Less-than-expected weight loss in normal-weight women undergoing caloric restriction and exercise is accompanied by preservation of fat-free mass and metabolic adaptations.

BACKGROUND/OBJECTIVES: Normal-weight women frequently restrict their caloric intake and exercise, but little is known about the effects on body weight, body composition and metabolic adaptations in this population. SUBJECTS/METHODS: We conducted a secondary analysis of data from a randomized controlled trial in sedentary normal-weight women. Women were assigned to a severe energy deficit (SEV: -1062±80 kcal per day; n=9), a moderate energy deficit (MOD: -633±71 kcal per day; n=7) or energy balance (BAL; n=9) while exercising five times per week for 3 months. Outcome variables included changes in body weight, body composition, resting metabolic rate (RMR) and metabolic hormones associated with energy conservation. RESULTS: Weight loss occurred in SEV (-3.7±0.9 kg, P<0.001) and MOD (-2.7±0.8 kg; P=0.003), but weight loss was significantly less than predicted (SEV: -11.1±1.0 kg; MOD: -6.5±1.1 kg; both P<0.001 vs actual). Fat mass declined in SEV (P<0.001) and MOD (P=0.006), whereas fat-free mass remained unchanged in all groups (P>0.33). RMR decreased by -6±2% in MOD (P=0.020). In SEV, RMR did not change on a group level (P=0.66), but participants whose RMR declined lost more weight (P=0.020) and had a higher baseline RMR (P=0.026) than those whose RMR did not decrease. Characteristic changes in leptin (P=0.003), tri-iodothyronine (P=0.013), insulin-like growth factor-1 (P=0.016) and ghrelin (P=0.049) occurred only in SEV. The energy deficit and adaptive changes in RMR explained 54% of the observed weight loss. CONCLUSIONS: In normal-weight women, caloric restriction and exercise resulted in less-than-predicted weight loss. In contrast to previous literature, weight loss consisted almost exclusively of fat mass, whereas fat-free mass was preserved.

Unique effects of energy versus estrogen deficiency on multiple components of bone strength in exercising women.

Many female athletes are energy and/or estrogen deficient, but the independent effects on bone health have not been isolated. Energy deficiency was detrimental at the tibia while estrogen deficiency was detrimental at the radius. Nutrition must be considered alongside menstrual recovery when addressing compromised bone health in female athletes. INTRODUCTION: The purpose of this study was to describe volumetric bone mineral density (vBMD), bone geometry, and estimated bone strength in exercising women (n = 60) grouped according to energy status (energy replete (EnR: n = 30) vs. energy deficient (EnD: n = 30)) and estrogen status (estrogen replete (E2R: n = 33) vs. estrogen deficient (E2D: n = 27)), resulting in four distinct groups: EnR + E2R (n = 17), EnR + E2D (n = 13), EnD + E2R (n = 16), EnD + E2D (n = 14). METHODS: Energy status was determined using the ratio of measured to predicted resting energy expenditure (mREE/pREE). Estrogen status was based on self-reported menstrual status confirmed by daily evaluation of urinary estrone-1-glucoronide (E1G), pregnanediol glucuronide (PdG), and luteinizing hormone (LH). Eumenorrheic women were considered E2R, amenorrheic women were E2D, and oligomenorrheic women were categorized based on history of menses in the past year. Bone was assessed using peripheral quantitative computed tomography (pQCT). RESULTS: EnD women exhibited lower total vBMD, trabecular vBMD, cortical area, and BSI at the distal tibia and lower total vBMD, smaller cortical area and cortical thickness, and larger endosteal circumference at the proximal tibia compared to EnR women (p < 0.042). E2D women had lower total and cortical vBMD, larger total and trabecular area, and lower BSI at the distal radius and lower cortical vBMD at the proximal radius compared to E2R women (p < 0.023). Energy and estrogen interacted to affect total and trabecular area at the distal tibia (p < 0.021). CONCLUSIONS: Efforts to correct energy deficiency, which in turn may promote reproductive health, are warranted in order to address the unique contributions of energy status versus estrogen status to bone health.

Postprandial peptide YY is lower in young college-aged women with high dietary cognitive restraint.

Acylated ghrelin and peptide YY (PYY3-36) are involved in appetite-regulation and energy homeostasis. These gastrointestinal hormones provide peripheral signals to the central nervous system to regulate appetite and short term food intake, and interact with leptin and insulin to regulate energy balance. Dietary restraint is an eating behavior phenotype that manifests as a conscious cognitive control of food intake in order to achieve or sustain a desired body weight. The purpose of the current study was to determine if college-aged women (18 to 25 years) with different eating behavior phenotypes, i.e., high vs normal dietary restraint, differ with respect to circulating concentrations of gastrointestinal hormones during and following a test meal. We hypothesized that women with high dietary cognitive restraint [High CR (score ≥ 13, n=13)] would have elevated active ghrelin and PYY3-36 concentrations after a test meal compared to women with normal dietary cognitive restraint [Normal CR (score < 13, n=30)]. Gastrointestinal hormones were assessed before (-15 and 0 min) and after (10, 15, 20, 30, 60, 90, 120 and 180 min) the consumption of a mixed composition meal (5.0 kcal per kg/body weight). In contrast to our hypothesis, mean PYY3-36 concentrations (p=0.042), peak PYY3-36 concentrations (p=0.047), and PYY3-36 area under the curve (p=0.035) were lower in the High CR group compared to the Normal CR group after controlling for body mass index. No group differences were observed with respect to acylated ghrelin before or after the meal. In conclusion, PYY3-36 concentrations were suppressed in the women with High CR compared to the women with Normal CR. While the current study is cross-sectional and cause/effect of high dietary restraint and suppressed PYY3-36 concentrations cannot be determined, we speculate that these women with high cognitive restraint may be prone to weight gain or weight re-gain related to the suppressed circulating PYY after a meal. Further investigations need to explore the relationship between dietary cognitive restraint, circulating PYY, and weight gain.

Exercise lowers estrogen and progesterone levels in premenopausal women at high risk of breast cancer.

Experimental and clinical data support a role for estrogens in the development and growth of breast cancer, and lowered estrogen exposure reduces breast cancer recurrence and new diagnoses in high-risk women. There is varied evidence that increased physical activity is associated with breast cancer risk reduction in both pre- and postmenopausal women, perhaps via lowered estrogen levels. The purpose of this study was to assess whether exercise intervention in premenopausal women at increased breast cancer risk reduces estrogen or progesterone levels. Seven healthy premenopausal women at high risk for breast cancer completed a seven-menstrual-cycle study. The study began with two preintervention cycles of baseline measurement of hormone levels via daily first-morning urine collection, allowing calculation of average area under the curve (AUC) hormone exposure across the menstrual cycle. Participants then began five cycles of exercise training to a maintenance level of 300 min per week at 80-85% of maximal aerobic capacity. During the last two exercise cycles, urinary estradiol and progesterone levels were again measured daily. Total estrogen exposure declined by 18.9% and total progesterone exposure by 23.7%. The declines were mostly due to decreased luteal phase levels, although menstrual cycle and luteal phase lengths were unchanged. The study demonstrated the feasibility of daily urine samples and AUC measurement to assess hormone exposure in experimental studies of the impact of interventions on ovarian hormones. The results suggest value in exercise interventions to reduce hormone levels in high-risk women with few side effects and the potential for incremental benefits to surgical or pharmacologic interventions.

Estrogen and peptide YY are associated with bone mineral density in premenopausal exercising women.

BACKGROUND: In women with anorexia nervosa, elevated fasting peptide YY (PYY) is associated with decreased bone mineral density (BMD). Prior research from our lab has demonstrated that fasting total PYY concentrations are elevated in exercising women with amenorrhea compared to ovulatory exercising women. PURPOSE: The purpose of this study was to assess the association between fasting total PYY, average monthly estrogen exposure and BMD in non-obese premenopausal exercising women. METHODS: Daily urine samples were collected and assessed for metabolites of estrone 1-glucuronide (E1G) and pregnandiol glucuronide (PdG) for at least one menstrual cycle if ovulatory or a 28-day monitoring period if amenorrheic. Fasting serum samples were pooled over the measurement period and analyzed for total PYY and leptin. BMD and body composition were assessed by dual-energy X-ray absorptiometry. Multiple regression analyses were performed to determine whether measures of body composition, estrogen status, exercise minutes, leptin and PYY explained a significant amount of the variance in BMD at multiple sites. RESULTS: Premenopausal exercising women aged 23.8±0.9years with a mean BMI of 21.2±0.4kg/m(2) exercised 346±48min/week and had a peak oxygen uptake of 49.1±1.8mL/kg/min. Thirty-nine percent (17/44) of the women had amenorrhea. Fasting total PYY concentrations were negatively associated with total body BMD (p=0.033) and total hip BMD (p=0.043). Mean E1G concentrations were positively associated with total body BMD (p=0.033) and lumbar spine (L2-L4) BMD (p=0.047). The proportion of variance in lumbar spine (L2-L4) BMD explained by body weight and E1G cycle mean was 16.4% (R(2)=0.204, p=0.012). The proportion of variance in hip BMD explained by PYY cycle mean was 8.6% (R(2)=0.109, p=0.033). The proportion of variance in total body BMD explained by body weight and E1G cycle mean was 21.9% (R(2)=0.257, p=0.003). CONCLUSION: PYY, mean E1G and body weight are associated with BMD in premenopausal exercising women. Thus, elevated PYY and suppressed estrogen concentrations are associated with, and could be directly contributing to, low BMD in exercising women with amenorrhea, despite regular physical activity.

Circulating leptin concentrations do not distinguish menstrual status in exercising women.

BACKGROUND: Low concentrations of leptin secondary to low body fat or other modulators are thought to be a key signal whereby an energy deficit suppresses the reproductive axis in exercising women resulting in functional hypothalamic amenorrhea (FHA). The purpose of this study was to first examine leptin concentrations in exercising women with and without FHA to address whether there is a threshold concentration of leptin below which reproductive function is suppressed. Secondly, we examined the role of adiposity and other possible modulators of leptin to ascertain whether leptin regulation differs depending on reproductive status. METHODS: This study assessed 50 exercising, premenopausal women (aged 18-30 years) over the course of one menstrual cycle (eumenorrheic women) or one 28-day monitoring period (amenorrheic women). Quantification of daily urinary ovarian steroids and menstrual history were used to determine menstrual status. Body composition was assessed using dual energy X-ray absorptiometry, and leptin was determined by enzyme-linked immunoassay. Key modulators of leptin such as serum insulin concentration, carbohydrate intake, glucose availability, indirect indices of sympathetic nervous activity and other factors were assessed using linear regression. RESULTS: Percentage body fat (%BF) (21.0 ± 1.0 versus 26.8 ± 0.7%; P < 0.001) and leptin concentration (4.8 ± 0.8 versus 9.6 ± 0.9 ng/ml; P < 0.001) were lower in the exercising women with amenorrhea (ExAmen; n = 24) compared with the exercising ovulatory women (ExOvul; n = 26). However, the ranges in leptin were similar for each group (ExAmen: 0.30-16.98 ng/ml; ExOvul: 2.57-18.28 ng/ml), and after adjusting for adiposity the difference in leptin concentration was no longer significant. Significant predictors of log leptin in ExAmen included %BF (ß = 0.826, P < 0.001), log insulin (ß = 0.308, P = 0.012) and log glycerol (ß = 0.258, P = 0.030), but in ExOvul only %BF predicted leptin. CONCLUSIONS These data suggest that leptin concentrations per se are not associated with FHA in exercising women, but the modulation of leptin concentrations may differ depending on reproductive status.

Estrogen and progesterone exposure is reduced in response to energy deficiency in women aged 25-40 years.

BACKGROUND: Alterations in circulating steroids are believed to be important mediators of the impact that diet and exercise have on breast cancer risk and changes in bone density. This study aimed to test the hypothesis that moderate exercise training combined with caloric restriction would produce significant menstrual disturbances and alterations in ovarian steroids in premenopausal women. METHODS: Sedentary premenopausal women (25-40 years; body mass index: 23.6 +/- 0.6 kg/m(2)) assigned to either a light conditioning (LC, n = 9) or an exercise combined with caloric restriction group (EX + CR, n = 24) were studied for one screening, one baseline and four intervention periods equivalent to the length of subjects' menstrual cycles. Exercise consisted of supervised training sessions, i.e. two LC or four EX + CR times per week, 30-60 min at a moderate intensity. The EX + CR group was prescribed a diet representing a caloric restriction of 20-35% below baseline energy requirements, whereas the LC group remained eucaloric. Ovarian steroid exposure was determined with daily urinary estrone-1- and pregnanediol glucuronides (E1G and PdG, respectively) and mid-cycle urinary LH measures. Fitness, body composition, and serum sex hormone binding globulin (SHBG) and serum estradiol (E2) were assessed repeatedly. RESULTS: The intervention produced significant increases in VO(2) max and decreases in both body weight (-3.7 +/- 0.5 kg; ranged from -8.8 to +1.8 kg) and percent body fat (-4.5 +/- 0.7%; ranged from -12 to +0.3%), which were attributable primarily to changes in the EX + CR subjects (time x group; P < 0.05). Serum E2 and urinary E1G and PdG concentrations declined significantly across the intervention period (time; P < 0.05), whereas SHBG increased transiently (time; P < 0.05) in the EX + CR subjects, with no significant changes observed in the LC group. The decrease in E1G area under the curve was significantly related to the daily energy deficit (R =0.61; P = 0.003), not the amount of weight lost. There was no significant impact of the intervention on menstrual cyclicity or the incidence of menstrual disturbances in either group. CONCLUSIONS: A moderate aerobic exercise training program combined with modest weight loss in accordance with recommended guidelines produces significant reductions in ovarian steroid exposure without disrupting menstrual cyclicity in premenopausal women aged 25-40 years. Exposure to a daily energy deficit is a stronger predictor of the decline in estrogen exposure than decreases in body weight.

Effects of aerobic exercise training on cognitive function and cortical vascularity in monkeys.

This study examined whether regular exercise training, at a level that would be recommended for middle-aged people interested in improving fitness could lead to improved cognitive performance and increased blood flow to the brain in another primate species. Adult female cynomolgus monkeys were trained to run on treadmills for 1 h a day, 5 days a week, for a 5 month period (n=16; 1.9+/-0.4 miles/day). A sedentary control group sat daily on immobile treadmills (n=8). Half of the runners had an additional sedentary period for 3 months at the end of the exercise period (n=8). In all groups, half of the monkeys were middle-aged (10-12 years old) and half were more mature (15-17 years old). Starting the fifth week of exercise training, monkeys underwent cognitive testing using the Wisconsin General Testing Apparatus (WGTA). Regardless of age, the exercising group learned to use the WGTA significantly faster (4.6+/-3.4 days) compared to controls (8.3+/-4.8 days; P=0.05). At the end of 5 months of running monkeys showed increased fitness, and the vascular volume fraction in the motor cortex in mature adult running monkeys was increased significantly compared to controls (P=0.029). However, increased vascular volume did not remain apparent after a 3-month sedentary period. These findings indicate that the level of exercise associated with improved fitness in middle-aged humans is sufficient to increase both the rate of learning and blood flow to the cerebral cortex, at least during the period of regular exercise.

High prevalence of subtle and severe menstrual disturbances in exercising women: confirmation using daily hormone measures.

BACKGROUND: The identification of subtle menstrual cycle disturbances requires daily hormone assessments. In contrast, the identification of severe menstrual disturbances, such as amenorrhea and oligomenorrhea, can be established by clinical observation. The primary purpose of this study was to determine the frequency of subtle menstrual disturbances, defined as luteal phase defects (LPD) or anovulation, in exercising women, with menstrual cycles of 26-35 days, who engage in a variety of sports, both recreational and competitive. Secondly, the prevalence of oligomenorrhea and amenorrhea was also determined via measurement of daily urinary ovarian steroids rather than self report alone. METHODS: Menstrual status was documented by daily measurements of estrone and pregnanediol glucuronide and luteinizing hormone across two to three consecutive cycles and subsequently categorized as ovulatory (Ovul), LPD, anovulatory (Anov), oligomenorrheic (Oligo) and amenorrheic (Amen) in sedentary (Sed) and exercising (Ex) women. RESULTS: Sed (n = 20) and Ex women (n = 67) were of similar (P > 0.05) age (26.3 +/- 0.8 years), weight (59.3 +/- 1.8 kg), body mass index (22.0 +/- 0.6 kg/m2), age of menarche (12.8 +/- 0.3 years) and gynecological maturity (13.4 +/- 0.9 years). The Sed group exercised less (P < 0.001) (96.7 +/- 39.1 versus 457.1 +/- 30.5 min/week) and had a lower peak oxygen uptake (34.4 +/- 1.4 versus 44.3 +/- 0.6 ml/kg/min) than the Ex group. Among the menstrual cycles studied in the Sed group, the prevalence of subtle menstrual disturbances was only 4.2% (2/48); 95.8% (46/48) of the observed menstrual cycles were ovulatory. This finding stands in stark contrast to that observed in the Ex group where only 50% (60/120) of the observed menstrual cycles were ovulatory and as many as 50% (60/120) were abnormal. Of the abnormal cycles in the Ex group, 29.2% (35/120) were classified as LPD (short, inadequate or both) and 20.8% (25/120) were classified as Anov. Among the cycles of Ex women with severe menstrual disturbances, 3.5% (3/86) of the cycles were Oligo and 33.7% (29/86) were Amen. No cycles of Sed women (0/20) displayed either Oligo or Amen. CONCLUSIONS: This study suggests that approximately half of exercising women experience subtle menstrual disturbances, i.e. LPD and anovulation, and that one third of exercising women may be amenorrheic. Estimates of the prevalence of subtle menstrual disturbances in exercising women determined by the presence or absence of short or long cycles does not identify these disturbances. In light of known clinical consequences of menstrual disturbances, these findings underscore the lack of reliability of normal menstrual intervals and self report to infer menstrual status.

Meal energy content is related to features of meal-related ghrelin profiles across a typical day of eating in non-obese premenopausal women.

UNLABELLED: Some features of the meal-related profile of ghrelin correspond to acute energy intake, suggesting a role in short-term energy homeostasis. Yet, no studies have examined this relationship across a typical day of eating when effects of time of day and or cumulative energy intake may also exist. AIM OF STUDY: To examine the relation between ghrelin and acute energy intake by quantifying changes in ghrelin over 24 hours in response to three typical meals and a snack occurring throughout the day. METHODS: Fourteen non-obese women consumed three meals and a snack at specific times; total ghrelin was measured repeatedly over 24 hours. RESULTS: Significant correlations existed between: 1) meal calories and the post-meal trough (r = - 0.36; p < 0.05), and 2) the sum of breakfast and lunch calories and subsequent dinner rise (r = - 0.45; p < 0.02) and 3) the sum of breakfast and lunch calories and dinner peak (r = - 0.54; p < 0.003). Thus, as energy intake increased across the day, pre-meal rises of subsequent meals were reduced. CONCLUSION: Meal-related profiles of ghrelin are not only associated with the energy content of specific meals, but also with the accumulated calories prior to a subsequent meal, suggesting a role in the modulation of acute energy homeostasis.

Acute effects of moderate intensity resistance exercise on bone cell activity.

Resistance exercise has positive effects on bone mass, but little is known about the mechanisms by which this occurs. The purpose of this study was to determine if a single bout of moderate intensity resistance exercise alters biochemical markers of bone cell activity. Indices of bone turnover were measured in nine healthy, untrained men (21.9 +/- 1.2 yrs old), before and following a single 45 minute session of resistance exercise, and during a control trial. A cross-over design was used so that all participants performed both trials in random order. Blood samples were collected immediately before, immediately after, and at 1, 8, 24, and 48 hours post exercise and analyzed for bone-specific alkaline phosphatase (BAP), type I collagen propeptide (PICP), and type I collagen N-telopeptide (sNTX). Urine from the second morning void was collected over four days (day before, day of, and two days following exercise) and analyzed for type I collagen N-telopeptide (uNTX). Exercise resulted in a significant increase (p < 0.05) in the ratio of biochemical markers of bone formation to bone resorption eight hours post exercise, largely due to a decrease in sNTX. Markers return to baseline within 24 hrs. These data suggest that moderate intensity resistance training acutely reduces bone resorption, leading to a favorable change in overall bone turnover, for at least 8 hours post exercise in untrained young men. Further work is needed to determine if long-term benefits to bone strength follow with persistent training.

Circulating ghrelin is sensitive to changes in body weight during a diet and exercise program in normal-weight young women.

Ghrelin is directly involved with short-term regulation of energy balance. Although circulating levels of ghrelin are elevated in anorexia nervosa and reduced in obesity, the role of ghrelin in regulating long-term energy balance in healthy women has not been investigated. We examined the effects of a 3-month energy deficit-imposing diet and exercise intervention on circulating ghrelin in normal-weight, healthy women. Body composition, resting metabolic rate, and serum ghrelin were measured at pre-, mid-, and postintervention in controls (n = 7), who performed no exercise, and exercising women who remained weight stable (n = 5) or lost weight (n = 10). Exercise training occurred five times per week, and subjects were fed a specific diet. Ghrelin significantly increased over time (770 +/- 296 to 1322 +/- 664 pmol/liter) in the weight-loss group compared with the controls and the weight-stable group (P < 0.05). Changes in ghrelin were negatively correlated with changes in body weight (r = -0.61; P < 0.05). Body fat, body weight, and resting metabolic rate significantly decreased in the weight-loss group before the increase in ghrelin. These findings suggest that ghrelin responds in a compensatory manner to changes in energy homeostasis in healthy young women, and that ghrelin exhibits particular sensitivity to changes in body weight.

The relationship of natural killer cell counts, perforin mRNA and CD2 expression to post-exercise natural killer cell activity in humans.

The aim of this study was to further investigate the mechanism of suppression of natural killer (NK) cell cytotoxic activity in peripheral blood following strenuous exercise. Blood was collected for analysis of NK cell concentration, cytotoxic activity, CD2 surface expression and perforin gene expression from runners (RUN, n=6) and resting controls (CONTROL, n=4) pre-exercise, 0, 1.5, 5, and 24 h following a 60-min treadmill run at 80% of VO2 peak. Natural killer cytotoxic activity, measured using a whole blood chromium release assay, fluctuated minimally in the CONTROL group and increased by 63% and decreased by 43% 0 and 1.5 h post-exercise, respectively, in the RUN group (group x time, P < 0.001). Lytic index (cytotoxic activity per cell) did not change. Perforin mRNA, measured using quantitative real-time polymerase chain reaction (QRT-PCR) decreased from pre- to post-exercise and remained decreased through 24 h. The decrease from pre- to 0 h post-exercise was seen predominately in the RUN group and was inversely correlated (r=- 0.95) to pre-exercise perforin mRNA. The NK cell surface expression of CD2 (lymphocyte function-associated antigen-2) was determined using fluorescent antibodies and flow cytometry. There was no change in the proportion of NK cells expressing CD2 or CD2 density. We conclude that (1) numerical redistribution accounted for most of the change in NK cytotoxic activity following a strenuous run, (2) decrease in perforin gene expression during the run was inversely related to pre-exercise levels but did not parallel changes in cytotoxic activity, and (3) CD2 surface expression was not affected by exercise.

Evidence for a causal role of low energy availability in the induction of menstrual cycle disturbances during strenuous exercise training.

Cross-sectional and short-term prospective studies in humans support the concept that low energy availability, and not other factors associated with exercise, causes the development of exercise-induced reproductive dysfunction. To rigorously test this hypothesis, we performed a longitudinal study, examining the role of low energy availability on both the development and the reversal of exercise-induced amenorrhea, using a monkey model (Macaca fascicularis). Eight adult female monkeys developed amenorrhea (defined as absence of menses for at least 100 d, with low and unchanging concentrations of LH, FSH, E2, and P4) after gradually increasing their daily exercise to 12.3 +/- 0.9 km/d of running over a 7- to 24-month period. Food intake remained constant during exercise training. To test whether amenorrhea is caused by low energy availability, four of the eight amenorrheic monkeys were provided with supplemental calories (138-181% of calorie intake during amenorrhea) while they maintained their daily training. All four monkeys exhibited increased reproductive hormone levels and reestablished ovulatory cycles, with recovery times for circulating gonadotropin levels ranging from 12-57 d from the initiation of supplemental feeding. The rapidity of recovery within the reproductive axis in a given monkey was directly related to the amount of energy that was consumed during the period of supplemental feeding (r = -0.97; P < 0.05). Repeated measurements of plasma T3 concentrations, a marker of cellular energy availability, revealed a tight correlation between the changes in reproductive function and T3 levels, such that T3 significantly decreased (27%) with the induction and significantly increased (18%) with the reversal of amenorrhea (P < 0.05). These data provide strong evidence that low energy availability plays a causal role in the development of exercise-induced amenorrhea.

Longitudinal changes in reproductive hormones and menstrual cyclicity in cynomolgus monkeys during strenuous exercise training: abrupt transition to exercise-induced amenorrhea.

Cross-sectional studies of exercise-induced reproductive dysfunction have documented a high proportion of menstrual cycle disturbances in women involved in strenuous exercise training. However, longitudinal studies have been needed to examine individual susceptibility to exercise-induced reproductive dysfunction and to elucidate the progression of changes in reproductive function that occur with strenuous exercise training. Using the female cynomolgus monkey (Macaca fascicularis), we documented changes in menstrual cyclicity and patterns of LH, FSH, estradiol, and progesterone secretion as the animals developed exercise-induced amenorrhea. As monkeys gradually increased running to 12.3 +/- 0.9 km/day, body weight did not change significantly although food intake remained constant. The time spent training until amenorrhea developed varied widely among animals (7-24 months; mean = 14.3 +/- 2.2 months) and was not correlated with initial body weight, training distance, or food intake. Consistent changes in function of the reproductive axis occurred abruptly, one to two menstrual cycles before the development of amenorrhea. These included significant declines in plasma reproductive hormone concentrations, an increase in follicular phase length, and a decrease in luteal phase progesterone secretion. These data document a high level of interindividual variability in the development of exercise-induced reproductive dysfunction, delineate the progression of changes in reproductive hormone secretion that occur with exercise training, and illustrate an abrupt transition from normal cyclicity to an amenorrheic state in exercising individuals, that is not necessarily associated with weight loss.

The role of exercise in the prevention and treatment of osteoporosis and osteoarthritis.

Osteoporosis and osteoarthritis are two distinctly different rheumatic conditions that target elderly, primarily female, populations. This article examines the scientific evidence supporting the use of exercise as a specific therapeutic modality, the general physiologic and psychological benefits of exercise, and the exercise programs currently recommended to combat these prevalent musculoskeletal disorders. Exercise is a valuable adjunct to treatment programs aimed at alleviating the risks and symptoms of osteoporosis and osteoarthritis. In addition to its potential impact on the disease processes themselves, exercise improves general health and well being, enhances quality of life, and preserves physical independence.

Effects of short-term strenuous endurance exercise upon corpus luteum function.

PURPOSE: The present study tested whether short-term, abruptly initiated training can cause corpus luteum dysfunction when exercise is limited to either the follicular or luteal phase of the cycle. METHODS: Reproductive hormone excretion and menstrual characteristics were studied in sedentary women who exercised only during the follicular (N = 5) or the luteal (N = 4) phase. Six women served as controls, three of whom exercised at a low volume and three who remained sedentary. Weekly progressive increments in exercise volume continued until either ovulation (follicular group) or menses (luteal group) occurred. Physical activity and nutrient intake were closely monitored with the intent to maintain body weight. RESULTS: No luteal phase disturbances occurred in any of the control subjects, whereas 40% of follicular and 50% of luteal exercisers experienced luteal defects. The proportion of menstrual cycles disrupted was not different between luteal and follicular exercisers (50% vs 30%, respectively) but was significantly greater than the proportion of cycles disrupted in control subjects (P < 0.05). CONCLUSIONS: These results suggest that exposure to abrupt onset of training can alter luteal function, regardless of the menstrual cycle phase in which exercise occurs. This study also demonstrates that a relatively low volume of exercise suffices to induce mild disturbances in luteal function.

Stimulation of luteinizing hormone secretion by food intake: evidence against a role for insulin.

In adult male rhesus monkeys, 1 day of fasting leads to a profound suppression of LH secretion that is rapidly reversed with refeeding. To test the hypothesis that changes in insulin secretion during fasting and refeeding mediate the changes in LH secretion, blood samples for LH measurement were obtained between 0900-2400 h from adult male rhesus monkeys (n = 9) on 1) a day when monkeys were refed their normal meal after a day of fasting, and 2) a day when monkeys were refed their normal meal, but endogenous insulin secretion was suppressed. Diazoxide (7.5-9.5 mg/kg.h) caused a 40-99% suppression of postmeal insulin secretion. However, no significant differences in LH pulse frequency, pulse amplitude, or mean serum LH levels were detected between control and diazoxide trials, even in animals in which insulin was markedly suppressed. Further, no correlation existed between the degree of insulin suppression and the magnitude of the meal-induced stimulation of LH. We conclude that meal-induced insulin secretion does not provide the stimulus mediating the meal-induced increase in LH secretion.

Strenuous exercise with caloric restriction: effect on luteinizing hormone secretion.

To test whether strenuous exercise with and without caloric restriction alters LH secretion, and whether these changes are apparent in the immediate post-exercise period, LH pulse parameters were studied in four moderately trained eumenorrheic women over three successive menstrual cycles. Blood samples were obtained 5 h before and 5 h after 90 min of running at 74% VO2max. Each test was preceded by a 7-d treatment of controlled diet and exercise (74% VO2max). During CONTROL, subjects were eucaloric on days 1-7, and performed no exercise on days 5-7. During STTI (short-term training increase), subjects were eucaloric and completed 90 min runs on days 5-7. During DIET/STTI, subjects consumed 60% of the calories necessary to maintain weight on days 1-7, and exercised as in STTI. A significant decrease in overall (0700-1830 h) LH pulse frequency during DIET/STTI compared with CONTROL and STTI treatments was observed. No changes were found in mean serum LH levels or peak amplitude. These results suggest that high-volume training combined with caloric restriction may predispose one to exercise-induced changes in LH pulse frequency, while adequate caloric intake may prevent these changes.