Cardiovascular disease (CVD) is the primary cause of mortality worldwide. Cardiac autonomic dysfunction seems to be related to the genesis of several CVDs and is also linked to the increased risk of mortality in CVD patients. The quantification of heart rate decrement after exercise - known as heart rate recovery (HRR) - is a simple tool for assessing cardiac autonomic activity in healthy and CVD patients. Furthermore, since The Cleveland Clinic studies, HRR has also been used as a powerful index for predicting mortality. For these reasons, in recent years, the scientific community has been interested in proposing methods and protocols to investigate HRR and understand its underlying mechanisms. The aim of this review is to discuss current knowledge about HRR, including its potential primary and secondary physiological determinants, as well as its role in predicting mortality. Published data show that HRR can be modelled by an exponential curve, with a fast and a slow decay component. HRR may be influenced by population and exercise characteristics. The fast component mainly seems to be dictated by the cardiac parasympathetic reactivation, probably promoted by the deactivation of central command and mechanoreflex inputs immediately after exercise cessation. On the other hand, the slow phase of HRR may be determined by cardiac sympathetic withdrawal, possibly via the deactivation of metaboreflex and thermoregulatory mechanisms. All these pathways seem to be impaired in CVD, helping to explain the slower HRR in such patients and the increased rate of mortality in individuals who present a slower HRR.

Introduction:The acute blood pressure (BP) decrease is greater after evening than morning exercise, suggesting that evening training may have a greater hypotensive effect. Objective: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 3 groups: morning training (MT); evening training (ET); and control (C). Training groups cycled for 45min 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/week for 10 weeks. Clinic and ambulatory BP, hemodynamic, and autonomic mechanisms were evaluate d before and after the interventions. Clinic assessments were performed in the morning (7-9a.m.) and evening (6-8p.m.). Between-within ANOVAs were used (P≤0.05). Results: Only ET decreased clinic systolic BP differently from C and MT (morning assessment -5±6 mmHg and evening assessment -8±7 mmHg, P<0.05). Only ET reduced 24h and asleep diastolic BP differently from C and MT (-3±5 and -3±4 mmHg, respectively, P<0.05). Systemic vascular resistance (SVR) 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 SVR and vasomotor sympathetic modulation. Aerobic training conducted at both times of day increases baroreflex sensitivity, but with greater after ET.

Patients with Parkinson disease (PD) present blunted nocturnal blood pressure fall and similar ambulatory blood pressure variability (ABPV) measured by standard deviation (SD) and coefficient of variation (CV) compared with healthy subjects. However, these classical indices of ABPV have limited validity in individuals with circadian blood pressure alterations. New indices, such as the average of daytime and night-time standard deviation weighted by the duration of the daytime and night-time intervals (SD ) and the average real variability (ARV), remove the influence of the daytime and the night-time periods on ABPV. This study assessed ABPV by SD and ARV in PD. Twenty-one patients with PD (11 men, 66 ± 2 years, stages 2-3 of modified Hoehn & Yahr) and 21 matched controls without Parkinson disease (9 men, 64 ± 1 years old) underwent blood pressure monitoring for 24 h. ABPV was analysed by 24 h, daytime and night-time SD and CV, and by the SD and ARV. Systolic/diastolic 24-h and night-time SD and CV were similar between the patients with PD and the controls. The patients with PD presented higher daytime systolic/diastolic CV and SD than the controls (10·4 ± 0·9/12·3 ± 0·8 versus 7·0 ± 0·3/9·9 ± 0·5%, P<0·05; 12·6 ± 1·0/9·1 ± 0·5 versus 8·6 ± 0·4/7·5 ± 0·3 mmHg, P<0·05, respectively) as well as higher systolic/diastolic SD (10·9 ± 0·8/8·2 ± 0·5 versus 8·2 ± 0·3/7·1 ± 0·2 mmHg, P<0·05, respectively) and ARV (8·8 ± 0·6/6·9 ± 0·3 versus 7·2 ± 0·2/6·0 ± 0·2 mmHg, P<0·05, respectively). In conclusion, patients with PD have higher ABPV than control subjects as assessed by SD , CV , SD and AVR.

Heart rate (HR) recovery (HRR) and variability (HRV) after exercise are non-invasive tools used to assess cardiac autonomic regulation and cardiovascular prognosis. Autonomic recovery is slower after evening than morning exercise in healthy individuals, but this influence is unknown in subjects with autonomic dysfunction, although it may affect prognostic evaluation. This study compared post-exercise HRR and HRV after maximal morning and evening exercise in pre-hypertensive men. Ten volunteers randomly underwent two maximal exercise tests conducted in the morning (8-10 a.m.) and evening (6-8 p.m.). HRR60s (HR reduction at 60 s of recovery - prognostic index), T30 (short-term time-constant of HRR - parasympathetic reactivation marker), rMSSD30s (square root of the mean of the sum of the squares of differences between adjacent R-R intervals on subsequent 30 s segments - parasympathetic reactivation marker), and HRRτ (time constant of the first order exponential fitting of HRR - marker of sympathetic withdraw and parasympathetic reactivation) were measured. Paired t-test and two-way ANOVA were used. HRR60s and HRRτ were similar after exercise in the morning and evening (27 ± 7 vs. 29 ± 7 bpm, p = 0.111, and 79 ± 14 vs. 96 ± 29 s, p = 0.119, respectively). T30 was significantly greater after evening exercise (405 ± 215 vs. 295 ± 119 s, p = 0.002) and rMSSD30s was lower in the evening (main factor session, p = 0.009). In conclusion, in pre-hypertensive men, the prognostic index of HRR, HRR60s, is not affected by the time of day when exercise is conducted. However, post-exercise parasympathetic reactivation, evaluated by T30 and rMSSD30s, is blunted after evening exercise.

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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 AE 8 years) and 25 NT (45 AE 8 years) men randomly underwent two exercise sessions (30 min of cycling at 70% VO 2peak ) 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, shortterm time constant of HRR (T30) and the time constant of the HRR after exponential fitting (HRRs). 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 = 39AE12 versus 36 AE 10 bpm, P≤0Á05) and increased postexercise HRV (lnRMSSD = 1Á8 AE 0Á7 versus 1Á6 AE 0Á7 ms, P≤0Á05). 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.

The role of metaboreflex on heart rate recovery after exercise (HRR) is controversial. It is speculated that this mechanism is active in exercises with larger muscle masses, however it has not been tested after a typical aerobic exercise. The aim of this study was to evaluate the influence of metaboreflex on HRR. 12 healthy middle‐aged men randomly underwent 2 sessions consisting of an exercise (cycle ergometer, 70% VO2peak, 30 min) followed by 5 min of recovery. In each session, the recovery was performed with (occlusion) or without (control) leg circulatory occlusion (cuffs at the hips inflated to supra‐systolic pressure). ECG was registered and HRR was assessed by: heart rate reduction after 60 (HRR60s) and 300s (HRR300s) of recovery; short‐term time constant of HRR (T30); time constant of the HRR after exponential fitting (HRRτ); and mean values of HR in segments of 30s (HR30s). Heart rate variability (HRV) was assessed by the root mean square residual (RMS) and square root of mean squared differences of successive R–R intervals (rMSSD) on subsequent 30‐s segments. Paired T‐test, Wilcoxon test and ANOVA were employed. HRR60s (25 ± 7 vs. 22 ± 12 beats.min‐1, p = 0.69), T30 (284 ± 155 vs. 309 ± 253 s, p = 0.89) and HRRτ (120 ± 45 vs. 107 ± 103 s, p = 0.75) were similar between control and occlusion sessions, respectively. HRR300s was significantly lower in occlusion session (30 ± 13 vs. 38 ± 14, p = 0.05). There was no session vs. time interaction for the rMSSD index (p = 0.46), while HR30s and RMS had significant time vs. session interactions (p = 0.00 and 0.01, respectively), showing slower decrease of HR30s and slower increase of RMS in the occlusion session. In conclusion, metaboreflex activation delays HRR, particularly at the slower phase of HRR.Funding: FAPESP 2013/044997‐0 and 2013/05519‐4; CAPES PROEX

Objective:American guidelines included dynamic resistance exercise (DRE) and isometric handgrip (IH) in hypertension treatment. A single session of DRE decreases blood pressure (BP) during the recovery period, which has been described as post-exercise hypotension (PEH). However, the occurrence of PEH after a session of IH is controversial and the post-exercise effects of the association of DRE and IH, in a combined resistance exercise (CRE), has not been evaluated. Thus, this study investigated the effects of DRE, IH and CRE on post-exercise BP and its hemodynamic, autonomic and vascular mechanisms.Design and method:Seventy medicated hypertensive men (52 ± 8 years) were randomly allocated to perform 1 of 4 interventions: DRE (8 exercises, 3 sets, 50%1RM, repetitions until moderate fatigue), IH (4 sets, 2 min-unilateral contraction, 30% MVC), CRE (DRE + IH) and control (CO - seated resting). Office BP, systemic hemodynamics (CO2 rebreathing technique), cardiovascular autonomic modulation [spectral analysis of heart rate (HR) and BP variabilities] and brachial vascular parameters (ultrasound) were evaluated before and after the interventions. Thus, the responses to interventions (post – pre-intervention values) were calculated and compared among the groups by ANOVAs with significance level set at P < 0.05.Results:Responses to IH were similar to CO, showing that a single session of IH did not promote PEH, and did not affect any of the BP mechanisms. On the other hand, DRE and CRE induced responses significantly different from IH and CO. DRE and CRE significantly decreased systolic BP, diastolic BP, mean BP, stroke volume and cardiac baroreflex sensitivity, while they significantly increased HR, brachial artery diameter, blood flow and vascular conductance during the post-exercise period. Additionally, DRE significantly decreased post-exercise cardiac vagal modulation (HFR-R, nu) and increased cardiac sympathovagal balance (LF/HF).Conclusions:DRE, but not IH, elicits PEH, which is accompanied by vasodilation and increased HR, via a higher sympathovagal balance and lower baroreflex sensitivity. The addition of IH to DRE, in a CRE, does not potentiate PEH and did not change its mechanisms.