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C De Crée

Publications and source records attributed to C De Crée.

18 recordsLinked to original sources
PubMed2000

Interactions between homocyst(e)ine and nitric oxide during acute submaximal exercise in adult males.

Experimental studies investigating the effects of exercise on plasma total homocyst(e)ine (H[e]) levels in humans are almost non-existent. H(e) has been demonstrated to represent an independent risk factor for cardiovascular disease. The exact mechanism through which H(e) exerts its effects on the arteries is unknown but it is thought to involve nitric oxide (NO). The present study was designed to assess the effects of acute submaximal exercise on H(e) while levels of NO inhalation were manipulated using an air-filter mask. The study was completed by seven male volunteers, aged 21.6+/-1.3 yr (X+/-SD), VO2max: 48.6+/-7.6 mL x kg(-1) x min(-1). During two separate occasions the subjects performed a 1-hour bout of submaximal exercise on a stationary cycle ergometer at 60% of their VO2max. The two trials were completed in random order (with and without mask). Data were collected before (PRE) and after (POST) the acute exercise bouts. Plasma H(e) was directly measured by HPLC and NO by quantifying the enzymatic oxidation to nitrite (NO2-) & nitrate (NO3-). Mean H(e) concentrations were 10.89+/-2.05 nmol/mL (PRE) & 11.21+/-1.81 nmol/mL (POST) and were not significantly altered by submaximal exercise. When wearing a mask, the correlation of the PRE/POST H(e) differences with the PRE/ POST differences in NO3- were 0.77 (P=0.07). No correlation was found between either H(e) and NO2- or between NO2- and NO3-. However, a significant correlation (r= - 0.86, P= 0.03) was also observed between H(e) and NO2- but only for the post-exercise values when wearing a mask. The results suggest that: (1) plasma H(e) levels are not affected by acute submaximal exercise; (2) there is insufficient evidence to support the view that plasma H(e) levels are being mediated by NO during either rest or exercise.

Adult↗
PubMed1999

Influence of exercise and menstrual cycle phase on plasma homocyst(e)ine levels in young women--a prospective study.

Plasma total homocysteine (tHcy) has been identified as an independent risk factor for cardiovascular diseases (CVD). The difference in tHcy between the sexes has most often been related to the sex hormones, but also to a higher muscle mass in men. The purpose of this study was to assess the effects of acute exercise, brief exhaustive training, and menstrual cycle phase on circulating plasma tHcy concentrations. Fifteen untrained eumenorrheic women (mean age [+/-SD]: 18.7+/-0.4 yr, body fat: 25.8+/-3.4%, VO2max: 43.8+/-2.3 ml x kg(-1) x min(-1)) volunteered for the present study, which covered two menstrual cycles. During the second cycle the subjects participated in two exhaustive 5-day training programs on a cycle ergometer: one in the follicular (FPh) and one in the luteal phase (LPh). Pre- and posttraining plasma tHcy and total estrogen (E) responses were determined in blood samples obtained immediately before, during and immediately after incremental exercise to exhaustion. tHcy levels showed a large between-subject variation, but differences between FPh and LPh levels were consistent (P=0.063). Mean tHcy levels at rest were 9.44+/-1.65 micromol/L and 8.93+/-1.71 micromol/L during the FPh and LPh, respectively. Brief exhaustive training did not elicit any changes in plasma tHcy concentrations, although posttraining LPh E levels were lower (P<0.01). Overall, the differences between FPh and LPh values for tHcy and E were attenuated by training. Acute exercise increased plasma tHcy concentrations (P<0.001). At exhaustion, tHcy levels increased by 17% and 16% during the FPh and LPh, respectively. This was also significantly above tHcy levels at submaximal exercise (P=0.044). After a short period of training tHcy levels did not increase as much during acute exercise as they did before training; however, the increments were still significant (P=0.048). In conclusion, acute exercise in women produces significant increases in plasma tHcy concentrations, whereas brief exhaustive training does not significantly alter plasma tHcy levels. Our findings also suggest that plasma tHcy concentrations are menstrual cycle phase-dependent and that there is a close association between estrogen status and tHcy levels.

Adolescent↗
PubMed1998

Responsiveness of plasma 2- and 4-hydroxycatecholestrogens to training and to graduate submaximal and maximal exercise in an untrained woman. Interuniversity Project on Reproductive Endocrinology in Women and Exercise.

A single-subject experimental design was used to obtain some preliminary findings on the plasma responses of catecholestrogens (CE) to acute exercise and brief, but exhaustive training on a cycle ergometer. One previously untrained eumenorrheic female (body fat: 26% VO2max: 43.3 ml x kg(-1) x min[-1]) participated in this study. Resting CE levels were for "total" (unconjugated + conjugated) 2-hydroxyestrogens (2-OHE) 162pg/ ml and 350 pg/ml in the follicular (FPh) and luteal phase (LPh), respectively. Plasma total 4-hydroxyestrogen (4-OHE) levels were 41 pg/ml in the FPh and 66 pg/ml in the LPh. For "total" 2-methoxyestrogens (2-MeOE), we found 257 pgl/ml in the FPh and 374 pg/ml in the LPh. Resting levels of 2-hydroxy CE following a period of brief, intensive training were decreased during the LPh (2-OHE: -38%; 2-MeOE: -19%), whereas 4-hydroxy CE were unaffected. After training, the formation of CE as expressed by the 2-OHE:E and 4-OHE:E ratios, was increased by 75% and 200% at rest, respectively. CE activity or O-methylation, as estimated from the 2-MeOE:2-OHE ratio, was higher following training (FPh: +22%; LPh: +30%). During acute exercise before training, we observed a small rise proportional to the exercise intensity in the plasma "total" primary estrogen concentrations (FPh: +28%; LPh: +16%), and no changes in either 2-OHE or 2 MeOE levels. Plasma concentrations of 4-OHE, however, doubled during maximal exercise intensity. The 2-OHE:E and 2-MeOE:2-OHE ratios did not alter during incremental exercise. Training effects on acute exercise responses were only noticed for 4-OHE, which contrary to pre-training conditions, now progressively decreased. The major findings of this study are that in response to training: a) during rest, a greater proportion of CE are formed from a lower amount of precursor hormone, b) the rate of O-methylation of CE increases.

Adult↗
PubMed1998

Sex steroid metabolism and menstrual irregularities in the exercising female. A review.

This article aims to clarify why, and by which mechanisms, exercise may influence the normal menstrual cycle. Therefore, the vast amount of literature on this subject is reviewed and a critical appraisal of the most widespread hypotheses if offered. The strikingly low body mass which frequently accompanies exercise-related menstrual irregularities (ERMI) has led some authors to develop a hypothesis which postulates that a critical percentage of body fat is essential to trigger normal menstruation. The relevance of any reference to anorexia nervosa to support this view lacks consistency: female athletes differ in many ways from patients with anorexia nervosa, not least in their excellent physical status which is essential to deliver first-class performances. ERMI is not identical to the so-called female athlete triad, a complicated pathology that involves ERMI, premature osteoporosis and disordered eating. ERMI itself does not seem to have any substantial pathological effects as long as attention is paid to preventing osteoporosis or stress fractures which may result from prolonged hypo-estrogenaemia. In the female athlete with ERMI who wishes to conceive, the accompanying subfertility may necessitate a response other than a prompt reduction in training intensity, as this is hardly a first choice for any top athlete. During recent years, a number of prospective studies have greatly contributed to our understanding of the complexity of the mechanisms involved in ERMI. Older hypotheses, such as those considering hyperprolactinaemia as the cornerstone of ERMI, have now been firmly rejected. The present hypotheses emphasise the importance of caloric deficiency and limited energy availability, although they still fail to identify the actual mechanism that causes ERMI. There is, however, evidence that ERMI is produced by a disturbance of the hypothalamic gonadotrophin-releasing hormone oscillator. This disturbance is caused by either an insufficient estrogen or progesterone feedback or by an imbalance of local opioid peptide and catecholamine activities mediated by gamma-aminobutyric acid (GABA), corticotrophin-releasing hormone and insulin-like growth factor-1. More recent experiments have also linked ERMI with changes in steroid metabolism, in particular, an increasing activity of catecholestrogens possibly leading to enhanced intracerebral noradrenaline (norepinephrine) levels that may interfere with normal gonadotrophin release. This article demonstrates that the outcome of the many studies of ERMI is characterised by much controversy and numerous methodological flaws. The importance and complexity of some recent findings necessitate a comprehensive study which links older and newer findings within a critical perspective.

Adipose Tissue↗
PubMed1997

4-Hydroxycatecholestrogen metabolism responses to exercise and training: possible implications for menstrual cycle irregularities and breast cancer.

OBJECTIVE: To investigate the behavior of C4-substituted estrogens, the so-called catecholestrogens, in response to acute exercise and training. The 4-hydroxyestrogens are known to have both a strong estrogenic potency and affinity for catechol-O-methyltransferase (COMT), the enzyme that deactivates catecholamines. DESIGN: A prospective trial covering three menstrual cycles: a control cycle, a moderate training cycle, and a heavy training cycle. PARTICIPANT(S): Six untrained, healthy, eumenorrheic women (mean pretraining maximum oxygen uptake: 40.9 +/- 4.9 mL/kg per minute, body fat: 27.9% +/- 3.6%) volunteered for this study. INTERVENTION(S): An incremental exercise test to exhaustion on a cycle ergometer, in the follicular and luteal phases, before and after a brief but exhaustive training program. MAIN OUTCOME MEASURE(S): Hormone measurements included follicular and luteal phase plasma E2, LH, catecholamines, PRL, total unconjugated and conjugated estrogens, total 4-hydroxyestrogens (4-OHE), and 4-hydroxyestrogen-monomethylethers (4-MeOE). RESULT(S): Pretraining baseline 4-OHE levels were significantly higher in the luteal phase (66 +/- 9 pg/mL; mean +/- SEM) than in the follicular phase (51 +/- 7 pg/mL). Pretraining and post-training baseline 4-MeOE values were below minimal detection limits (< 35 pg/mL). During incremental exercise, catecholamines, PRL, E2, unconjugated and conjugated estrogens, 4-OHE, and 4-MeOE always increased (the increases in 4-OHE during exercise were more pronounced before training, contrary to the 4-MeOE being most increased after training). The baseline 4-MeOE:4-OHE ratio (a measure of catecholestrogen activity) significantly increased with progressive training. CONCLUSION(S): Because 4-OHE have been shown to be able to control the hypothalamic gonadotropin oscillator and to stimulate the luteolytic prostaglandin PGF2 alpha, the acute exercise-induced increases of 4-OHE and their positive correlation with lactate levels may indicate a key process in the pathogenesis of exercise-associated menstrual irregularities. In addition, 4-OHE, when insufficiently O-methylated, are known to be capable of raising mutagenic superoxide free radicals and causing DNA damage that may lead to breast cancer. The results of the present study also may be of significance for the apparent protective effects of sports participation against cancer of the breast.

Adult↗
PubMed1997

Exercise-induced changes in enzymatic O-methylation of catecholestrogens by erythrocytes of eumenorrheic women.

The present study was designed to assess the effects of acute exercise and short-term intensive training on catechol-O-methyltransferase (COMT) activity. COMT inactivates catecholamines and converts primary catecholestrogens (CE) into their O-methylated form yielding the 2- (2-MeOE) and 4-methoxyestrogens (4-MeOE). Blood samples were obtained from 15 previously untrained eumenorrheic women (mean +/- SE, VO2max: 43.8 mL x kg-1 x min-1 +/- 0.6) before and after a 5-d intensive training period, at rest and during incremental exercise. COMT activity was determined in the erythrocytes (RBC-COMT) after incubation of blood lysate with primary CE. The formation of both 2- and 4-MeOE was significantly higher (P < 0.05) during the luteal (LPh) than during the follicular phase (FPh). The amount of 2-MeOE formed (FPh: 4.2 +/- 0.2%; LPh: 4.9 +/- 0.2%) was significantly greater than the produced amount of 4-MeOE (FPh: 1.4 +/- 0.1%; LPh: 1.5 +/- 0.1%) (P < 0.05). Both before and after training, incremental exercise did not significantly alter RBC-COMT activity although we observed a trend for RBC-COMT activity increasing proportionally with the exercise intensity. After a brief period of exhaustive training, during rest the formation of 2-MeOE (FPh: +16.7%, LPh: +15.7%) and 4-MeOE (FPh: +28.6%; LPh: +40%) was significantly (P < 0.05) increased. The results of the present study are consistent with earlier findings reporting increased plasma concentrations of O-methylated CE following training. It is concluded that RBC-COMT activity is increased by brief intensive training, but not by acute exercise. We speculate that an increase in COMT-catalyzed O-methylation of CE may indicate that less COMT is available to deactivate norepinephrine.

Adolescent↗
PubMed1997

Plasma 2-hydroxycatecholestrogen responses to acute submaximal and maximal exercise in untrained women.

Exercise-induced menstrual problems are accompanied by an increase in catecholestrogen (CE) formation. It has been hypothesized that hypoestrogenemia may be secondary to an increased turnover from estrogens to CE, which then may disrupt luteinizing hormone release. In addition, the strong affinity of CE for the catecholamine-deactivating enzyme catechol-O-methyltransferase (COMT) has led to speculations about their possible role in safeguarding norepinephrine from premature decomposition during exercise. We investigated whether acute exercise on a cycle ergometer produces any changes in CE homeostasis. Nine untrained eumenorrheic women (body fat, 24.8 +/- 3.1%) volunteered for this study. Baseline plasma CE averages for total 2-hydroxyestrogens (2-OHE) were 218 +/- 29 (SE) pg/ml during the follicular phase (FPh) and 420 +/- 58 pg/ml during the luteal phase (LPh). 2-Methoxyestrogens (2-MeOE) measured 257 +/- 17 pg/ml in the FPh and 339 +/- 39 pg/ml in the LPh. During incremental exercise, total estrogens (E) increased, but 2-OHE and 2-MeOE levels did not significantly change in either phase. The 2-OHE/E ratio (measure of CE turnover) decreased during exercise in both menstrual phases, whereas the 2-MeOE/2-OHE ratio (correlates with COMT activity) did not significantly change. These findings suggest that there is insufficient evidence to conclude that brief incremental exercise in untrained eumenorrheic females acutely produces increased CE formation.

Adult↗
PubMed1997

Effects of a training program on resting plasma 2-hydroxycatecholestrogen levels in eumenorrheic women.

Catecholestrogens (CE) represent a major metabolic pathway in estrogen metabolism. Previous information on CE and training is limited to two cross-sectional studies that did not involve standardized training. Our purpose, by means of a prospective design, was to evaluate the effects of a brief, exhaustive training program on resting plasma concentrations of 2-hydroxy CE. The experimental design spanned two menstrual cycles; a control cycle and a training cycle. The subjects were nine previously untrained, eumenorrheic women [body fat: 24.8 +/- 1.0 (SE) %]. Data were collected during the follicular (FPh) and the luteal phases (LPh). Posttraining FPh and LPh tests were held the day after the last day of a 5-day period of training on a cycle ergometer. Total 2-hydroxyestrogens (2-OHE) averaged 200 +/- 29 pg/ml during the FPh and 420 +/- 54 pg/ml during the LPh (P < 0.05). Levels of total 2-methoxyestrogens (2-MeOE) were 237 +/- 32 pg/ml during the FPh and 339 +/- 26 pg/ml during the LPh (P < 0.05). After training, although the plasma levels of 2-OHE significantly decreased (21%; P < 0.05) during the LPh, the actual CE formation (as estimated from the 2-OHE-to-total estrogens ratio) increased (+ 29%; P < 0.05). CE activity, as expressed by the 2-MeOE-to-2-OHE ratio, showed significantly higher values in both phases (FPh, + 14%; LPh, + 13%; P < 0.05). At the same time, resting levels of norepinephrine (NE) were increased by 42% (P < 0.05). CE strongly inhibit biological decomposition of NE by catechol-O-methyltransferase (COMT). Results of the present study suggest that, in response to training, CE are increasingly competing with the enzyme COMT, thus preventing premature NE deactivation.

Adult↗
PubMed1997

Responses of catecholestrogen metabolism to acute graded exercise in normal menstruating women before and after training.

It has been hypothesized that exercise-related hypo-estrogenemia occurs as a consequence of increased competition of catecholestrogens (CE) for catechol-O-methyltransferase (COMT). This may result in higher norepinephrine (NE) concentrations, which could interfere with normal gonadotropin pulsatility. The present study investigates the effects of training on CE responses to acute exercise stress. Nine untrained eumenorrheic women (mean percentage of body fat +/-SD: 24.8 +/- 3.1%) volunteered for an intensive 5-day training program. Resting, submaximal, and maximal (tmax) exercise plasma CE, estrogen, and catecholamine responses were determined pre- and post training in both the follicular (FPh) and luteal phase (LPh). Acute exercise stress increased total primary estrogens (E) but had little effect on total 2-hydroxyestrogens (2-OHE) and 2-hydroxyestrogen-monomethylethers (2-MeOE) (= O-methylated CE after competition for catechol-O-methyltransferase). This pattern was not significantly changed by training. However, posttraining LPh mean (+/-SE) plasma E, 2-OHE, and 2-MeOE concentrations were significantly lower (P < 0.05) at each exercise intensity (for 2-OHE: 332 +/- 47 vs. 422 +/- 57 pg/mL at tmax; for 2-MeOE: 317 +/- 26 vs. 354 +/- 34 pg/mL at tmax). Training produced opposite effects on 2-OHE:E ratios (an estimation of CE formation) during acute exercise in the FPh (reduction) and LPh (increase). The 2-MeOE:2-OHE ratio (an estimation of CE activity) showed significantly higher values at tmax in both menstrual phases after training (FPh: +11%; LPh: +23%; P < 0.05). After training, NE values were significantly higher (P < 0.05). The major findings of this study were that: training lowers absolute concentrations of plasma estrogens and CE; the acute exercise challenge altered plasma estrogens but had little effect on CE; estimation of the formation and activity of CE suggests that formation and O-methylation of CE proportionately increases. These findings may be of importance for NE-mediated effects on gonadotropin release.

Adolescent↗
PubMed1995

Hypoestrogenemia and rhabdomyelysis (myoglobinuria) in the female judoist: a new worrying phenomenon?

It is now well established that strenuous engagement in aerobic endurance sports may cause menstrual problems and hypoestrogenemia-related phenomena, such as osteoporosis. The present study was designed to assess whether the competitive practice of female judoists produces specific physiological changes in menstruation and bone and muscle metabolism. A test group of 17 white female judoists (mean VO2max, 50.9 +/- 2.8 mL/kg.min; mean percent body fat, 16.3 +/- 3.3%), a reference group of oarswomen, and a group of sedentary women participated in this study. Specific metabolic parameters were determined before and after a heavy 5-week pre-Olympic training period. With regard to anthropometrical characteristics, after a period of intensive training, female judoists significantly differed (P < 0.05) from their pretraining values for percent body fat (-2.2%) and number of oligomenorrheic individuals (+28.4%). Mean baseline posttraining luteal phase plasma levels of estrone (78 +/- 26 pmol/L), estradiol (85 +/- 70 pmol/L), LH (7.6 +/- 2.8 IU/L), and progesterone (13.4 +/- 3.1 nmol/L) were significantly lower than those in both reference groups, although pretraining values did not significantly differ from those in a group of oarswomen. Luteal phase posttraining urinary parameters of muscular catabolism (3-methylhistidine, 367 +/- 30 mmol/day) and collagen turnover (hydroxyproline, 678 +/- 14 mumol/L) were significantly higher than those in a group of oarswomen (3- methylhistidine, 183 +/- 18 mmol/day; hydroxyproline, 196 +/- 21 micrograms/mL). Total plasma spontaneous monocyte interleukin-1 activity, an experimental parameter for bone turnover and formation, was significantly higher (P < 0.05) in both female judoists (15.8 +/- 3.0% max) and oarswomen (7.1 +/- 1.8% max) than in sedentary women (5.2 +/- 2.2% max). These findings were accompanied by a subjective feeling of musculotendinous soreness and fatigue. Posttraining values for blood diagnostic enzymes, such as creatinine phosphokinase, glutamic oxalacetic transaminase, lactic dehydrogenase, and uric acid exceeded 2-5 times maximal normal laboratory reference values. We believe that these overtraining-like findings should be further examined to study the eventual causal relationship between hypoestrogenemia and rhabdomyelysis (myoglobinuria) and to fully understand the extent of these results and their importance to the female athlete's health.

Adolescent↗
PubMed1991

Failure to induce ovulation with clomiphene citrate and bromocriptine in luteal deficient women athletes.

This study was designed with a three-fold aim: to assess ovarian function of women athletes with menstrual irregularities (AMI); to evaluate the potentiality of clomiphene citrate and bromocriptine for the induction of ovulation in these women; and to show that ultrasound scanning offers a suitable technique for ovarian screening in healthy and high-performance athletes. Our small test group consisted of 11 women, mainly track athletes, with AMI. There was no significant difference in age at menarche (13.2 yrs +/- 0.2), percent of ideal body weight (92% +/- 4), or percent of body fat (12.3% +/- 2.8) among the subjects. Plasma estradiol values were low (mean: 22 pg/ml +/- 0.8), as those of plasma progesterone (2.85 ng/ml +/- 2.10), LH (5.6 mIU/ml +/- 0.8), and prolactin (10.89 ng/ml +/- 5.56). The mean distance run per week (35 km +/- 15) was relatively high considering the presence of 4 non-runners. All menstrual irregularities were attributed to exercise. A short luteal phase (7 days +/- 1.5 for a cycle with a mean duration of 25 days +/- 1.8) was found in all subjects. We failed to observe the presence of a corpus luteum in 9 out of 11 women. A two-month administration of clomiphene citrate (150 mg/d for 5 days) or bromocriptine (2.5 mg/d) did not succeed in provoking ovulation in any of these women. Ultrasonographic observations showed a continuously hypo-estrogenic endometrium with a consecutively developing and regressive follicle. Our data emphasize the difficulties inherent in the restoration of menstrual function in women athletes with AMI. In addition, the usefulness of ultrasound in screening ovarian function was confirmed.

Adolescent↗
PubMed1990

The monitoring of the menstrual status of female athletes by salivary steroid determination and ultrasonography.

This study was designed to evaluate whether traditional plasma hormone determinations can be adequately replaced by measurements of salivary hormones. Eleven young sportswomen with menstrual irregularities attributed to strenuous physical exercise participated in this study. Mean body weight expressed as a percentage of ideal body weight was 92%, SD 4%. Their mean weekly training distance was 35 km, SD 15. Basal plasma endocrinological measurements revealed a hypo-oestrogenic status (mean plasma oestradiol values: 22 pg.ml-1, SD 8.8), and a deficient luteal phase (mean plasma progesterone: 2.9 ng.ml-1, SD 2.1). Pre-exercise salivary sex steroids were low. Salivary progesterone levels were 39.3 pg.ml-1, SD 9.5 (normal ranges in saliva: 25-60 pg.ml-1), salivary oestrone (E1) was 12.2 pg.ml-1, SD 2.3 (normal ranges in saliva: 7.5-25 pg.ml-1), and salivary oestradiol (E2) less than 1.9 pg.ml-1, SD 1.1 (normally 1.0-10.0 pg.ml-1). After a 21-km run, all salivary steroids appeared to increase. Mean salivary testosterone levels increased by 15.2% and salivary progesterone by 14.8%. Mean salivary oestrogens also increased (E1: +13.9%; E2: +21.1%). These findings confirm the results of earlier studies which found higher post-exercise plasma sex steroid levels. Since salivary measurements are believed to reflect non-protein-bound, thus free steroid levels, the results obtained by these techniques may provide a more realistic picture of the hormonal effects of physical exercise. In future, more accurate, cost-effective and easier techniques for salivary measurements may offer additional advantages.

Adolescent↗
PubMed1990

The possible involvement of endogenous opioid peptides and catecholestrogens in provoking menstrual irregularities in women athletes.

It is well known that women athletes engaged in strenuous physical exercise and endurance training may develop "athletic menstrual irregularities" (AMI). Although many studies have appeared dealing with the immediate endocrinological and physiological changes in these women, the underlying mechanisms have remained unknown to date. A number of hypotheses have been put forward, the most well-known among them, for example, defending the existence of a critical percent of body fat necessary to trigger or maintain normal menstruation. All these theories have, however, their own, sometimes numerous, methodological inaccuracies and a teleological way of investigation. Spectacular, and perhaps promising new developments concern the possible involvement of endogenous opioid peptides and catecholestrogens in these processes. In basal circumstances beta-endorphin, the most well-known endogenous substance with opiate-like activity, may decrease LH levels by suppressing hypothalamic GnRH. This phenomenon is, however, only observed during the estrogen-dominant late-follicular and mid-luteal phases. As for catecholestrogens, it appears essential to differentiate between, for example, the 2- and 4-hydroxy derivatives of both estrone and estradiol. While some of these catecholestrogens obviously seem to suppress LH levels, others seem to potentiate and induce the LH surge. In any case, similar to beta-endorphin, these activities of catecholestrogens appear to depend upon the essential presence of a sufficiently estrogenic environment. In addition, both endogenous opioid peptides and some of the catecholestrogens appear to be able to suppress prolactin release, probably by interfering with its inhibiting factor dopamine. Other effects of catecholestrogens may include the control of the luteolysis-potent prostaglandin F2 alpha. Although a number of studies have investigated the behaviour of beta-endorphin during and post-exercise, similar studies investigating catecholestrogens as to their relation to physical exercise are almost nonexistent. This, in association with the numerous methodological inaccuracies of various studies, makes it difficult to draw any firm conclusion. As to formulate new hypotheses, the only reasonable suggestion considers the possible existence of a complex feedback system including catecholestrogens and endogenous opioid peptides. Furthermore, recommendations made in this survey may be helpful in designing new, perhaps more firmly supported and appropriate future studies.

Adipose Tissue↗
PubMed1989

Endogenous opioid peptides in the control of the normal menstrual cycle and their possible role in athletic menstrual irregularities.

The remarkable morphinic capacities of endogenous opioid peptides give these agents particular and interesting properties. They can be found on different locations throughout the human body, where they bind to specific receptors. By means of various agonists and antagonists it was shown that endogenous opioids possibly play a prominent role in the control of hypophyseal secretions. The menstrual cycle is thought to represent one of the most important phenomena in which these agents are involved. In the presence of a steroid-sufficient environment (that is to say, in the luteal phase) beta-endorphin exerts a tonic inhibition on the secretion of GnRH and thereby on the LH-release. Moreover, the regulation of prolactin is probably under the control of endorphins interfering via dopamine (PIF). It becomes possible to explain a number of menstrual dysfunctions in this manner. The increased plasma concentrations of beta-endorphin, which are found after physical exercise, give rise to speculations as to their involvement in the frequently appearing menstrual irregularity in women athletes. The hypothesis proposing prolactin as being entirely responsible for these phenomena is unconvincing. We believe that endogenous opioid peptides could have a possible inhibitory effect on the GnRH-LH-axis. At this moment, methodological inaccuracies and differences of various studies make it very difficult to arrive at any firm conclusion.

Endorphins↗
PubMed1988

Suitability of cyproterone acetate in the treatment of osteoporosis associated with athletic amenorrhea.

The effectiveness of the antiandrogenic agent cyproterone acetate (CA) in its contraceptive form (2 mg CA + 50 micrograms ethinyl estradiol) in the treatment of osteoporosis associated with athletic amenorrhea was studied in seven high-performance athletes. Four women with similar characteristics served as controls. Their mean age was 21.9 years +/- 3.9. Training was started at a mean age of 14.0 years +/- 2.0. The mean training intensity expressed as kilometers run per week was 35 +/- 15. Mineral density was primarily affected by the hypoestrogenic status of these athletes (= 22 pg/ml +/- 8.8 in the midluteal phase). All participants showed low serum progesterone (= 2.85 ng/ml +/- 2.10) and LH profiles (= 5.6 mlU/ml +/- 0.8) during the midluteal phase. Cyproterone acetate was administered for 8 months to treat the increased bone loss in seven women athletes. Vertebral density appeared to be increased with 9.5% +/- 2.45% (mean +/- SD) while cortical base mineral content measured at the radius was not significantly changed. Our results demonstrate that cyproterone acetate administered in combination with estrogens provides a suitable therapeutic agent in the management of osteoporosis due to a hypoestrogenic status. This treatment could substitute other contraceptive agents. Moreover, women with the most severe estrogen deficiency showed a more pronounced reaction to this therapy.

Adolescent↗