We tested hypothesis that aerobic exercise with blood flow restriction (BFR) induced postexercise hypotension (PEH), and the reduction in blood pressure (BP) was due to peripheral vasodilation via the histamine receptors. Ten male subjects participated in this study. The subjects were randomly assigned to walk for 10 min at 6.4 km/h, 0% grade with or without BFR after taking histamine receptor blockade. Following exercise, BP was measured at 10 min interval for 60 min. Heart rate (HR), stroke volume (SV), cardiac output (CO), mean arterial pressure (MAP), and total peripheral resistance (TPR) were evaluated. Our results indicated that MAP was significantly lowered immediately after exercise at 20 min, 30 min, and 40 min before the blockade as opposed to after the blockade. A significant reduction in diastolic BP (DBP) occurred. There were no significant differences in HR, SV, CO, and TPR between before the blockade and after the blockade. MAP was substantially decreased at 20 min, 30 min, and 40 min before the blockade compared to resting (−3.2 ± 2.2, −3.3 ± 2.8, and −2.9 ± 2.5, respectively) while increasing MAP after the blockade. The current study demonstrated that low-intensity aerobic exercise with BFR lowered MAP via histamine receptor-induced peripheral vasodilation. In conclusion, BFR exercise training using short periods and low intensity would be greatly beneficial as a potential treatment to lower BP.

Evidence has suggested that post-exercise heart rate recovery (PHRR) is a useful tool in evaluating cardiac autonomic function. Altered cardiac autonomic function is characterized by heightened sympathetic activation and the abnormal reactivation of the parasympathetic nervous system and is associated with delayed HRR. Although grape seed extract (GSE) supplementation has been shown to increase nitric oxide production and modify sympathetic output, there is limited evidence on its potential beneficial effects on PHRR. We investigated the effect of GSE supplementation on PHRR during sympathetic overactivation induced by muscle metaboreflex activation (MMA) in young individuals. Participants were randomly assigned, via a double-blind, cross-over design, to either receive GSE (300 mg, two capsules) or PL (300 mg, two capsules), with a washout period of at least 72 h. between trials. A submaximal exercise test was performed using a cycle ergometer combined with an isometric handgrip exercise using a handgrip dynamometer and blood flow occlusion by placing a cuff over the brachial artery of the dominant arm. PHRR was measured at 5 s. intervals throughout the experiment. The PHRR was evaluated between GSE and PL at every min. for 300 s. PHRR kinetics significantly improved following GSE supplementation (74.3 ± 7.5 s) compared with the PL condition (86.2 ± 10.4 s). Our results suggest that GSE is effective in improving HRR kinetics during heightened sympathetic activity induced by MMA in young individuals (p = 0.034; ES = 0.4). Thus, regular treatment with GSE may provide a nonpharmacological intervention to reduce sympathetic hyperactivity in conditions where excessive sympathetic activity is consistently present.