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BACKGROUND: Low cardiorespiratory fitness is associated with poor prognosis in individuals with coronary artery disease and after coronary artery bypass grafting surgery. Thus, we comment about a meta-analysis that adds important information about the effect of exercise training on cardiac autonomic function in individuals following coronary artery bypass grafting surgery. MAIN BODY: The study by Kushwaha et al. showed positive effects for heart rate variability and heart rate recovery in subjects after coronary artery bypass grafting surgery in response to acute physical training. These data are relevant, since heart rate variability is an independent predictor of for all-cause and cardiovascular mortality for individuals with cardiovascular disorders. Additionally, attenuated heart rate recovery is associated with increased risk for the same outcomes. Moreover, we summarize the quantitative data from studies that compared the effect of physical training in comparison with control group in cardiorespiratory fitness in adults following coronary artery bypass grafting. CONCLUSIONS: Our findings suggest that improvements in peak oxygen consumption result in an additional benefit in adults following coronary artery bypass grafting. Considered that, the increased cardiorespiratory fitness is an independent predictor of longer survival in coronary artery disease.

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Different exercise models have been used in patients with type 2 diabetes mellitus (T2D), like moderate intensity continuous training (MICT) and high intensity interval training (HIIT); however, their effects on autonomic modulation are unknown. The present study aimed to compare the effects of different exercise modes on autonomic modulation in patients with T2D. In total, 44 adults with >5 years of T2D diagnosis were recruited and stratified into three groups: HIIT-30:30 (n = 15, age 59.13 ± 5.57 years) that performed 20 repetitions of 30 s at 100% of VO2peak with passive recovery, HIIT-2:2 (n = 14, age 61.20 ± 2.88) that performed 5 repetitions of 2 min at 100% of VO2peak with passive recovery, and MICT (n = 15, age 58.50 ± 5.26) that performed 14 min of continuous exercise at 70% of VO2peak. All participants underwent anamnesis and evaluation of cardiorespiratory fitness and cardiac autonomic modulation. All protocols were equated by total distance and were performed two times per week for 8 weeks. Group × time interactions were observed for resting heart rate (HRrest) [F(2.82) = 3.641; p = 0.031] and SDNN [F(2.82) = 3.462; p = 0.036]. Only the HIIT-30:30 group significantly reduced SDNN (p = 0.002 and 0.025, respectively). HRrest reduced more in the HIIT-30:30 group compared with the MICT group (p = 0.038). Group × time interactions were also observed for offTAU [F(2.82) = 3.146; p = 0.048] and offTMR [F(2.82) = 4.424; p = 0.015]. The MICT group presented increased values of offTAU compared with the HIIT-30:30 and HIIT-2:2 groups (p = 0.001 and 0.013, respectively), representing a slower HR response after eight weeks of intervention. HIIT, specially HIIT-30:30, represents a promising measure for improving autonomic modulation in patients with T2D.

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OBJECTIVES: To determine whether the time for peak exercise heart rate to return to resting heart rate after the 6-minute walk test (6MWT) can predict cardiac events in patients with heart failure (HF) within 2 years. DESIGN: Prospective cohort study. SETTING: HF outpatient facility at a tertiary teaching hospital. PARTICIPANTS: Seventy-six patients with HF, New York Heart Association functional classification II and III, and left ventricular ejection fraction <50%. MAIN OUTCOME MEASURES: Patients used a heart rate monitor to measure the time for peak exercise heart rate to return to resting heart rate after the 6MWT. Data were analysed using Polar Pro-Trainer 5 software (Kempele, Finland). Patients were followed for >2 years for cardiac events (hospitalisations and death). RESULTS: Thirty-four patients had cardiac events during the 2-year follow-up period. However, there was a significant difference in the time to return to resting heart rate between the groups with and without cardiac events {with 3.6 (SD 1.1) vs without 2.8 (SD 1.1) minutes; mean difference of 0.79 (95% confidence interval (CI) of the difference 0.28 to 1.28; P=0.003}. No significant differences between patients with and without cardiac events were found for mean walking distance, mean heart rate recovery at 1minute and mean heart rate recovery at 2minutes. The receiver operating curve discriminated between patients with and without cardiac events (área under the curve 0.71, 95% CI 0.61 to 0.81; P<0.001). Using logistic regression analysis, prolonged time to return to resting heart rate (≥3minutes) independently increased the risk for cardiac events 6.9-fold (95% CI 2.34 to 20.12; P<0.001). The Kaplan-Meier curve showed more cardiac events in patients with prolonged time to return to resting heart rate (P=0.028). CONCLUSIONS: Prolonged time to return to resting heart rate (≥3minutes) after the 6MWT was an independent predictor of cardiac events in patients with HF.

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Introduction: Type 2 diabetes (T2D) is characterized by a metabolic disorder that elevates blood glucose concentration. Chronic hyperglycemia has been associated with several complications in patients with T2D, one of which is cardiac autonomic dysfunction that can be assessed from heart rate variability (HRV) and heart rate recovery (HRR) response, both associated with many aspects of health and fitness, including severe cardiovascular outcomes. Objective: To evaluate the effects of T2D on cardiac autonomic modulation by means of HRV and HRR measurements. Materials and Methods: This study has an observational with case-control characteristic and involved ninety-three middle-aged adults stratified into two groups (control group - CG, n = 34; diabetes group - DG, n = 59). After signing the free and informed consent form, the patients were submitted to the evaluation protocols, performed biochemical tests to confirm the diagnosis of T2D, collection of R-R intervals for HRV analysis and cardiopulmonary effort test to quantify HRR. Results: At rest, the DG showed a reduction in global HRV (SDNN= 19.31 ± 11.72 vs CG 43.09 ± 12.74, p < 0.0001), lower parasympathetic modulation (RMSSD= 20.49 ± 14.68 vs 52.41 ± 19.50, PNN50 = 4.76 ± 10.53 vs 31.24 ± 19.24, 2VD%= 19.97 ± 10.30 vs 28.81 ± 9.77, p < 0.0001 for both indices) and higher HRrest when compared to CG. After interruption of physical exercise, a slowed heart rate response was observed in the DG when compared to the CG. Finally, a simple linear regression showed that fasting glycemia was able to predict cardiac autonomic involvement in volunteers with T2D. Conclusion: Patients with T2D presented lower parasympathetic modulation at rest and slowed HRR after physical exercise, which may be associated with higher cardiovascular risks. The findings show the glycemic profile as an important predictor of impaired cardiac autonomic modulation.

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There are several methods to assess the function of the autonomic nervous system. Among them, heart rate recovery (HRR) is an accepted, easy, low-cost technique. Different pathological conditions have been related to the development of autonomic dysfunction. Our study aimed to evaluate the relationship between HRR and HRR-derived parameters in ambulatory patients with asthma or type 2 diabetes followed at the National Institutes of Health in Mexico City. A total of 78 participants, 50 women and, 28 men were enrolled; anthropometric, respiratory evaluations, and fasting blood samples were taken before participants performed a 6-min walking test (6MWT). Abnormal HRR was defined as a drop of ≤8 and ≤11 beats/min at 1 or 2 min and correlated negatively with basal oxygen saturation at 1 min. Heart rate at 1 min, correlated negatively with final oxygen saturation (p < 0.01). Statistically significant negative correlations were also observed between red cell count and white blood cell count and HOMA-IR with a p < 0.01. Since discrete hematological but significant changes correlated with HRR and HRR-derived parameters, we consider that these measures are helpful in clinical settings to identify subclinical autonomic dysfunction that permits us to prevent or anticipate chronic and fatal clinical outcomes.

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Objective: The present study sought to expand upon prior investigations of the relationship between the post-exercise heart rate recovery (HRR) and the cardiac autonomic responsiveness after orthostatic stress test.Method: HRR at the 1st, 3rd, and 5th min after maximal exercise test were correlated with relative change (Δ%) of time-domain (CV, pNN50, and rMSSD) and frequency-domain (TP, LF, HF, and LF/HF ratio) indices of heart rate variability (HRV) after active orthostatic test in 46 healthy men. Statistical analysis employed non-parametric tests with a p-value set at 5%.Results: HRR at 1st min correlated with Δ%pNN50 (rs:0.36 - p = .02). In the 3rd and 5th min, these measures correlated with Δ%pNN50, Δ%rMSSD, Δ%CV, Δ%TP, and Δ%HF indices (rs:0.33, 0.59 - p ≤ .05). Coefficient of HRR at the 1st min correlated with Δ%pNN50, Δ%rMSSD, and Δ%HF (rs:0.28, 0.45 - p ≤ .05). The 3rd and 5th min showed correlation with Δ%pNN50, Δ%rMSSD, Δ%HF, Δ%CV, and Δ%TP (rs:0.37, 0.64 - p ≤ .05). No correlation was found with indices combined sympathetic-parasympathetic modulation and HRR. After the sample was divided into high and low parasympathetic responsiveness subgroups after the orthostatic test, faster HRR was associated with the degree of parasympathetic responsiveness (reduction) following postural change (p ≤ .05).Conclusion: HRR throughout the 1st to 5th min is positively correlated with parasympathetic responsiveness and overall cardiac autonomic modulation of HRV after the orthostatic stress test, and faster HRR is positively correlated with the relative degree of parasympathetic responsiveness after the active postural change at rest in healthy men.

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BACKGROUND: Inflammation caused by chronic lung disease in childhood may lead to delayed heart rate recovery (HRR) however, there is lack of evidence on HRR in this population. The aim was to assess HRR after functional capacity testing in asthmatic children and adolescents and to compare with severity and disease control. METHOD: This was a study secondary to a randomized control trial. The modified shuttle test (MST) was performed to assess functional capacity and HRR. This is an externally cadenced test in which the distance walked is the outcome. HRR was assessed after MST and was defined as HR at exercise peak minus HR in the second minute after the end of exercise. Asthma control was assessed by the Asthma Control Test (ACT). Data normality was tested by Shapiro Wilk and the comparison between groups was made by Student's t test or Mann Whitney test for numerical variables, and by Chi-square test for categorical variables. Statistical significance was considered when p < 0.05. SPSS version 20 was used in the analyzes. RESULTS: The sample included 77 patients diagnosed with asthma (asthma group - AG) who were regularly treated for asthma. Control group (CG) consisted of 44 volunteers considered healthy, matched in age and gender to AG. The median age of CG was 12 (10-14) years and in AG 11 (9-13 years) being classified as mild to moderate asthmatic, and 57% of the sample had controlled asthma by ACT. Distance walked in the CG was 952 ± 286 m and AG 799 ± 313 m, p = 0.001. HRR was more efficient in CG (79 ± 15 bpm) compared to AG (69 ± 12 bpm), p = 0.001. The mild (69 ± 12 beats) and severe (72 ± 15 beats) AG presented worse HRR compared to control group (79 ± 15 bpm), p < 0.05. CONCLUSIONS: Asthmatic children and adolescents have delayed HRR after modified Shuttle test compared to their peers, suggesting that asthma leads to autonomic nervous system imbalance. TRIAL REGISTRATION: Registered in Clinical Trials under number NCT02383069 and approved by the Universidade Nove de Julho - UNINOVE Research Ethics Committee, protocol number 738192/2014.

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Abstract Aims: The purpose of this study was to evaluate the acute effects of different resistance exercise (RE) volumes on postexercise cardiac autonomic modulation in men. Methods: Ten young men (25.5 ± 4.9 years, 24.8 ± 2.1 kg/m2) performed 3 trials of RE with 1, 2 or 3 sets (48-72 h between each trial) of 10-12 repetitions (70% of the one-maximum repetition) of bench press, leg press, and barbell row. Heart rate variability (HRV) was assessed at the 1st and 5th minutes of recovery (fast phase) and 3 consecutive 5-minute intervals from the 5th to 20th minute of recovery (slow phase). Parasympathetic and global modulations were assessed using the SD1 and SD2 indices of HRV, respectively. The comparison of the interventions was performed using the Friedman and Wilcoxon tests (p<0.05). Results: Lower parasympathetic modulation was identified after 2 and 3 sets compared to 1 set in both the fast and slow recovery phases (p= 0.004-0.05). Lower global modulation was identified after 3 sets compared to 1 set in both fast and slow recovery phases (p= 0.005-0.01). No differences in post-exercise parasympathetic and global modulation were observed between 2 and 3 sets. Conclusion: We concluded that 2 and 3 sets of RE compared to 1 set promoted higher autonomic reduction on the post-exercise phase, which should be considered by coaches when prescribing an RE program for untrained participants or intend to manipulate the postexercise organic recovery.

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KEY POINTS: Dysfunction of post-exercise cardiac autonomic control is associated with increased mortality risk in healthy adults and in patients with cardiorespiratory diseases. The afferent mechanisms that regulate the post-exercise cardiac autonomic control remain unclear. We found that afferent signals from carotid chemoreceptors restrain the post-exercise cardiac autonomic control in healthy adults and patients with pulmonary arterial hypertension (PAH). Patients with PAH had higher carotid chemoreflex sensitivity, and the magnitude of carotid chemoreceptor restraint of autonomic control was greater in patients with PAH as compared to healthy adults. The results demonstrate that the carotid chemoreceptors contribute to the regulation of post-exercise cardiac autonomic control, and suggest that the carotid chemoreceptors may be a potential target to treat post-exercise cardiac autonomic dysfunction in patients with PAH. ABSTRACT: Dysfunction of post-exercise cardiac autonomic control predicts mortality, but its underlying mechanisms remain unclear. We tested whether carotid chemoreflex activity restrains post-exercise cardiac autonomic control in healthy adults (HA), and whether such restraint is greater in patients with pulmonary arterial hypertension (PAH) who may have both altered carotid chemoreflex and altered post-exercise cardiac autonomic control. Twenty non-hypoxaemic patients with PAH and 13 age- and sex-matched HA pedalled until 90% of peak work rate observed in a symptom-limited ramp-incremental exercise test. Recovery consisted of unloaded pedalling for 5 min followed by seated rest for 6 min. During recovery, subjects randomly inhaled either 100% O2 (hyperoxia) to inhibit the carotid chemoreceptor activity, or 21% O2 (normoxia) as control. Post-exercise cardiac autonomic control was examined via heart rate (HR) recovery (HRR; HR change after 30, 60, 120 and 300 s of recovery, using linear and non-linear regressions of HR decay) and HR variability (HRV; time and spectral domain analyses). As expected, the PAH group had higher carotid chemosensitivity and worse post-exercise HRR and HRV than HA. Hyperoxia increased HRR at 30, 60 and 120 s and absolute spectral power HRV in both groups. Additionally, hyperoxia resulted in an accelerated linear HR decay and increased time domain HRV during active recovery only in the PAH group. In conclusion, the carotid chemoreceptors restrained recovery of cardiac autonomic control from exercise in HA and in patients with PAH, with the restraint greater for some autonomic indexes in patients with PAH.

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The aim of the present study was to compare differences in heart rate response following a treadmill exercise test in elderly obese women categorized into groups based on relative handgrip strength. Eighty-eight obese elderly women who were between the ages of 60 and 87 participated in the study and were categorized and enrolled to one of two groups based on lower (< 1.51 m2) or higher (≥ 1.51 m2) relative handgrip strength, respectively. The heart rate recovery in the first and second minutes following the treadmill exercise test and the chronotropic index were compared between groups. The higher relative handgrip strength group presented a significantly higher peak heart rate during exercise and a quicker heart rate recovery following exercise versus the lower relative handgrip strength group (p<0.05). Furthermore, there was a tendency (p=0.059) toward a significantly greater chronotropic index in the higher versus the lower relative handgrip strength group. In conclusion, elderly women with greater relative handgrip strength also demonstrated a better heart rate response during and following exercise, possibly indicating better autonomic balance. The relative handgrip strength might be an important and inexpensive tool for the elderly obese women to indirect assess cardiovascular health.

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Heart rate recovery (HRR) is a strong mortality predictor. Exercise training (ET) and ß-blocker therapy have significant impact on the HRR of patients following myocardial infarction (MI). However, the combination of ET and ß-blocker therapy, as well as its effectiveness in patients with a more compromised HRR (≤12 bpm), has been under-studied. Male patients (n = 64) post-MI were divided: Training + ß-blocker (n = 19), Training (n = 15), ß-blocker (n = 11) and Control (n = 19). Participants performed an ergometric test before and after 3 months of intervention. HRR was obtained during 5 min of recovery and corrected by the cardiac reserve (HRRcorrCR ). Compared to pre-intervention, HRRcorrCR was significantly increased during the 1st and 2nd minutes of recovery in the Training + ß-blocker group (70·5% and 37·5%, respectively; P<0·05). A significant improvement, lasting from the 1st to the 4th minute of recovery, was also observed in the Training group (47%, 50%, 25% and 8·7%, respectively; P<0·05). In contrast, the ß-blocker group showed a reduction in HRRcorrCR during the 2nd and 3rd minutes of recovery (-21·2% and -16·3%, respectively; P<0·05). In addition, interventions involving ET (Training + ßb, Training) were significantly more effective in patients with a pre-intervention HRR ≤ 12 bpm than for patients with HRR > 12 bpm. Combination of ß-blocker therapy with ET does not compromise the effect of training and instead promotes HRR and aerobic capacity improvement. In addition, this combination is particularly beneficial for individuals presenting with a more compromised HRR. However, chronic administration of ß-blocker therapy alone did not promote improvement in HRR or aerobic capacity.

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Heart rate recovery (HRR) is a strong mortality predictor. Exercise training (ET) and β-blocker therapy have significant impact on the HRR of patients following myocardial infarction (MI). However, the combination of ET and β-blocker therapy, as well as its effectiveness in patients with a more compromised HRR (≤12 bpm), has been under-studied. Male patients (n = 64) post-MI were divided: Training + β-blocker (n = 19), Training (n = 15), β-blocker (n = 11) and Control (n = 19). Participants performed an ergometric test before and after 3 months of intervention. HRR was obtained during 5 min of recovery and corrected by the cardiac reserve (HRRcorrCR ). Compared to pre-intervention, HRRcorrCR was significantly increased during the 1st and 2nd minutes of recovery in the Training + β-blocker group (70·5% and 37·5%, respectively; P 12 bpm. Combination of β-blocker therapy with ET does not compromise the effect of training and instead promotes HRR and aerobic capacity improvement. In addition, this combination is particularly beneficial for individuals presenting with a more compromised HRR. However, chronic administration of β-blocker therapy alone did not promote improvement in HRR or aerobic capacity.

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Post-exercise heart rate (HR) recovery (HRR) presents a biphasic pattern, which is mediated by parasympathetic reactivation and sympathetic withdrawal. Several mechanisms regulate these post-exercise autonomic responses and thermoregulation has been proposed to play an important role. The aim of this study was to test the effects of heat stress on HRR and HR variability (HRV) after aerobic exercise in healthy subjects. Twelve healthy males (25 ± 1 years, 23.8 ± 0.5 kg/m2) performed 14 min of moderate-intensity cycling exercise (40-60% HRreserve) followed by 5 min of loadless active recovery in two conditions: heat stress (HS) and normothermia (NT). In HS, subjects dressed in a whole-body water-perfused tube-lined suit to increase internal temperature (Tc) by ~1°C. In NT, subjects did not wear the suit. HR, core and skin temperatures (Tc and Tsk), mean arterial pressure (MAP) skin blood flow (SKBF), and cutaneous vascular conductance (CVC) were measured throughout and analyzed during post-exercise recovery. HRR was assessed through calculations of HR decay after 60 and 300 s of recovery (HRR60s and HRR300s), and the short- and long-term time constants of HRR (T30 and HRRt). Post-exercise HRV was examined via calculations of RMSSD (root mean square of successive RR intervals) and RMS (root mean square residual of RR intervals). The HS protocol promoted significant thermal stress and hemodynamic adjustments during the recovery (HS-NT differences: Tc = +0.7 ± 0.3°C; Tsk = +3.2 ± 1.5°C; MAP = -12 ± 14 mmHg; SKBF = +90 ± 80 a.u; CVC = +1.5 ± 1.3 a.u./mmHg). HRR and post-exercise HRV were significantly delayed in HS (e.g., HRR60s = 27 ± 9 vs. 44 ± 12 bpm, P < 0.01; HRR300s = 39 ± 12 vs. 59 ± 16 bpm, P < 0.01). The effects of heat stress (e.g., the HS-NT differences) on HRR were associated with its effects on thermal and hemodynamic responses. In conclusion, heat stress delays HRR, and this effect seems to be mediated by an attenuated parasympathetic reactivation and sympathetic withdrawal after exercise. In addition, the impact of heat stress on HRR is related to the magnitude of the heat stress-induced thermal stress and hemodynamic changes.

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JUSTIFICATIVE: The relationship between post-exercise heart-rate recovery (HRR) and resting cardiac autonomic modulation is an incompletely explored issue. OBJECTIVE: To correlate HRR with resting supine and orthostatic autonomic status. METHOD: HRR at the 1st, 3th, and 5th min following maximal treadmill exercise were correlated with 5-min time-domain (CV, pNN50 and rMSSD) and frequency-domain (TP, LF, HF, LFn, HFn, and LF/HF ratio) indices of heart-rate variability (HRV) in both supine and standing positions in 31 healthy physically active non-athletes men. Statistical analysis employed non-parametric tests with two-tailed p value set at 5 %. RESULTS: Absolute HRR and Δ %HRR at each post-exercise time did not correlated with HRV in supine position, as well as at 1st min in standing position. At the 3rd min and 5th min, these measures negatively correlated with pNN50, rMSSD, TP, and HF indices, and only in the 5th min, they showed negative correlation with HFn and positive correlation with LF, LFn, and LF/HF ratio in the standing position. Coefficient of HRR (CHRR) at the 1st min negatively correlated with pNN50 and rMSSD and at 3rd and 5th min showed positive correlation with LFn and LF/HF ratio in supine position. With HRV indices in standing position CHRR from the 1st to 5th min showed the same respective negative and positive correlations as the other measures. CONCLUSION: HRR from the 1st to 5th min post-exercise negatively correlated with parasympathetic modulation in resting orthostatic, but showed no correlation in supine position. At the 3rd and 5th min, a positive correlation with combined sympathetic-parasympathetic modulation in both positions was observed.

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This study aimed to assess the blood pressure (BP), cardiac autonomic modulation at rest, in physical exercise and in the recovery in untrained eutrophic (E) and overweight (O) youth. The body mass index (BMI), waist circumference (WC), systolic BP-SBP (E: 109.80 ± 10.05; O: 121.85 ± 6.98 mmHg) and diastolic BP - DBP (E: 65.90 ± 7.28; O: 73.14 ± 12.22 mmHg) were higher in overweight and the heart rate recovery (%HRR) was lower as compared with E volunteers. The BMI was associated with SBP (r= 0.54), DBP (r= 0.65), load on the heart rate variability threshold - HRVT (r= -0.46), %HRR 2' (r= -0.48) and %HRR 5' (r= -0.48), and WC was associated with SBP (r= 0.54), DBP (r= 0.64) and HRR 2' (r= -0.49). The %HRR was associated to SBP, DBP and HRVT. In summary, the anthropometric variables, BP and cardiac autonomic modulation in the recovery are altered in overweight youth.

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PURPOSE: The main purpose of this study was to investigate parasympathetic reactivation of the heart [evaluated through heart rate recovery (HRR) and HR variability (HRV)] after maximal cardiopulmonary exercise testing (CPET) using three different exercise modalities. METHODS: Twenty healthy men, aged 17 to 28 yr, performed three maximal CPETs (cycling, walking, and running) separated by 72 h and in a randomized, counter-balanced order. HRR was determined from the absolute differences between HRpeak and HR at 1-3 min after exercise. The root mean square of successive R-R differences calculated for consecutive 30-s windows (rMSSD30s) was calculated to assess the parasympathetic reactivation after maximal CPET. RESULTS: Lower HRpeak, VO2peak and energy expenditure were observed after the cycling CPET than the walking and running CPETs (P < 0.001). Both HRR and rMSSD30s were significantly greater during recovery from the cycling CPET compared to the walking and running CPETs (P < 0.001). Furthermore, Δ rMSSD (i.e. resting minus postexercise rMSSD every 30 s into the recovery period) was positively related to the resting high-frequency component (HF), rMSSD, and standard deviation of all normal R-R intervals (SDNN) (rs = 0.89 to 0.98; P < 0.001), and negatively related to the resting low-frequency component (LF) and sympathovagal balance (LF:HF ratio) after all exercise conditions (rs = -0.73 to -0.79 and -0.86 to -0.90, respectively; P < 0.001). CONCLUSIONS: These findings support that parasympathetic reactivation after maximal CPET (as assessed by HRR and rMSSD30s) depends on exercise modality and cardiac autonomic control at rest.

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STUDY OBJECTIVES: The attenuation of heart rate recovery after maximal exercise (ΔHRR) is independently impaired by obstructive sleep apnea (OSA) and metabolic syndrome (MetS). Therefore, we tested the hypotheses: (1) MetS + OSA restrains ΔHRR; and (2) Sympathetic hyperactivation is involved in this impairment. DESIGN: Cross-sectional study. PARTICIPANTS: We studied 60 outpatients in whom MetS had been newly diagnosed (ATP III), divided according to apnea-hypopnea index (AHI) ≥ 15 events/h in MetS + OSA (n = 30, 49 ± 1.7 y) and AHI < 15 events/h in MetS - OSA (n = 30, 46 ± 1.4 y). Normal age-matched healthy control subjects (C) without MetS and OSA were also enrolled (n = 16, 46 ± 1.7 y). INTERVENTIONS: Polysomnography, microneurography, cardiopulmonary exercise test. MEASUREMENTS AND RESULTS: We evaluated OSA (AHI - polysomnography), muscle sympathetic nerve activity (MSNA - microneurography) and cardiac autonomic activity (LF = low frequency, HF = high frequency, LF/HF = sympathovagal balance) based on spectral analysis of heart rate (HR) variability. ΔHRR was calculated (peak HR minus HR at first, second, and fourth minute of recovery) after cardiopulmonary exercise test. MetS + OSA had higher MSNA and LF, and lower HF than MetS - OSA and C. Similar impairment occurred in MetS - OSA versus C (interaction, P < 0.01). MetS + OSA had attenuated ΔHRR at first, second, and at fourth minute than did C, and attenuated ΔHRR at fourth minute than did MetS - OSA (interaction, P < 0.001). Compared with C, MetS - OSA had attenuated ΔHRR at second and fourth min (interaction, P < 0.001). Further analysis showed association of the ΔHRR (first, second, and fourth minute) and AHI, MSNA, LF and HF components (P < 0.05 for all associations). CONCLUSIONS: The attenuation of heart rate recovery after maximal exercise is impaired to a greater degree where metabolic syndrome (MetS) is associated with moderate to severe obstructive sleep apnea (OSA) than by MetS with no or mild or no OSA. This is at least partly explained by sympathetic hyperactivity.

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Previous studies have suggested that physical activity (PA) levels and cardiorespiratory fitness (CRF) impact on the autonomic control of heart rate (HR). However, previous studies evaluating PA levels did not discriminate between incidental PA and regular exercise. We hypothesized that incidental PA "per se" would influence cardiac autonomic indices as assessed via HR variability (HRV) and HR recovery (HRR) in non-exercisers. Thus, the objective of this study was to investigate the relationships between objective PA levels, CRF, and cardiac autonomic indices in adult, regular non-exercising female workers. After familiarization with procedures and evaluation of body composition, 21 women completed a submaximal cycling test and evaluation of HRR on four different days. Resting (2-min seated and standing) and ambulatory (4-h) HRV were also recorded. Levels of PA were assessed by accelerometry over five consecutive days (i.e., Wednesday to Sunday). Maximum oxygen consumption (VO2max) was measured as an index of CRF. As reliability was low to moderate for most HR measures, relationships between these and PA and CRF were examined using the 4-day average measures. Significant correlations were identified between post-exercise HRR in the first min with various PA indices (daily moderate PA, daily vigorous PA, and the sum of vigorous and very vigorous daily PA). Additionally, VO2max was significantly correlated to HRV but not to HRR. The current results indicated that CRF was influential in enhancing HRV while incidental or non-exercise based PA was associated with greater autonomic reactivation in adult overweight women. Therefore, both CRF and non-exercise based PA contribute significant but diverse effects on cardiac health. The use of 4-day averages instead of single measures for evaluation of autonomic control of HR may provide a better indication of regular cardiac autonomic function that remains to be refined.

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BACKGROUND: Although substantial evidence relates reduced exercise heart rate (HR) reserve and recovery to a higher risk of all-cause mortality, a combined indicator of these variables has not been explored. Our aim was to combine HR reserve and recovery into a single index and to assess its utility to predict all-cause mortality. DESIGN: Retrospective cohort analysis. METHODS: Participants were 1476 subjects (937 males) aged between 41 and 79 years who completed a maximal cycle cardiopulmonary exercise test while not using medication with negative chronotropic effects or having an implantable cardiac pacemaker. HR reserve (HR maximum - HR resting) and recovery (HR maximum - HR at 1-min post exercise) were calculated and divided into quintiles. Quintile rankings were summed yielding an exercise HR gradient (EHRG) ranging from 2 to 10, reflecting the magnitude of on- and off-HR transients to exercise. Survival analyses were undertaken using EHRG scores and HR reserve and recovery in the lowest quintiles (Q1). RESULTS: During a mean follow up of 7.3 years, 44 participants died (3.1%). There was an inverse trend for EHRG scores and death rate (p < 0.05) that increased from 1.2% to 13.5%, respectively, for scores 10 and 2. An EHRG score of 2 was a better predictor of all-cause mortality than either Q1 for HR reserve (<80 bpm) or HR recovery alone (<27 bpm): age-adjusted hazard ratios: 3.53 (p = 0.011), 2.52 (p < 0.05), and 2.57 (p < 0.05), respectively. CONCLUSIONS: EHRG, a novel index combining HR reserve and HR recovery, is a better indicator of mortality risk than either response alone.

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