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

Abstract

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...

Fear and C-reactive protein cosynergize annual pulse increases in healthy adults

“…Cholinergic status values improved pulse predictions even when controlled for all other risk factors in men but not in women (24), compatible with the antiinflammatory effect of cholinergic signaling (14) as well as with previous reports of protective acetylcholine effects on ischemic myocardium (26), and with the pulse improvement effects of the AChE inhibitor pyridostigmine (27).…”

Relationship between Resting Heart Rate Variability and Heart Rate Recovery from Exercise in College-Aged Men

“…Dewland, Androne, Lee, Lampert, and Katz (2007) found no relationship between resting HRV and HRR from maximal exercise.…”

In search of the optimal measure for assessment of parasympathetic control of heart rate

“…Dewland et al utilized the acetylcholinesterase inhibitor pyridostigmine to augment parasympathetic signaling at the sinoatrial node in ten sedentary subjects (mean age 37 ± 7 years, mean VO 2max 29.4 ± 6.2 ml/kg per min) and ten endurance-trained athletes (mean age 27 ± 8 years, mean VO 2max 53.3 ± 11.3 ml/kg per min). These investigators demonstrated that pyridostigmine increased HRR in sedentary subjects, but not in trained athletes, and did not alter HRV in either group [7].…”

“…Dewland et al utilized the acetylcholinesterase inhibitor pyridostigmine to augment parasympathetic signaling at the sinoatrial node in ten sedentary subjects (mean age 37 ± 7 years, mean VO 2max 29.4 ± 6.2 ml/kg per min) and ten endurance-trained athletes (mean age 27 ± 8 years, mean VO 2max 53.3 ± 11.3 ml/kg per min). These investigators demonstrated that pyridostigmine increased HRR in sedentary subjects, but not in trained athletes, and did not alter HRV in either group [7].In this issue, Esco et al [8] report the findings of a crosssectional study that further supports the viewpoint that HRV and HRR are independent measures of parasympathetic function. The investigators recruited a sample of 66 healthy subjects (mean age 22.74 ± 3.64 years, mean VO 2max 46.39 ± 8.23 ml/kg per min) and demonstrated no association between any time domain or frequency-domain measure of HRV and HRR in this population.…”

“…One plausible explanation is that HRV measures parasympathetic modulation of heart rate (primarily related to the phasic changes in acetylcholine concentrations associated with the respiratory cycle), while HRR measures the parasympathetic tone (the mean level of acetylcholine at the sinoatrial node) [5,7]. It is also possible that both of these measures are influenced by other unmeasured central and peripheral factors that modulate heart rate oscillations.…”