Investigating the Effects of Ultraendurance Running on Athletes' Heart Rate and Blood Pressure.

Abstract

Background While the effects of exercise on the cardiovascular system are well documented, ultra-endurance sports involve distances beyond the scope of traditional marathons and have grown in popularity at a staggering pace in recent years. While short-termhigh-intensity exercise stimulates sympathetic rises in heart rate (HR) and blood pressure (BP), the depletion of fluid and electrolyte reserves characteristic of ultra-endurance sports may contribute to decreases in overall BP after the race. If decompensation of the autonomic safety net occurs, orthostatic hypotension as a result of fluid loss during an event may cause fatigue, dizziness, syncope, or collapse. Methodology Subjects were recruited by emails sent to race participants and at pre-race meetings, and no participants were excluded from the study. We observed BP and HR changes in subjects before and after ultramarathon activity in both supine and standing positions over multiple races of variant length and terrain from 50 to 240 km from 2013 to 2018. Participants entered races in Florida, with a mean age of 43.8 andan average body mass index (BMI) of 21.2. In addition to pre-race and post-race measurements, positional post-race BPs and HRs were analyzed for orthostatic trends. Results Of those who participated, 140 completed the events and post-race HRandBPmeasurements were recorded. The mean systolic blood pressure (SBP) increase from pre-race to post-race standing was 21 mmHg, while the mean diastolic blood pressure (DBP) rise was 13 mmHg. While in a supine position, there was a 15 mmHg increase in SBPfrom pre-race to post-race, along with a 7 mmHg rise in diastolic pressure. Post-race supine to standing average BP change was insignificant. In the supine position, the mean HR increased by 20 beats per minute (bpm) after the race and by 27 bpm while standing. After the race, the average increase in HR supine to standing was 15 bpm. Conclusions The SBP changed much more notably than diastolic pressures likely due to the increase in stroke volume associated with the sympathetic response during exercise. HR values also climbed as a result of exercise stress in the setting of catecholamine release, and the combined influence contributed to increased cardiac output despite water and electrolyte loss during the event. Post-race, no trends of orthostatic hypotension were noted either with HR or BP when rising from a supine position. The significance of the contribution of fluid intake during the race to compensatory mechanisms under neural control requires further study.