Increased resting ventilation (VE) and hypoxic and hypercapnic ventilatory responses occur during pregnancy in association with elevations in female hormones and metabolic rate. To determine whether increases in progestin, estrogen, and metabolic rate produced a rise in VE and hypoxic ventilatory response (HVR) similar in magnitude to that observed at full-term pregnancy, we studied 12 postmenopausal women after 1 wk of treatment with placebo, progestin (20 mg tid medroxyprogesterone acetate), estrogen (1.25 mg bid conjugated equine estrogens), and combined progestin and estrogen. Progestin alone or with estrogen raised VE at rest and decreased end-tidal PCO2 (PETCO2) by 3.9 +/- 0.8 and 3.3 +/- 0.6 Torr, respectively (both P less than 0.05), accounting for approximately one-fourth of the rise in VE and three-fourths of the PETCO2 reduction seen at full-term pregnancy. The addition of mild exercise sufficient to raise metabolic rate by 33-36% produced the remaining three-fourths of the rise in VE but no further decline in PETCO2. Combined progestin and estrogen raised HVR and hypercapnic ventilatory response more consistently than progestin alone and could account for one-half of the increase in HVR seen at full-term pregnancy. Mild exercise alone did not raise HVR, but when exercise was combined with progestin and estrogen administration, HVR rose by amounts equal to that seen at full-term pregnancy. We concluded that female hormones together with mild elevation in metabolic rate were likely responsible for the pregnancy-associated increases in VE and HVR.

Women exhibit sleep-disordered breathing syndromes less commonly than men before but not after the age of menopause, suggesting that female hormones may exert a protective effect. We sought to determine whether combined progestin and estrogen treatment decreased sleep-disordered breathing in healthy postmenopausal women. Nine ovarihysterectomized women [50 +/- 2 (SE) yr of age] were studied after 1 wk of treatment with placebo (lactose) or combined progestin and estrogen (medroxyprogesterone acetate, 20 mg tid, and Premarin, 1.25 mg bid). Subjects showed few respiratory disturbances during placebo treatment. Despite this, combined progestin and estrogen administration reduced the number of sleep-disordered breathing episodes in every subject, decreasing the average number of episodes per subject from 15 +/- 4 to 3 +/- 1. The duration of hypopneas also decreased with hormone treatment. Thus the presence of progestin and estrogen may be involved in protecting premenopausal women against sleep-disordered breathing.

Fetal liver slices have a remarkably high rate of lipogenesis anaerobically as well as aerobically, shown by the incorporation of carbon-14 from pyruvate into lipids. In contrast, slices of adult or 1-day-old liver have a much lower lipogenetic rate anaerobically than aerobically. Fractionation of the fetal liver lipids showed that phospholipid and glyceride fatty acids are synthesized at essentially equal rates aerobically and anaerobically but cholesterol synthesis is much slower in nitrogen than in oxygen. Fetal liver slices have a respiratory quotient of about 1.5, further evidence of rapid lipogenesis. Lactate production by fetal liver is 90% greater in nitrogen than in oxygen; that of adult liver is only 30% greater. Fetal liver metabolizes anaerobically much more pyruvate carbonyl carbon to carbon dioxide than adult liver does. Direct evidence from the rate of conversion of labeled glucose to labeled pyruvate showed that the glycolytic enzymes of fetal liver respond to anaerobiosis more effectively than those of adult liver. Thus the aging of fetal tissue to adult includes a loss of a) the high rate of glycogen deposition, b) the high rate of activity of one or more glycolytic enzymes which are rate-limiting in the adult, and c) the high rate of lipogenesis which is evident anaerobically as well as aerobically.

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