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Clinical Endocrinology (2005) 63, 530–536
Adaptation of the hypothalamic-pituitary hormones during
intensive endurance training
T. Bobbert*†, L. Brechtel¶, K. Mai*†, B. Otto‡, C. Maser-Gluth§, A. F. H. Pfeiffer*†, J. Spranger*† and S. Diederich** *Department of Endocrinology, Diabetes and Nutrition, Charité University Medicine Berlin, Campus Benjamin Franklin, Berlin, †Department of Clinical Nutrition, Germany Institute of Human Nutrition Potsdam, Nuthetal, ‡Medical Department, University Hospital Innenstadt, Munich, §Steroid Laboratory, Department of Pharmacology, University of Heidelberg, Heidelberg, ¶Department of Sports Medicine, Humboldt University Berlin, Berlin, Germany, **Endokrinologikum Berlin, Centre for Endocrine and Metabolic Diseases Berlin, Germany (Received 18 April 2005; returned for revision 1 June 2005; finally revised 7 June 2005; accepted 25 August 2005) Objective Physical activity leads to changes in the hypothalamic-
pituitary hormonal system. However, acute and long-term adaptations
have not yet been precisely characterized. In this study, the changes
of the hormonal system as a result of marathon training and running
Introduction
a marathon were examined. In particular, we focused on adaptations Physical activity is known to induce various endocrine changes1,2 of the hypothalamic-pituitary-adrenocortical (HPA) axis, regarding such as an activation of the hypothalamic-pituitary-adrenocortical the activation or inactivation of cortisol to cortisone by the 11β- (HPA) system3–5 but varies between acute and long-term adapta- hydroxysteroid-dehydrogenase system (11β-HSD).
tions.6 In particular, relatively short-term intensive physical activity Design Patient measurements: 8 healthy women and 11 healthy
leads to increased plasma levels of glucocorticoids like cortisol. This men volunteered for this study. Blood samples, 24-h urine and a is apparently required to cope with the higher demand of energy as dexamethasone suppression test were analysed for metabolic a result of the acute stress, e.g. running a marathon.7 Data concerning and hormonal parameters at five different dates 12 weeks around long-term physical activity or endurance training are not conclusive.
In some studies it was suggested that chronic stress or physical training Results Cortisol and ACTH values decreased significantly 2 days
leads to a pseudo-Cushing’s syndrome with elevated cortisol levels after the marathon, whereas the activity of the whole body 11β-HSD-1 or insufficient suppression in the dexamethasone suppression test.8,9 was up-regulated. An increased suppression of cortisol levels was On the other hand there are also studies that showed a decrease in observed in the dexamethasone suppression test after 6 weeks of cortisol levels after long-term endurance training or competition.10,11 reduced training levels. Ghrelin was elevated 2 days after the marathon.
Furthermore, in some studies no changes in cortisol metabolism Only minor changes in the other hypothalamic-pituitary-hormonal were found.12 In addition to the mechanism of the cortisol synthesis axes could be observed. However, the free androgen index increased or production in response to exercise, there is no information about significantly after 6 weeks of reduced training.
the activation or inactivation of cortisol to its inactive metabolite, Conclusions The HPA system appeared to become chronically
cortisone, by the 11β-hydroxysteroid-dehydrogenase system (11β- activated by continuous physical training and therefore less sensitive HSD).13,14 The NADP+/ H-dependent 11β-HSD type 1 (11β-HSD-1) to the dexamethasone suppression test. The acute stress of the mar- enzyme functions in vitro as a bidirectional oxidoreductase and athon led to a central exhaustion of the HPA system with a paracrine is expressed ubiquitously. In vivo, 11β-HSD-1 acts mainly as a counteraction by the activation of the 11β-HSD system. Changes in reductase and activates inactive cortisone to cortisol. Thereby it is the other hypothalamic-pituitary hormonal axes were the result of believed that 11β-HSD-1 modulates intracellular concentrations of long-term differences in training levels and were not altered by the active glucocorticoids and occupancy of the glucocorticoid-receptor.
The main function of 11β-HSD-2 is the protection of the unselectivemineralocorticoid receptor, which has similar affinity to cortisol andaldosterone. This isoenzyme converts large amounts of cortisol toinactive cortisone, thus allowing the less concentrated aldosterone Correspondence: Thomas Bobbert, Department of Endocrinology, Diabetes to bind to the mineralocorticoid receptor.
and Nutrition, Charité University Medicine Berlin, Campus Benjamin Besides the changes in glucocorticoid secretion and metabolism Franklin, Hindenburgdamm 30, 12200 Berlin, Germany. Tel.: +4930/8445 4125; Fax: +4930/8445 4204. E-mail: [email protected] following physical activity, the response of other hypothalamic-pituitary Endurance training and pituitary hormones hormones to endurance training are still not clear. The changes C-reactive protein (CRP). The volunteers received 1 mg dexametha- in the growth hormone /insulin-like growth factor-I (GH / IGF-I) sone, which they were asked to take at 12:00 h on the same day. At axis as a result of endurance training seem to depend on many 8:00 h of the second day, blood samples were taken for cortisol and factors. Short-term activity leads to an increase of GH, IGF-1 and IGF-BP3,15,16 whereas there is little information about chronic phys-ical activity. In elderly men, no differences in IGF-I, GH and IGF- BP3 levels were found between endurance-trained and normal men.
However, IGF-BP1/2 levels were slightly different in both groups.17 After sampling in ethylenediaminetetraacetic acid or serum tubes, A recently discovered hormone, with strong GH-releasing prop- blood was immediately chilled on ice and centrifuged; aliquots were erties, is ghrelin.18 Ghrelin, a 28-amino acid peptide, is produced by frozen at −20 °C until assayed. Blood samples were analysed for cor- the enterocrine cells of the gastric mucosa. It is the natural ligand tisol, ACTH, testosterone, SHBG, LH, FSH, IGF-1, IGF-BP3, TSH, of GH secretagogue receptor and stimulates GH secretion more fT4 by the full automatic chemiluminiscence-immunoassay system potently than GH-releasing hormone (GHRH).19 In addition, ghrelin IMMULITE from DPC Biermann (Bad Nauheim, Germany). Free also stimulates the release of corticotropin releasing hormone androgen index was calculated by FAI = testosterone × 100/SHBG.
(CRH), vasopressin, ACTH, cortisol, prolactin and aldosterone,19–21 CRP was measured with COBAS MIRA from Roche (Lörrach, whereas its own secretion seems to be inhibited by somatostatin.22,23 Germany). Free cortisone, free cortisol, tetrahydrocortisol (THF), Short-term exercise did not lead to changes in ghrelin levels.24 The αTHF and tetrahydrocortisone (THE) concentrations in 24-h urine effects of prolonged exercise are unknown.
samples were analysed by RIA.25 11β-HSD-1 activity was calculated by The aim of this study was to assess the adaptations of the the ratio (THF + αTHF)/THE, and 11β-HSD-2 activity by the ratio hypothalamic-pituitary hormonal system to endurance training and Plasma ghrelin was analysed in all samples from individual sub- jects in duplicate in the same assay. Immunoreactive total humanplasma ghrelin was measured by RIA (Phoenix Pharmaceuticals, Materials and methods
Mountain View, CA, USA). Intra- and interassay CV was 5·3% and13·6%, respectively.26 Eight healthy women between 26 and 55 years old and 11 healthy men between 30 and 66 years old volunteered for this study. The BMIwas 21·6 ± 1·1 kg/m2 and 24·0 ± 1·6 kg/m2 for the female and for the Statistical calculations were performed with  11·0 (SPSS Inc., male athletes, respectively. The VO max was 42·9 ± 2·1 ml/kg for the female athletes and 48·3 ± 1·8 ml/kg * min for the male All values are given as mean value and standard error. Paired athletes. A training log over the whole study period of 12 weeks was analysis was performed by Wilcoxon test. An alpha-error below 5% carried out by each runner. All volunteers trained the whole time in was considered statistically significant.
Berlin at an altitude of about 80 m above sea level and all participantswere requested not to change nutritive behaviour.
All volunteers were screened for serious health problems or use of any drugs by interview, and an examination was performed by an In the time before the marathon, there was a significantly higher experienced sports physician. The experimental protocol was training level (date 2: 57·5 ± 4·3 km/week, date 4: 20·5 ± 4·0 km/ approved by the institutional review board, and all subjects gave week, P < 0·05), which is shown by the number of kilometres per week (Fig. 1). The 42.195 kilometres of the marathon are notincluded in training amounts at date 3 (28·44 ± 5·1 km/week).
The data for ACTH and cortisol are shown in Fig. 2. There was a significant decrease of ACTH (date 1: 21·5 ± 2·1 ng/l, date 3: 16·7 ± Metabolic parameters were analysed at five different dates around 1·4 ng / l, date 5: 23·3 ± 3·2 ng/ml, P < 0·05) and cortisol (date 1: 483·5 ± 37·0 nmol/l, date 3: 370·7 ± 25·8 nmol/l, date 5: 446·6 ± 43·3 nmol / l, P < 0·05) 2 days after the marathon, but no differences were observed in relation to high and low training levels. All ACTH Date 3: 2 days after real,- Berlin marathon and cortisol values were in the physiological normal range.
The results of the dexamethasone suppression test showed signi- ficantly lower levels of cortisol 6 weeks after the marathon with lower The participants came at 2 days between 8:00 and 9:00 h for blood training levels (Fig. 3). Significant differences were seen only in date withdrawal. Before the first day they also collected urine for 24 h. At 5 (date 1: 40·2 ± 4·5 nmol/l, P = 0·008, date 5: 31·6 ± 3·7 nmol/l, date 1, blood samples were taken for basal values of cortisol, ACTH, P = 0·037). No differences were found in relation to the marathon total testosterone, sex hormone binding globulin (SHBG), LH, FSH, insulin-like growth factor-1 (IGF-1), insulin-like growth factor- Values for 11β-HSD-1 activity and 11β-HSD-2 activity are shown binding protein 3 (IGF-BP3), TSH, free thyroxine (fT4), ghrelin and in Fig. 4. Whereas the activity of the 11β-HSD-2 appeared to 2005 Blackwell Publishing Ltd, Clinical Endocrinology, 63, 530–536
Fig. 1 Kilometres per week between the five examinations (date 1: 6 weeks
Fig. 3 Cortisol after 1 mg dexamethasone suppression test. Significant
before marathon, date 2: 10 days before marathon, date 3: 2 days after real,- changes were marked with brackets. (date 1: 6 weeks before marathon, Berlin marathon (training amounts did not include the 42.195 kilometres date 2: 10 days before marathon, date 3: 2 days after real,- Berlin marathon, of the marathon), date 4: 10 days after marathon, date 5: 6 weeks after date 4: 10 days after marathon, date 5: 6 weeks after marathon).
marathon). After the marathon there was a significant decrease in running intensity (P < 0·05).
Fig. 2 Changes of ACTH and cortisol levels in relation to the marathon.
Fig. 4 Activity of HSD 1(circles) and HSD 2 (squares) in 24-h urine.
Significant changes (P < 0·05) in relation to date 3 (2 days after marathon) Significant changes in relation to date 3 (2 days after marathon) were marked were marked with * (date 1: 6 weeks before marathon, date 2: 10 days before with brackets. (date 1: 6 weeks before marathon, date 2: 10 days before marathon, date 3: 2 days after real,- Berlin marathon, date 4: 10 days after marathon, date 3: 2 days after real,- Berlin marathon, date 4: 10 days after marathon, date 5: 6 weeks after marathon).
marathon, date 5: 6 weeks after marathon).
be unaffected, the activity of the 11β-HSD-1 was significantly higher 3: 141·0 ± 8·8 µg/l, P = 0·036) and IGF-BP3 (date 3: 3·7 ± 0·2 mg/l, 2 days after the marathon (date 2: 1·18 ± 0·09, P = 0·013, date 4: date 5: 4·2 ± 0·2 mg/l, P = 0·045).
Ghrelin levels were basically not different during the study (Fig. 5).
Thyroid-stimulating hormone was significantly lower 6 weeks Only in relation to 6 weeks after the marathon was there a slight differ- after the marathon (date 1: 1·13 ± 0·2 mU/l, date 5: 1·03 ± 0·16 mU/l, ence (date 3: 588·4 ± 51·8 ng/l, date 5: 512·17 ± 41·8 ng/l, P = 0·031).
P = 0·024), but free T4 showed no significant changes (date 1: 22·5 ± Changes in sex hormones were studied only for men, because of 0·8 pmol / l, date 5: 23·3 ± 0·7 pmol/l, P = 0·205). TSH and fT4 values different cycle times in female volunteers. In male volunteers, no were in the physiological normal range, but TSH was in a lower normal changes were observed for LH and FSH (data not shown). However, range, whereas fT4 was in the high normal range at all time points.
there was a significant increase from all dates to date 5 of the free IGF-1 and IGF-BP3 were also unaltered in the observed 12 weeks androgen index (FAI) (date 1: 38·3 ± 3·4, date 2: 41·7 ± 3·3, date 3: (IGF-1: date 1: 132·1 ± 8·7 µg/l, date 3: 141·2 ± 8·8 µg/l, date 5: 46·0 ± 6·4, date 4: 51·1 ± 3·4, date 5: 58·9 ± 9·5, P < 0·05), which was 147·9 ± 11·5 µg/l, P > 0·05; IGF-BP3: date 1: 4·1 ± 0·2 mg/l, date 3: calculated by testosterone (date 1: 15·4 ± 1·5 nmol/l, date 2: 16·2 ± 4·0 ± 0·1 mg/l, date 5: 4·3 ± 0·2 mg/l, P > 0·05). Only in men did we 1·3 nmol / l, date 3: 17·3 ± 1·6 nmol/l, date 4: 19·4 ± 1·8 nmol/l, date find a significant increase of IGF-1 (date 1: 126·7 ± 9·0 µg/l, date 5: 21·8 ± 2·9 nmol/l) and SHBG values (date 1: 40·0 ± 4·5 nmol/l, 2005 Blackwell Publishing Ltd, Clinical Endocrinology, 63, 530–536
Endurance training and pituitary hormones Fig. 5 Plasma samples were taken at all five dates in the morning and were
Fig. 7 CRP levels at all dates. CRP at date 3 (2 days after the marathon)
analysed for ghrelin. Significant changes were marked with brackets. (date was significant higher compared with all other dates. (date 1: 6 weeks before 1: 6 weeks before marathon, date 2: 10 days before marathon, date 3: 2 days marathon, date 2: 10 days before marathon, date 3: 2 days after real,- after real,- Berlin marathon, date 4: 10 days after marathon, date 5: 6 weeks Berlin marathon, date 4: 10 days after marathon, date 5: 6 weeks after lower basal cortisol levels after endurance training.10,11 In this studyno changes in basal cortisol or ACTH basal levels between a hightraining status (at date 1 or 2) and a low training status (at date 4or 5) were found. However, there was a trend to an up-regulationof the HPA system, because the dexamethasone suppression test,which is an indicator for the sensitivity of the HPA system, showedsignificant lower levels of cortisol after 6 weeks of lower traininglevels in relation to high training levels. In combination with theresults of unaltered basal cortisol levels, it seems that the sensitivityof the HPA axis is changed. At a training status with an elevated train-ing amount, the HPA axis is more resistant to dexamethasone thanin a moderate training status with only a few kilometres per week.
Similar results were found in a cross-sectional study performed inendurance-trained and untrained men, although a dexamethasone-CRH test was applied in this study.9 It is also known that the tissue Fig. 6 For all male volunteers, free androgen index was calculated by
sensitivity to glucocorticoids in endurance-trained men is decreased.27 testosterone × 100/SHBG. FAI at date 5 (6 weeks after marathon) was Changes in sensitivity to glucocorticoids may explain the discrep- significantly higher compared with all other dates. (date 1: 6 weeks before ancy between repeated and prolonged exercise-induced HPA axis marathon, date 2: 10 days before marathon, date 3: 2 days after real,- Berlin activation and the lack of metabolic consequences of such increased marathon, date 4: 10 days after marathon, date 5: 6 weeks after marathon).
We found reduced plasma levels of cortisol and ACTH 2 days after date 2: 39·1 ± 4·5 nmol/l, date 3: 37·4 ± 4·3 nmol/l, date 4: 37·9 ± 4·4 the marathon. This was probably an acute effect of the marathon and nmol / l, date 5: 37·4 ± 4·3 nmol/l) (Fig. 6).
not related to training changes. The results suggest that the extreme We also aimed to detect general inflammation or possible infec- physical stress of the marathon7 causes a short-term exhaustion of tions. Therefore, CRP was measured at all time points (Fig. 7). There was a significant increase of CRP in the physiological normal range As a result of the exhaustion of the ACTH-cortisol axis after the 2 days after the marathon (date 3: 5·4 ± 0·6 mg/l, P < 0·005).
marathon, the tissues expressing 11β-HSD-1 may regulate cortisolmetabolism against the low-circulating cortisol levels. Indeed, theactivity of the 11β-HSD-1 was increased 2 days after the marathon, Discussion
whereas the activity of the 11β-HSD-2 was slightly reduced. Thus, In this study, the effects of intensive endurance training on the the impaired sensitivity of the systemic HPA axis appears to be coun- hypothalamic-pituitary axis were examined.
terbalanced by increased availability of cortisol by increased local Previous reports suggested that endurance training is associated activation from cortisone to the more active cortisol. Similar results with subclinical hypercortisolism,3,8 whereas others reported even are found in the circadian rhythm of the 11β-HSD activity. Low 2005 Blackwell Publishing Ltd, Clinical Endocrinology, 63, 530–536
cortisol values at midnight are maybe compensated by a higher activ- androgen index (FAI) was significantly higher after reduction of endurance exercise. Changes in testosterone values through physical Generally, CRP levels were relatively low in the investigated indi- activity depend of the kind of training. Lower testosterone levels have viduals, which was probably to the result of the ongoing endurance been shown in endurance-trained men compared with sedentary training.29,30 The extreme physical stress during the marathon caused controls,41,42 whereas resistance-trained persons seem to have higher a substantial increase of CRP values as detected 2 days after the race.
basal testosterone levels.43,44 Thereby endurance- and resistant- Although elevation of CRP usually indicates an ongoing systemic trained persons had lower testosterone levels than sedentary control inflammatory reaction31 we found no elevated cortisol levels like subjects.45 It is also known that high cortisol levels, e.g. in patients that found in ill persons.32 Interestingly, there were no differences with Cushing’s syndrome, lead to a suppression of the gonadal axis between high and low training levels. However, the time periods with the with lowered values for testosterone.46 The present study supports respective training levels may have been too short to see any changes.
the previously found results. Thereby this lowered testosterone level Although there was a trend towards higher ghrelin levels directly does not seem to induce pathological reactions like decreased bone after the marathon, no dramatic differences were seen. This result is density47 or decreased physical fitness.48 Furthermore, testosterone in line with a recent publication showing that acute exercise does not concentrations have been shown to increase after an acute bout change circulating ghrelin levels in humans.24 The slightly increased of resistance or endurance exercise.49,50 In response to prolonged ghrelin levels 2 days after the marathon could be still a sign of a negative endurance exercise (e.g. running a marathon), testosterone levels energy balance after the marathon, which is known to induce higher will typically decline.51,52 In this study, the time after the marathon (2 days) was probably too long to see any acute changes resulting The changes of IGF-1 and IGF-BP3 were not significant, but there was a trend towards increasing levels of IGF-1 and IGF-BP3 during In summary, this study has shown acute and prolonged changes lower training levels. However, these findings are only significant in in pituitary hormone axes as a result of marathon training and run- men, but not in women. One year of endurance training above the ning a marathon. In particular, the adaptations in the HPA system lactate threshold has been shown to cause an increase in basal 24-h showed decreased levels of cortisol after the marathon and decreased pulsatile GH release.35 Interestingly, subjects training below the lac- sensitivity of glucocorticoid-regulation during a stage of high training tate threshold did not show any change in the GH release, indicating intensity. Furthermore, cortisol metabolism by the 11β-HSD system is that training intensity may be important in regulating the GH axis.
altered after the marathon. Concerning the acute down-regulation Therefore, the study group was perhaps too inhomogeneous to see any of ACTH and cortisol after the marathon, further studies with differences in the hypothalamic-pituitary-growth hormone axis.
dynamic testing (CRH test, metyrapone test) would be interesting.
We found no acute effect 2 days after the marathon, whereas otherstudies have shown that IGF-1 and IGF-BP3 increase after acute Acknowledgements
exercise.36,37 However, the duration of the postexercise elevation ofIGF-1 and IGF-BP3 might be short and we thus might have missed We thank Petra Exner and Katrin Sprengel for excellent technical a peak directly after the marathon. Additionally in our study, all assistance. JS was supported by the BMBF (0313036B), the Eli-Lilly investigated individuals had a relatively high training status and the International Foundation (ELIF21001) and the German Diabetes IGF-1/IGF-BP3 levels might have reached a relative plateau, explain- Association (DDG021006). We thank also the real,- Berlin marathon ing that there was no additional increase after the acute exercise.
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