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SHORT-TERM SALT LOADING DOES NOT INFLUENCE HEART RATE VARIABILITY DURING SUBMAXIMAL EXERCISE AND RECOVERY

Abstract

Braxton A. Linder1, Joseph C. Watso2, Matthew C. Babcock3, Kamilla U. Pollin4, William B. Farquhar, FACSM5, Austin T. Robinson1. 1Auburn University, Auburn, AL. 2University of Texas, Dallas, TX. 3University of Colorado Denver-Anschultz Campus, Aurora, CO. 4Veteran Affairs Medical Center, Washington, DC. 5University of Delaware, Newark, DE.

Introduction: Heart rate variability (HRV) is the change in time intervals between consecutive heartbeats and represents autonomic control of hemodynamic responses. Dietary salt consumption may affect HRV by altering hemodynamic responses during dynamic exercise. Additionally, acute exercise reduces HRV as the body increases heart rate to meet physiological demands. However, it is unclear if dietary salt influences HRV during dynamic exercise. Therefore, this analysis aims to assess the effects of a short-term high salt load (HS) on HRV measures at rest, during submaximal exercise, and during recovery from exercise. Methods: Using a randomized, crossover, blinded design, 20 young adults (Females = 9, age: 24 ± 4 yrs, blood pressure: 110 ± 10/64 ± 8 mmHg) consumed HS (3900 mg sodium) or placebo (PLA; dextrose) capsules with their habitual diets for 10 days each separated by ≥ two weeks. On day 10 of the interventions, we assessed participants’ electrocardiograms for 10 minutes of rest, 50 minutes of cycling at 60% VO2max, and 5 minutes of recovery. We quantified HRV using normal RR intervals to assess the standard deviation of normal-to-normal RR intervals (SDNN) and the natural log of root mean square of successive NN interval differences (LnRMSSD). We visually inspected RR intervals and analyzed them using the Labchart 8.1.19 HRV module and included RR intervals if they fell within acceptable resting and maximal physiological parameters. We ran statistical analyses in Jamovi 2.0.0.0 using repeated measures two-way ANOVA with significance set to p < 0.05. Results: Acute exercise reduced the average RR interval (p < 0.001 for time) but there was no main effect of diet or interaction (PLA vs HS; baseline: 1092 ± 201 vs. 1095 ± 184 ms, exercise: 420 ± 53 vs 416 ± 37 ms, recovery: 904 ± 133 vs. 936 ± 159 ms). Similarly, acute exercise reduced SDNN (p < 0.001) and there was no diet or interaction effect (PLA vs HS, baseline: 88.8 ± 42.5 vs. 109.4 ± 52.7 ms, exercise: 47.3 ± 32.4 vs. 61.4 ± 35.4 ms, recovery: 104.9 ± 32.0 vs. 110.3 ± 29.2 ms). These findings were consistent with LnRMSSD as there was a significant time effect (p < 0.001) but no diet or interaction effect (PLA vs HS, baseline: 86.0 ± 8.7 vs. 89.6 ± 10.8, exercise: 72.8 ± 20.2 vs. 78.0± 23.8, recovery: 83.7 ± 12.9 vs. 87.2 ± 12.3). Conclusions: As expected, HRV was significantly reduced by acute exercise. However, a short-term high salt load did not affect baseline, exercise, or recovery HRV measures in healthy young adults. Funding: American College of Sports Medicine Foundation Doctoral Student Research Grant 17‐00521 (Babcock), Supported by NIH grants R01HL128388, P20 GM113125, and K01HL147998

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