Activation of Mechanoreflex, but not Central Command, Delays Heart Rate Recovery after Exercise in Healthy Men.

This study tested the hypotheses that activation of central command and muscle mechanoreflex during post-exercise recovery delays fast-phase heart rate recovery with little influence on the slow phase. Twenty-five healthy men underwent three submaximal cycling bouts, each followed by a different 5-min recovery protocol: active (cycling generated by the own subject), passive (cycling generated by external force) and inactive (no-cycling). Heart rate recovery was assessed by the heart rate decay from peak exercise to 30 s and 60 s of recovery (HRR30s, HRR60s fast phase) and from 60 s-to-300 s of recovery (HRR60-300s slow phase). The effect of central command was examined by comparing active and passive recoveries (with and without central command activation) and the effect of mechanoreflex was assessed by comparing passive and inactive recoveries (with and without mechanoreflex activation). Heart rate recovery was similar between active and passive recoveries, regardless of the phase. Heart rate recovery was slower in the passive than inactive recovery in the fast phase (HRR60s=20±8vs.27 ±10 bpm, p<0.01), but not in the slow phase (HRR60-300s=13±8vs.10±8 bpm, p=0.11). In conclusion, activation of mechanoreflex, but not central command, during recovery delays fast-phase heart rate recovery. These results elucidate important neural mechanisms behind heart rate recovery regulation.

Effects of postexercise cooling on heart rate recovery in normotensive and hypertensive men.

BACKGROUND: Postexercise heart rate recovery (HRR) is determined by cardiac autonomic restoration after exercise and is reduced in hypertension. Postexercise cooling accelerates HRR in healthy subjects, but its effects in a population with cardiac autonomic dysfunction, such as hypertensives (HT), may be blunted. This study assessed and compared the effects of postexercise cooling on HRR and cardiac autonomic regulation in HT and normotensive (NT) subjects. METHODS: Twenty-three never-treated HT (43 ± 8 years) and 25 NT (45 ± 8 years) men randomly underwent two exercise sessions (30 min of cycling at 70% VO2peak ) followed by 15 min of recovery. In one randomly allocated session, a fan was turned on in front of the subject during the recovery (cooling), while in the other session, no cooling was performed (control). HRR was assessed by heart rate reductions after 60 s (HRR60s) and 300 s (HRR300s) of recovery, short-term time constant of HRR (T30) and the time constant of the HRR after exponential fitting (HRRτ). HRV was assessed using time- and frequency-domain indices. RESULTS: HRR and HRV responses in the cooling and control sessions were similar between the HT and NT. Thus, in both groups, postexercise cooling equally accelerated HRR (HRR300s = 39±12 versus 36 ± 10 bpm, P≤0·05) and increased postexercise HRV (lnRMSSD = 1·8 ± 0·7 versus 1·6 ± 0·7 ms, P≤0·05). CONCLUSION: Differently from the hypothesis, postexercise cooling produced similar improvements in HRR in HT and NT men, likely by an acceleration of cardiac parasympathetic reactivation and sympathetic withdrawal. These results suggest that postexercise cooling equally accelerates HRR in hypertensive and normotensive subjects.

Metaboreflex activation delays heart rate recovery after aerobic exercise in never-treated hypertensive 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. 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% 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-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.