Abstract
Previous studies have shown that IHG and rhythmic handgrip training can reduce arterial blood pressure (ABP), especially in hypertensive subjects. The mechanisms underlying these effects are unclear, but it has been proposed that IHG training achieves its effects mainly by decreasing sympathetic activity. However, in hypertensive patients, IHG decreases plasma markers of oxidative stress. Thus, we tested the hypothesis in young normotensive men, that IHG improves endothelial function remotely, in the non‐trained arm. In 10 recreationally‐active men (18–25 years), we used laser Doppler fluximetry on the non‐dominant forearm to record changes in cutaneous red cell flux (RCF) evoked by iontophoresis of acetylcholine (ACh, 8 × 20s pulses: 7 at 100 μA, 8th at 200 μA, at 60s intervals), and following release of arterial occlusion for 3 min (reactive hyperaemia) before and after IHG training of the dominant forearm. IHG training comprised 4×3 min contractions at 30% Maximum voluntary contraction (MVC) at 5 min intervals, 4 days/week for 4 weeks. Before and after IHG training, we tested the contribution of COX products to dilator responses. IHG training did not affect resting ABP: 124±1.8/70±1.7 vs 125±1.8/72±1.6 mmHg. As expected, MVC was increased in the trained arm (29.0±1.3 vs 33.5±1.5Kg: P<0.05, paired t‐test), but not in the contralateral arm (26±0.9 vs 27.1±2.6Kg). Before training, ACh‐induced dilator responses were unaltered by COX inhibition with aspirin (600mg p.o.): maximum RCF 192.2±5.5 vs 182.6±4.7 PU respectively), suggesting any contribution of COX dilator and constrictor products was balanced. By contrast, aspirin attenuated peak reactive hyperaemia from 92.9±2.5 to 75.07± 2.58PU (P<0.05 : RMANOVA) indicating a contribution of COX dilator products. After IHG training, neither the magnitude of ACh‐induced dilatation, nor reactive hyperaemia was changed, but aspirin now augmented the ACh response: maximum RCF 192.6±4.1 increased to 227.5±5.2PU (P<0.001), but had no effect on reactive hyperaemia (92.1±2.3 vs 91.8±3.6PU). These results suggest that in young normotensive men, IHG training of one arm has no effect on ABP and no net effect on the magnitude of endothelial‐dependent dilatation remotely, but does change the balance of influence of vasoconstrictor and dilator COX products. We propose that during IHG training, the contribution of COX dilator products to endothelium‐dependent, agonist‐evoked dilatation and reactive hyperaemia is attenuated and replaced with the influence of another dilator such as nitric oxide, leaving vasoconstrictor COX products limiting even greater agonist‐induced dilatation.Support or Funding InformationAlexander S. Onassis Public Benefit Foundation
Published Version
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