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Articles in PresS, published online ahead of print May 17, 2002
J Appl Physiol, 10.1152/jap.01103.2001
Submitted on November 2, 2001
Accepted on May 13, 2002
1 Department of Anesthesiology and General Clinical Research Center, Mayo Clinic and Foundation, Rochester, MN, USA
2 Department of Exercise and Movement Science, University of Oregon, Eugene, OR, USA
* To whom correspondence should be addressed. E-mail: halliwill.john{at}mayo.edu.
We tested the hypothesis that acute hypoxia would alter the sensitivity of arterial baroreflex control of both heart rate and sympathetic vasoconstrictor outflow. In 16 healthy, non-smoking, normotensive subjects (8 women, 8 men, 20 - 33 yrs), we assessed baroreflex control of heart rate and muscle sympathetic nerve activity using the modified Oxford technique during both normoxia and hypoxia (12 % O2). Compared to normoxia, hypoxia reduced arterial oxygen saturation levels from 96.8 ± 0.3 to 80.7 ± 1.4 % (P < 0.001), increased heart rate from 59.8 ± 2.4 to 79.4 ± 2.9 beats/min (P < 0.001), increased mean arterial pressure from 96.7 ± 2.5 to 105.0 ± 3.3 mmHg (P = 0.002), and increased sympathetic activity 126 ± 58 % (P < 0.05). The sensitivity for baroreflex control of both heart rate and sympathetic activity was not altered by hypoxia (heart rate: - 1.02 ± 0.09 vs - 1.02 ± 0.11 beats/min/mmHg; nerve activity: - 5.6 ± 0.9 vs - 6.2 ± 0.9 integrated activity/beat/mmHg; both P > 0.05). Acute exposure to hypoxia reset baroreflex control of both heart rate and sympathetic activity to higher pressures without changes in baroreflex sensitivity.
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