Metaboreflex activation delays heart rate recovery after aerobic exercise in never‐treated hypertensive men. (21st September 2016)

• Record Type: Journal Article
• Authors: Peçanha, Tiago; de Brito, Leandro Campos; Fecchio, Rafael Yokoyama; de Sousa, Patricia Nascimento; da Silva Junior, Natan Daniel; de Abreu, Andrea Pio; da Silva, Giovanio Vieira; Mion‐Junior, Décio; Forjaz, Cláudia Lúcia de Moraes
• Is Part Of: Journal of physiology. Volume 594:Number 21(2016:Nov.)
• Page Start: 6211
• Page End: 6223
• Publication Date: 2016-09-21
• Subjects: baroreflex sensitivity -- exercise pressor reflex -- hypertension; Physiology -- Periodicals; 612.005
• DOI: 10.1113/JP272851
• Languages: English
• ISSNs: 0022-3751

Abstract

Abstract : Key points: Recent evidence indicates that metaboreflex regulates heart rate recovery after exercise (HRR). An increased metaboreflex activity during the post‐exercise period might help to explain the reduced HRR observed in hypertensive subjects. Using lower limb circulatory occlusion, the present study showed that metaboreflex activation during the post‐exercise period delayed HRR in never‐treated hypertensive men compared to normotensives. These findings may be relevant for understanding the physiological mechanisms associated with autonomic dysfunction in hypertensive men. Abstract: 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% V ̇ O 2 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 –1 and 2.1 ± 1.2 vs . 3.2 ± 2.4 ms mmHg −1, 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 –1 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. Key points: Recent evidence indicates that metaboreflex regulates heart rate recovery after exercise (HRR). An increased metaboreflex activity during the post‐exercise period might help to explain the reduced HRR observed in hypertensive subjects. Using lower limb circulatory occlusion, the present study showed that metaboreflex activation during the post‐exercise period delayed HRR in never‐treated hypertensive men compared to normotensives. These findings may be relevant for understanding the physiological mechanisms associated with autonomic dysfunction in hypertensive men.