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Biomedical subjects

W C Adams

Publications and source records attributed to W C Adams.

At least 19 recordsLinked to original sources
PubMed1995

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.

Adolescent↗
PubMed1992

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)

Adult↗
PubMed1991

Enhanced vagal baroreflex response during 24 h after acute exercise.

We evaluated carotid-cardiac baroreflex responses in eight normotensive men (25-41 yr) on two different test days, each separated by at least 1 wk. On one day, baroreflex response was tested before and at 3, 6, 12, 18, and 24 h after graded supine cycle exercise to volitional exhaustion. On another day, this 24-h protocol was repeated with no exercise (control). Beat-to-beat R-R intervals were measured during external application of graded pressures to the carotid sinuses from 40 to -65 mmHg; changes of R-R intervals were plotted against carotid pressure (systolic pressure minus neck chamber pressure). The maximum slope of the response relationship increased (P less than 0.05) from preexercise to 12 h (3.7 +/- 0.4 to 7.1 +/- 0.7 ms/mmHg) and remained significantly elevated through 24 h. The range of the R-R response was also increased from 217 +/- 24 to 274 +/- 32 ms (P less than 0.05). No significant differences were observed during the control 24-h period. An acute bout of graded exercise designed to elicit exhaustion increases the sensitivity and range of the carotid-cardiac baroreflex response for 24 h and enhances its capacity to buffer against hypotension by increasing heart rate. These results may represent an underlying mechanism that contributes to blood pressure stability after intense exercise.

Adult↗
PubMed1991

Impairment of carotid-cardiac vagal baroreflex in wheelchair-dependent quadriplegics.

The incidence of orthostatic hypotension can increase after prolonged exposure to chair rest and bedrest and is associated with post-bed rest impairment of the carotid-cardiac baroreflex response. We therefore hypothesized that the hypotension observed in humans confined to wheelchairs may be manifested by a reduced baroreflex sensitivity. We compared baroreflex responses of 16 wheelchair-dependent (WCD) quadriplegics with those of 15 able-bodied subjects (ABS) matched for age, height, and weight. Beat-to-beat R-R intervals were measured during application of graded pressures from 40 to -65 mmHg using a neck chamber for noninvasive stimulation of the carotid baroreceptors. Changes of R-R intervals were plotted against carotid distending pressures. The maximum slope of the stimulus-response relationship was greater (P less than 0.0001) in ABS (6.1 +/- 0.6 ms/mmHg) than in WCD (2.6 +/- 0.4 ms/mmHg). The range of the R-R interval response, i.e., the capacity to buffer blood pressure changes, was only 138 +/- 19 ms in WCD compared with 253 +/- 19 ms in ABS (P less than 0.001). Mean sitting systolic-to-diastolic blood pressures in WCD (92/60 mmHg) were less (P less than 0.0001) than in ABS (120/77 mmHg), although there were no significant differences between groups in supine resting blood pressures. Chronic loss of stimulation to carotid baroreceptors by routine standing posture is associated with attenuated sensitivity and reduced buffer capacity of the arterial baroreflex and hypotension during sitting in WCD patients.

Adult↗
PubMed1991

Circulating hormone concentrations in hypothyroid rats with induced polycystic ovaries.

The induction of polycystic ovaries in hypothyroid rats by human chorionic gonadotropin (hCG) has been studied for many years. A complete understanding of this phenomenon requires information regarding the circulating levels of the hormones of the hypophyseal-gonadal axis. In this study, serum prolactin (PRL), luteinizing hormone (LH), estradiol, testosterone, and progesterone were measured by radioimmunoassay at intervals during the 40-day period in which large ovarian cysts were induced in hypothyroid rats by daily injections of hCG. After 20 injections, ovaries increased in weight 10-fold, and well-developed ovarian cysts were present, accompanied by lutein tissue; cyst development continued for the subsequent 20 days of hCG. Both PRL and LH rose during the first 5 days of treatment and were maintained at high levels from day 20 on. The pattern of change of gonadal steroids showed greater increases with hCG in hypothyroid than in euthyroid rats. Levels of estradiol in hypothyroid, hCG-injected rats increased in parallel to ovarian hypertrophy, whereas progesterone was high in initial stages and then declined. Testosterone increased in both euthyroid and hypothyroid animals, with no clear pattern coincident with cyst formation. The data suggest that the formation of polycystic ovaries in the hypothyroid rat is associated with high levels of PRL and LH followed by elevations of estradiol, which may serve to maintain continuous PRL, as well as LH, stimulation of the ovary.

Animals↗
PubMed1990

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)

Adult↗
PubMed1989

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)

Adult↗
PubMed1989

Acute ozone exposure increases plasma prostaglandin F2 alpha in ozone-sensitive human subjects.

Twenty O3-sensitive and 2O O3-nonsensitive subjects participated in a study to investigate the effects of disparate O3 sensitivity on plasma prostaglandin F2 alpha) responses consequent to exposure to ambient O3 concentrations. Subjects were selected from a pool of 75 normal healthy college-aged males who had been previously exposed to 0.35 ppm O3 for 1 h at an exercising VE of 60 L/min. The selection criterion used was the observed decrement in FEV1 after the O3 exposure: O3-sensitive, FEV1 decrement greater than 24%; O3-nonsensitive, FEV1 decrement less than 11%. Each subject was exposed to filtered air and to 0.20 and 0.35 ppm O3 for 80 min while exercising at a VE of 50 L/min. These experimental protocols were divided into two 40-min sessions separated by a period of 4 to 10 min. PGF2 alpha, FVC, FEV1, and FEF25-75 were evaluated before, during, and after each protocol. SGaw and Vtg were measured before and after each protocol. Plasma PGF2 alpha was significantly increased in the O3-sensitive group during and after the 0.35-ppm O3 exposure.

Adult↗
PubMed1989

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)

Adult↗
PubMed1989

Progesterone inhibits the uterotrophic effect of relaxin in immature rats.

Injection of progesterone for 3 days before treatment with relaxin inhibited the trophic effect of the peptide in both estrogen-primed and unprimed uteri. The depression in collagen concentration and increase in apparent rate of proline incorporation into collagen induced by relaxin alone were also eliminated, indicating a fundamental blockade of the effect of relaxin in this experimental design as well as a close association of changes in collagen concentration with tissue hypertrophy. The effect of relaxin on incorporation of proline into soluble protein was not blocked by progesterone, however, suggesting a separate mechanism for this anabolic effect of relaxin.

Animals↗
PubMed1988

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.

Adipose Tissue↗
PubMed1987

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.

Adult↗
PubMed1987

Indomethacin pretreatment reduces ozone-induced pulmonary function decrements in human subjects.

We studied whether O3-induced pulmonary function decrements could be inhibited by the prostaglandin synthetase inhibitor, indomethacin, in healthy human subjects. Fourteen college-age males completed six 1-h exposure protocols consisting of no drug, placebo, and indomethacin (Indocin SR 75 mg every 12 h for 5 days) pretreatments, with filtered air and O3 (0.35 ppm) exposures within each pretreatment. Pretreatments were delivered weekly in random order in a double-blind fashion. Ozone and filtered air exposures, separated by 72 h, were delivered in random order in a single-blind fashion. Exposures consisted of 1-h exercise on a bicycle ergometer with work loads set to elicit a mean minute ventilation of 60 L/min. Statistical analysis revealed significant (p less than 0.05) across pretreatment effects for FVC and FEV1, with no drug versus indomethacin and placebo versus indomethacin comparisons being significant. These findings suggest that cyclooxygenase products of arachidonic acid, which are sensitive to indomethacin inhibition, play a prominent role in the development of pulmonary function decrements consequent to acute O3 exposure.

Adult↗
PubMed1987

Effects of porcine relaxins upon uterine hypertrophy and protein metabolism in mice.

Two variant forms of porcine relaxin (B and C) are active in producing relaxation of the guinea pig pubic symphysis and in effecting uterine growth in rats. Only relaxin B, however, is active in the mouse pubic ligament assay. These two hormones were compared in mice for their effects upon uterine growth and incorporation of radioactively labeled proline into soluble protein and collagen in vitro and in vivo. Both relaxin B and relaxin C produced an early (3-hr) elevation in in vitro protein synthesis and a later (6-hr) increase in collagen incorporation of proline at the time when the uterotrophic effect was maximal. In vivo effects of relaxin C on the uterus were in some cases greater than relaxin B in contrast to the complete inactivity of the former upon the pubic ligament of the mouse. These findings suggest a high degree of tissue specificity for relaxin stimulation, a variability in responsiveness among tissues in the same animal, and perhaps a primary role of relaxin in uterine function with pelvic relaxation representing a secondary function which has developed in certain species.

Animals↗
PubMed1986

Hormonal changes during the early development of ovarian cysts in the rat.

The daily administration of human chorionic gonadotropin (hCG) to rats with thiouracil-induced hypothyroidism results in the development of cystic ovaries. This study was undertaken to delineate hormonal changes during the first 48 h of hCG treatment. Groups of euthyroid and hypothyroid rats were injected daily with hCG or saline for up to two days and killed at 0, 12, 24, or 48 h after the initial hCG injection. Sera were analyzed for progesterone (P), testosterone (T), 17 beta-estradiol (E2), and prolactin (Prl) by specific radioimmunoassay (RIA). Serum levels of these hormones were not significantly different in the euthyroid and hypothyroid rats. However, P was significantly elevated at 12, 24, and 48 h in the hypothyroid/hCG rats. T and Prl were significantly elevated at 12 and 48 h in the hypothyroid/hCG rats. T levels were also elevated at 12 and 48 h in the euthyroid rats receiving hCG. In contrast, hCG had no effect on P and Prl levels in the euthyroid rats. E2 levels were undetectable in the euthyroid and hypothyroid rats. The administration of hCG increased E2 in both the euthyroid and hypothyroid rats at 48 h with significantly more E2 detected in the hypothyroid rats. These results show that ovarian steroids and Prl levels increase during the early stages of cyst induction and suggest they may be important in triggering ovarian cyst formation.

Animals↗
PubMed1986

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.

Adaptation, Physiological↗
PubMed1986

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.

Adult↗