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Biomedical subjects

A B Loucks

Publications and source records attributed to A B Loucks.

27 records · Page 2Linked to original sources
PubMed1989

Alterations in the hypothalamic-pituitary-ovarian and the hypothalamic-pituitary-adrenal axes in athletic women.

The functional integrity of the hypothalamic-pituitary-ovarian and hypothalamic-pituitary-adrenal axes was assessed by determining pulsatile LH, ACTH, and cortisol secretion during the early follicular phase in athletic women with regular menstrual cycles (CA; n = 9), athletic women with amenorrhea (AA; n = 9), and regularly cyclic sedentary women (CS; n = 8). The CA and AA women were not significantly different in body composition, exercise training, psychometric tests, or dietary consumption. The CA women had shorter luteal phases (P less than 0.05) and lower urinary excretion of pregnanediol glucuronide than the CS women. In the AA women, urinary estrone glucuronide, pregnanediol glucuronide, and LH excretion were low throughout a 30-day period. The CA women had a 24-h pattern of pulsatile LH secretion characterized by reduced frequency (P less than 0.05) and increased amplitude (P less than 0.05), yielding an overall increased 24-h mean level (P less than 0.05), but interpulse intervals similar to those in the CS women. During sleep, LH pulse frequency slowed in the CS and CA women, while pulse amplitude increased and the mean serum LH level decreased in both groups. The AA women had even fewer pulses (P less than 0.05) of normal amplitude occurring at much more variable (P less than 0.01) interpulse intervals. Sleep-associated changes in LH pulsatility were absent. Responses to a 10-microgram bolus GnRH dose revealed blunted (P less than 0.05) FSH release in CA and augmented (P less than 0.05) LH release in AA women. The groups did not differ in any 24-h ACTH pulse pattern parameter or in cortisol pulse frequencies. Yet, early morning (0200-0800 h) serum cortisol levels were higher (P less than 0.05) in both groups of athletes, and this elevation was extended through the day (0800-2000 h; P less than 0.001) and evening (2000-0200 h; P less than 0.05) in the AA women. The plasma ACTH and serum cortisol responses to bolus human CRH administration were blunted in the CA and AA women [change from baseline (delta) in ACTH, P less than 0.05 and P less than 0.01; delta cortisol, P less than 0.01 and P less than 0.01, respectively], but adrenal sensitivity (delta cortisol/delta ACTH ratio) was increased (P less than 0.05). The plasma ACTH and serum cortisol responses to meals also were blunted in the athletic groups (P less than 0.05).(ABSTRACT TRUNCATED AT 400 WORDS)

Adrenocorticotropic Hormone↗
PubMed1986

Does exercise training affect reproductive hormones in women?

In recent years, reproductive disorders in athletes have been observed in increasing numbers and proportions as larger numbers of women are participating in more strenuous athletic activities. Clinical problems with infertility and decreased bone density have been reported in this group, which has prided itself on its health. Hypoestrogenic women, including amenorrheic athletes, should definitely seek medical treatment for the prevention of osteoporosis, but before women sacrifice the many benefits of strenuous exercise, it is appropriate to consider the strength of the evidence that exercise training in particular, rather than other, extraneous aspects of athletic training, is responsible for the hormonal changes associated with reproductive disorders. This review has examined this first link in the postulated causal chain between exercise and these clinical conditions. In this review, only those studies that have compared trained or highly trained women with untrained or less-trained women, either cross-sectionally or longitudinally have been considered. In assessing the credibility of the reported results, we have found that the extensive precautions, painstaking techniques, and powerful protocols required for studying the question have only slowly been appreciated and never fully implemented by investigators. As a result, most of the published results are of little value. The few studies less susceptible to such criticism are consistent in their observations of gonadotropin and ovarian steroid suppression in women participating in athletic training. Nevertheless, even these results may have been biased by confounding factors, and thus at the present time the first link in the causal chain of events from exercise training to infertility and fractures cannot be regarded as proven. If the observed suppression of reproductive hormones is, indeed, due to exercise training, it may be dependent upon either the intensity of exercise training or the rate at which the intensity is increased. A dependence upon the rate at which exercise intensity is increased may explain why large proportions of athletes at all exercise intensity levels remain eumenorrheic. If future studies eliminate the biasing effects of known confounding factors and confirm that the female reproductive system can be suppressed by exercise training in particular, then additional research will be needed to determine the training intensity or rate of change in intensity required for these effects to occur. Research will also be needed to determine how gynecologic age, body composition, diet, and psychologic status may exaggerate or attenuate these effects.(ABSTRACT TRUNCATED AT 400 WORDS)

Cross-Sectional Studies↗
PubMed1985

Athletic amenorrhea: a review.

Secondary amenorrhea in athletes is reviewed with respect to its incidence, treatment, associated characteristics, proposed mechanisms, and endocrine profile. Athletic amenorrhea is classified within the general category of chronic anovulation syndrome, but no mechanism has been demonstrated. The wide range in observed incidences (1-44%) is due to the lack of a standard definition for secondary amenorrhea and differences between the populations surveyed. The currently recommended treatment is outlined briefly. Several descriptive characteristics of amenorrheic athletes have led to a variety of proposed mechanisms involving body composition, training regimen, reproductive maturity, sport specificity, diet, and psychological stress. Basal hormone concentrations in eumenorrheic women after training and in amenorrheic athletes, as well as transitory endocrine responses to exercise, are the basis for evaluating these proposals. Methodological errors which have led to conflicting results are identified, and the proposed mechanisms are evaluated on the basis of the presently available data.

Adolescent↗
PubMed1984

Exercise-induced stress responses of amenorrheic and eumenorrheic runners.

The role of stress in exercise-associated amenorrhea was investigated. Sex hormones [FSH, LH, androstenedione (A), testosterone, estrone, and 17 beta-estradiol (E2)], stress hormones [dehydroepiandrosterone, cortisol (F), PRL, norepinephrine, and epinephrine] and psychological status (Profile of Mood States and State-Trait Anxiety Inventory) were measured at rest and in response to a 40-min 80% of maximal aerobic power (VO2max) run in highly trained eumenorrheic (n = 8) and amenorrheic (n = 7) women runners matched for fatness [eumenorrheic, 16.5 +/- 2.3% (+/- SD); amenorrheic, 14.9 +/- 4.8] and maximal aerobic power (eumenorrheic, 58.9 +/- 5.7 ml/kg X min; amenorrheic, 59.8 +/- 4.6). Eumenorrheic runners were tested between days 3 and 8 of the follicular phase. At rest, decreased plasma FSH, LH, and E2 concentrations were found in amenorrheic women [eumenorrheic FSH, 10.5 +/- 4.1 mIU/ml; amenorrheic FSH, 4.9 +/- 1.6 (P less than 0.01); eumenorrheic LH, 14.1 +/- 6.1 mIU/ml; amenorrheic LH, 5.1 +/- 1.7 (P less than 0.01); eumenorrheic E2, 20 +/- 9 pg/ml; amenorrheic E2, 7 +/- 6 (P less than 0.05)]. Other sex and stress hormones and psychological measurements were similar in the two groups and were within the normal range. Ventilatory, cardiovascular, thermoregulatory, and psychological responses to the submaximal run were identical. Among eumenorrheic women, all stress hormones and A increased after exercise, but PRL, F, and A were unchanged among amenorrheic women. Estrone, E2, and testosterone did not change in either group. These observations are inconsistent with a general stress hypothesis of exercise-associated amenorrhea as well as with more specific hyperprolactinemic and hyperandrogenic hypotheses. In amenorrheic women, failure of PRL to increase in response to exercise may be due to their lack of E2, while failure of F and A to increase may indicate reduced adrenal 3 beta-hydroxysteroid dehydrogenase/isomerase activity.

Adolescent↗
PubMed1982

Sweating sensitivity and capacity of women in relation to age.

Ten postmenopausal and ten younger women rested for 2 h in a 40 degrees C, 22.2-Torr vapor pressure environment. Sweating response was monitored by resistance hygrometry for onset, a platform balance for whole-body sweat rate, and five individual capsules for regional sweat rate. Other variables measured included forearm blood flow, heart rate (HR), mean skin (Tsk) and rectal (Tre) temperatures, sweat electrolytes (Na+ and K+), oxygen uptake, and plasma volume changes. Preliminary tests included maximal aerobic power (VO2max) and percent body fat. Heat stress did not elicit any significant differences in sweating response between age groups. Indices of heat strain, Tre and HR, were also similar for both groups. The only significant difference between younger and older women was a higher Na+ concentration in the forearm sweat of postmenopausal women. No thermoregulatory responses were related to age, but both sweat rate (r = 0.48) and peak Tsk (r = -0.43) were related to VO2max. For healthy, active, older women aging did not diminish the functional capacity of the sweating mechanism to cope with heat stress while resting in this specific thermal environment.

Adult↗
PubMed1979

Response of women mountaineers to maximal exercise during hypoxia.

Eight members of the American Women's Himalayan Expedition, ranging in age from 20-49, performed maximal exercise on a treadmill under normoxic and acute hypoxic (12.58% O2) conditions. Normoxic values for VO2 max were above average for all subjects and did not decline with age. The mean decrease in VO2 max (26.7%) during hypoxia was equivalent to that reported for younger males, which suggests that age was not a factor in response to hypoxia. Maximal heart rate, respiratory exchange ratio, oxygen pulse, and walk time were lower in hypoxia while ventilatory equivalent and blood lactate were higher. VEmax BTPS, was the same under both conditions. The combination of laboratory results and field observations by the Expedition physician suggest that women are capable of performing hard work at high altitude if they are in good condition and properly acclimatized.

Adult↗