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 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.

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.

Higher mitochondrial fatty acid oxidation following intermittent versus continuous endurance exercise training

1998 ◽  
Vol 76 (9) ◽  
pp. 891-894 ◽  
Author(s):  
P D Chilibeck ◽  
G J Bell ◽  
R P Farrar ◽  
T P Martin
Keyword(s):  
Fatty Acid ◽  
Exercise Training ◽  
Fatty Acid Oxidation ◽  
Endurance Exercise ◽  
High Intensity ◽  
Treadmill Running ◽  
Acid Oxidation ◽  
Interval Exercise ◽  
Endurance Exercise Training ◽  
Mitochondrial Fatty Acid

It has been well documented that skeletal muscle fatty acid oxidation can be elevated by continuous endurance exercise training. However, it remains questionable whether similar adaptations can be induced with intermittent interval exercise training. This study was undertaken to directly compare the rates of fatty acid oxidation in isolated subsarcolemmal (SS) and intermyofibrillar (IMF) mitochondria following these different exercise training regimes. Mitochondria were isolated from the gastrocnemius-plantaris muscles of male Sprague-Dawley rats following exercise training 6 days per week for 12 weeks. Exercise training consisted of either continuous, submaximal, endurance treadmill running (n = 10) or intermittent, high intensity, interval running (n = 10). Both modes of training enhanced the oxidation of palmityl-carnitine-malate in both mitochondrial populations (p < 0.05). However, the increase associated with the intermittent, high intensity exercise training was significantly greater than that achieved with the continuous exercise training (p < 0.05). Also, the increases associated with the IMF mitochondria were greater than the SS mitochondria (p < 0.05). These data suggest that high intensity, intermittent interval exercise training is more effective for stimulation of fatty acid oxidation than continuous submaximal exercise training and that this adaptation occurs preferentially within IMF mitochondria.Key words: muscle, subsarcolemmal mitochondria, intermyofibrillar mitochondria.

THE EFFECTS OF ENDURANCE EXERCISE TRAINING ON INTRAMUSCULAR SUBSTRATE USE DURING PROLONGED SUBMAXIMAL EXERCISE

1985 ◽  
Vol 17 (2) ◽  
pp. 259-260 ◽  
Author(s):  
B. F. Hurley ◽  
P. M. Nemeth ◽  
W. H. Martin ◽  
G. P. Dalaky ◽  
J. M. Hagberg ◽  
...  
Keyword(s):  
Exercise Training ◽  
Endurance Exercise ◽  
Submaximal Exercise ◽  
Substrate Use ◽  
Endurance Exercise Training

Skeletal muscle biochemical adaptations to exercise training in miniature swine

1997 ◽  
Vol 82 (6) ◽  
pp. 1862-1868 ◽  
Author(s):  
Richard M. McAllister ◽  
Brian L. Reiter ◽  
John F. Amann ◽  
M. Harold Laughlin
Keyword(s):  
Skeletal Muscle ◽  
Antioxidant Enzymes ◽  
Lactate Dehydrogenase ◽  
Exercise Training ◽  
Endurance Exercise ◽  
Oxidative Capacity ◽  
Treadmill Running ◽  
Miniature Swine ◽  
Endurance Exercise Training ◽  
Hydroxyacyl Coa Dehydrogenase

McAllister, Richard M., Brian L. Reiter, John F. Amann, and M. Harold Laughlin. Skeletal muscle biochemical adaptations to exercise training in miniature swine. J. Appl. Physiol. 82(6): 1862–1868, 1997.—The primary purpose of this study was to test the hypothesis that endurance exercise training induces increased oxidative capacity in porcine skeletal muscle. To test this hypothesis, female miniature swine were either trained by treadmill running 5 days/wk over 16–20 wk (Trn; n = 35) or pen confined (Sed; n = 33). Myocardial hypertrophy, lower heart rates during submaximal stages of a maximal treadmill running test, and increased running time to exhaustion during that test were indicative of training efficacy. A variety of skeletal muscles were sampled and subsequently assayed for the enzymes citrate synthase (CS), 3-hydroxyacyl-CoA dehydrogenase, and lactate dehydrogenase and for antioxidant enzymes. Fiber type composition of a representative muscle was also determined histochemically. The largest increase in CS activity (62%) was found in the gluteus maximus muscle (Sed, 14.7 ± 1.1 μmol ⋅ min−1 ⋅ g−1; Trn, 23.9 ± 1.0; P < 0.0005). Muscles exhibiting increased CS activity, however, were located primarily in the forelimb; ankle and knee extensor and respiratory muscles were unchanged with training. Only two muscles exhibited higher 3-hydroxyacyl-CoA dehydrogenase activity in Trn compared with Sed. Lactate dehydrogenase activity was unchanged with training, as were activities of antioxidant enzymes. Histochemical analysis of the triceps brachii muscle (long head) revealed lower type IIB fiber numbers in Trn (Sed, 42 ± 6%; Trn, 10 ± 4; P < 0.01) and greater type IID/X fiber numbers (Sed, 11 ± 2; Trn, 22 ± 3; P < 0.025). These findings indicate that porcine skeletal muscle adapts to endurance exercise training in a manner similar to muscle of humans and other animal models, with increased oxidative capacity. Specific muscles exhibiting these adaptations, however, differ between the miniature swine and other species.

Endurance exercise training has a minimal effect on resting heart rate: the HERITAGE study

1996 ◽  
Vol 28 (7) ◽  
pp. 829-835 ◽  
Author(s):  
JACK H. WILMORE ◽  
PHILIP R. STANFORTH ◽  
JACQUES GAGNON ◽  
ARTHUR S. LEON ◽  
D. C. RAO ◽  
...  
Keyword(s):  
Heart Rate ◽  
Exercise Training ◽  
Endurance Exercise ◽  
Minimal Effect ◽  
Resting Heart Rate ◽  
Endurance Exercise Training

Cardiac autonomic neural remodeling and susceptibility to sudden cardiac death: effect of endurance exercise training

2009 ◽  
Vol 297 (4) ◽  
pp. H1171-H1193 ◽  
Author(s):  
George E. Billman
Keyword(s):  
Myocardial Infarction ◽  
Sudden Cardiac Death ◽  
Ventricular Fibrillation ◽  
Exercise Training ◽  
Endurance Exercise ◽  
Cardiac Death ◽  
Endurance Exercise Training ◽  
Cardiac Autonomic Regulation ◽  
Parasympathetic Regulation ◽  
Neural Remodeling

Sudden cardiac death resulting from ventricular tachyarrhythmias remains the leading cause of death in industrially developed countries, accounting for between 300,000 and 500,000 deaths each year in the United States. Yet, despite the enormity of this problem, both the identification of factors contributing to ventricular fibrillation as well as the development of safe and effective antiarrhythmic agents remain elusive. Subnormal cardiac parasympathetic regulation coupled with an elevated cardiac sympathetic activation may allow for the formation of malignant ventricular arrhythmias. In particular, myocardial infarction can reduce cardiac parasympathetic regulation and alter β-adrenoceptor subtype expression enhancing β2-adrenoceptor sensitivity that can lead to intracellular calcium dysregulation and arrhythmias. As such, myocardial infarction can induce a remodeling of cardiac autonomic regulation that may be required to maintain cardiac pump function. If alterations in cardiac autonomic regulation play an important role in the genesis of life-threatening arrhythmias, then one would predict that interventions designed to either augment parasympathetic activity and/or reduce cardiac adrenergic activity would also protect against ventricular fibrillation. Recently, studies using a canine model of sudden death demonstrate that endurance exercise training (treadmill running) enhanced cardiac parasympathetic regulation (increased heart rate variability), restored a more normal β-adrenoceptor balance (i.e., reduced β2-adrenoceptor sensitivity and expression), and protected against ventricular fibrillation induced by acute myocardial ischemia. Thus exercise training may reverse the autonomic neural remodeling induced by myocardial infarction and thereby enhance the electrical stability of the heart in individuals shown to be at an increased risk for sudden cardiac death.

Endurance Exercise Training Improves Heart Rate Recovery in Patients with COPD

2013 ◽  
Vol 11 (2) ◽  
pp. 190-196 ◽  
Author(s):  
Elena Gimeno-Santos ◽  
Diego A. Rodriguez ◽  
Anael Barberan-Garcia ◽  
Isabel Blanco ◽  
Jordi Vilaró ◽  
...  
Keyword(s):  
Heart Rate ◽  
Exercise Training ◽  
Endurance Exercise ◽  
Heart Rate Recovery ◽  
Endurance Exercise Training
Sign in / Sign up

Export Citation Format

Share Document