Abstract
Heart rate (HR) responds to exercise by increasing during exercise and recovering after exercise. As such, HR is an important predictor of mortality that researchers believe is modulated by the autonomic nervous system. However, the mechanistic basis underlying inter-individual differences has yet to be explained. Here, we perform a large-scale genome-wide analysis of HR increase and HR recovery in 58,818 UK Biobank individuals. Twenty-five independent SNPs in 23 loci are identified to be associated (p < 8.3 × 10−9) with HR increase or HR recovery. A total of 36 candidate causal genes are prioritized that are enriched for pathways related to neuron biology. No evidence is found of a causal relationship with mortality or cardiovascular diseases. However, a nominal association with parental lifespan requires further study. In conclusion, the findings provide new biological and clinical insight into the mechanistic underpinnings of HR response to exercise. The results also underscore the role of the autonomous nervous system in HR recovery.
Highlights
Heart rate (HR) responds to exercise by increasing during exercise and recovering after exercise
The goals of the current study study are to (1) provide genetic heritability estimates among variables of the HR profile during exercise; (2) identify genetic variants and the underlying candidate causal genes associated with HR increase and HR recovery at 10, 20, 30, 40, and 50 s; and (3) obtain insights into pleiotropy and the clinical consequences of HR increase and HR recovery
Participants from the UK Biobank exercised for ~350 (±44.9) seconds; the mean duration of the recovery phase was 52.6 (±1.7) seconds
Summary
Heart rate (HR) responds to exercise by increasing during exercise and recovering after exercise. The first data linking electrocardiographic changes in response to exercise with mortality was presented in 1975 This data indicated that a low-peak heart-rate (HR) response during exercise was associated with an increased risk of cardiac death[2]. The hypothesis linking HR recovery to mortality arose from work that associated components of the autonomic nervous system with sudden cardiac death[11], as well as studies of decreased vagal activity[12,13]. The goals of the current study study are to (1) provide (shared) genetic heritability estimates among variables of the HR profile during exercise; (2) identify genetic variants and the underlying candidate causal genes associated with HR increase and HR recovery at 10, 20, 30, 40, and 50 s; and (3) obtain insights into pleiotropy and the clinical consequences of HR increase and HR recovery. The results improve our understanding of HR regulation in response to exercise from a genetics perspective
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