Key result
Exposure to 3454 m altitude for 2 weeks increased resting heart rate from 64 to 74 bpm (P=0.007), an effect abolished by parasympathetic inhibition with glycopyrrolate.
Why the study?
Does high altitude exposure increase resting heart rate via parasympathetic withdrawal or sympathetic activation in healthy lowlanders?
Population
7 healthy lowlanders
Comparison
15-18 days of exposure to 3454 m high altitude… vs Measurements taken at sea level with the same…
Design
Other
Follow-up
15-18 days
Authors
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Parasympathetic withdrawal accounts for tachycardia in chronic hypoxia; leaves open applicability beyond small lowlander cohorts.
Does high altitude exposure increase resting heart rate via parasympathetic withdrawal or sympathetic activation in healthy lowlanders?
Absolute Event Rate: 74% vs 64%
p-value: p=0.007
Reduced cardiac parasympathetic activity, rather than sympathetic activation, is the primary mechanism underlying elevated resting heart rate after 2 weeks of exposure to chronic hypoxia.
Siebenmann et al. (2016) studied Healthy lowlanders (n=7). High altitude exposure (3454 m) and pharmacological autonomic blockade vs. Sea level was evaluated on Resting heart rate (p=0.007). Exposure to 3454 m altitude for 2 weeks increased resting heart rate from 64 to 74 bpm (P=0.007), an effect abolished by parasympathetic inhibition with glycopyrrolate.
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