The Mechanism of Bradycardia Evoked by Physical Training

Frick, M H; Elovainio, R.; Somer, T

doi:10.1159/000165849

Cited by 96 publications

(33 citation statements)

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“…In the first place, exercise involves adrenergic stimulation of the heart to a much greater degree than pacing. Furthermore, the decrease in catecholamine concentration in hearts of conditioned rats (30) and the attenuated effect of autonomic blockade on exercise tachycardia in conditioned humans (31) suggest that adrenergic stimulation of the heart during exercise may be less after conditioning.…”

Section: Resultsmentioning

confidence: 99%

Investigation of the Physiological Basis for Increased Exercise Threshold for Angina Pectoris after Physical Conditioning

Sim¹,

Neill²

1974

J. Clin. Invest.

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A B S T R A C T Eight patients with coronary heart disease and exertional angina pectoris successfully completed an 11-15 wk program of endurance exercise conditioning. Angina threshold was determined by upright bicycle ergometer exercise and by atrial pacing. The product of heart rate and arterial systolic blood pressure at the exercise angina threshold was higher after conditioning, suggesting that conditioning increased the maximum myocardial 02 supply during exercise. However, when angina was induced by atrial pacing, heart rate, arterial blood pressure, coronary blood flow, and myocardial 02 consumption at the angina threshold were the same before and after conditioning. Myocardial lactate extraction during atrial pacing was abnormal in the same five patients before and after conditioning. Conditioning caused no detectable changes in coronary collaterals as judged by coronary arteriograms.The increase in exercise angina threshold appeared to be due to a functional adaptation in either myocardial 02 supply or the relationship between hemodynamic work and myocardial 02 consumption. The adaptation was limited to exercise, and did not occur during a different stress to myocardial 02 supply, atrial pacing.

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Section: Resultsmentioning

confidence: 99%

Investigation of the Physiological Basis for Increased Exercise Threshold for Angina Pectoris after Physical Conditioning

Sim¹,

Neill²

1974

J. Clin. Invest.

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“…This suggests a reduced cardiac vagal control accompanying physiologic aging may result essentially from progressive deconditioning (Goldsmith et al, 1997). Greater resting cardiac vagal tone is a distinguishing characteristic of physically fit individuals (Ekblom et al, 1973;Frick et al, 1967;Shi et al, 1995;Smith et al, 1989) and a vagally mediated resting bradycardia is observed in younger as well as older humans after exercise training (Stratton et al, 1994). Moreover, our prior work shows that older fit individuals can display baroreflex-mediated cardiac vagal control similar to young individuals (Hunt et al, 2001).…”

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confidence: 92%

Effects of fitness and age on the response to vagotonic atropine

Lee¹,

Picard²,

Beske³

et al. 2008

Autonomic Neuroscience

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Previous work indicates compromised cardiac vagal control plays a prominent role in reducing arterial baroreflex gain with age, however older fit individuals display cardiovagal baroreflex responses similar to young individuals. The purpose of this study was to test the hypothesis that chronic aerobic exercise mitigates against age-related declines in cardiac parasympathetic receptor function. In forty-four young and old (fit and unfit) individuals, we used the parasympathomimetic responses to low doses of atropine to probe cardiac cholinergic receptor responses. Data was collected before and after eight doses of atropine sulfate from 0.4 to 7.2 ug/kg. Chronotropic responses were assessed from average RR intervals and heart rate variabilities were derived in time and frequency domains. All subjects exhibited bradycardia with at least one dose of atropine and peak bradycardia occurred at a similar dose in each group. However, changes in heart rate variability did not consistently track the chronotropic responses within subjects (r-square from 0.90 down to 0). As expected, basal RR interval was longer in the fit groups and was unaffected by age. However, the degree of RR interval lengthening with parasympathomimetic atropine was unaffected by physical fitness and was significantly less in all older subjects. These data indicate there are certain prepotent age-related declines in the cardiac parasympathetic system that cannot be prevented by regular physical activity. Keywordsatropine; vagal; heart rate variability; muscarinic receptor Our previous work indicates a decline in cardiac parasympathetic neural control compromises baroreflex gain with age (Kaushal et al., 2002) and this decline can be offset by regular physical activity (Hunt et al., 2001). This suggests a reduced cardiac vagal control accompanying physiologic aging may result essentially from progressive deconditioning (Goldsmith et al., 1997). Greater resting cardiac vagal tone is a distinguishing characteristic of physically fit individuals (Ekblom et al., 1973;Frick et al., 1967;Shi et al., 1995;Smith et al., 1989) and a vagally mediated resting bradycardia is observed in younger as well as older humans after exercise training (Stratton et al., 1994). Moreover, our prior work shows that older fit individuals can display baroreflex-mediated cardiac vagal control similar to young individuals (Hunt et al., 2001). In these individuals, baroreflex responses are maintained despite age-related Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. Atropine sulfate is routinely used to probe the cardiac parasympathe...

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“…The mechanism for the decrease in the intrinsic heart rate might be digitalis-induced long-term changes in autonomic nervous system activity (Gillis & Quest, 1979). This occurs in athletes, whose intrinsic heart rate decreases during training (Frick et al, 1967), though digoxin induces no diastolic volume changes in the heart.…”

Section: Effect Of Digoxin During Autonomic Blockadementioning

confidence: 99%

Effect of digoxin on the heart in normal subjects: influence of isometric exercise and autonomic blockade: a noninvasive study.

Partanen

Heikkilä

Pellinen

et al. 1988

Brit J Clinical Pharma

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1 Eight healthy subjects were studied before digoxin and after successive therapy periods of 1 week 0.125, 0.25 and 0.50 mg of digoxin. The mean serum concentrations (± s. d.) were 0.4 ± 0.2, 0.6 ± 0.3 and 1.4 ± 0.5 nmol I-1, respectively. The effects of digitalis were studied by echocardiography and systolic time intervals at rest and after 3 min handgrip exercise. Effects of simultaneous autonomic blockade induced by atropine and propranolol were also examined. 2 Digoxin in increasing doses slowed the heart rate at rest; with the daily dose of 0.50 mg from 63 ± 10 to 53 ± 6 beats min-', and fractional shortening rose from 28 ± 6 to 33 ± 3% (P < 0.05 for both). Preload, afterload and cardiac output did not change. The electromechanic systolic time index (QS2I) decreased (P < 0.001) and the observed alteration of QS2I was dose-related.3 The influence of digoxin was similar during isometric exercise, except for unchanged fractional shortening. 4 During autonomic blockade digoxin slowed the intrinsic heart rate from 93 ± 6 to 86 ± 6 beats min-' (0.25 mg) and to 83 ± 6 beats min-' (0.50 mg) (P < 0.01 for both). QS2I was shortened (P < 0.01). Echocardiographically determined ejection phase indices remained unchanged. 5 When handgrip stress was induced during autonomic blockade, digoxin evoked a clearcut increase in contractile function, resembling the effects of digoxin alone at rest. Thus, fractional shortening increased by 14% and QS21 decreased by 16 ms (P < 0.01 for both). 6 We conclude that digoxin increases the contractility in normal heart without changes in loading conditions. The rise in inotropy at rest is obvious from both fractional shortening by echo and systolic time intervals. The same takes place during handgrip with autonomic blockade, when the heart lacks sympathetic support. The influence of long-term digoxin on heart rate is partly direct without autonomic mediation. The effect of digoxin is dosedependent.Keywords digoxin isometric exercise autonomic blockade left ventricular contractility echocardiography systolic time intervals

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The Mechanism of Bradycardia Evoked by Physical Training

Cited by 96 publications

References 0 publications

Investigation of the Physiological Basis for Increased Exercise Threshold for Angina Pectoris after Physical Conditioning

Investigation of the Physiological Basis for Increased Exercise Threshold for Angina Pectoris after Physical Conditioning

Effects of fitness and age on the response to vagotonic atropine

Effect of digoxin on the heart in normal subjects: influence of isometric exercise and autonomic blockade: a noninvasive study.

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