Heart Rate Recovery after Maximal Exercise Is Associated with Acetylcholine Receptor M2 (CHRM2) Gene Polymorphism

Hautala, Arto J.; Rankinen, Tuomo; Kiviniemi, Antti M.; Mäkikallio, Timo H.; Huikuri, Heikki V.; Bouchard, Claude; Tulppo, Mikko P.

doi:10.1249/00005768-200605001-01096

Cited by 20 publications

(27 citation statements)

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“…Physical training is unlikely to alter renal excretion of pyridostigmine (48), but other effects of training, including reduced fat mass, increased basal metabolic rate, and longer duration of exercise testing in the study protocol, may have altered other aspects of pyridostigmine metabolism and thereby contributed to our findings. Moreover, individual differences in pyridostigmine pharmacokinetics related to age, sex, body habitus, or genetic factors are potential confounders that should be assessed in future studies (5,27,37,39). Resting autonomic tone was not formally evaluated by pharmacological blockade with atropine in either cohort.…”

Section: Discussionmentioning

confidence: 99%

Effect of acetylcholinesterase inhibition with pyridostigmine on cardiac parasympathetic function in sedentary adults and trained athletes

Dewland¹,

Androne²,

Lee³

et al. 2007

American Journal of Physiology-Heart and Circulatory Physiology

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Dewland TA, Androne AS, Lee FA, Lampert RJ, Katz SD. Effect of acetylcholinesterase inhibition with pyridostigmine on cardiac parasympathetic function in sedentary adults and trained athletes. Am J Physiol Heart Circ Physiol 293: H86-H92, 2007. First published February 23, 2007 doi:10.1152/ajpheart.01339.2006.-Heart rate variability and postexercise heart rate recovery are used to assess cardiac parasympathetic tone in human studies, but in some cases these indexes appear to yield discordant information. We utilized pyridostigmine, an acetylcholinesterase inhibitor that selectively augments the parasympathetic efferent signal, to further characterize parasympathetic regulation of rest and postexercise heart rate. We measured time-and frequency-domain indexes of resting heart rate variability and postexercise heart rate recovery in 10 sedentary adults and 10 aerobically trained athletes after a single oral dose of pyridostigmine (30 mg) and matching placebo in randomized, doubleblind, crossover trial. In sedentary adults, pyridostigmine decreased resting heart rate [from 66.7 (SD 12.6) to 58.1 beats/min (SD 7.6), P ϭ 0.005 vs. placebo] and increased postexercise heart rate recovery at 1 min [from 40.7 (SD 10.9) to 45.1 beats/min (SD 8.8), P ϭ 0.02 vs. placebo]. In trained athletes, pyridostigmine did not change resting heart rate or postexercise heart rate recovery when compared with placebo. Time-and frequency-domain indexes of resting heart rate variability did not differ after pyridostigmine versus placebo in either cohort and were not significantly associated with postexercise heart rate recovery in either cohort. The divergent effects of pyridostigmine on resting and postexercise measures of cardiac parasympathetic function in sedentary subjects confirm that these measures characterize distinct aspects of cardiac parasympathetic regulation. The lesser effect of pyridostigmine on either measure of cardiac parasympathetic tone in the trained athletes indicates that the enhanced parasympathetic tone associated with exercise training is at least partially attributable to adaptations in the efferent parasympathetic pathway. heart rate variability; heart rate recovery; parasympathetic nervous system; exercise RESTING HEART RATE VARIABILITY and postexercise heart rate recovery are used in human studies to assess cardiac parasympathetic tone (1,30,47). The high-frequency (HF) component of resting heart rate variability quantifies short-term changes in heart rate caused by the effects of central and peripheral respiratory reflexes on vagal efferent activity during a resting steady state with low sympathetic activation (1). Postexercise heart rate recovery assesses the complex interaction of baroreceptor and central command signals that mediate a rapid deceleration of heart rate in the setting of autonomic flux, profound exercise-induced sympathetic stimulation, and high minute ventilation (30).Parasympathetic efferent control of heart rate is ultimately mediated by cholinergic signaling at the sinoatrial node. Acetyl...

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Section: Discussionmentioning

confidence: 99%

Effect of acetylcholinesterase inhibition with pyridostigmine on cardiac parasympathetic function in sedentary adults and trained athletes

Dewland¹,

Androne²,

Lee³

et al. 2007

American Journal of Physiology-Heart and Circulatory Physiology

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“…1,2,[11][12][13] These articles were read and the reference lists were checked. Based on this analysis, 7 other articles were found that met the inclusion criteria [14][15][16][17][18][19][20] but had been missed using the original databases and search terms. Therefore, 12 articles were included as part of the current systematic review.…”

Section: Study Selection: Inclusion and Exclusion Criteriamentioning

confidence: 99%

A Systematic Review on Heart-Rate Recovery to Monitor Changes in Training Status in Athletes

Daanen¹,

Lamberts²,

Kallen³

et al. 2012

International Journal of Sports Physiology and Performance

190

152

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Heart-rate recovery (HRR) can be defined as the rate at which heart rate declines, usually within minutes after the cessation of physical exercise. [1][2][3] The autonomic nervous system (ANS) regulates both the initial increase in heart rate after the start of physical activity and the decrease in heart rate immediately after physical activity ends. The ANS is composed of a parasympathetic and a sympathetic branch that operate in a reciprocal and inverse manner: An increase in heart rate is caused by an increase in sympathetic activity combined with decreased parasympathetic drive, whereas HRR is characterized by parasympathetic reactivation and sympathetic withdrawal. [3][4][5][6][7] Cardiac output is adjusted during exercise based on the metabolic demand. The regulation occurs by intrinsic autoregulation of cardiac pumping (the so-called Frank-Starling law of the heart) and by sympathetic activation and parasympathetic deactivation, which increases heart rate and the contraction force of mainly the left ventricle. 8 Increased sympathetic activity combined with parasympathetic withdrawal (eg, during exercise) leads to reduced skin blood flow and increased blood flow to the muscles. 9 When the exercise stops, cardiac output is reduced by intrinsic autoregulation (by the ANS), more specifically by parasympathetic nervous system reactivation and inhibition of sympathetic impulses.Although it is well documented that changes in HRR coincide well with changes in training status in patient populations, 10 to our knowledge a systematic review on the use of HRR in athletes is missing. HRR may be an indicator of fitness, which is currently generally expressed in terms of VO 2max or VO 2peak , the maximum oxygen uptake during exhaustive exercise. Although VO 2max has a strong relationship with training status in a general population, it loses its predictive value for aerobic performance in already well-trained and elite athletes. 2 In addition, the typical error of measurement of VO 2max is relatively high, which makes VO 2max unreliable to monitor training changes over time. 2 In contrast, parameters such as HRR, peak power output, and/or peak treadmill running speed have lower typical errors of measurements, which makes them more sensitive to detect changes in training status.Therefore, the aim of this study was to conduct a systematic review on the use of HRR in athletes to track long-term changes in training status. Methods Data SourcesAn electronic literature search was performed in the digital databases of Scopus, EMBASE, and PubMed. The search terms used were a combination of heart/pulse rate(s), recovery/deceleration, (physical) exercise, and health(y) subjects/population. This search yielded 90 scientific articles (see Figure 1). Heart-rate recovery (HRR) has been proposed as a marker of autonomic function and training status in athletes. The authors performed a systematic review of studies that examined HRR after training. Five cross-sectional studies and 8 studies investigating changes over time (longitudinal)...

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“…Whereas this polymorphism has major effects on the transcription of CHRM2, its potential impact on tachycardic responses to muscarinic receptor antagonists has not been investigated. The effects of two polymorphisms located in intron 5 (rs324640) or the 3Ј-untranslated region (rs8191992) of CHRM2, originally identified in a study on alcohol dependence and major depressive syndromes (Wang et al, 2004), were analyzed in volunteers undergoing maximal exercise testing (Hautala et al, 2006). A highly significant difference in heart rate recovery of 12 beats/min was observed in association with the various alleles of these SNPs.…”

Section: A Muscarinic Acetylcholine Receptorsmentioning

confidence: 99%

Pharmacogenomics of G Protein-Coupled Receptor Ligands in Cardiovascular Medicine

Rosskopf

Michel²

2008

Pharmacol Rev

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Heart Rate Recovery after Maximal Exercise Is Associated with Acetylcholine Receptor M2 (CHRM2) Gene Polymorphism

Cited by 20 publications

References 0 publications

Effect of acetylcholinesterase inhibition with pyridostigmine on cardiac parasympathetic function in sedentary adults and trained athletes

Effect of acetylcholinesterase inhibition with pyridostigmine on cardiac parasympathetic function in sedentary adults and trained athletes

A Systematic Review on Heart-Rate Recovery to Monitor Changes in Training Status in Athletes

Pharmacogenomics of G Protein-Coupled Receptor Ligands in Cardiovascular Medicine

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