Krishnan R. Rajagopal

Obstructive Sleep Apnea in Hypothyroidism

To determine the incidence and frequency of sleep apnea in persons with hypothyroidism, 11 consecutive patients with newly diagnosed disease were studied before and during thyroid hormone replacement therapy. Nine patients had episodes of apnea, with the number of episodes per hour of sleep ranging from 17 to 176 (mean, 71.8). Six of the nine patients were obese and had 99.5 episodes per hour compared with 16.3 episodes per hour in the 3 nonobese patients (p less than 0.02). After 3 to 12 months of thyroxine replacement therapy, mean apnea frequency decreased from 71.8 +/- 18.0 (SE) to 12.7 +/- 6.1 episodes per hour, without reduction in body weight. There were fewer changes in sleep stage per hour during treatment (22.1 +/- 4.9) than pretreatment (57.6 +/- 14.5). Carbon dioxide response tests done under non-loaded and flow-resistive loaded conditions before and during thyroxine replacement therapy showed increases in the loaded respiratory effort and ventilation during thyroxine treatment. Sleep apnea episodes are common in persons with untreated hypothyroidism, even with normal lung function. Thyroxine replacement therapy decreases apnea frequency, even without change in body weight.

Exercise responses prior to pregnancy and in the postpartum state.

Increased women in the work force and requirements for maximal employee productivity have necessitated examination of the optimal time for parturients to resume normal activities. This prospective study was designed to determine whether prepregnancy measures of aerobic capacity are regained by 4-8 wk postpartum. Weight, percent body fat, recall energy expenditure, and exercise responses via a stage 1, graded cycle ergometer exercise test were determined in 11 subjects (mean age = 27.56 +/- 2.2) in a postabsorptive state prior to pregnancy and 4-8 wk postpartum. Subject characteristics were compared by the Students t-test and differences across workloads and time by analysis of variance with repeated measures. Prepregnant weight (mean = 58.80 +/- 7.26 kg) was significantly less (P less than 0.05) than postpartum weight (mean = 62.81 +/- 9.12 kg), and prepregnant energy expenditure (1352 +/- 453 kJ) per day was significantly higher (P less than 0.05) than in the postpartum period (274 +/- 333 kJ). Maximal oxygen uptake was significantly higher (35.2 +/- 0.7 vs 30.5 +/- 2.0 ml.kg-1min-1) in the prepregnant as compared with the postpartum period. Further, heart rate at 125 and 150 W was significantly lower prepregnancy as compared with postpregnancy. Results support a detraining effect in the early postpartum period. Whether this detraining is an inevitable factor associated with pregnancy or whether exercising throughout pregnancy can ameliorate the decline in aerobic capacity postpartum is uncertain.

An analysis of respiratory drive components during flow-resistive respiratory loading

Inspiratory flow-resistive loading normally causes an additional respiratory drive that limits the resistance-induced decrease in minute ventilation (load compensation). Occlusion pressures (P100) were measured during CO2 rebreathing with and without added inspiratory loads in normal persons and persons with obstructive sleep apnea (OSA). At each point obtained during loaded breathing, the additional drive due to resistive loading was determined by subtracting CO2-dependent drive (estimated from the nonloaded run) from total drive. In normal subjects, the additional drive correlated with each of four different estimates of load magnitude. In OSA subjects, there was no significant increase in drive due to loading and ventilation decreased markedly during loading. The relationships among ventilation rate, load, and drive, with and without load compensation, were analyzed using a 4-quadrant feedback control diagram. The diagram enables the prediction of ventilation rate for any end-tidal CO2 in the loaded and nonloaded cases, and the flow decrement that will occur as a result of added inspiratory resistance.