Slower Heart Rate Recovery Research Articles

Reply to Morton. Heart-rate responses to exercise in patients with diabetes with acute or chronic autonomic dysfunction

We thank Dr Morton for his interest in our paper on the utility of post-exercise heart-rate recovery for cardiac autonomic neuropathy assessment and for elucidating this interesting case study highlighting the related issue of chronotropism. Slower heart-rate recovery in patients with vs. without cardiac autonomic neuropathy in our study coincided with (but was still independent of) a blunted heartrate response to exercise. The significance of this relative chronotropic incompetence is highlighted by its associations with adverse outcomes and exercise intolerance.Morton’s case provides a compelling argument that hypoglycaemia triggers acute chronotropic incompetence in patients with diabetes...

Attenuated Heart Rate Recovery is Associated with Sympathetic Hyperactivity in Patients with Metabolic Syndrome and Obstructive Sleep Apnea

Obstructive sleep apnea (OSA) and metabolic syndrome (MetS) are independently associated with impaired heart rate recovery (HRR) after maximal exercise. We tested the hypotheses that: 1) MetS+OSA would have an additive effect on attenuation of HRR; 2) The sympathetic hyperactivation would be involved on slower HRR. Newly diagnosed MetS (ATP III) patients, sedentary were divided into: MetS+OSA (n=18, 49±2y) and MetS‐OSA (n=21, 44±2y). Normal individuals were also studied (C, n=13, 47±2y). OSA was characterized by apnea‐hypopnea index (AHI) >;15events/h (polysomnography). Muscle sympathetic nerve activity (MSNA, microneurography), heart rate (EKG), low (LF) and high (HF) frequency power bands and sympatho‐vagal balance (LF/HF‐Spectral analysis) were measured. The HRR was calculated (HRpeak minus HHR at 1st, 2nd, 4th min). MetS+OSA had higher MSNA, LF and LF/HF compared with MetS‐OSA and C. MSNA was higher in MetS‐OSA than in C. HF power was lower in MetS+OSA compared with MetS‐OSA and C. HRR at 1st, 2nd min was lower in MetS+OSA compared with C (P<0.01) and lower at 4th min compared with Met‐OSA and C (P<0.01). Further analyses showed an association between MSNA levels and HRR (P<0.01). In conclusion, OSA exacerbates the attenuation of HRR after maximal exercise in patients with MetS. In addition, the attenuation of HRR is associated with sympathetic hyperactivation.(FAPESP#2011/17533–6)

HEART RATE RECOVERY PREDICTS CLINICAL WORSENING IN PATIENTS WITH CONGENITAL HEART DISEASE ASSOCIATED PULMONARY ARTERIAL HYPERTENSION

Slow heart rate recovery (HRR) after exercise has been shown to be a predictor of mortality in patients with chronic cardiopulmonary diseases. The ability of HRR to predict clinical worsening in congenital heart disease associated pulmonary arterial hypertension (PAH) remains unexplored. Our aim was

Do Interleukin-1β Levels Correlate with MIBG and Exercise Parameters in Heart Failure?

Interleukin 1β (IL 1β) levels are associated with prognosis in heart failure. The cardiac adrenergic activity as assessed by metaiodobenzylguanidine (I123 MIBG) scintigraphy along with exercise parameters are important predictors of prognosis. The relationship between these variables is not fully established. To evaluate the association of IL 1β levels with exercise and I123 MIBG parameters. Cross-sectional observational study evaluating 25 consecutive patients with heart failure and ejection fraction lower than 45% by means of: determination of IL 1β levels; I123 MIBG parameters [early and late heart/mediastinum ratio, washout rate (WO)]; and treadmill exercise test using the ramp protocol. The patients were divided into two groups according to their IL 1β levels (normal vs. increased). The group with increased levels showed lower double-product reserve (DPR); lower functional capacity (FC); slower heart rate recovery at the first (HRR 1º) and second minute (HRR 2º); and higher WO. In the univariate analysis, all variables correlated with IL 1β; DPR: r = 0.203, p = 0.024; FC: r = 0.181, p = 0.034; HRR 1º: r = 0.182, p = 0.034; HRR 2º: r = 0.204, p = 0.023; WO: r = 0.263, p = 0.009. In the multivariate analysis, only WO maintained a significant correlation (r² = 0.263, p = 0.009). Adrenergic overactivity was the main determinant of IL 1β levels, thus demonstrating that an excessive sympathetic activity influences the systemic inflammatory response. Exercise test variables were not able to identify patients with high IL 1β levels.

Heart Rate Recovery Is Impaired After Maximal Exercise Challenge in Pediatric Sickle Cell Anemia

AbstractAbstract ▪3220▪This icon denotes a clinically relevant abstractSlow heart rate recovery (HRR) after exercise, particularly at 1 and 2 minutes during recovery, is a strong indicator of autonomic nervous system (ANS) imbalance and represents an important risk factor for increased cardiovascular morbidity and mortality in the general population. Recent evidence suggests cardiovascular ANS dysfunction and vagal tone impairment also exist in individuals with sickle cell anemia (SCA). Despite the known impact of disease burden on exercise capacity and overall fitness in SCA, post-exercise HRR has not previously been studied in this population. The objective of this study was to examine HRR in the post-exercise recovery phase following maximal exercise testing in a cohort of children and young adults with SCA. Methods We prospectively performed maximal cardiopulmonary exercise testing using a ramp, cycle ergometry protocol in 60 subjects with SCA (hemoglobin SS and S-β0 thalassemia) and 20 controls without SCA or sickle cell trait matched for race and gender. Data from standard 12-lead electrocardiography (ECG) was assessed during a 10-minute recovery phase, and HR and corrected QT (QTc) interval measured from tracings obtained at 1-minute intervals. A single investigator performed all measurements manually using leads II, V5, and V6. Final values were averaged from 3 independent measurements. The difference between maximal HR and both HR at 1-minute (ΔHR1min) and 2-minute (ΔHR2min) recovery was our primary outcome. Between-group differences were compared using Mann-Whitney U testing (IBM, SPSS V20). The relationship between ΔHR1min and exercise parameters was examined using Spearman’s rank correlation coefficient. Results Post-exercise ECG data from 58 subjects with SCA (median age 15.5 years) and 20 controls without SCA (median age 12 years) were interpretable for this analysis. A total of 30/58 (52%) and 22/58 (38%) subjects were male and on hydroxyurea, respectively. There was no significant difference in median baseline HR or QTc interval in subjects versus controls. Median peak HR was also not significantly different in the 2 groups. When compared to controls, subjects with SCA demonstrated significantly lower HR reserve (100 vs. 111 bpm, p = 0.005), representing the difference between peak and baseline HR. Impaired HRR, defined by slower declines in HR during recovery, was also evident among subjects with SCA following maximal exercise challenge. Although the absolute HR measured at each minute of recovery did not differ significantly in the 2 groups, subjects demonstrated significantly smaller median ΔHR1min (21 vs. 33 bpm, p < 0.0001) and ΔHR2min (39 vs. 51 bpm, p = 0.003), even after adjustment for age between groups. Significantly smaller ΔHR values were also noted in subjects at each minute up to 8 minutes throughout recovery. When compared to subjects not on hydroxyurea, subjects on treatment had significantly greater median ΔHR1min (25 vs. 19 bpm, p = 0.037) but similar ΔHR2min. In subjects with SCA, ΔHR1min correlated inversely with age (−0.41, p = 0.001) and directly with peak oxygen consumption (peak VO2) (0.30, p = 0.03) and oxygen delivery (ΔVO2/Δwork rate) (0.46, p < 0.0001), but not with baseline QTc interval or hemoglobin. Through mono-exponential curve fitting, we found that the time constant associated with HR decline over the first 5 minutes of recovery was greater in subjects with SCA versus controls (T = 128 sec, 95% CI [123, 134] versus 104 sec, 95% [97, 110]). Conclusions Compared to controls without SCA, children and young adults with SCA demonstrate impaired HRR following maximal cardiopulmonary exercise testing, as evidenced by smaller decrements in HR at 1 and 2 minutes during recovery and exponential time constants that indicate a longer period of time over which HR declines. Slower HRR is also associated with decreased fitness and measures of oxygen delivery during exercise testing in subjects with SCA. Although the mechanisms are not well understood, prolonged HRR in this population may in part be explained by ANS imbalance, suggesting either inadequate sympathetic withdrawal or suboptimal parasympathetic reactivation in the post-exercise period. Future studies should focus on delineating the role of the ANS in post-exercise HRR and assessing the prognostic potential of this marker as it relates to disease severity and outcomes in SCA. Disclosures:No relevant conflicts of interest to declare.

Influence of mental workload on muscle endurance, fatigue, and recovery during intermittent static work

Most occupational tasks involve some level of mental/cognitive processing in addition to physical work; however, the etiology of work-related musculoskeletal disorders (WMSDs) due to these demands remains unclear. The aim of this study was to quantify the interactive effects of physical and mental workload on muscle endurance, fatigue, and recovery during intermittent work. Twelve participants, balanced by gender, performed intermittent static shoulder abductions to exhaustion at 15, 35, and 55% of individual maximal voluntary contraction (MVC), in the absence (control) and presence (concurrent) of a mental arithmetic task. Changes in muscular capacity were determined using endurance time, strength decline, electromyographic (EMG) fatigue indicators, muscle oxygenation, and heart rate measures. Muscular recovery was quantified through changes in strength and physiological responses. Mental workload was associated with shorter endurance times, specifically at 35% MVC, and greater strength decline. EMG and oxygenation measures showed similar changes during fatigue manifestation during concurrent conditions compared to the control, despite shorter endurance times. Moreover, decreased heart rate variability during concurrent demand conditions indicated increased mental stress. Although strength recovery was not influenced by mental workload, a slower heart rate recovery was observed after concurrent demand conditions. The findings from this study provide fundamental evidence that physical capacity (fatigability and recovery) is adversely affected by mental workload. Thus, it is critical to determine or evaluate occupational demands based on modified muscular capacity (due to mental workload) to reduce risk of WMSD development.

Genetic contributions to acute autonomic stress responsiveness in children

Identification of genetic factors that influence stress reactivity is important in order to link environmental demands, particularly adversity to disease outcome. There is ample literature on genetic contribution to the endocrine stress response, while evidence for genetic contribution to individual differences in autonomic nervous system function is sparse and produced conflicting results. Here, we investigated the influence of two polymorphisms in the Catechol-o-methyltransferase (COMT) and serotonin transporter (5-HTT; SCL6A4) gene. We examined the autonomic stress response to the Trier Social Stress Test for Children in 115 children. Salivary α-amylase (sAA) was obtained prior to the stressor and repeatedly during recovery as a marker of autonomic reactivity. Furthermore, heart rate (HR) and heart rate variability (HRV) were monitored continuously. We found differences in ANS stress response associated with each polymorphism (all p<.05). Children with the L variant of 5-HTTLPR showed a higher increase and sharper recovery of sAA in response to stress than those with S variants. For HR, we found differences associated with COMT, i.e. children carrying at least one met allele showed lower mean HR increase and slower HR recovery in response to the stressor compared to those with two val alleles (p<.001) as well as a significant decrease in heart rate variability (p<.05). Our findings indicate that these two polymorphisms do indeed influence the ANS response to stress. This study provides further evidence for the crucial role of genetic factors in the modulation of differences in the acute stress response during childhood.

Two-minute heart rate recovery after cycle ergometer exercise and all-cause mortality in middle-aged men

A slow heart rate recovery (HRR) after an exercise test is associated with an increased risk of all-cause mortality in asymptomatic individuals, but the data regarding additional prognostic information provided by HRR beyond other exercise test variables are inconsistent. We investigated the prognostic significance of HRR for premature death, particularly in relation to other exercise test variables. The study subjects were a representative population-based sample of 1102 men (42-61 years of age) without cardiovascular disease, cancer or diabetes. HRR was defined as the difference between maximal HR and HR 2 min after a maximal symptom-limited exercise test using a cycle ergometer. The association between HRR and premature mortality was examined with Cox regression models. During an average follow-up of 18 years, 238 deaths occurred. HRR was an independent predictor of death [for a decrease of 12 beats min(-1) , relative risk (RR) 1.16, 95% CI 1.02-1.33, P = 0.02] after adjustment for age and established risk factors. When added in a Cox model with chronotropic response (decrease of 12 beats min(-1) , RR 1.09, 95% CI 0.93-1.27, P = 0.26) or cardiorespiratory fitness (decrease of 12 beats min(-1) , RR 1.12, 95% CI 0.98-1.30, P = 0.08), the association between a slow HRR and an increased risk of death was clearly weaker. A slow 2-min HRR after a cycle ergometer exercise test was an independent predictor of death in healthy middle-aged men after accounting for demographic and clinical characteristics. However, it was no longer predictive after accounting for chronotropic response and exercise capacity.

The effect of major depression on postexercise cardiovascular recovery

Major depressive disorder (MDD) is associated with increased cardiovascular (CV) mortality. Dysfunctional autonomic control of the CV system may represent a mechanism explaining this relationship. Poor CV recovery after exercise, indicative of dysfunctional autonomic control of the CV system, predicts CV events and death. This is the first study to examine the association between MDD and postexercise CV recovery. Some 886 patients underwent exercise stress tests. Heart rate (HR), systolic blood pressure, and diastolic blood pressure were measured at rest, peak exercise, 1 min, and 5 min after exercise. Patients with MDD had slower HR recovery (p=.026) 1 min after exercise than non-MDD patients. No other effects of MDD were found. MDD is accompanied by a dysregulation in autonomic control of exercise-related CV recovery, suggesting that depressed individuals have a slow parasympathetic recovery from exercise.

Effects of explicit and implicit perseverative cognition on cardiac recovery after cognitive stress

Slow cardiovascular (CV) recovery after stress is a predictor of adverse CV outcomes. Perseverative cognition (PC) about stress has been hypothesized to co-determine slow recovery. In the present study, it was investigated whether two types of trait PC, i.e. trait worry and trait rumination, predicted delayed cardiac recovery after a cognitive stressor. Furthermore, it was examined whether explicit state PC (i.e. negative intrusive thoughts) or implicit state PC (i.e. automatic vigilance) additionally predicted delayed cardiac recovery. Fifty-nine participants performed a stressful task, which consisted of an unsolvable synonym task. After a 6-minute recovery period, participants reported on their level of negative intrusive thoughts (i.e. explicit state PC), and performed a lexical decision task (LDT) to measure automatic vigilance for task-related information (i.e. implicit state PC). Cardiac activity was continuously measured using heart rate (HR) and heart rate variability (HRV). Trait worry and rumination were measured by the Penn State Worry Questionnaire (PSWQ) and the Ruminative Response Scale (RRS), respectively. The results showed that high trait worriers had a slower HR recovery from the cognitive stressor compared to low trait worriers. They also showed delayed HRV recovery, but only when the tendency to dwell upon one's negative mood (the ‘brooding’ subscale of the RRS) was low. Slow HR recovery was associated with high levels of negative intrusive thoughts and with automatic vigilance, but in the unexpected direction for the latter. These results provide evidence that delayed cardiac recovery is associated with trait as well as state PC, and suggest that brooding attenuates the HRV suppressing effect of high trait worry.

Heart rate recovery after exercise and incidence of type 2 diabetes in men

We tested that slow heart rate recovery (HRR) after exercise testing, indicative of decreased parasympathetic nervous system activity, is associated with the development of type 2 diabetes in 1,813 healthy men. Heart rate recovery was calculated as the difference between maximum heart rate during the exercise test and heart rate 1 min after cessation of the exercise test. During an average of 6.4 years of follow-up, 64 (3.5%) subjects developed type 2 diabetes. The unadjusted relative risk (RR) of developing incident diabetes in the slowest versus the fastest HRR quartile was 3.13 (95% CI, 1.28-7.65). However, the association was no longer significant after adjustment for diabetes risk factors and baseline glucose (RR = 2.28, 95% CI, 0.87-5.95). Slow HRR is associated with the development of type 2 diabetes, but these relationships were largely explained by baseline fasting glucose in healthy men.

Interactive effect of long-term mental stress and cardiac stress reactivity on carotid intima-media thickness: The Cardiovascular Risk in Young Finns study

The present study examined the interaction between vital exhaustion and cardiac reactivity and recovery on preclinical atherosclerosis assessed by carotid intima-media thickness (IMT) in young men and women. We measured heart rate (HR), respiratory sinus arrhythmia (RSA), and pre-ejection period (PEP) in response to mental arithmetic and speech tasks. Vital exhaustion and carotid IMT were also measured. Significant associations were observed for men aged 28–37 years, but not for men aged 22–25 years, nor for women in these age groups. It was shown that, among highly exhausted men in the older age group, lower HR reactivity was related to greater IMT. Our results also imply that, among non-exhausted men in this age group, slow HR and RSA recovery after acute stress predicted higher IMT. These results suggest that long-term stress as assessed by vital exhaustion is a risk only if it has resulted in ineffective cardiac stress reactivity. Autonomic imbalance resulting from chronic stress may be the common mechanism linking vital exhaustion and cardiac responsiveness to an increased risk of atherosclerosis.

Correlates of Heart Rate Recovery in Healthy Young- to Middle-Aged Adults

Slow heart rate recovery (HRR) from a graded exercise treadmill test (GXT) is a marker of impaired parasympathetic reactivation associated with elevated mortality in patients symptomatic for coronary heart disease (CHD). Little is known about changes in HRR over time in adults free from CHD, or about demographic, behavioral, and clinical factors associated with the development of slow HRR. PURPOSE: To describe change in HRR over 20 years, and test the hypothesis that participants with less favorable CHD risk factors during young adulthood are more likely to develop slow HRR over follow-up. METHODS: Participants from the Coronary Artery Risk Development in Young Adults (CARDIA) study who were aged 18 to 30 years in 1985–86 underwent symptom-limited maximal GXT using a modified Balke protocol at the baseline and 20-year (2005-06) examinations. HRR was calculated as the difference between maximum heart rate (HR) and HR 2 minutes following cessation of the GXT in 2,556 participants (56% female, 44% black). Slow HRR was defined as 2-minute HRR < 22 beats/min (bpm). RESULTS: After excluding 56 participants (2.2%) with slow HRR at baseline, mean HRR was 43 bpm (SD = 11). Over 20 years, HRR declined to 39 bpm (SD = 12) and incident slow HRR occurred in 142 participants (5.7%). In a multivariable model adjusting for GXT duration and maximum HR, only low education, smoking, BMI and high blood pressure were significantly associated with incident slow HRR (Table). There were no differences in the incidence of slow HRR by sex and race when GXT performance was taken into account.Table: Multivariable-adjusted baseline characteristics and incident slow HRR over 20 yearsCONCLUSIONS: HRR declines with aging in all asymptomatic adults, but the 20-year incidence of clinically slow HRR is most strongly associated with traditional CHD risk factors.

The association of heart rate recovery immediately after exercise with coronary artery calcium: the coronary artery risk development in young adults study

We tested whether slower heart rate recovery (HRR) following graded exercise treadmill testing (GXT) was associated with the presence of coronary artery calcium (CAC). Participants (n = 2,648) ages 18–30 years at baseline examination underwent GXT, followed by CAC screening 15 years later. Slow HRR was not associated with higher odds of testing positive (yes/no) for CAC at year 15 (OR = 0.99, p = 0.91 per standard deviation change in HRR). Slow HRR in young adulthood is not associated with the presence of CAC at middle age.

Relation of Heart Rate Recovery After Exercise to C-Reactive Protein and White Blood Cell Count

This study was conducted to test the hypothesis that slow and abnormal heart rate recovery (HRR), an indicator of decreased autonomic nervous system activity, after exercise is associated with inflammatory markers. Subjects who underwent exercise treadmill testing (n = 5,527, mean age 50.4 +/- 8.5 years) were studied in a cross-sectional design. HRR was calculated as the difference between maximum heart rate during the test and heart rate 1 minute after the cessation of exercise. Abnormal HRR was defined as < or =12 beats/min. Subjects with abnormal HRR had higher levels of log C-reactive protein (CRP; 1.38 +/- 0.6 vs 1.11 +/- 0.4 mg/dl, p <0.001) and higher white blood cell counts (6.9 +/- 2.1 vs 6.2 +/- 1.7 x 10(9) cells/L, p <0.001) than those with normal HRR. HRR was associated with CRP (r = -0.21, p <0.001) and white blood cell count (r = -0.19, p <0.001). HRR was independently associated with CRP (beta = -0.13, p = 0.001) in a stepwise multiple regression. In a logistic multivariate model, the group within the highest quartile of CRP (odds ratio 1.54, 95% confidence interval 1.05 to 2.27) was more likely to have abnormal HRR than those within the lowest quartile. In conclusion, slow and abnormal HRR after exercise testing is associated with inflammatory markers, which could contribute to the high incidence of cardiovascular disease in these subjects.

Evaluation of Autonomic Function Underlying Slow Postexercise Heart Rate Recovery

The reduction in heart rate (HR) during the first minute of recovery immediately after a graded maximal exercise stress test (GXT) has recently been found to be a powerful and independent predictor of cardiovascular and all-cause mortality. Reduced vagal activity has been postulated as the cause, but this has not been proven in a population with slow HR recovery (HRR). To investigate autonomic contributions to HRR using time-frequency analysis in a group of individuals demonstrating slow HRR. HRR was defined as the difference in HR between peak exercise and 1 min later; a value < or = 18 bpm was set as threshold and considered abnormal. A modified continuous wavelet transform (CWT) was used to perform time-dependent spectral analysis during the baseline steady state and the following non-steady-state conditions created by GXT. This method provides dynamic measures of low-frequency (LF) and high-frequency (HF) peaks associated with autonomic activity. Individuals (N = 20) with a previous slow HRR underwent a second GXT within 3 months after their initial test. An additional eight subjects whose first GXT disclosed normal HRR were taken as a control group. Seven of 20 subjects demonstrated slow HRR (14 +/- 5 bpm) on the repeat test, and 13 subjects displayed normal HRR (29 +/- 5 bpm). Subjects with slow HRR in both GXT displayed significantly (P < 0.05) lower HF and LF fluctuations during recovery than those with normal HRR. Attenuated HRR after GXT, assessed by CWT, is indeed associated with abnormal vagal reactivation and prolonged sympathetic stimulation after termination of maximal exercise.

Slow heart rate recovery after exercise is associated with carotid atherosclerosis

ObjectiveSlow heart rate recovery (HRR) after exercise is an estimate of impaired parasympathetic tone and predictor of all-cause and cardiovascular mortality. Carotid atherosclerosis is associated with high risk of developing coronary heart disease (CHD) and stroke. We tested the hypothesis that slow HRR is associated with carotid atherosclerosis in a cross-sectional study of 12,712 middle-aged men (age 49.1±8.9 years). MethodsCarotid atherosclerosis was measured using B-mode ultrasonography and defined as stenosis >25% and/or intima–media thickness >1.2mm. HRR was calculated as the difference between peak heart rate during a graded exercise treadmill test and heart rate 2min after cessation of exercise. ResultsThe prevalence of carotid atherosclerosis was 8.4%. The prevalence of atherosclerosis was significantly higher among subjects in the lowest (<44bpm) versus the highest (>61bpm) quartile of HRR (14.4% versus 4.1%, p<0.001). In multivariable logistic regression models adjusted for established CHD risk factors, inflammatory markers, and exercise capacity, subjects in the lowest quartile of HRR (<44bpm) were 1.50 times (95% CI: 1.13–2.00) more likely to have carotid atherosclerosis than subjects in the highest quartile (HRR>61bpm). ConclusionsSlow heart rate recovery after exercise, an index of decreased parasympathetic activity, is associated with carotid atherosclerosis independent of established risk factors in middle-age men.

Gender-Specific Prediction of Cardiac Disease

Current guidelines recommend targeting the intensity of preventive cardiovascular interventions to the level of the patient's risk, which is usually obtained from a global risk score such as the Framingham equations. However, a large proportion of asymptomatic U.S. women (approximately 80-90%) are classified as low risk by the Framingham score, although they have a 1 in 2 chance of dying from cardiovascular disease (CVD) during their lifetime. A promising avenue for improving CVD risk stratification has come from recent studies evaluating the prognostic value of exercise testing in asymptomatic populations using test variables that are not related to exercise-induced ST-segment depression. In particular, it has been shown that 2 easily obtained noninvasive measures, low exercise capacity and slow heart rate recovery, have been linked to increased CVD and all-cause death in both women and men. These 2 simple yet powerful measures of risk that are readily available are useful tools for the practicing cardiologist who desires more accurate assessment of risk in a female patient, particularly if she is deemed as intermediate risk by the Framingham score. In addition, both exercise capacity and heart rate recovery are at least partially modifiable by regular physical activity. Exercise recommendations of at least 30 minutes of moderate physical activity most days of the week have been associated with 30% to 50% reductions in coronary events and coronary mortality and should be recommended to all patients regardless of their Framingham risk score.

Abstract 188: Abnormal Heart Rate Responses to Exercise and Susceptibility to Ventricular Fibrillation: Effect of Endurance Exercise Training

BACKGROUND : Both a large heart rate (HR) increase at exercise onset and a slow heart rate recovery following the termination of exercise have been linked to an increased susceptibility to ventricular fibrillation (VF). Endurance exercise training can enhance cardiac vagal and reduce cardiac sympathetic regulation and could, thereby, improve the exercise HR response and decrease the risk for VF. METHODS : To test this hypothesis, a 2-min coronary occlusion was made during the last min of an 18-min exercise test in dogs with healed myocardial infarctions: 20 had VF (S, susceptible) and 13 did not (R, resistant). On a previous day, HR and heart rate variability (HRV, 0.24 to 1.04 Hz frequency component; an index of cardiac vagal activity) responses to submaximal exercise were measured before and 30, 60 &amp; 120s after exercise onset and 30, 60 &amp; 120s following the termination of exercise. RESULTS : Larger HR increases and a slower HR recovery (ANOVA, both P&lt;0.01) were noted in the susceptible dogs (HR: 30s after exercise onset, S 179 ± 8.4 vs. R 156.8 ± 3.4 beats/min; 30s post exercise, S 186 ± 7.8 vs. R 164.2 ± 5.7 beats/min). These HR differences were accompanied by corresponding differences in cardiac vagal activity (HRV: 30s after exercise onset, S 4.0 ± 0.4 vs. R 4.8 ± 04 ln ms 2 ; 30s post exercise, S 2.4 ± 0.3 vs. R 3.8 3 0.4 ln ms 2 ). The dogs then received either a 10-wk exercise program (treadmill running; S n = 9; R n = 8) or an equivalent sedentary period (S n = 11; R n = 5). After 10-weeks, the response to exercise was not altered in the sedentary animals. In contrast, exercise training increased cardiac vagal activity such that HR at exercise onset was reduced while HR recovery increased. As a result, differences were no longer noted between the groups (30s after exercise onset: HR, S 151.4 ± 6.6 vs. R 149.5 ± 7.3 beats/min; HRV, S 5.8 ± 0.4 vs. R 5.6 ± 0.4 ln ms 2 ; 30s post exercise: HR, S 159.4 ± 7.7 vs. R 153.5 ± 5.3 beats/min; HRV, S 4.0 ± 0.6 vs. R 4.9 ± 0.5 ln ms 2 ). After training, the exercise plus ischemia tested provoked VF in sedentary but not trained susceptible dogs. CONCLUSION : Endurance exercise training can alter cardiac autonomic balance (increased cardiac vagal activity) to restore a more normal heart rate regulation and could, thereby, prevent ventricular fibrillation in high-risk individuals.

Effect of endurance exercise training on heart rate onset and heart rate recovery responses to submaximal exercise in animals susceptible to ventricular fibrillation

Both a large heart rate (HR) increase at exercise onset and a slow heart rate (HR) recovery following the termination of exercise have been linked to an increased risk for ventricular fibrillation (VF) in patients with coronary artery disease. Endurance exercise training can alter cardiac autonomic regulation. Therefore, it is possible that this intervention could restore a more normal HR regulation in high-risk individuals. To test this hypothesis, HR and HR variability (HRV, 0.24- to 1.04-Hz frequency component; an index of cardiac vagal activity) responses to submaximal exercise were measured 30, 60, and 120 s after exercise onset and 30, 60, and 120 s following the termination of exercise in dogs with healed myocardial infarctions known to be susceptible (n = 19) to VF (induced by a 2-min coronary occlusion during the last minute of a submaximal exercise test). These studies were then repeated after either a 10-wk exercise program (treadmill running, n = 10) or an equivalent sedentary period (n = 9). After 10 wk, the response to exercise was not altered in the sedentary animals. In contrast, endurance exercise increased indexes of cardiac vagal activity such that HR at exercise onset was reduced (30 s after exercise onset: HR pretraining 179 +/- 8.4 vs. posttraining 151.4 +/- 6.6 beats/min; HRV pretraining 4.0 +/- 0.4 vs. posttraining 5.8 +/- 0.4 ln ms(2)), whereas HR recovery 30 s after the termination of exercise increased (HR pretraining 186 +/- 7.8 vs. posttraining 159.4 +/- 7.7 beats/min; HRV pretraining 2.4 +/- 0.3 vs. posttraining 4.0 +/- 0.6 ln ms(2)). Thus endurance exercise training restored a more normal HR regulation in dogs susceptible to VF.