Registered report: A pilot investigation of acute exercise response among girls and young women with and without eating disorders

Exercise is well appreciated as a therapeutic approach to improve health. While chronic exercise training can change metabolism, even a single exercise session can have significant effects upon metabolism. Responses of adipose tissue lipolysis and skeletal muscle triacylglycerol (TAG) utilization have been well-appreciated as components of the acute exercise response. However, there are other central components of the physiological response to be considered, as well. A robust and growing body of literature depicts a rapid responsiveness of hepatic TAG content to single bouts of exercise, and there is a remaining need to incorporate this information into our overall understanding of how exercise affects the liver. TAG content in the liver increases during an exercise session and can continue to rise for a few hours afterwards, followed by a fairly rapid return to baseline. We summarize evidence that rapid responsiveness of hepatic TAG content to metabolic stress is a fundamental component of the exercise response. Adipose tissue lipolysis and plasma free fatty acid concentration are likely the major metabolic controllers of enhanced lipid storage in the liver after each exercise bout, and we discuss nutritional impacts as well as health implications. While traditionally clinicians would be merely concerned with hepatic lipids in overnight-fasted, rested individuals, it is now apparent that the content of hepatic TAG fluctuates in response to metabolic challenges such as exercise, and these responses likely exert significant impacts on health and cellular homeostasis.

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Corticotrophin-releasing hormone does not inhibit growth hormone-releasing hormone-induced release of growth hormone in control subjects but is effective in patients with eating disorders

Journal of Endocrinology ◽

10.1677/joe.0.1400327 ◽

1994 ◽

Vol 140 (2) ◽

pp. 327-332 ◽

Cited By ~ 7

Author(s):

M Rolla ◽

A Andreoni ◽

D Bellitti ◽

M Ferdeghini ◽

E Ghigo ◽

...

Keyword(s):

Growth Hormone ◽

Eating Disorders ◽

Young Women ◽

Animal Studies ◽

Area Under The Curve ◽

Inhibitory Influence ◽

Releasing Hormone ◽

Gh Secretion ◽

Not Otherwise Specified ◽

Normal Women

Abstract Previous studies have shown that corticotrophin-releasing hormone (CRH) inhibits GH secretion in response to GH-releasing hormone (GHRH) in normal women and men, and animal studies suggest that this effect is mediated by an increased release of somatostatin from the hypothalamus. It has been reported that there are abnormalities in the neuroendocrine regulation of the hypothalamo-pituitary-somatotrophic axis and the hypothalamo-pituitary-adrenocortical axis in patients with eating disorders. The present study therefore investigated the ability of CRH to inhibit the GH response to GHRH in eight young women with anorexia nervosa (AN) and in seven young women with eating disorders which were not otherwise specified (NOS). We also compared the effect of CRH in the patients with the response it caused in ten control women. In contrast to a previous report, combined i.v. administration of 50 μg human CRH (hCRH) and 50 μg GHRH(1–29) caused a GH response in control women which was higher, although not significantly so, than that induced by GHRH alone (area under the curve (AUC) 988·5 ±506·0 compared with 1568·4 ±795·6 (s.e.m.) ng/ml per 120 min for GHRH alone and GHRH plus hCRH respectively). Conversely, the administration of hCRH given together with GHRH markedly inhibited the GH response induced by the latter in both AN patients (AUC 2253·0 ±385·7 compared with 1224·4 ±265·7 ng/ml per 120 min for GHRH and GHRH plus hCRH respectively; P<0·005 and NOS patients (AUC 2827·4±281·1 compared with 308·5 ± 183·4 ng/ml per 120 min for GHRH and GHRH plus hCRH respectively; P<0·0001). These results (1) refute the suggestion that there is an inhibitory influence of CRH over GH secretion under normal conditions, (2) indicate that this inhibitory influence exists in patients with eating disorders, and (3) imply that, in the latter, hypothalamic somatostatinergic function is, at least in part, preserved. Journal of Endocrinology (1994) 140, 327–332

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The Body Project

10.1093/med:psych/9780199859245.001.0001 ◽

2015 ◽

Cited By ~ 3

Author(s):

Eric Stice ◽

Paul Rohde ◽

Heather Shaw

Keyword(s):

Eating Disorders ◽

Eating Disorder ◽

Young Women ◽

Prevention Program ◽

Evidence Base ◽

The Body ◽

Thin Ideal ◽

Eating Disorder Prevention ◽

Body Project ◽

Disorder Prevention

The Body Project is an empirically based eating disorder prevention program that offers young women an opportunity to critically consider the costs of pursuing the ultra-thin ideal promoted in the mass media, and it improves body acceptance and reduces risk for developing eating disorders. Young women with elevated body dissatisfaction are recruited for group sessions in which they participate in a series of verbal, written, and behavioral exercises in which they consider the negative effects of pursuing the thin-ideal. This online resource provides information on the significance of body image and eating disorders, the intervention theory, the evidence base which supports the theory, recruitment and training procedures, solutions to common challenges, and a new program aimed at reducing obesity onset, as well as intervention scripts and participant handouts. It is the only currently available eating disorder prevention program that has been shown to reduce risk for onset of eating disorders and received support in trials conducted by several independent research groups.

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