CLINICAL SICKNESS AT ALTITUDE AFFECTS THE HEART RATE RESPONSE
DiPasquale, D. M., Strangman, G. E., & Muza, S. R. (2013). Altitude vs. hypoxia: comparing the effects of exercise in hypobaric and normobaric hypoxia on resting heart rate. Medicine & Science in Sports & Exercise, 45(5), Supplement abstract number 2706.
This study compared the effects of exercise in hypobaric hypoxia (at altitude) and normobaric hypoxia (reduced oxygen pressure at low altitude) on resting heart rate. Ss completed two of six possible conditions: exposure to low altitude (300 m) and hypobaric hypoxia (4,400 m), or normobaric hypoxia (ambient PO2 = 91 mmHg), and cycling at 50% heart-rate reserve for either 10 or 60 minutes. Exposures lasted eight hours and exercise was completed by 1.25 hours into the exposure. Resting heart rate, oxygen saturation, and end-tidal carbon dioxide were measured before exposure, 1.5, 4.0, and 6.5 hours into exposure, and one hour post-exposure for 5-10 minutes with means calculated from the final two minutes. Ss also completed the Environmental Symptoms Questionnaire at those times. An AMS-C score of 0.7 or greater indicated clinical sickness.
For resting heart rate, i) in normobaric hypoxia it was significantly higher than when at low altitude; ii) in hypobaric hypoxia it was significantly higher than when at low altitude, iii) it was higher at 60 minutes of exercise compared to when at 10 minutes of exercise, and iv) it increased in the presence of AMS-C. Similar results were found when eliminating the time point closest to the completion of exercise, as well as when considering only the last exposure time point, suggesting that the observed effects on resting heart rate were not due to recovery from exercise.
Implication. Normobaric hypoxia alone had about the same effect on resting heart rate as 50 minutes of exercise in normobaric conditions. The effect of hypobaric hypoxia on resting heart rate was double the effect of normobaric hypoxia and exercise. The presence of AMS-C had the largest single effect, seeming to be independent of the other effects. These results suggest that elevated resting heart rate in AMS-C is not solely due to compensation for exposure to hypoxia or previous exercise. It is hypothesized that the mechanism responsible for AMS may have an associated effect of increasing resting heart rate.
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