Relationship of polycystic ovary induction to prolactin secretion: prevention of cyst formation by bromocriptine in the rat.

PRL levels were measured over 30 days of cyst induction in the rat. Polycystic ovaries (PCO) were induced by dietary incorporation of thiouracil (Thio) for 30 days and injection of 10 IU hCG sc for the last 20 days of the experimental period. Animals were killed at specific intervals 24 hours after the last injection. Ovaries and thyroids were removed and weighed. Sera were analyzed for PRL by RIA. PRL levels increased in animals receiving Thio plus hCG by day 30 compared to animals receiving Thio alone. The increase in PRL in the Thio, hCG-stimulated group coincides with formation of follicular cysts. Administration of bromocriptine (1 mg/day) concurrent with hCG during the last 20 days of Thio-feeding significantly suppressed ovarian weight gain and PCO formation. Serum PRL levels in bromocriptine-treated rats were significantly reduced compared to the PCO group yet were also significantly greater than all control groups at day 30. These findings suggest that PRL is important to the etiology of ovarian cysts in the rat.

Effects of ozone inhalation during exercise in selected patients with heart disease.

Although epidemiologic evidence suggests that patients with heart and lung disease are more vulnerable to the acute toxic effects of photochemical air pollution, no laboratory studies have been reported in patients with coronary heart disease. In the present investigation, six male volunteers, ages 46 to 64 years, with clinically documented coronary heart disease and a well-defined symptomatic angina pectoris threshold, served as subjects. Each patient was exposed on three 40-minute occasions to either filtered air or ozone at concentrations of 0.20 or 0.30 parts per million (ppm), while walking on a treadmill at workloads simulating their regularly prescribed exercise training regimen. Results of standard pulmonary function tests and periodic observations of exercise ventilation, respiratory metabolism, electrocardiographic changes, hemodynamic response, and clinical signs and symptoms were recorded. Analysis of variance revealed that none of the patients' physiologic responses to ozone exposure were statistically significant. Furthermore, neither onset of angina pain or ischemic changes were related to ozone exposure in a dose-dependent fashion. Hence, the patients not only failed to exhibit any unexpected cardiovascular strain while exposed to ozone during exercise, but also evidenced no significant pulmonary function impairment or exercise ventilatory pattern alteration, as has been observed in clinically normal subjects exercising at similar ozone concentration levels. This apparent incongruity may be due to the fact that acute ozone toxicity is more closely related to the total amount of ozone inhaled, which is a function of pulmonary ventilation volume and exposure time, as well as ozone concentration. In the patients with angina, symptom-limited exercise tolerance resulted in a lower total amount of ozone inhaled than that observed to effect ozone toxicity in clinically normal subjects who exercised at greater intensities and for longer durations. Patients with angina appear to be no more susceptible to ozone toxicity than are clinically normal subjects at the effective doses imposed. However, had the patients exercised longer, they might well have evidenced pulmonary function impairment and/or cardiovascular strain. Hence, caution is advised in generalizing these observations to other conditions and patient groups.

Enhanced response to ozone exposure during the follicular phase of the menstrual cycle.

Exposure to ozone (O3), a toxic component of photochemical smog, results in significant airway inflammation, respiratory discomfort, and pulmonary function impairment. These effects can be reduced via pretreatment with anti-inflammatory agents. Progesterone, a gonadal steroid, is known to reduce general inflammation in the uterine endometrium. However, it is not known whether fluctuations in blood levels of progesterone, which are experienced during the normal female menstrual cycle, could alter O3 inflammatory-induced pulmonary responses. In this study, we tested the hypothesis that young, adult females are more responsive to O3 inhalation with respect to pulmonary function impairment during their follicular (F) menstrual phase when progesterone levels are lowest than during their mid-luteal (ML) phase when progesterone levels are highest. Nine subjects with normal ovarian function were exposed in random order for 1 hr each to filtered air and to 0.30 ppm O3 in their F and ML menstrual phases. Ozone responsiveness was measured by percent change in pulmonary function from pre- to postexposure. Significant gas concentration effects (filtered air versus O3) were observed for forced vital capacity (FVC), forced expiratory volume in 1 sec (FEV1), and forced expiratory flow between 25 and 75% of FVC (FEF25-75; p < .05). More importantly, the pulmonary function flow rates, FEV1 and FEF25-75, showed a significant menstrual phase and gas concentration interaction effect, with larger decrements observed in the F menstrual phase when progesterone concentrations were significantly lower. We conclude that young, adult females appear to be more responsive to acute O3 exposure during the F phase than during the ML phase of their menstrual cycles.(ABSTRACT TRUNCATED AT 250 WORDS)

Effects of ozone exposure on four consecutive days on work performance and VO2max.

The effects of 4 consecutive days of 1-h exposure to 0.35 ppm ozone (O3) on maximal O2 uptake (VO2max), performance time, pulmonary function, and subjective symptom responses were studied in eight aerobically trained males. Each subject was first exposed in random order to filtered air (FA) and 0.35 ppm O3 while exercising on a bicycle ergometer for 50 min at a work load eliciting minute ventilation of approximately 60 1/min. A rapidly incremented VO2max test to volitional fatigue was completed within 10 min following each of these exposures, as well as on day 4 of the consecutive daily exposures to O3. Initial exposure to O3 induced the occurrence of subjective symptoms, as well as significant pulmonary function impairment and decrements in maximal exercise performance time (from 253 to 211 s) and VO2max (from 3.85 to 3.62 l/min). Following the fourth consecutive day of exposure to O3, pulmonary function impairment was not significantly different from initial exposure to O3, although subjective symptom severity was significantly reduced. Exercise performance time (239 s) and VO2max (3.79 l/min) on the fourth consecutive daily exposure to O3 were not significantly different from FA values. These data indicate no significant adaptation to initial O3 exposure-induced pulmonary function impairment following four consecutive daily exposures to O3, although reduced subjective symptom severity and enhanced exercise performance time on day 4 suggest an habituation effect. Our results also suggest that O3 adaptation may be a more complex phenomena than identified previously.

Ozone inhalation effects in females varying widely in lung size: comparison with males.

It has been suggested that lung size accounts for observed gender differences in responsiveness to the same total inhaled dose of O3. To test the hypothesis that lung size is a determinant of magnitude of response within a gender, two groups of 14 healthy young adult females differing significantly in forced vital capacity [FVC; i.e., small-lung group mean = 3.74 liters (range 3.2-4.0) and large-lung group mean = 5.11 liters (range 4.5-6.2] were exposed for 1 h to filtered air (FA) and to 0.18 and 0.30 ppm O3. On each occasion, subjects exercised continuously on a cycle ergometer at a work rate that elicited a mean minute ventilation of approximately 47 l/min. For the small-lung group [mean total lung capacity (TLC) = 4.52 liters] exercise O2 uptake was 67% of maximal O2 uptake (VO2max), and that for the large-lung group (TLC 6.37 liters) was 61% of VO2max. Statistical analysis revealed significant decrements for both groups in FVC, forced expiratory volume in 1 s (FEV1.0), and forced expiratory flow rate in the middle half of FVC on exposure to 0.18 and 0.30 ppm O3. Exercise respiratory frequency increased, and tidal volume decreased significantly in both groups in response to 0.18 and 0.30 ppm O3 exposure. On exposure to 0.30 ppm O3, the number of individual subjective symptoms reported and their severity were significantly greater for both groups than those reported for the FA and 0.18 ppm O3 exposures. Both groups evidenced similar percent changes in pulmonary function and exercise ventilation response, and in subjective symptom response.(ABSTRACT TRUNCATED AT 250 WORDS)

Ozone inhalation effects consequent to continuous exercise in females: comparison to males.

Exposure to ozone (O3) at ambient photochemical smog alert levels has been shown to cause alteration in pulmonary function and exercise response in humans, but there is a paucity of data on females. The initial purpose of the present investigation was to study the effects of O3 inhalation on pulmonary function and selected exercise respiratory metabolism and breathing pattern responses in young adult females. Six female subjects exercised continuously on a bicycle ergometer for 1 h on 10 occasions at one of three intensities, while exposed to 0.0, 0.20, 0.30, or 0.40 ppm O3. Forced expiratory volume and flow rates and residual volume (RV) were measured before and immediately following each protocol. During exercise, expired minute ventilation (VE), respiratory frequency (fR), tidal volume, O2 uptake (VO2), and heart rate (HR) were measured every 10 min. O3 dose-dependent decrements were observed for forced vital capacity (FVC), forced expiratory volume in 1 s (FEV1.0), and forced expiratory flow rate during the middle half of FVC, coupled with an increase in RV and altered exercise ventilatory pattern. There was also an increased VE but no significant O3 effect on VO2 or HR. Comparison of the females' responses to those of a group of young adult males (previously studied) at the same total O3 effective dose (i.e., expressed as the simple product of O3 concentration, VE, and exposure time) revealed significantly greater effects on FVC, FEV1.0, and fR for the females. With VE reduced for females as a function of exercise intensity at the same percent of maximum VO2, these differences were considerably attenuated, although not negated.(ABSTRACT TRUNCATED AT 250 WORDS)

Effects of NO2 alone and in combination with O3 on young men and women.

Previous studies of 2 h of exposure to NO2 at high urban atmospheric levels (i.e., 0.50-1.0 ppm), utilizing light-to-moderate exercise for up to 1 h have failed to demonstrate significant pulmonary dysfunction in healthy humans. To test the hypothesis that heavy sustained exercise would elicit pulmonary dysfunction on exposure to 0.60 ppm NO2 and/or enhance the effects of exposure to 0.30 ppm O3, 40 aerobically trained young adults (20 males and 20 females) completed 1 h of continuous exercise at work rates eliciting a mean minute ventilation of 70 and 50 l/min for the males and females, respectively. Exposures to filtered air, 0.60 ppm NO2, 0.30 ppm O3, and 0.60 ppm NO2 plus 0.30 ppm O3 were randomly delivered via an obligatory mouthpiece inhalation system. Treatment effects were assessed by standard pulmonary function tests and exercise ventilatory and subjective symptoms response. Two-way analysis of variance with repeated measures and post hoc analyses revealed a statistically significant (P less than 0.05) effect of O3 on forced expiratory parameters, specific airway resistance, exercise ventilatory response, and reported subjective symptoms of respiratory discomfort. In contrast, no significant effect of NO2 was observed nor was there any significant interaction of NO2 and O3 in combination. There were no significant differences between male and female responses to gas mixture treatments. It was concluded that inhalation of 0.60 ppm NO2 for 1 h while engaged in heavy sustained exercise does not elicit effects evidenced by measurement techniques used in this study nor evoke additive effects beyond those induced by 0.30 ppm O3 in healthy young adults.

O.35 ppm O3 exposure induces hyperresponsiveness on 24-h reexposure to 0.20 ppm O3.

Pulmonary function hyperresponsiveness, defined as enhanced response on reexposure to O3, compared with initial O3 exposure, has been previously noted in consecutive day exposures to high ambient O3 concentrations (i.e., 0.32-0.42 ppm). Effects of consecutive-day exposure to lower O3 concentrations (0.20-0.25 ppm) have yielded equivocal results. To examine the occurrence of hyperresponsiveness at two levels of O3 exposure, 15 aerobically trained males completed seven 1-h exposures of continuous exercise at work rates eliciting a mean minute ventilation of 60 1/min. Three sets of consecutive-day exposures, involving day 1/day 2 exposures to 0.20/0.20 ppm O3, 0.35/0.20 ppm O3, and 0.35/0.35 ppm O3, were randomly delivered via an obligatory mouthpiece inhalation system. A filtered-air exposure was randomly placed 24 h before one of the three sets. Treatment effects were assessed by standard pulmonary function tests, exercise ventilatory pattern (i.e., respiratory frequency, f; and tidal volume, VT) changes and subjective symptom (SS) response. Initial O3 exposures to 0.35 and 0.20 ppm had a statistically significant effect, compared with filtered air, on all measurements. On reexposure to 0.35 ppm O3 24 h after an initial 0.35 ppm O3 exposure, significant hyperresponsiveness was demonstrated for forced vital capacity (FVC), forced expiratory volume in 1 s (FEV1), f, VT, and total SS score. Exposure to 0.20 ppm O3 24 h after 0.35 ppm O3 exposure, however, resulted in significantly enhanced responses (compared with initial 0.20 ppm O3 exposure) only for FEV1, f, and VT.(ABSTRACT TRUNCATED AT 250 WORDS)

Effects of varied air velocity on sweating and evaporative rates during exercise.

This study was designed to determine the extent to which changes in the evaporative power of the environment (Emax) affect sweating and evaporative rates. Six male subjects undertook four 60-min bouts of cycle ergometer exercise at 56% maximal O2 uptake (VO2max).Emax was varied by differences in ambient temperature and airflow; two exercise bouts took place at 24 degrees C and two at 35 degrees C, with air velocity at < 0.2 and 3.0 m/s in both. Total sweat production was estimated from body weight loss, whereas whole body evaporative rate was measured continuously from a Potter beam balance. Body core temperature was measured continuously from a thermocouple in the esophagus (T(es)), with mean skin temperature (Tsk) computed each minute from thermocouples at eight sites. Total body sweat loss was significantly greater (P < 0.05) in the 0.2- than in the 3.0-m/s condition at both 24 and 35 degrees C. Tsk was higher (P < 0.05) in the still-air conditions at both temperatures, but final T(es) was significantly higher (P < 0.05) in still air only in the 35 degrees C environment. Thus the reduced Emax in still air caused a greater heat storage, thereby stimulating a greater total sweat loss. However, in part because of reduced skin wettedness, the slope of the sweat rate-to-T(es) relation at 35 degrees C in the 3.0-m/s condition was 118% that at 0.2 m/s (P < 0.005).(ABSTRACT TRUNCATED AT 250 WORDS)

Effects of ozone exposure at ambient air pollution episode levels on exercise performance.

Ozone is a principal component of photochemical air pollution endogenous to numerous metropolitan areas, which may induce irritant effects on the respiratory tract which impair pulmonary function, result in subjective symptoms of respiratory discomfort, including cough and shortness of breath, and can limit exercise performance. The effects of moderate ambient photochemical air pollution observed in a mobile laboratory have also been shown to be similar to those induced in laboratory chamber exposures to the same level of ozone alone. The metabolic demand of exercise increases minute ventilation (VE) and thus, the rate of ozone inhalation over that at rest. Potentially, exercise can also enhance the effects of ozone by: (a) reducing nasal passage absorption; (b) increasing the uniformity of ventilation throughout the lungs; and (c) replacing reacted ozone at a faster rate. However, results from 2-hour intermittent exercise and 1-hour continuous exercise exposures at the same total ventilation and ozone concentration have been shown to yield similar pulmonary function effects. It has been shown via significant variation in exercise intensity, and thus VE, that the simple product of ozone concentration, VE and exposure time (termed the ozone effective dose) predicts pulmonary function and exercise ventilatory pattern (induced rapid, shallow breathing) effects more precisely than ozone concentration alone. Better prediction of pulmonary function effects has been achieved via multiple regression analysis in which ozone concentration is given a greater weighting than VE and exposure time. Light intermittent exercise was first studied in 2-hour laboratory exposures to ozone at concentrations rarely seen in the ambient environment. In recent studies, heavy continuous exercise has been used in 1-hour exposures to ozone at levels routinely observed in photochemical episodes (less than or equal to 0.35 ppm). Statistically significant impairment of exercise performance has been observed at 0.18 ppm, a level reached for 1 hour, or more, on about 180 days per year in the Los Angeles basin. Responses of subpopulation groups, such as children, young adult females, older adults, and those with pre-existing pulmonary disease are not notably different from those of young adult males provided that the ozone effective dose is proportional to body size. Conversely, highly trained endurance athletes demonstrate significant responses at rather low ozone concentrations due to their ability to sustain very high VE over prolonged periods.(ABSTRACT TRUNCATED AT 400 WORDS)

Reduced exercise time in competitive simulations consequent to low level ozone exposure.

Ten highly trained endurance athletes were studied to determine the effects of exposure to low ozone (O3) concentrations on simulated competitive endurance performance and associated physiological and subjective symptom responses. Each subject was randomly exposed to filtered air (FA), and to 0.12, 0.18, and 0.24 ppm O3 while performing a 1 h competitive simulation protocol on a bicycle ergometer. Endurance performance was evaluated by the number of subjects unable to complete rides (last 30 min at an intense work load of approximately 86% VO2max). All subjects completed the FA exposure, whereas one, five, and seven subjects did not complete the 0.12, 0.18, and 0.24 ppm O3 exposures, respectively. Statistical analysis indicated a significant (P less than 0.05) increase in the inability of subjects to complete the competitive simulations with increasing O3 concentration, including a significant difference between the 0.24 ppm O3 and FA exposure. Significant decreases (P less than 0.05) were also observed following the 0.18 and 0.24 ppm O3 exposures, respectively, in forced vital capacity (-7.8 and -9.9%), and forced expiratory volume in 1 s (-5.8 and -10.5%). No significant O3 effect was observed for exercise respiratory metabolism or ventilatory pattern responses. However, the number of reported subjective symptoms increased significantly following the 0.18 and 0.24 ppm O3 protocols. These data demonstrate significant decrements in simulated competitive endurance performance and in pulmonary function, with accompanying enhanced subjective symptoms, following exposure to low O3 levels commonly observed in numerous metropolitan environments during the summer months.

Effect of bone density on body composition estimates in young adult black and white women.

Bone mineral content (BMC) and density (BMD) by dual x-ray absorptiometry, total body water (TBW) by the deuterium oxide (D2O) dilution technique, and body density (Bd) by hydrostatic weighing were measured in 26 black (B) and 26 white (W) young adult women. Both groups were similar in age, height, weight, and total skinfolds; however, black subjects had significantly higher BMC and BMD. Formulas to estimate percent body fat (%BF) from Bd included Siri's two-component equation for the reference man, which assumes a fat free body density (FFBd) of 1.100 g.ml-1, and an adjusted two-component formula that assumes a lower FFBd of 1.095 g.ml-1. Percent body fat was also predicted from TBW and by several multicomponent models that corrected for individual subject variation in measured BMC and TBW. The two groups did not differ significantly in %BF predictions by any of the methods. However, the difference in %BF between the groups was halved with the four-component model (B = 21.9%; W = 23.6%) as compared with that calculated from the Siri two-component densitometric model (B = 21.2%; W = 24.2%). Within each racial group, %BF was not significantly different when predicted by two-component or multicomponent models. However, %BF of individuals with the highest and lowest BMD was substantially under- and overpredicted, respectively, by Siri's equation.(ABSTRACT TRUNCATED AT 250 WORDS)

Wet bulb globe temperature index and performance in competitive distance runners.

In 1974 two sets of heat stress guidelines, each based on the wet bulb globe temperature (WBGT) index, were designed for men's National Collegiate Athletic Association (NCAA) Championship Division I distance running competitions. One set of guidelines was established to minimize the chance of heat injury during distance running events. A second set was designed to predict heat stress related performance decrements. During the time the heat injury guidelines were used (1974-1993), no heat injuries were reported. The purpose of this study was to assess the accuracy of the performance decrement guidelines and determine whether the WBGT indices were linearly related to men's championship distance running performance. WBGT index data were collected during the 1500-, 3000-steeplechase (SC), 5000-, and 10,000-m events at men's NCAA Division I Track and Field Championships held from 1974 to 1981 (excluding 1975). These data were compared to the average running performance of the top six finishers in each event. Analysis of the accuracy of the NCAA performance decrement guidelines revealed four unexpected performances out of 28 predictions. Pearson product-moment correlation and linear regression analyses between the WBGT indices and performance revealed statistically significant linear relationships for the 3000-SC and 10,000-m events (P < 0.05). A significant linear relationship was also found when the 1500-, 3000-SC, 5000-, and 10,000-m results were pooled (P < 0.05). In conclusion, the NCAA guidelines were effective in preventing heat injury and fairly successful in predicting performance. However, a linear relationship between WBGT indices and distance running performance did not exist in all running events.

Effects of physical activity, body weight and composition, and muscular strength on bone density in young women.

OBJECTIVE: The purpose of this study was to examine the relationship between body weight and composition, muscular strength, physical activity, and bone mineral density (BMD) in eumenorrheic college-aged women. METHODS: BMD and bone mineral content (BMC) of the total body, and BMD of the lumbar spine (L2-L4) and femoral neck (via dual energy x-ray absorptiometry), as well as body composition and muscular strength, were measured in 60 college-aged women. The women were divided into three groups: 1) low body weight athletes involved in weight-bearing, collegiate sports (N = 20), 2) matched low body weight and sedentary (N = 20), and 3) average body weight and sedentary (N = 20). All groups were matched for height, age, and age at menarche. RESULTS: The athletes had significantly greater (P < 0.05) (mean +/- SD) total body BMD (1.164 +/- 0.06 g x cm[-2]), L2-L4 BMD (1.240 +/- 0.13 g x cm[-2]), femoral neck BMD (1.144 +/- 0.13 g x cm[-2]) and total body BMC (2.44 +/- 0.30 kg) than the low body weight, sedentary (LWS) group, but were only greater than the average body weight sedentary group (AWS) for femoral neck BMD. Significant correlations were found between lean body mass (LBM) and all BMD variables (P < 0.001). A significant correlation (P < 0.01) was found between fat mass and all BMD variables in the sedentary subjects alone (N = 40), but with inclusion of the athletes (N = 60), none of the correlations between fat mass and BMD were significant. Arm and leg strength isometric torque values corrected for muscle + bone cross-sectional area (M + B CSA) were not significantly different between the athletes and LWS group, but the athletes were greater (P < 0.05) than the AWS group for both arm and leg strength/M + B CSA. No significant, site-specific correlations were found between strength/M + B and BMD. CONCLUSIONS: In summary, the athletes had significantly greater BMD, BMC, and LBM than the LWS group and, except for a greater femoral neck BMD, similar BMD, BMC, and LBM as the AWS group. These results suggest that LBM and weight-bearing exercise both enhance BMD in eumenorrheic young adult women.

Effects of run-training and swim-training at similar absolute intensities on treadmill VO2max.

Thirty-seven sedentary males, aged 28-35 yr, were either run-trained, swim-trained, or served as controls in an 11 1/2-wk training study. Runners and swimmers exercised once a d, 3 d.wk, at a heart rate (HR) intensity equivalent to 75% of their treadmill VO2max. Treadmill maximal oxygen consumption (VO2max), submaximal cardiorespiratory response, and body composition parameters were measured before and following the training period. Runners, swimmers, and controls experienced a significant increase in treadmill VO2max over the 11 1/2-wk study period. The 28 and 25% increases observed for the runners and swimmers, respectively, were significantly greater than the 5% increase observed for the controls (P less than 0.0001). Runners and swimmers did not differ significantly from each other with respect to this increase in VO2max; nor did they demonstrate significant changes in respiratory exchange ratio (RER) at VO2max between tests. The run-trained and swim-trained groups both experienced a decrease in HR at a standard submaximal walking workload but did not differ significantly from each other. Controls showed no significant change in submaximal exercise response. A significant difference was observed among groups (P less than 0.01) for change in percent body fat. Changes in lean and fat weight over the training period were significant for both the runners (P less than 0.002) and swimmers (P less than 0.03) but not for the controls.(ABSTRACT TRUNCATED AT 250 WORDS)

Peak torque per unit cross-sectional area differs between strength-trained and untrained young adults.

It is unclear whether gender differences in the relative strength of the upper and lower body are due to differences in muscle mass distribution or dissimilarity of use. There is also controversy as to whether prolonged resistance training increases strength per unit cross-sectional area (CSA). To help resolve these questions, maximum isometric torque per unit muscle and bone (M+B) CSA was measured in the upper arm and thigh of 26 trained (13 males; 13 females) and 26 untrained (13 males; 13 females) young adults. Muscle and bone CSA values were calculated from limb circumferences and skinfolds. Maximal isometric torque values were recorded by a LIDO isokinetic dynamometer. There was no significant difference (P > 0.05) in mean upper arm or thigh torque per unit M+B CSA between the trained males and trained females, or between the untrained males and untrained females. However, mean torque per unit M+B CSA was significantly higher for the trained subjects of both genders compared with the untrained subjects of both genders for the upper arm (28.9%; P < 0.0001) and thigh (18.8%; P < 0.0001). These results suggest that muscle quality (peak torque/CSA) is equal between genders, and that the increase in muscle strength per unit area that occurs with resistance training is not gender-dependent.

Body composition analysis by bioelectrical impedance: effect of skin temperature.

Bioelectrical impedance analysis (BIA) was used to estimate body water and composition under both cool (14.4 degrees C, dry bulb) and warm (35.0 degrees C) ambient conditions in eight healthy adult men. The prediction equation provided with the commercially available instrument (RJL Systems) was used with the BIA measurements to estimate body composition. Skin temperature increased from 24.1 +/- 1.81 degrees C in the cool condition to 33.4 +/- 1.36 degrees C in the warm condition. (Mean increase was 9.3 +/- 1.75 degrees C, t = 15.05, P less than 0.01). The corresponding BIA resistances were 461 +/- 48 omega and 426 +/- 47 omega, respectively. (Mean reduction was 35.0 +/- 9.8 omega, t = 10.13, P less than 0.01). This resulted in a significant increase in predicted total body water (cool 47.4 +/- 5.5 l vs. warm 49.9 +/- 5.6 l, t = 3.88, P less than 0.01). Consequently, predicted fat mass was significantly lower in the warm than in the cool condition (8.8 +/- 3.2 kg vs. 11.0 +/- 3.7 kg; mean difference 2.23 +/- 0.69 kg, t = 9.22, P less than 0.01). These findings indicate that varying skin temperature by altering ambient temperature significantly changes resistance measurements and the estimation of total body water and percent fat by BIA. The observed changes in resistance are consistent with an apparent expansion of conductor volume in the warm environment and a reduction in the cooler condition. In this regard, the temperature-induced change in resistance could be due to alterations in cutaneous blood flow and/or compartmental distribution of body water. Thus, BIA measurements should be taken only under well-standardized ambient conditions.

Bone density and cyclic ovarian function in trained runners and active controls.

This study was conducted to determine whether rigorous exercise training adversely affects ovarian hormone levels and bone health in cyclically menstruating trained runners. Ovarian hormones, bone mineral density (BMD), body composition, 3-d diet records, 3-d estimated energy expenditure, and menstrual histories were evaluated in 10 trained collegiate runners and 10 moderately active controls. The trained runners had lower total body calcium per kg of soft lean tissue measured by DEXA (P = 0.045). Half of the trained runners had experienced stress fractures compared with only one of the moderately active controls. The trained runners' lumbar (L2-L4) BMD (1.178 g.cm-2) was not significantly different from that of the active controls (1.283 g.cm-2) (P = 0.074) but, for all subjects combined, there wasa significant inverse relation between L2-L4 BMD and distance run per week (P = 0.036). Further, adding age, body weight, percent body fat, daily energy intake, and daily calcium intake to a stepwise multiple regression analysis did not significantly improve predictive precision. The trained runners consumed nearly twice the amount of calcium (1089 mg.d-1 vs 641 mg.d-1, respectively; P = 0.036), while intake of other nutrients did not differ significantly between groups. Urinary estrone conjugates (E1C) were lower in the trained runners during the early follicular phase (P = 0.028), while pregnanediol-3-glucuronide (PdG) was not significantly different between groups during the luteal phase (P = 0.213). Thus, it appears that lower estrogen production, especially during the early follicular phase, and not progesterone, is associated with lower whole body calcium per kg of soft lean tissue and, probably, L2-L4 BMD. Results of this study also suggest that regular menstrual cycles do not imply normal ovarian hormone function in young women who are engaged in either recreational or competitive running.

Ozone dose-response effects of varied equivalent minute ventilation rates.

While it is well known that exercise minute ventilation (V(E)) results in greater pulmonary function and subjective symptoms (SS) responses upon exposure to a given ozone (O3) dose, the magnitude of V(E) increase to produce a significant forced expiratory volume in 1 s (FEV1.0) response compared to that observed at a lower exercise V(E) for the same O3 concentration and exposure time is unclear, especially in prolonged (i.e., >2 h) exposures. Further, in prolonged exposures, the relationship of body size to FEV1.0 response to a given O3 exposure dose has not been systematically examined. In the present study, 30 young adults were exposed on four occasions for 6 h (during a 6.6-h period) to constant 03 levels of zero (filtered air, FA) or 0.12 parts per million (ppm). At the latter concentration, exercise V(E) was varied in exposures to 17, 20, and 23 l min(-1) m(-2) of BSA, respectively, for each individual to achieve an equivalent ventilation rate, EVR). In the FA exposure, EVR was 23 l min(-1) m2. Percent changes in FEV1.0 for the three 0.12 ppm O3 exposures were significantly greater than that for FA, but did not differ significantly from each other. For the 6.6-h exposures, exercise EVR at or in excess of 17 l min(-1) m(-2), SS values were significantly greater than those observed for the FA protocol. Further, SS values at 6.6 h of exposure to 0.12 ppm O3 for the exercise EVR of 23 l min(-1) m(-2) protocol were significantly greater than for the 0.12 ppm O3 exercise EVR of 17 l min(-1) m(-2) protocol. To achieve a widened EVR, two 1-h exposures to 0.30 ppm O3 with continuous exercise (CE) at a level necessitating an EVR of 17 and approximately 34 l min(-1) m(-2), respectively, were completed by each subject. All postexposure pulmonary function and SS responses were significantly greater for the higher 1-h EVR protocol. In all exposures with significant O3-induced changes in FEV1.0 and SS, it was found that the smaller subjects who exercised at the lowest absolute V(E) had significantly smaller responses than did the larger subjects. These results strongly suggest that for the O3 concentrations and exposure durations used in this study, the effect of V(E) on O3-induced FEV1.0 and SS responses is not body-size-dependent.

Effects of hypovolemia and posture on responses to the Valsalva maneuver.

INTRODUCTION: We tested the hypotheses that hypovolemia would result in attenuated elevation in blood pressure, greater baroreflex-mediated tachycardia, and reduced capacity for vasoconstriction during a Valsalva maneuver (VM). METHODS: Heart rate (HR) and mean arterial pressure (MAP) were measured beat-by-beat before strain, during a 15-s VM strain at 30 mmHg expiratory pressure, and post-strain. Eight subjects performed three VM trials in each of three postures (supine, sitting, and standing) under two experimental conditions (normovolemic and hypovolemic). Hypovolemia was acutely induced by a bolus injection of 30 mg furosemide. Each experimental condition was conducted on a different day, separated by one week. delta MAP was used in analyses of phase I, late phase II (an indicator of vasoconstriction) and phase III of VM. The ratio delta HR/delta MAP, an index of nonspecific baroreflex control of HR, was used in analysis of early phase II and phase IV of the VM. RESULTS: Compared to normovolemia, hypovolemia resulted in 12% lower plasma volume (p = 0.0001). delta MAP for both phase I and phase III of the VM differed between postures (p = 0.0132 and p = 0.0003, respectively) and was lower in the hypovolemic condition than in the normovolemic condition for phase I in the standing posture (-5 mmHg, p = 0.0385). CONCLUSIONS: HR and blood pressure responses to alterations in intrathoracic pressure are affected by fluid redistribution (posture change), but not by circulating blood volume. Therefore, our results did not support our hypothesis that hypovolemia would result in attenuated elevation in blood pressure, greater baroreflex-mediated tachycardia, and reduced capacity for vasoconstriction during a Valsalva maneuver. However, moderate hypovolemia can be specifically predicted by the phase I response to a VM performed in the standing posture.