5 bpm, P<0.05). Only evening exercise increased sympathovagal balance (+1.5±1.6, P<0.05) and calf blood flow responses to reactive hyperemia (+120±179 vs. -70±188 U, P<0.05). In conclusion, PEH occurs after exercise conducted at both times of day, but the systolic hypotensive effect is greater after morning exercise when circadian variations are considered. This greater effect is accompanied by a reduction of cardiac output due to a smaller increase in heart rate and cardiac sympathovagal balance.

Muscle metaboreflex influences heart rate (HR) regulation after aerobic exercise. Therefore, increased metaboreflex sensitivity may help to explain the delayed HR recovery (HRR) reported in hypertension. The present study assessed and compared the effect of metaboreflex activation after exercise on HRR, cardiac baroreflex sensitivity (cBRS) and heart rate variability (HRV) in normotensive (NT) and hypertensive (HT) men. Twenty-three never-treated HT and 25 NT men randomly underwent two-cycle ergometer exercise sessions (30 min, 70% V̇O2 peak ) followed by 5 min of inactive recovery performed with (occlusion) or without (control) leg circulatory occlusion (bilateral thigh cuffs inflated to a suprasystolic pressure). HRR was assessed via HR reduction after 30, 60 and 300 s of recovery (HRR30s, HRR60s and HRR300s), as well as by the analysis of short- and long-term time constants of HRR. cBRS was assessed by sequence technique and HRV by the root mean square residual and the root mean square of successive differences between adjacent RR intervals on subsequent 30 s segments. Data were analysed using two- and three-way ANOVA. HRR60s and cBRS were significant and similarly reduced in both groups in the occlusion compared to the control session (combined values: 20 ± 10 vs. 26 ± 9 beats min and 2.1 ± 1.2 vs. 3.2 ± 2.4 ms mmHg , respectively, P < 0.05). HRR300s and HRV were also reduced in the occlusion session, although these reductions were significantly greater in HT compared to NT (-16 ± 11 vs. -8 ± 15 beats min for HRR300s, P < 0.05). The results support the role of metaboreflex in HRR and suggest that increased metaboreflex sensitivity may partially explain the delayed HRR observed in HT men.

. Effects of oral N-acetylcysteine on walking capacity, leg reactive hyperemia, and inflammatory and angiogenic mediators in patients with intermittent claudication.