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Thesis (doctoral)--Rijksuniversiteit te Utrecht.

Thesis (M.S.)--University of Wisconsin--Madison, 1982. / Typescript. eContent provider-neutral record in process. Description based on print version record. Includes bibliographical references (leaves 55-58).

Thesis (doctoral)--Ludwig Maximilians-Universität zu München, 1979.

Women with exercise associated amenorrhea display a disturbance in basal and exercise levels of reproductive, anti-reproductive and stress hormones. Co-incident with chronic exercise are other factors, which alone, also affect the menstrual cycle. Therefore, amenorrheic runners (AR), regularly menstruating runners (RMR) and regularly menstruating sedentary controls (RMSC) were compared for plasma progesterone levels, plasma lipid levels, menstrual cycle characteristics, physical characteristics and nutritional adequacy to determine if the difference in menstrual status could be explained, and to determine whether exercise alone could be attributed as the cause of menstrual cycle disturbances.Plasma progesterone levels were significantly lower in the AR group (. 28 + .02 ng/ml) than in the RMR group (.41 + .06 ng/ml) and the RMSC group (.49 + .06 ng/ml) in the follicular phase. Regularly menstruating runners demonstrated lower plasma progesterone levels in the luteal phase (9.76 + 1.05 ng/ml) than RMSC subjects (10.24 + 2.21 ng/ml). Regularly menstruating runners had a significantly shorter luteal phase length relative to their cycle length (.35 + .01) than RMSC subjects (.46 + .01). Mean age, incidence of parity, age of menarche, height, weight, body composition, max V02 and number of miles run per week did not differ between the RMR and AR subjects. Amenorrheic runners took in significantly less fat, red meat, phosphorous and total calories than the RMR subjects. Serum LDL-C was significantly higher in the AR subjects (89.2 + 9.7 mg/dl) than in the RMR subjects in both the luteal (67.8+ 3.4 mg/dl) and follicular (66.8+ 5.6 mg/dl) phases. Serum HDL-C was significantly higher in the RMR subjects in both the luteal (62.9+ 4.1 mg/dl) and follicular (59.2+ 2.9 mg/dl) phase, and in the AR subjects (63.9+ 4.2 mg/dl), than in the RMSC subjects in the luteal (49.2+ 5.9 mg/dl) and follicular (47.2+ 2.4 mg/dl) phase. Serum VLDL-C did not differ between any groups.This investigation demonstrates that hormonal and lipid level alterations with exercise are significantly different in the amenorrheic runner. However, regularly menstruating runners display alterations which may represent and intermediate or potential phase of menstrual cycle disturbances. The nutritional inadequacy or energy imbalance separates amenorrheic runners from regularly menstruating runners. Thus, it appears that exercise alone is not enough to cause the hormonal disturbances that trigger amenorrhea, and, that exercise associated amenorrhea is not unlike other amenorrheas of hypothalamic origin.

The influence of estrogen deficiency in physically active women with functional hypothalamic amenorrhea (ExFHA) on cardiovascular regulation is unknown. Three mechanistic studies compared cardiovascular responses to exercise and orthostatic stress in ExFHA women with responses in physically active (ExOv) and sedentary (SedOv) eumenorrheic ovulatory women. Measures included calf blood flow (BF), brachial artery (BA) endothelial dependent and independent function, shear rate (SR), vascular resistance (VR), blood pressure (BP), heart rate (HR), HR variability (HRV), muscle sympathetic nervous activity (MSNA), and serum renin-angiotensin-aldosterone system (RAAS) components. Study one examined the effects of a single bout of dynamic exercise on vascular function in ExFHA (n=12), ExOv (n=14), and SedOv (n=15) women. Pre-exercise, calf BF and BA endothelium-dependent flow-mediated vasodilation (FMD%) were lower (p<0.05) in ExFHA versus ovulatory women in association with higher (p<0.05) calf VR and lower (p<0.05) SR, respectively. Endothelium-independent vasodilation, assessed at baseline only, was also lower (p<0.05) in ExFHA. Post-exercise, calf BF was increased and VR decreased (p<0.05) in ExFHA women, similar (p>0.05) to that observed in ovulatory women. FMD% and SR were augmented (p<0.05) post-exercise, but both remained lower (p<0.05) in ExFHA versus ovulatory women (p<0.05). Study two investigated neurohumoral (MSNA and RAAS) BP regulation during orthostatic stress in ExFHA (n=12) and ExOv (n=17) women. Baseline systolic BP was lower (p<0.05) in ExFHA versus ExOv. Neurohumoral measures did not differ (p>0.05) between the groups at baseline. However, during hypotensive stimuli, MSNA increased to a greater extent (p<0.05), yet angiotensin II and renin were not activated in ExFHA women. Study three examined autonomic control of HR during orthostatic stress in ExFHA (n=11), ExOv (n=17), and SedOv (n=17) women. Lower HR (p<0.05) at rest and during orthostatic stress in ExFHA was associated with markedly elevated (p<0.05) HRV due to higher (p<0.05) parasympathetic modulation. Sympathetic modulation did not differ (p>0.05) between the groups. These studies indicate altered cardiovascular regulation in otherwise healthy ExFHA women. The influence of estrogen deficiency per se in these alterations are not clear, but in light of the etiology of amenorrhea, it is likely that complex interactions between estrogen and energy deficiency and exercise training are involved.

The influence of estrogen deficiency in physically active women with functional hypothalamic amenorrhea (ExFHA) on cardiovascular regulation is unknown. Three mechanistic studies compared cardiovascular responses to exercise and orthostatic stress in ExFHA women with responses in physically active (ExOv) and sedentary (SedOv) eumenorrheic ovulatory women. Measures included calf blood flow (BF), brachial artery (BA) endothelial dependent and independent function, shear rate (SR), vascular resistance (VR), blood pressure (BP), heart rate (HR), HR variability (HRV), muscle sympathetic nervous activity (MSNA), and serum renin-angiotensin-aldosterone system (RAAS) components. Study one examined the effects of a single bout of dynamic exercise on vascular function in ExFHA (n=12), ExOv (n=14), and SedOv (n=15) women. Pre-exercise, calf BF and BA endothelium-dependent flow-mediated vasodilation (FMD%) were lower (p<0.05) in ExFHA versus ovulatory women in association with higher (p<0.05) calf VR and lower (p<0.05) SR, respectively. Endothelium-independent vasodilation, assessed at baseline only, was also lower (p<0.05) in ExFHA. Post-exercise, calf BF was increased and VR decreased (p<0.05) in ExFHA women, similar (p>0.05) to that observed in ovulatory women. FMD% and SR were augmented (p<0.05) post-exercise, but both remained lower (p<0.05) in ExFHA versus ovulatory women (p<0.05). Study two investigated neurohumoral (MSNA and RAAS) BP regulation during orthostatic stress in ExFHA (n=12) and ExOv (n=17) women. Baseline systolic BP was lower (p<0.05) in ExFHA versus ExOv. Neurohumoral measures did not differ (p>0.05) between the groups at baseline. However, during hypotensive stimuli, MSNA increased to a greater extent (p<0.05), yet angiotensin II and renin were not activated in ExFHA women. Study three examined autonomic control of HR during orthostatic stress in ExFHA (n=11), ExOv (n=17), and SedOv (n=17) women. Lower HR (p<0.05) at rest and during orthostatic stress in ExFHA was associated with markedly elevated (p<0.05) HRV due to higher (p<0.05) parasympathetic modulation. Sympathetic modulation did not differ (p>0.05) between the groups. These studies indicate altered cardiovascular regulation in otherwise healthy ExFHA women. The influence of estrogen deficiency per se in these alterations are not clear, but in light of the etiology of amenorrhea, it is likely that complex interactions between estrogen and energy deficiency and exercise training are involved.

Background: Past studies suggest that inadequate energy intake (EI) is directly related to menstrual dysfunction (MD) in active females. Inadequate EI causes activation of the hypothalamic-pituitary-adrenal axis, disrupting the normal hormonal signaling of reproductive cycling and resulting in MD. However, studies have also demonstrated similar EI in athletes, but with different menstrual function. Traditionally, energy balance has been evaluated in 24-hour time periods. Recent research suggests there is benefit to analyzing energy balance at smaller intervals to better address physiologic response in real time. It is possible that women who meet their daily EI needs could still, therefore, experience MD if the majority of the day is spent in energy deficit. Objective: The purpose of this study is to determine whether within-day energy balance is a factor in menstrual status in active adult females. Methods: Twenty active females tracked hourly EI and energy expenditure over three days. A two-page survey was utilized to obtain information on training, health, and menstrual status. Participants were also asked to respond to several questions regarding eating habits and attitude towards food. Within-day energy balance was calculated and evaluated using NutriTimingTM software. Collected energy balance data were analyzed for associations with menstrual status. Results: Participants spent more hours in a catabolic state (energy balance less than zero) than in an anabolic state (20.5 hrs vs 3.5 hrs) and averaged a caloric deficit of -504 kcal over 24-hours. Nine subjects (45%) had experienced loss of menses for greater than 3 months (LoM>3mos), indicative of amenorrhea. Hours spent in energy surplus >400 kcal was inversely correlated with LoM>3mos (r = -0.463; P = 0.04). The impact of number of miles run per week and menstrual dysfunction, based on a quartile stratification of miles run, were analyzed using an ANOVA with Tamhane non-parametric post hoc test. Significant differences were found between the upper two quartiles of distance run per week and LoM>3mos (P = 0.048). There was no relationship between end-of-day energy balance and Lom>3mos. Conclusion: Researchers and healthcare professionals would do well to examine energy balance in an hour-by-hour manner as it is has implications for MD. This would help to clarify whether within-day energy balance is a factor in MD, and allow for the development of appropriate intervention strategies to improve health and athletic outcomes for active women.

Thesis (M.S.)--University of Wisconsin--La Crosse, 2009. / Includes bibliographical references.

Thesis (M.S.)--State University of New York, College at Brockport, 2002. / Includes bibliographical references (leaves 94-100). Also available online (PDF file) by a subscription to the set or by purchasing the individual file.