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Biomedical subjects

C L Otis

Publications and source records attributed to C L Otis.

5 recordsLinked to original sources

American College of Sports Medicine position stand. The Female Athlete Triad.

The Female Athlete Triad is a syndrome occurring in physically active girls and women. Its interrelated components are disordered eating, amenorrhea, and osteoporosis. Pressure placed on young women to achieve or maintain unrealistically low body weight underlies development of the Triad. Adolescents and women training in sports in which low body weight is emphasized for athletic activity or appearance are at greatest risk. Girls and women with one component of the Triad should be screened for the others. Alone or in combination, Female Athlete Triad disorders can decrease physical performance and cause morbidity and mortality. More research is needed on its causes, prevalence, treatment, and consequences. All individuals working with physically active girls and women should be educated about the Female Athlete Triad and develop plans to prevent, recognize, treat, and reduce its risks.

Adolescent

Exercise-associated amenorrhea.

Currently, more is unknown than is known about the complex interactions of exercise and the female reproductive system. Three types of menstrual changes are observed in athletes: luteal phase deficiency, anovulation, and exercise-associated amenorrhea. This article presents a clinically oriented update on the hypothesized causes, evaluation, and management of menstrual changes in active women.

Amenorrhea

Epinephrine-induced alterations in urinary cyclic AMP in hyper- and hypothyroidism.

Although ratios of urinary cyclic AMP (cAMP) to creatinine were found in this study to be elevated in hyperthyroidism, as previously reported, this elevation appears to result primarily from a decrease in the rate of urinary creatinine excretion associated with the hyperthyroid state and not to be due to an increase in the urinary cAMP production rate. Indeed, there was no significant alteration observed in the urinary cAMP excretion found in 15 hyper-, 12 eu-, and 5 hypothyroid subjects. However, a slight, but significant increase in the 24-hour urinary cAMP excretion was noted in ambulating hyperthyroid subjects (8.5 +/- 2.4 muMol/day; normal 5.2 +/- 1.6 muMol/day; P less than .05). In contrast, the effect of the infusion of 0.05 mug/kg/min of epinephrine over a 2-hour period, resulted in a significantly greater rise in urinary cAMP excretion in hyperthyroid patients (0.83 +/- 0.07 muMol/h) compared to euthyroid subjects (0.53 +/- 0.4 muMol/h; P less than .005). Furthermore, hypothyroid subjects had no significant rise in urinary cAMP excretion after epinephrine infusion (P less than .001). Cardiovascular end-organ response to the epinephrine infusion was also greater in the hyperthyroid subjects and virtually absent in the hypothyroid group. These results suggest that there may be a significant alteration in the cAMP generating systems in states of thyroid hormone excess or insufficiency, and that provocative stimuli, such as epinephrine, may have its end-organ response modified by thyroid hormone effects on adenylate cyclase-cyclic AMP generating systems.

Adult