Supraventricular Arrhythmias in Athletes: Basic Mechanisms and New Directions

D’Souza, Alicia; Trussell, Tariq; Morris, Gwilym M.; Dobrzynski, Halina; Boyett, Mark R.

doi:10.1152/physiol.00009.2019

Cited by 15 publications

(11 citation statements)

References 132 publications

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“…These findings are contested by studies in rodents (e.g., Aschar-Sobbi et al, 2015) and dogs (Billman et al, 2015) where training induced intrinsic slowing was not observed and instead a role for high vagal tone was determined. The evidence for intrinsic vs. autonomic mechanisms in underlying training-induced sinus bradycardia has been extensively reviewed by our group (Boyett et al, 2013(Boyett et al, , 2017D'Souza et al, 2015D'Souza et al, , 2019 and we posit that non-uniform methodology (species, drug doses, and training modalities) contribute to the reported discrepancies. Furthermore, based on our present results we advance that both vagally mediated and intrinsic SAN remodeling-based mechanisms of the HR adaptation to training may be reconciled: we speculate that (currently uncharacterized) training-induced alterations in sympathetic and/or parasympathetic input may trigger transcriptional remodeling of SAN ion channels, leading to a decrease in intrinsic automaticity as observed.…”

Section: Impact Of the Studymentioning

confidence: 91%

Genetic Ablation of G Protein-Gated Inwardly Rectifying K+ Channels Prevents Training-Induced Sinus Bradycardia

et al. 2021

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Background: Endurance athletes are prone to bradyarrhythmias, which in the long-term may underscore the increased incidence of pacemaker implantation reported in this population. Our previous work in rodent models has shown training-induced sinus bradycardia to be due to microRNA (miR)-mediated transcriptional remodeling of the HCN4 channel, leading to a reduction of the “funny” (If) current in the sinoatrial node (SAN).Objective: To test if genetic ablation of G-protein-gated inwardly rectifying potassium channel, also known as IKACh channels prevents sinus bradycardia induced by intensive exercise training in mice.Methods: Control wild-type (WT) and mice lacking GIRK4 (Girk4–/–), an integral subunit of IKACh were assigned to trained or sedentary groups. Mice in the trained group underwent 1-h exercise swimming twice a day for 28 days, 7 days per week. We performed electrocardiogram recordings and echocardiography in both groups at baseline, during and after the training period. At training cessation, mice were euthanized and SAN tissues were isolated for patch clamp recordings in isolated SAN cells and molecular profiling by quantitative PCR (qPCR) and western blotting.Results: At swimming cessation trained WT mice presented with a significantly lower resting HR that was reversible by acute IKACh block whereas Girk4–/– mice failed to develop a training-induced sinus bradycardia. In line with HR reduction, action potential rate, density of If, as well as of T- and L-type Ca2+ currents (ICaT and ICaL) were significantly reduced only in SAN cells obtained from WT-trained mice. If reduction in WT mice was concomitant with downregulation of HCN4 transcript and protein, attributable to increased expression of corresponding repressor microRNAs (miRs) whereas reduced ICaL in WT mice was associated with reduced Cav1.3 protein levels. Strikingly, IKACh ablation suppressed all training-induced molecular remodeling observed in WT mice.Conclusion: Genetic ablation of cardiac IKACh in mice prevents exercise-induced sinus bradycardia by suppressing training induced remodeling of inward currents If, ICaT and ICaL due in part to the prevention of miR-mediated transcriptional remodeling of HCN4 and likely post transcriptional remodeling of Cav1.3. Strategies targeting cardiac IKACh may therefore represent an alternative to pacemaker implantation for bradyarrhythmias seen in some veteran athletes.

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Section: Impact Of the Studymentioning

confidence: 91%

Genetic Ablation of G Protein-Gated Inwardly Rectifying K+ Channels Prevents Training-Induced Sinus Bradycardia

et al. 2021

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“…Supraventricular arrhythmia number post high-volume endurance exercise was also related to baseline supraventricular number. This result is not unexpected, considering that high volume endurance exercise is accepted as a factor contributing to the development of supraventricular arrhythmias ( D’Souza et al, 2019 ), including bradyarrhythmia, atrioventricular block ( Baldesberger et al, 2008 ) and atrial fibrillation ( Andersen et al, 2013 ; Myrstad et al, 2014 ). Further, supraventricular arrhythmias can have serious quality of life and sport participation consequences in athletes ( D’Souza et al, 2019 ), although in the general population it has been suggested that they are common and rarely life threatening ( Blomstrom-Lundqvist et al, 2003 ).…”

Section: Discussionmentioning

confidence: 79%

Sympathovagal Balance Is a Strong Predictor of Post High-Volume Endurance Exercise Cardiac Arrhythmia

et al. 2022

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Regular physical activity is important for cardiovascular health. However, high-volume endurance exercise has been associated with increased number of electrocardiogram (ECG) abnormalities, including disturbances in cardiac rhythm (arrhythmias) and abnormalities in ECG pattern. The aim of this study was to assess if heart rate variability (HRV) is associated with ECG abnormalities. Fifteen participants with previous cycling experience completed a 21-day high-volume endurance exercise cycle over 3,515 km. Participants wore a 5-lead Holter monitor for 24 h pre- and post-exercise, which was used to quantify ECG abnormalities and export sinus R-to-R intervals (NN) used to calculate HRV characteristics. As noise is prevalent in 24-h HRV recordings, both 24-h and heart rate collected during stable periods of time (i.e., deep sleep) were examined. Participants experienced significantly more arrhythmias post high-volume endurance exercise (median = 35) compared to pre (median = 12; p = 0.041). All 24-h and deep sleep HRV outcomes were not different pre-to-post high-volume endurance exercise (p > 0.05). Strong and significant associations with arrhythmia number post-exercise were found for total arrhythmia (total arrhythmia number pre-exercise, ρ = 0.79; age, ρ = 0.73), supraventricular arrhythmia (supraventricular arrhythmia number pre-exercise: ρ = 0.74; age: ρ = 0.66), and ventricular arrhythmia (age: ρ = 0.54). As a result, age and arrhythmia number pre-exercise were controlled for in hierarchical regression, which revealed that only deep sleep derived low frequency to high frequency (LF/HF) ratio post high-volume endurance exercise predicted post total arrhythmia number (B = 0.63, R2Δ = 34%, p = 0.013) and supraventricular arrhythmia number (B = 0.77, R2Δ = 69%, p < 0.001). In this study of recreationally active people, only deep sleep derived LF/HF ratio was associated with more total and supraventricular arrhythmias after high-volume endurance exercise. This finding suggests that measurement of sympathovagal balance during deep sleep might be useful to monitor arrhythmia risk after prolonged high-volume endurance exercise performance.

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“…Physiologically, HRA was related to sinus node innervated by autonomic nervous system, which modulated heart rhythm through neurotransmitter release [26]. This was the reason that the disturbed HRA could provide diagnostic evidences for many pathologies [7,8,27].…”

Section: Resultsmentioning

confidence: 99%

The effect of passive lower limb training on heart rate asymmetry

Shi

et al. 2022

Physiol. Meas.

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Objective: Heart rate asymmetry (HRA) is an approach for quantitatively assessing the uneven distribution of heart rate accelerations and decelerations for sinus rhythm. We aimed to investigate whether automatic regulation led to HRA alternation during passive lower limb training. Methods: Thirty healthy participants were recruited in this study. The protocol included a baseline (Pre-E) and three passive lower limb training trials (E1, E2 and E3) with a randomized order. Several variance-based HRA variables were established. Heart rate variability (HRV) parameters, i.e., mean RR, SDNN, RMSSD, LF (n.u.), HF (n.u.) and VLF (ms2), and HRA variables, i.e., SD1a, SD1d, SD2a, SD2d, SDNNa and SDNNd, were calculated by using 5-min RR time series, as well as the normalized HRA variables, i.e., C1a, C1d, C2a, C2d, Ca and Cd. Results: Our results showed that the performance of HRA was distinguished. The normalized HRA was observed with significant changes in E1, E2 and E3 compared to Pre -E. Moreover, parts of non-normalized HRA variables correlated with HRV parameters, which indicated that HRA might benefit in assessing cardiovascular modulation in passive lower limb training. Conclusions: In summary, this study suggested that passive training led to significant HRA alternation and the application of HRA gave us the possibility for autonomic assessment.

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Supraventricular Arrhythmias in Athletes: Basic Mechanisms and New Directions

Cited by 15 publications

References 132 publications

Genetic Ablation of G Protein-Gated Inwardly Rectifying K+ Channels Prevents Training-Induced Sinus Bradycardia

Genetic Ablation of G Protein-Gated Inwardly Rectifying K+ Channels Prevents Training-Induced Sinus Bradycardia

Sympathovagal Balance Is a Strong Predictor of Post High-Volume Endurance Exercise Cardiac Arrhythmia

The effect of passive lower limb training on heart rate asymmetry

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