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Articles in PresS, published online ahead of print September 13, 2002
J Appl Physiol, 10.1152/jap.00264.2002
Submitted on March 27, 2002
Accepted on September 10, 2002
1 Sleep Research Laboratory, Division of Pulmonary, Critical Care and Sleep Medicine, Department of Internal Medicine, John D. Dingell VAMC, Wayne State University, Detroit, MI, USA
2 Division of Reproductive Endocrinology and Infertility, Department of Obstetrics & Gynecology, Wayne State University, Detroit, MI, USA
* To whom correspondence should be addressed. E-mail: jrowley{at}intmed.wayne.edu.
The hypocapnic apneic threshold (AT) is lower in females relative to males. To test the hypothesis that the gender difference in AT was due to testosterone, we determined the AT during NREM sleep in 8 healthy non-snoring pre-menopausal females before and after 10 to 12 days of transdermal testosterone. Hypocapnia was induced via nasal mechanical ventilation (MV) for 3 minutes with tidal volumes ranging from 175-215% above eupneic tidal volume and respiratory frequency matched to eupneic frequency. Cessation of MV resulted in hypocapnic central apnea or hypopnea depending on the magnitude of hypocapnia. Nadir minute ventilation as a percentage of control (%VE) was plotted against the change in end-tidal CO2 (PETCO2); %VE was given a value of zero during central apnea. The AT was defined as the PETCO2 at which the apnea closest to the last hypopnea occurred; hypocapnic ventilatory response (HPVR) was defined as the slope of the linear regression VE v. PETCO2. Both the AT (39.5±2.9 mmHg v. 42.1±3.0 mmHg, p=0.002) and HPVR (0.20±0.05 %VE/mmHg v. 0.33±0.11 %VE/mmHg, p=0.016) increased with testosterone administration. We conclude that testosterone administration increases AT in pre-menopausal females suggesting that the increased breathing instability during sleep in men is related to the presence of testosterone.
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