Heart rate response to onset of exercise: evidence for enhanced cardiac sympathetic activity in animals susceptible to ventricular fibrillation

2006 ◽  
Vol 291 (1) ◽  
pp. H429-H435 ◽  
Author(s):  
George E. Billman
Keyword(s):  
Heart Rate ◽  
Ventricular Fibrillation ◽  
Activity Index ◽  
Frequency Component ◽  
Treadmill Running ◽  
Vagal Activity ◽  
Circumflex Artery ◽  
Left Circumflex Artery ◽  
Increased Risk ◽  
Exercise Onset

A large heart rate (HR) increase at the onset of exercise has been linked to an increased risk for adverse cardiovascular events, including cardiac death. However, the relationship between changes in cardiac autonomic regulation induced by exercise onset and the confirmed susceptibility to ventricular fibrillation (VF) has not been established. Therefore, a retrospective analysis of the HR response to exercise onset was made in mongrel dogs with healed myocardial infarctions that were either susceptible (S, n = 131) or resistant (R, n = 114) to VF (induced by a 2-min occlusion of the left circumflex artery during the last minute of exercise). The ECG was recorded, and time series analysis of HR variability (vagal activity index, the 0.24–1.04-Hz frequency component of R-R interval variability) was measured before and 30, 60, and 120 s after the onset of exercise (treadmill running). Exercise elicited significantly (ANOVA, P < 0.0001) greater increases in HR in susceptible dogs at all three times (e.g., at 60 s: R, 46.8 ± 2.3 vs. S, 57.1 ± 2.2 beats/min). However, the vagal activity index decreased to a similar extent in both groups of dogs (at 60 s: R, −2.8 ± 0.1 vs. S, −3.0 ± 0.2 ln ms2). β-Adrenoceptor blockade (BB, propranolol 1.0 mg/kg iv) reduced the HR increase and eliminated the differences noted between the groups [at 60 s: R ( n = 26), 40.4 ± 3.2 vs. S ( n = 31), 37.5 ± 2.4 beats/min]. After BB, exercise once again elicited similar declines in vagal activity in both groups (at 60 s: R, −3.6 ± 0.5 vs. S, −3.2 ± 0.4 ln ms2). When considered together, these data suggest that at the onset of exercise HR increases to a greater extent in animals prone to VF compared with dogs resistant to this malignant arrhythmia due to an enhanced cardiac sympathetic activation in the susceptible dogs.

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

2007 ◽  
Vol 102 (1) ◽  
pp. 231-240 ◽  
Author(s):  
George E. Billman ◽  
Monica Kukielka
Keyword(s):  
Heart Rate ◽  
Ventricular Fibrillation ◽  
Exercise Training ◽  
Endurance Exercise ◽  
Submaximal Exercise ◽  
Treadmill Running ◽  
Vagal Activity ◽  
Endurance Exercise Training ◽  
Increased Risk ◽  
Exercise Onset

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 ms2), 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 ms2). Thus endurance exercise training restored a more normal HR regulation in dogs susceptible to VF.

Heart rate recovery after exercise: a predictor of ventricular fibrillation susceptibility after myocardial infarction

2005 ◽  
Vol 288 (4) ◽  
pp. H1763-H1769 ◽  
Author(s):  
Lauren L. Smith ◽  
Monica Kukielka ◽  
George E. Billman
Keyword(s):  
Myocardial Infarction ◽  
Heart Rate ◽  
Ventricular Fibrillation ◽  
Heart Rate Recovery ◽  
Treadmill Running ◽  
Vagal Activity ◽  
Circumflex Artery ◽  
Left Circumflex Artery ◽  
Exercise Treadmill ◽  
Parasympathetic Tone

Heart rate recovery after exercise, thought to be related to cardiac parasympathetic tone, has been shown to be a prognostic tool for all-cause mortality. However, the relationship between this variable and confirmed susceptibility to ventricular fibrillation (VF) has not been established. Therefore, myocardial ischemia was induced with a 2-min occlusion of the left circumflex artery during the last minute of exercise in mongrel dogs with myocardial infarction ( n = 105 dogs). VF was induced in 66 animals (susceptible), whereas the remaining 39 dogs had no arrhythmias (resistant). On a previous day, ECG was recorded and a time-series analysis of heart rate variability was measured 30, 60, and 120 s after submaximal exercise (treadmill running). The heart rate recovery was significantly greater in resistant dogs than in susceptible dogs at all three times, with the most dramatic difference at the 30-s mark (change from maximum: 48.1 ± 3.6 beats/min, resistant dogs; 31.0 ± 2.2 beats/min, susceptible dogs). Correspondingly, indexes of parasympathetic tone increased to a significantly greater extent in resistant dogs at 30 and 60 s after exercise. These differences were eliminated by atropine pretreatment. When considered together, these data suggest that resistant animals exhibit a more rapid recovery of vagal activity after exercise than those susceptible to VF. As such, postexercise heart rate recovery may help identify patients with a high risk for VF following myocardial infarction.

Exercise training normalizes β-adrenoceptor expression in dogs susceptible to ventricular fibrillation

2007 ◽  
Vol 293 (5) ◽  
pp. H2702-H2709 ◽  
Author(s):  
Bethany J. Holycross ◽  
Monica Kukielka ◽  
Yoshinori Nishijima ◽  
Ruth A. Altschuld ◽  
Cynthia A. Carnes ◽  
...  
Keyword(s):  
Gene Expression ◽  
Ventricular Fibrillation ◽  
Exercise Training ◽  
Left Ventricular ◽  
Treadmill Running ◽  
Rt Pcr ◽  
Circumflex Artery ◽  
Left Circumflex Artery ◽  
Protein Levels ◽  
Ventricular Tissue

Previous studies demonstrated an enhanced β2-adrenoceptor (AR) responsiveness in animals susceptible to ventricular fibrillation (VF) that was eliminated by exercise training. The present study investigated the effects of endurance exercise training on β1-AR and β2-AR expression in dogs susceptible to VF. Myocardial ischemia was induced by a 2-min occlusion of the left circumflex artery during the last minute of exercise in dogs with healed infarctions: 20 had VF [susceptible (S)] and 13 did not [resistant (R)]. These dogs were randomly assigned to either 10-wk exercise training [treadmill running; n = 9 (S) or 8 (R)] or an equivalent sedentary period [ n = 11 (S) or 5 (R)]. Left ventricular tissue β-AR protein and mRNA were quantified by Western blot analysis and RT-PCR, respectively. Because β2-ARs are located in caveolae, caveolin-3 was also quantified. β1-AR gene expression decreased (∼5-fold), β2-AR gene expression was not changed, and the ratio of β2-AR to β1-AR gene expression was significantly increased in susceptible compared with resistant dogs. β1-AR protein decreased (∼50%) and β2-AR protein increased (400%) in noncaveolar fractions of the cell membrane in susceptible dogs. Exercise training returned β1-AR gene expression to levels seen in resistant animals but did not alter β2-AR protein levels in susceptible dogs. These data suggest that β1-AR gene expression was decreased in susceptible dogs compared with resistant dogs and, further, that exercise training improves β1-AR gene expression, thereby restoring a more normal β-AR balance.

Cardiac vagal modulation of heart rate during prolonged submaximal exercise in animals with healed myocardial infarctions: effects of training

2006 ◽  
Vol 290 (4) ◽  
pp. H1680-H1685 ◽  
Author(s):  
Monica Kukielka ◽  
Douglas R. Seals ◽  
George E. Billman
Keyword(s):  
Heart Rate ◽  
Heart Rate Variability ◽  
Exercise Training ◽  
Submaximal Exercise ◽  
Treadmill Running ◽  
Myocardial Infarctions ◽  
Vagal Activity ◽  
Long Duration ◽  
Exercise Treadmill ◽  
Exercise Induced

The present study investigated the effects of long-duration exercise on heart rate variability [as a marker of cardiac vagal tone (VT)]. Heart rate variability (time series analysis) was measured in mongrel dogs ( n = 24) with healed myocardial infarctions during 1 h of submaximal exercise (treadmill running at 6.4 km/h at 10% grade). Long-duration exercise provoked a significant (ANOVA, all P < 0.01, means ± SD) increase in heart rate (1st min, 165.3 ± 15.6 vs. last min, 197.5 ± 21.5 beats/min) and significant reductions in high frequency (0.24 to 1.04 Hz) power (VT: 1st min, 3.7 ± 1.5 vs. last min, 1.0 ± 0.9 ln ms2), R-R interval range (1st min, 107.9 ± 38.3 vs. last min, 28.8 ± 13.2 ms), and R-R interval SD (1st min, 24.3 ± 7.7 vs. last min 6.3 ± 1.7 ms). Because endurance exercise training can increase cardiac vagal regulation, the studies were repeated after either a 10-wk exercise training ( n = 9) or a 10-wk sedentary period ( n = 7). After training was completed, long-duration exercise elicited smaller increases in heart rate (pretraining: 1st min, 156.0 ± 13.8 vs. last min, 189.6 ± 21.9 beats/min; and posttraining: 1st min, 149.8 ± 14.6 vs. last min, 172.7 ± 8.8 beats/min) and smaller reductions in heart rate variability (e.g., VT, pretraining: 1st min, 4.2 ± 1.7 vs. last min, 0.9 ± 1.1 ln ms2; and posttraining: 1st min, 4.8 ± 1.1 vs. last min, 2.0 ± 0.6 ln ms2). The response to long-duration exercise did not change in the sedentary animals. Thus the heart rate increase that accompanies long-duration exercise results, at least in part, from reductions in cardiac vagal regulation. Furthermore, exercise training attenuated these exercise-induced reductions in heart rate variability, suggesting maintenance of a higher cardiac vagal activity during exercise in the trained state.

Low-frequency component of the heart rate variability spectrum: a poor marker of sympathetic activity

1999 ◽  
Vol 276 (1) ◽  
pp. H215-H223 ◽  
Author(s):  
Melanie S. Houle ◽  
George E. Billman
Keyword(s):  
Heart Rate ◽  
Heart Rate Variability ◽  
Ventricular Fibrillation ◽  
Sympathetic Activity ◽  
Low Frequency ◽  
Frequency Component ◽  
Atropine Sulfate ◽  
Low Frequency Power ◽  
Heart Rate Variability Spectrum ◽  
Frequency Power

The low-frequency component of the heart rate variability spectrum (0.06–0.10 Hz) is often used as an accurate reflection of sympathetic activity. Therefore, interventions that enhance cardiac sympathetic drive, e.g., exercise and myocardial ischemia, should elicit increases in the low-frequency power. Furthermore, because an enhanced sympathetic activation has been linked to an increased propensity for malignant arrhythmias, one might also predict a greater low-frequency power in animals that are susceptible to ventricular fibrillation than in resistant animals. To test these hypotheses, a 2-min coronary occlusion was made during the last minute of exercise in 71 dogs with healed myocardial infarctions: 43 had ventricular fibrillation (susceptible) and 28 did not experience arrhythmias (resistant). Exercise or ischemia alone provoked significant heart rate increases in both groups of animals, with the largest increase in the susceptible animals. These heart rate increases were attenuated by β-adrenergic receptor blockade. Despite the sympathetically mediated increases in heart rate, the low-frequency power decreased, rather than increased, in both groups, with the largest decrease again in the susceptible animals: 4.0 ± 0.2 (susceptible) vs. 4.1 ± 0.2 ln ms2 (resistant) in preexercise control and 2.2 ± 0.2 (susceptible) vs. 2.9 ± 0.2 ln ms2 (resistant) at highest exercise level. In a similar manner the parasympathetic antagonist atropine sulfate elicited significant reductions in the low-frequency power. Although sympathetic nerve activity was not directly recorded, these data suggest that the low-frequency component of the heart rate power spectrum probably results from an interaction of the sympathetic and parasympathetic nervous systems and, as such, does not accurately reflect changes in the sympathetic activity.

scholarly journals Comparison of microalbuminuria and heart rate variability in prediction of cardiovascular complications in diabetic population: a pilot study

2017 ◽  
Vol 4 (3) ◽  
pp. 819
Author(s):  
K. Deepalakshmi ◽  
S. Vijayabaskaran ◽  
A. Murali
Keyword(s):  
Heart Rate ◽  
Heart Rate Variability ◽  
Statistical Significance ◽  
Vascular Complications ◽  
Cardiovascular Complications ◽  
P Value ◽  
Diabetic Patients ◽  
Vagal Activity ◽  
Autonomic Imbalance ◽  
Increased Risk

Background: Microalbuminuria is considered as an early marker and strongly associated with risk of cardiovascular complications in diabetic patients. Autonomic imbalance due to micro vascular damage to parasympathetic and sympathetic fibers results in reduced heart rate variability; also predicts increased risk for cardiovascular events in diabetics. Hence it is necessary to identify an early and effective predictor of diabetic micro vascular complications. Objective of the study was to compare heart rate variability of controls with type 2 diabetes with and without microalbuminuria.Methods: This comparative study was conducted among individuals without diabetes, hypertension and dyslipidemia (controls) and Type II diabetics with and without microalbuminuria (cases). Cases and controls were subjected to general clinical examination; microalbuminuria and HbA1C were noted. heart rate variability was assessed using digital physiograph. Frequency (HF, LF, LF/HF ratio) domain readings were noted.Results: Mann Whitney U test was employed to analyze nonparametric data. Diabetics with microalbuminuria when compared with controls showed statistically significant (p-value=0.015) reduction in vagal activity. When compared with diabetics without microalbuminuria (180.4±151.7) they showed reduction in HF with no statistical significance. When diabetic group without microalbuminuria (0.56±0.31) was compared with controls they showed alternation in LF/HF ratio which has no statistical significance. Diabetics with microalbuminuria when compared with controls showed a statistically significant (p-value=0.009) alternation in LF /HF ratio implying an autonomic imbalance.Conclusions: This study shows there is significant vagal inhibition and autonomic imbalance in diabetic patients with microalbuminuria compared to controls. To ascertain the role of HRV as an early predictor of cardiovascular complications we propose to conduct study with a larger sample size in future.

scholarly journals Testing the vagal withdrawal hypothesis during light exercise under autonomic blockade: a heart rate variability study

2018 ◽  
Vol 125 (6) ◽  
pp. 1804-1811 ◽  
Author(s):  
Timothée Fontolliet ◽  
Vincent Pichot ◽  
Aurélien Bringard ◽  
Nazzareno Fagoni ◽  
Alessandra Adami ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Heart Rate Variability ◽  
Baroreflex Sensitivity ◽  
Total Power ◽  
Vagal Activity ◽  
Arterial Blood ◽  
Exercise Onset ◽  
Autonomic Blockade ◽  
Vagal Withdrawal

We performed the first analysis of heart rate variability (HRV) at rest and during exercise under full autonomic blockade on the same subjects, to test the conjecture that vagal tone withdrawal occurs at exercise onset. We hypothesized that between rest and exercise there would be 1) no differences in total power (PTOT) under parasympathetic blockade, 2) a PTOT fall under β1-sympathetic blockade, and 3) no differences in PTOT under blockade of both autonomic nervous system branches. Seven men [24 (3) yr, mean (SD)] performed 5-min cycling (80 W) supine, preceded by 5-min rest during control and with administration of atropine, metoprolol, and atropine + metoprolol (double blockade). Heart rate and arterial blood pressure were continuously recorded. HRV and blood pressure variability were determined by power spectral analysis, and baroreflex sensitivity was determined by the sequence method. At rest, PTOT and the powers of low- and high-frequency components of HRV (LF and HF, respectively) were dramatically decreased with atropine and double blockade compared with control and metoprolol, with no effects on LF-to-HF ratio and on the normalized LF (LFnu) and HF (HFnu). During exercise, patterns were the same as at rest. Comparing exercise with rest, PTOT varied as hypothesized. For systolic and diastolic blood pressure, resting PTOT was the same in all conditions. During exercise, in all conditions, PTOT was lower than in control. Baroreflex sensitivity decreased under atropine and double blockade at rest and under control and metoprolol during exercise. The results support the hypothesis that vagal suppression determined disappearance of HRV during exercise. NEW & NOTEWORTHY This study provides the first demonstration, by systematic analysis of heart rate variability at rest and during exercise under full autonomic blockade on the same subjects, that suppression of vagal activity is responsible for the disappearance of spontaneous heart rate variability during exercise. This finding supports previous hypotheses on the role of vagal withdrawal in the control of the rapid cardiovascular response at exercise onset.

Postural Response of Low-Frequency Component of Heart Rate Variability Is an Increased Risk for Mortality in Patients With Coronary Artery Disease

CHEST Journal ◽  
2001 ◽  
Vol 120 (6) ◽  
pp. 1942-1952 ◽  
Author(s):  
Jun-ichiro Hayano ◽  
Seiji Mukai ◽  
Hidekatsu Fukuta ◽  
Seiichiro Sakata ◽  
Nobuyuki Ohte ◽  
...  
Keyword(s):  
Coronary Artery Disease ◽  
Heart Rate ◽  
Heart Rate Variability ◽  
Coronary Artery ◽  
Low Frequency ◽  
Frequency Component ◽  
Postural Response ◽  
Increased Risk ◽  
Artery Disease
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