Article Title



C. Poehling, J. Anderson, & T. Llewellyn
Nebraska Wesleyan University, Lincoln, NE

Heart rate variability (HRV) is defined by the asymmetric beat-to-beat intervals that exist in heart rate. The contraction phase, or R waves, on an electrocardiogram (EKG) can vary as much as up to ±0.75 seconds during rest, mostly due to the influence of the parasympathetic nervous system (PNS). Previously, we have found a trend suggesting that sedentary college students have a lower HRV compared to active students (p = 0.07). Much is understood about HRV when under the PNS (at rest), but less is known about HRV while under the sympathetic nervous system (SNS) during exercise. The purpose of this study was to examine HRV at rest, and during submaximal, and maximal exercise in collegiate distance runners. We hypothesized that there would be less variability in HR during exercise. Five collegiate runners (age 18-21) were recruited to participate in this study. The subjects were equipped with a standard Lead II EKG (Biopac) to record HRV at rest. Then, the subjects performed an incremental VO2max test while running on a treadmill. EKG was recorded throughout the exercise test, and HRV was later calculated during the submaximal and maximal exercise. To assess HRV, the standard deviation of R-R intervals (SDNN) was calculated at rest, and during submaximal and maximal exercise. A one-way ANOVA was used to determine HRV differences between the three states. The average R-R interval was 0.923 ± 0.121 s (66 bpm), 0.415 ± 0.02 s (144 bpm), and 0.322 ± 0.01 s (186 bpm) for rest, submaximal and maximal exercise, respectively. There were significant differences in SDNN from rest to submaximal (0.07 ± 0.03 to 0.01 ± 0.002 s, p < 0.05), and from rest to maximal exercise (0.07 ± 0.03 to 0.007 ± 0.002 s, p < 0.05). When comparing HRV between the resting and exercise states, it seems that the PNS influence at rest contributes to greater HRV, where as the SNS influence during both submaximal and maximal exercise corresponds to a reduced HRV. These effects are likely related to the enhanced automaticity affects of norepinephrine acting on its B1 receptor in the heart.

NACSM Professional Sponsor: Dr. Tamra Llewellyn

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