Morning versus Evening Aerobic Training Effects on Blood Pressure in Treated Hypertension

Introduction The acute blood pressure (BP) decrease is greater after evening than morning exercise, suggesting that evening training (ET) may have a greater hypotensive effect. Objective This study aimed to compare the hypotensive effect of aerobic training performed in the morning versus evening in treated hypertensives. Methods Fifty treated hypertensive men were randomly allocated to three groups: morning training (MT), ET, and control (C). Training groups cycled for 45 min at moderate intensity (progressing from the heart rate of the anaerobic threshold to 10% below the heart rate of the respiratory compensation point), while C stretched for 30 min. Interventions were conducted 3 times per week for 10 wk. Clinic and ambulatory BP and hemodynamic and autonomic mechanisms were evaluated before and after the interventions. Clinic assessments were performed in the morning (7:00-9:00 am) and evening (6:00-8:00 pm). Between-within ANOVA was used (P ≤ 0.05). Results Only ET decreased clinic systolic BP differently from C and MT (morning assessment -5 ± 6 mm Hg and evening assessment -8 ± 7 mm Hg, P < 0.05). Only ET reduced 24 h and asleep diastolic BP differently from C and MT (-3 ± 5 and -3 ± 4 mm Hg, respectively, P < 0.05). Systemic vascular resistance decreased from C only in ET (P = 0.03). Vasomotor sympathetic modulation decreased (P = 0.001) and baroreflex sensitivity (P < 0.02) increased from C in both training groups with greater changes in ET than MT. Conclusions In treated hypertensive men, aerobic training performed in the evening decreased clinic and ambulatory BP due to reductions in systemic vascular resistance and vasomotor sympathetic modulation. Aerobic training conducted at both times of day increases baroreflex sensitivity, but with greater after ET

Effects of post-exercise cooling on heart rate recovery in normotensive and hypertensive men

Background: Post-exercise heart rate recovery (HRR) is determined by cardiac autonomic restoration after exercise and is reduced in hypertension. Post-exercise 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 post-exercise cooling on HRR and cardiac autonomic regulation in HT and normotensive (NT) subjects. Methods: Twenty-three never-treated HT (43±8 ys) and 25 NT (45±8 ys) 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 (HRR60s) and 300s (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, post-exercise cooling equally accelerated HRR (HRR300s = 39±12 vs. 36±10 bpm, p≤0.05) and increased post44 exercise HRV (lnRMSSD = 1.8±0.7 vs. 1.6±0.7 ms, p≤0.05). Conclusion: Differently from the hypothesis, post-exercise 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 post-exercise cooling equally accelerates HRR in hypertensive and normotensive subjects

White-coat hypertension and normotension in the League of Hypertension of the Hospital das Clínicas, FMUSP: prevalence, clinical and demographic characteristics

OBJECTIVE: To assess the prevalence of white-coat normortension, white-coat hypertension, and white-coat effect. METHODS: We assessed 670 medical records of patients from the League of Hypertension of the Hospital das Clínicas of the Medical School of the University of São Paulo. White-coat hypertension (blood pressure at the medical office: mean of 3 measurements with the oscillometric device <FONT FACE=Symbol>&sup3;</FONT>140 or <FONT FACE=Symbol>&sup3;</FONT>90 mmHg, or both, and ambulatory blood pressure monitoring mean during wakefulness < 135/85) and white-coat normotension (office blood pressure < 140/90 and blood pressure during wakefulness on ambulatory blood pressure monitoring <FONT FACE=Symbol>&sup3;</FONT> 135/85) were analyzed in 183 patients taking no medication. The white-coat effect (difference between office and ambulatory blood pressure > 20 mmHg for systolic and 10 mmHg for diastolic) was analyzed in 487 patients on treatment, 374 of whom underwent multivariate analysis to identify the variables that better explain the white-coat effect. RESULTS: Prevalence of white-coat normotension was 12%, prevalence of white-coat hypertension was 20%, and prevalence of the white-coat effect was 27%. A significant correlation (p<0.05) was observed between white-coat hypertension and familial history of hypertension, and between the white-coat effect and sex, severity of the office diastolic blood pressure, and thickness of left ventricular posterior wall. CONCLUSION: White-coat hypertension, white-coat normotension, and white-coat effect should be considered in the diagnosis of hypertension

Activation of mechanoreflex 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 delay fast-phase heart rate recovery with little influence on 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 30s and 60s of recovery (HRR30s, HRR60s -fast-phase) and from 60s-to-300s 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- (HRR60s=20±8vs.27±10bpm, p<0.01), but not in the slow-phase (HRR60-300s=13±8vs.10±8bpm, 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