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Heat Exposure Elevates Plasma Immunoreactive Growth Hormone-Releasing Hormone Levels in Man*
Abstract
The effects of heat exposure on plasma levels of GH and GHRH were studied in six younger (31-46 yr) and six older (49-66 yr) normal men. For the GHRH RIA, 2-mL plasma samples were purified on Sep-Pak C18 cartridges, from which the mean recovery of synthetic GHRH-(1-44) was 62 +/- 10% (+/- SD; n = 8). Heat exposure (15 min) in a Finnish sauna bath at an ambient temperature of 72 C, led to an increase in plasma GH levels from 2 to 5 micrograms/L (P less than 0.01) at 30 min in the younger men. Their rectal temperature had risen by 0.2 C at 15 min. Plasma immunoreactive GHRH increased from 9 to 36 ng/L (P less than 0.05) 5 min after heat exposure, and it gradually fell to the initial levels by 45 min. The older men did not have a significant increase in plasma GH or GHRH levels in response to the heat exposure. Reverse phase high pressure liquid chromatography studies of plasma immunoreactive GHRH suggested that the major circulating GHRH immunoreactivity was GHRH-(1-40). We conclude that heat exposure-stimulated GH release in young adult men is mediated by GHRH, but in older men, GHRH and GH responses do not occur.
... specifically stimulates G H release in normal men (3)(4)(5) and it has been shown that increases in circulating concentrations of ir-GHRH are followed by GH release in some physiologic situations (6,7). However, only a little is known about the role of GHRH in the generation of the nocturnal rhythm of GH secretion. ...
... All samples from an individual child were analyzed in the same assay. Plasma ir-GHRH concentrations were measured by RIA as described in detail previously (6). Two mL of plasma were extracted using Sep-pak C 18 cartridges (Waters Inc., Milford MA). ...
... The eluate was evaporated and the residual assayed using a rabbit antiserum specific for the mid portion of GHRH and '251-GHRH 1-40 as tracer (1 8). Our HPLC analyses have shown that the major ir-GHRH species in the plasma samples eluates as synthetic human GHRH 1-40 (6). The sensitivity of the assay was 1 pg/tube. ...
To evaluate the role of growth hormone-releasing hormone (GHRH) in the physiologic release of growth hormone (GH) we studied the nocturnal secretion of immunoreactive GHRH (ir-GHRH) and its relationship to GH release and various stages of sleep in six prepubertal (three boys) and six pubertal children (two boys) with normal stature. Their ages ranged from 8.1 to 14.9 yr and their bone ages from 6.8 to 14.8 yr. Blood was withdrawn continuously between 2200-0600 h at a constant rate of 5 mL/20 min. The EEG was simultaneously registered. The ir-GHRH and GH data were analyzed by a discrete-pulse detection algorithm (Pulsar). The number of nocturnal ir-GHRH pulses varied from 0-8 (median 7) and the number of GH peaks from 2-6 (median 3). Pubertal children had significantly more (p less than 0.05) ir-GHRH pulses and the pulse amplitude was higher (p less than 0.05) than in the prepubertal children. There were no significant differences in the GH parameters between the two groups. The ir-GHRH peaks were not significantly related to any specific sleep stage. The majority of the GH pulses (71%) were associated with slow wave sleep (p less than 0.001). Two-thirds (69%) of the GHRH peaks preceded closely or coincided with GH pulses (p less than 0.02). Pubertal subjects had more isolated ir-GHRH peaks than prepubertal children (p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)
... They reported in the experimental group of 10 subjects the decrease in dynamic leg press 1-repetition maximum (RM) performance but no change in dynamic bench press 1RM, whereas no decrease muscular power in vertical jump. Sauna bathing has been reported to elevate serum levels of GH to 2-to 5-fold right after the sauna bath (4,18,21,22,32). Acute effects of sauna bathing (80-100°C) on serum cortisol levels are somewhat contradictory. ...
... Therefore, all the subjects were analyzed as one group in the GH 22kD analysis. Serum GH 22kD elevated significantly after 3 exercise loadings in MID and in all loadings including the sauna bath alone in POST, which supports the previous findings so that both the exercise (10,35) and sauna bath (18,21,22,32) can stimulate the anterior pituitary gland to secrete the GH 22kD pulse. Possible long-term effects of frequent sauna bathing on body composition, GH 22kD basal levels, and acute GH 22kD responses after the sauna may be interesting aspects to study in the future. ...
Rissanen, JA, Häkkinen, A, Laukkanen, J, Kraemer, WJ, and Häkkinen, K. Acute neuromuscular and hormonal responses to different exercise loadings followed by a sauna. J Strength Cond Res XX(X): 000-000, 2019-The purpose of this study was to investigate acute responses of endurance (E + SA), strength (S + SA), and combined endurance and strength exercise (C + SA) followed by a traditional sauna bath (70˚C70˚C, 18% relative humidity) on neuromuscular performance and serum hormone concentrations. Twenty-seven recreationally physically active men who were experienced with taking a sauna participated in the study. All the subjects performed a sauna bath only (SA) first as a control measurement followed by S + SA and E + SA (paired matched randomization) and C + SA. Subjects were measured PRE (before exercise), MID (immediately after exercise and before sauna), POST (after sauna), POST30min (30 minutes after sauna), and POST24h (24 hours after PRE). Maximal isometric leg press (ILPF max) and bench press (IBPF max) forces, maximal rate of force development (RFD) and countermovement vertical jump (CMVJ), serum testosterone (TES), cortisol (COR), and 22-kD growth hormone (GH 22kD) concentrations were measured. All exercise loadings followed by a sauna decreased ILPF max (29 to 215%) and RFD (220 to 226%) in POST. ILPF max , RFD, and CMVJ remained at significantly (p # 0.05) lowered levels after S + SA in POST24h. IBPF max decreased in POST in S + SA and C + SA and remained lowered in POST24h. SA decreased ILPF max and IBPF max in POST and POST30min and remained lowered in ILPF max (24.1%) at POST24h. GH 22kD , TES, and COR elevated significantly in all loadings measured in the afternoon in MID. SA only led to an elevation (15%) in TES in POST. The strength exercise followed by a sauna was the most fatiguing protocol for the neuromuscular performance. Traditional sauna bathing itself seems to be strenuous loading, and it may not be recommended 24 hours before the next training session. A sauna bath after the loadings did not further change the hormonal responses recorded after the exercise loadings.
... (17,18). No difference in initiated before temperatures existed in the women, suggesting the subjects had not experienced the menstrual temperature elevation and thus not confounded our results (10,23,24). This is important as shifting to a different menstrual cycle phase may also effect of secretion hormones especially if under thermal stress exposure (23). ...
... Specifically, ACTH increased by 80% after the first sauna bath, and by 40% after the last one. However, several Scandinavian authors observed a smaller increase of ACTH after heat exposure in sau- (10,23,24). On the other hand, non-Scandinavian authors observed that ACTH increased as much as 90-350% after sauna bath exposure, more in agreement with our data (9,13,25). ...
Introduction: The physiological responses to single and repeated hyperthermia exposure in men are well described in the literature, but less information is available on the effects of repeated thermal exposure in women. Aim of the study: The purpose of this study was to investigate the influence of single and repeated sauna exposure on selected endocrine responses in women. Methods: Ten healthy, eumenhorreic, female volunteers (19-21 yr old) were exposed to sauna bath seven times every second day. In all women the experiment started in the early follicular phase. Results: Body mass decreased by 0.68 kg and by 0.67 kg after the first and the last sauna respectively. Rectal temperature increased by 1.1°C and 0.8°C after the first and the last heat exposure. Plasma volume decreased by 4.6% after the first sauna, and by 6.1% after the last one. Statistically significant decrease in plasma T 3 concentration was observed after the last sauna exposure, whereas more than a threefold increase in hGH was observed after the first and more than twofold increase was noted after the last sauna. There were significant increases in ACTH and cortisol after each sauna bath, however the rise in these hormones was less pronounced after the last sauna. Conclusion: Less pronounced changes in core temperature as well as in the level of stress hormones may be the evident of adaptation to the thermal stress in women similar to that seen in men.
... Prolactin facilitates maternal adaptation to pregnancy and stimulates lactation postnatally, whilst GH promotes linear growth in childhood and might also increase cellular senescence in adulthood 33,34 . In sauna and warm water immersion studies in healthy human volunteers, exposure to temperatures in the range 44-85 °C acutely increased plasma concentrations of prolactin, whereas increases in plasma levels of GH occurred in younger but not older men [35][36][37] . Increases in prolactin and GH might form part of the stress response to heat exposure. ...
Climate change is increasing both seasonal temperatures and the frequency and severity of heat extremes. As the endocrine system facilitates physiological adaptations to temperature changes, diseases with an endocrinological basis have the potential to affect thermoregulation and increase the risk of heat injury. The effect of climate change and associated high temperature exposure on endocrine axis development and function, and on the prevalence and severity of diseases associated with hormone deficiency or excess, is unclear. This Perspective summarizes current knowledge relating to the hormonal effects of heat exposure in species ranging from rodents to humans. We also describe the potential effect of high temperature exposures on patients with endocrine diseases. Finally, we highlight the need for more basic science, clinical and epidemiological research into the effects of heat on endocrine function and health; this research could enable the development of interventions for people most at risk, in the context of rising environmental temperatures.
... The two anterior pituitary hormones with the most consistent responses during exposure to sauna are GH and PRL. GH increase has been documented in numerous studies [5,9,15]. Leppäluoto et al. [16] documented that the GH response was under control of the hypothalamic GH-releasing hormone (GHRH). ...
Sauna bath brings about numerous acute changes in hormone levels, partly akin to other stressful situations, partly specific for sauna. Norepinephrine increases in those accustomed to sauna bath. Sweating increases the production of antidiuretic hormone, and the renin–angiotensin system becomes activated. Of the anterior pituitary hormones, growth hormone (GH) and prolactin (PRL) secretion is increased. Also β-endorphin has been frequently reported to increase, whereas the responses of antidiuretic hormone and cortisol are variable, probably depending on the type of sauna exposure. Sperm production decreases in particular in sauna-naïve men, but reduced fertility has not been associated with regular sauna habits. Minor sex differences exist, the hormonal responses being somewhat greater in women. Sauna-naïve women may experience mild disturbances in menstrual cycle, but no effects on fertility have been reported. The hormone responses are short-lived, normalizing soon after sauna exposure during the recovery. Adaptation to regular sauna use plays an important role in the responses, which attenuate upon frequent exposure.
... Other conditions that increase circulating GHRH levels include the initial slow stage of sleep (914) and the sauna bath in young subjects (605). For other details on GHRH levels in GH hypo-and hypersecretory states, see Reference 749. ...
The secretion of growth hormone (GH) is regulated through a complex neuroendocrine control system, especially by the functional interplay of two hypothalamic hypophysiotropic hormones, GH-releasing hormone (GHRH) and somatostatin (SS), exerting stimulatory and inhibitory influences, respectively, on the somatotrope. The two hypothalamic neurohormones are subject to modulation by a host of neurotransmitters, especially the noradrenergic and cholinergic ones and other hypothalamic neuropeptides, and are the final mediators of metabolic, endocrine, neural, and immune influences for the secretion of GH. Since the identification of the GHRH peptide, recombinant DNA procedures have been used to characterize the corresponding cDNA and to clone GHRH receptor isoforms in rodent and human pituitaries. Parallel to research into the effects of SS and its analogs on endocrine and exocrine secretions, investigations into their mechanism of action have led to the discovery of five separate SS receptor genes encoding a family of G protein-coupled SS receptors, which are widely expressed in the pituitary, brain, and the periphery, and to the synthesis of analogs with subtype specificity. Better understanding of the function of GHRH, SS, and their receptors and, hence, of neural regulation of GH secretion in health and disease has been achieved with the discovery of a new class of fairly specific, orally active, small peptides and their congeners, the GH-releasing peptides, acting on specific, ubiquitous seven-transmembrane domain receptors, whose natural ligands are not yet known.
... The increased plasma GH concentration is also thought to be a reflection of a non-specific response to thermal stress and the HR [bpm] rehydration no rehydration reaction of hypothalamus to heat. This is associated with the increased secretion of somatoliberin which stimulates production of GH in somatotropic cells of the pituitary gland [20]. According to Leppaluoto et al. [16], heat exposure in a sauna leads do dehydration accompanied by the increased secretion of prolactin and GH. ...
The experiments were carried out in eight young males of mean age 23.1±1.4 years, mean body height 1855.0 cm, mean body mass 86.25.92 kg, and mean ‡O 2 max 4.30.92 l O 2 ·min-1. The subjects took a Finnish sauna bath twice at a week interval; the temperature of the bath was 90 o C and the relative humidity 35%. The total time of the bathing was divided into four 15-min exposures separated by 2-to 3-min breaks. On one day of the experiment the subjects received no drinking water during the bath, and on another day they were supplied with 1 l of non-carbonated mineral water of 25 o C divided into five 200-ml portions. Body mass was measured before and after the bath. Heart rate (HR), temperatures of the tympanic membrane (Tty) and forehead (Th), and blood levels of growth hormone (GH), cortisol (C), and testosterone (T) were estimated prior to entering the sauna and during the breaks. From the concentrations of testosterone and cortisol the anabolic-catabolic index (T/C) was calculated. The bath with no rehydration led to the significant reduction of the body mass approx. by 1.430.44 kg, i.e., by 1.69% of the initial mass. The bathing accompanied by rehydration resulted in an insignificant decrease in the body mass. In every case, the bath without rehydration led to the significant elevation of HR (i.e., from approx. 78 to approx. 135 bpm), while the bath with the supply of water resulted in the significantly (P<0.05) less pronounced increase in HR, i.e., to approx. 113 bpm. Tty was significantly elevated by 1.8 o C and by 1.5 o C as a result of bathing without and with the rehydration, respectively. Mean values of Th were lower in the subjects supplied with drinking water during the bath. The exposure to exogenous heat led to the significant (P<0.05) increase in GH and T and to the significant reduction in C; the latter effect was more pronounced in the rehydrated subjects. The magnitude of hormonal responses was affected by the supply of drinking water: the " peak " of GH after the sauna decreased from 6.24.92 ng/ml in the non-rehydrated subjects to 4.94.53 ng/ml in the rehydrated ones; in contrast, the testosterone level rose from 3.91.05 ng/ml in the non-rehydrated subjects to 4.70.87 ng/ml in the rehydrated ones. Finally, the sauna exposure stimulated anabolic metabolism: the T/C value increased from the initial range of 3.1-4.3 to
... Compared with previous reports, our domed sauna was more effective than a traditional one (21,22) in raising body temperature with less adverse effect on HR (23,24). This was because we could eliminate the possible harm of orthostatic hypotension by keeping participants supine until the eventual return of BP and because the changes in SBP in the older adults remained within the diurnal variation (25,26). ...
Thermal therapy has been used as adjuvant therapy in patients with cardiovascular disease. However, little is known about responses to thermal stress in older adults. We examined the effects of thermal stress in younger and older healthy Japanese individuals.
The study included 12 young (mean age, 22 years) and 12 older (mean age, 68 years) healthy adults and was performed under strict temperature and humidity control to minimize confounding. Participants lay supine throughout three consecutive 30-minute phases: Phase I (heating at 70°C in a dome-shaped sauna), Phase II (insulation in the sauna), and Phase III (cool down). Physiological parameters and subjective thermal sensations were compared within and between two age groups.
Mean skin temperature increased significantly in both age groups (Phase I) and after the first 10 minutes was higher among older adults (by 6.8°C vs 6.0°C among younger; p < .01). Mean rectal temperature increased by 0.6°C in both groups (Phase II). Mean heart rate increased significantly in both age groups (Phase II) and was higher among younger adults (by 21.4 vs 11.3 beats/min among older adults; p < .05). Both systolic (by 15.1 mmHg) and diastolic (by 10.5 mmHg) blood pressure dropped significantly among older adults (Phase I), returning to baseline in Phase III; no changes were noted among those younger. There was no between-group difference in fluid loss or thermal sensations.
Compared with younger adults, older adults are more likely to drop blood pressure in response to thermal stress but had similar fluid loss and subjective responses.
© The Author 2014. Published by Oxford University Press on behalf of The Gerontological Society of America. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com.
... ACTH increased three times after the first sauna bath, and almost four times after the last one. However, Scandinavian authors observed lower increase of ACTH after heat exposure in sauna (Kukkonen -Harjula et al. 1989, Laatikainen et al. 1988, Leppäluoto et al. 1987. Slovakian authors observed that ACTH hormone increased four times after sauna bath (Ježova et al. 1985(Ježova et al. , 1994. ...
... The cardiovascular effects of sauna bathing have been reviewed earlier (7,9 -12) and are summarized in Table 1. Skin temperature increases rapidly to about 40ЊC (5,9,13,14), whereas the increase in rectal temperature depends on heat exposure (15)(16)(17). Sweating begins quickly and reaches its maximum at about 15 minutes, with an average total secretion of 0.5 kg (6,9,18). Skin blood flow is increased from 5% to 10% so it becomes 50% to 70% of the cardiac output, while blood flow to internal organs decreases (12). ...
Although sauna bathing causes various acute, transient cardiovascular and hormonal changes, it is well tolerated by most healthy adults and children. Sauna bathing does not influence fertility and is safe during the uncomplicated pregnancies of healthy women. Some studies have suggested that long-term sauna bathing may help lower blood pressure in patients with hypertension and improve the left ventricular ejection fraction in patients with chronic congestive heart failure, but additional data are needed to confirm these findings. The transient improvements in pulmonary function that occur in the sauna may provide some relief to patients with asthma and chronic bronchitis. Sauna bathing may also alleviate pain and improve joint mobility in patients with rheumatic disease. Although sauna bathing does not cause drying of the skin-and may even benefit patients with psoriasis-sweating may increase itching in patients with atopic dermatitis. Contraindications to sauna bathing include unstable angina pectoris, recent myocardial infarction, and severe aortic stenosis. Sauna bathing is safe, however, for most people with coronary heart disease with stable angina pectoris or old myocardial infarction. Very few acute myocardial infarctions and sudden deaths occur in saunas, but alcohol consumption during sauna bathing increases the risk of hypotension, arrhythmia, and sudden death, and should be avoided.
... Ambient temperature affects some but not all pharmacological stimulators of GH secretion. Heat exposure increases GHRH secretion [18] but neither heat nor cold affects the GH response to insulin induced hypoglycaemia [19,20]. As the GH secretion in response to insulin induced hypoglycaemia are approximately three times greater than the response to heat alone, the mechanism by which heat induces GH secretion may be swamped by the effect of the hypoglycaemia [21]. ...
Ambient temperature alters exercise induced GH secretion. It is unknown whether temperature affects GH secretion at exercise intensities above the anaerobic threshold when other factors may override the relationship seen at lower intensities.
Cross-over study of ambient temperature on exercise induced GH in swimmers and rowers.
St Thomas Hospital, London.
Ten healthy men (age 21.7+/-0.8 yrs). Five swimmers and five rowers.
Forty-minute exercise test at 105% of anaerobic threshold at room temperature (RT) and at 4 degrees C.
Cutaneous and core body temperature. Serum GH concentration.
Cutaneous body temperature increased during exercise at RT but decreased in the cold. Although core temperature rose in both settings, the rise was greater at RT (p=0.021). GH increased at both temperatures but the onset was delayed by the cold. Peak GH tended to be higher at RT (17.4+/-3.6 microg/L vs. 9.5+/-1.5 microg/L, p=0.07). Total GH secretion was greater at RT (353.3+/-99.1 microg min/L) than 4 degrees C (128.3+/-21.0 microg min/L), p=0.038. Change in core temperature correlated with log peak GH (r=0.66, p=0.039) and log incremental GH (r=0.67, p=0.032) when exercising at 4 degrees C. There was no difference between swimmers and rowers.
Exercise at 4 degrees C reduces GH secretion during exercise at intensities above the anaerobic threshold. A change in core body temperature may be one mechanism by which exercise induces GH secretion. The difference in GH between swimmers and rowers during their respective events relates to the conditions under which they compete.
During aging, a progressive decline in the ability of an organism to maintain homeostasis occurs. The mechanism by which senescence of the endocrine system occurs is not known, but presumably involves both genetic and environmental components. In the hypothalamus, morphological changes occur in association with the aging process. In the rat, neurons are lost from areas that regulate temperature and gonadotropin secretion (1). In humans, there is marked enlargement of neurons in the supraoptic and paraventricular nuclei, but no loss of neurons from these areas (2). Parvicellular corticotropin-releasing hormone- (CRH), containing neurons in the paraventricular nucleus have been observed to be activated during the course of aging (3). However, with aging the number of neurons in the suprachiasmatic nucleus decreases (3).
The aim of the present study was to compare basic physiological, biochemical, and hormonal reactions in women who prior to the study had never had a sauna and who were subjected to a single or multiple (i.e., applied repeatedly over two weeks) thermal stress in a Finnish sauna and to evaluate these reactions in relation to the duration of the stress. Twenty healthy women tested in the present investigation were divided into two groups, each group having a sauna every two days for two weeks (i.e., seven exposures in total). The subjects from the first group bathed continuously for 30 min, while those from the second group bathed for 45 min with a five-min cooling break in the middle of the bath. The temperature and relative humidity in the sauna equalled to 80°C and 5-27%, respectively. All the physiological and biochemical tests were performed on the first and 14th days of the experiment both before and after the thermal exposure. The results indicate that the exposures to thermal stress led to reduction in the body mass which was more pronounced in group 2 (p<0.005) and to elevation of the tympanal temperature (Tty) which, in both groups, was smaller after the last visit to the sauna. The first bath in the sauna stimulated the heart rate (HR) to a similar extent in both groups of the subjects but after the last bath HR was significantly lower in group 2 (p<0.005). Enhanced secretion of the stress hormones (i.e., human growth hormone [hGH], corticotropin [ACTH] and cortisol) after the last bath in the sauna was less pronounced in group 2, whereas in group 1 the rates of elevation of hGH and ACTH were higher after the last than after the first visit to the sauna. In turn, stimulation of the production of hGH following the first sauna was significantly more pronounced (p<0.005) in group 2 than in group 1. Similar statistical difference was noted between the two groups with respect to changes in the concentration of TSH. Overall, the obtained results indicate that the 30-min continuous sauna bath is a greater stress for the organism than the 45-min bath with a 5-min break for cooling. The smaller elevations in the body temperature, HR, and serum levels of hGH, ACTH, and cortisol detected after the last sauna bath in women from group 2 suggest that in these subjects adaptive changes to thermal stress were more favourable than in those from group 1.
Study aim: To determine hormonal (growth hormone, cortisol and testosterone in blood) responses to a series of supramaximal cycle ergometer exercise bouts. Material and methods: Seven physical education students were subjected to two series of exercises, 5 bouts each, spaced by one week. The load in the first bout in each series amounted to 100% of work output recorded previously in the Wingate test, all other bouts amounting to 50%. In Series A and B, the loads were 10 and 5% of body mass (BM), respectively. Individual bouts were separated by 2-min intervals. Growth hormone (GH), cortisol (C), testosterone (T) and blood pH were determined in fingertip blood before the exercise, following Bouts 3 and 5, and 30 min after the exercise was discontinued. Results: Growth hormone, cortisol and testosterone concentrations increased significantly after both series of exertions. Conclusions: Repeated bouts of sprint-like exertions may be applied to design training protocols involving the desired kind of stimulation of the hormonal control, considering the necessary external load and exercise duration.
The sections in this article are:
This review focuses on the endocrine responses to thermal stimuli during passive heat or cold exposure, with particular reference to the relation of these responses to the changes in the body core temperature (T
core). Mild to moderate hyperthermia (<1°C rise in T
core) induces the release of growth hormone and prolactin (PRL). Moderate hypothermia (1°–2°C fall in T
core) suppresses PRL release. A positive correlation between plasma PRL and T
core suggests some role for PRL in thermoregulation. Hypothermia activates the hypothalamo-pituitary-thyroid (HPT) axis and releases thyrotropin-releasing hormone, thyroid-stimulating hormone (TSH), and thyroid hormones and increases the metabolic rate. Enhancement of extrathyroidal production of triiodothyronine (T3) from thyroxine (T4) may precede the TSH response to cold. Both severe hyperthermia and hypothermia (1°–3°C changes in T
core) activate the hypothalamo-pituitary-adrenal (HPA) axis and the sympathetic nervous system, resulting in release of corticotropin-releasing factor, adrenocorticotropic hormone, cortisol, and norepinephrine. The responses in the HPT axis and the HPA axis are not apparent in humans, as they are in rats, probably owing to the larger body mass of humans. Hyperthermia stimulates the renin-angiotensin-aldosterone system and the release of arginine vasopressin (AVP) and atrial natriuretic peptide, but this might be due to nonthermal factors. Diuresis due to suppression of AVP release is induced by cold. Gonadal response to thermal stimuli is possibly suppressive. The hormonal responses induced by thermal stress are mostly dependent on the change in T
core in humans; in small animals they are also dependent on the change in skin temperature.
The diagnosis of growth hormone deficiency (GHD) in adulthood has become increasingly important becauseof the approved indication for growth hormone (GH) substitution therapy in such patients. While GH stimulation tests are superior to single measurements of other growth factors or spontaneous GH secretion in the diagnosis in adults, the reproducibility and specificity of GH stimulatory tests are often described to be low. This is also the case with the insulin tolerance test. Many external factors, such as fasting, physical activity, heat exposure and sleep, are known to influence GH secretion. The stimulatory or inhibitory effect of these factors on GH secretion might, therefore, influence the GH provocative test and contribute to the variability in response. Age and body composition are also known to influence GH secretion, and these factors must be considered when evaluating GH test responses. However, age-related cut-off levels for GHD have not been defined. Obesity is still a complicating factor in the diagnosis of GHD, even though some GH tests have been able to distinguish between obesity and true GHD. Based on these complicating factors, the parameters of GH stimulatory tests are recommended to be defined and standardized to optimize reproducibility and specificity. Furthermore, such tests should be performed only in patients with firm evidence of pituitary disease.
Generally, the sauna bathing has been contraindicated for patients with chronic heart failure. However, it has been well tolerated and improved hemodynamics has been shown in patients with chronic heart failure after a single exposure and after a four-week period of sauna bathing (five days per week). Left ventricular ejection fraction increased from 24+/-7% to 31+/-9% and left ventricular end-diastolic dimension decreased from 66+/-6 mm to 62+/-5 mm after four weeks. In the present review, the mechanisms of action, the clinical data available to date and the possible beneficial effects of sauna bathing for patients with heart failure are discussed, as well as the precautions and the contraindications in this specific group of patients with chronic heart failure.
The process of aging is accompanied by a progressive reduction of biological dynamical sophistication, resulting in an increased probability of dysfunction, illness, and death. This loss of sophistication is inherent in all aging organisms. However, it may be possible to retard the rate of loss of biological complexity by introducing an increased amount of nonlinear, nonmonotonic external stimulation that challenges the organism and forces it to upregulate its biological processes. This can be achieved by exploiting the multiple effects of hormesis, through a wide range of challenges including physical, mental, and biological stress. Hormesis is widely encountered in biological systems, and its effects are also seen in humans. It is possible to use hormetic strategies (both conditioning hormesis and postexposure conditioning hormesis) to enhance the function of repair processes in aging humans and therefore prevent age-related chronic degenerative diseases and prolong healthy lifespan. Such techniques include dietary restriction and calorie restriction mimetics, intermittent fasting, environmental enrichment, cognitive and sense stimulation, sexuality-enhancing strategies, exposure to low or to high temperatures, and other physicochemical challenges. Current research supports the general principle that any type of a hormetic dose-response phenomenon has an effect that does not depend on the type of stressor and that it can affect any biological model. Therefore, novel types of innovative, mild, repeated stress or stimulation that challenge a biological system in a dose-response manner are likely to have an effect that, properly harnessed, can be used to delay, prevent, or reverse age-related changes in humans.
The secretion of growth hormone (GH) is regulated by a complex system that includes both neurotransmitters and feedback by hormonal and metabolic substrates. Over the last few years it has been recognized that GH release varies over a wide spectrum from deficient to excessive secretion. The diagnosis of GH deficiency is based on a combination of anthropometric and clinical signs on the one hand and an inadequate stimulated and/or spontaneous GH secretion on the other. There is no distinct boundary between deficient and sufficient GH secretion. The cut-off limit for normal GH release is accordingly relative and has increased over the past decade from 5 to 10 micrograms/l. The effect of GH therapy on growth can be evaluated only after treatment for at least 6 months. There is, therefore, an indisputable need for methods that would reflect growth response soon after the start of treatment. There are several promising biochemical candidates, e.g. the aminoterminal propeptide of type III procollagen, the carboxyterminal propeptide of procollagen I and the bone Gla-protein, which may turn out to be useful early indicators of the growth response to long-term GH therapy.
Hormonal response to Finnish sauna bath was investigated in 20 prepubertal children (age 5-10 years). Blood leukocyte count, plasma potassium, serum aldosterone, growth hormone and prolactin concentrations increased; plasma volume, plasma sodium, catecholamines, serum antidiuretic hormone, atrial natriuretic peptide (ANP), cortisol, and thyrotropin concentrations remained unchanged during sauna bath. One hour after sauna, serum thyrotropin, atrial natriuretic peptide and blood glucose concentrations decreased, whereas the rest of the hormones remained unchanged. Our results implicate that maintenance of homeothermia resulted in moderate hormonal changes in children during Finnish sauna bath which indicate similar adequate hormonal thermoregulatory adjustment as previously documented in adults.
Exercise-induced increases in blood somatotropin (hGH) have always been considered in terms of quantity of the circulating molecules. Knowing that the hypophysis can release several GH species, we investigated the differential release in blood of total hGH (hGHT) and the main hGH variant (hGH20K) molecules in six trained male swimmers exposed to three different conditions known to favor GH release in blood: 45 min--70% maximum oxygen uptake (VO2max) bicycling and swimming, and 20 min of sauna bathing. Based on the binding specificity of hGH antibodies, hGH20K was isolated then assayed using the Nichols immunoradiometric assay system. All three experimental conditions produced significant (P less than 0.001) elevations in blood hGHT and hGH20K. In all three cases, mean blood hGH20K contribution to blood hGHT was relatively constant (11.9, SE 0.7%). Rises in rectal temperature were not statistically related to the changes in blood hGHT. This demonstration of a relatively constant elevation in hGH20K during bicycling, swimming, and sauna bathing can hardly explain the large differences in blood hGHT responses reported in literature under similar conditions.
The secretion of growth hormone (GH) is regulated through a complex neuroendocrine control system, especially by the functional interplay of two hypothalamic hypophysiotropic hormones, GH-releasing hormone (GHRH) and somatostatin (SS), exerting stimulatory and inhibitory influences, respectively, on the somatotrope. The two hypothalamic neurohormones are subject to modulation by a host of neurotransmitters, especially the noradrenergic and cholinergic ones and other hypothalamic neuropeptides, and are the final mediators of metabolic, endocrine, neural, and immune influences for the secretion of GH. Since the identification of the GHRH peptide, recombinant DNA procedures have been used to characterize the corresponding cDNA and to clone GHRH receptor isoforms in rodent and human pituitaries. Parallel to research into the effects of SS and its analogs on endocrine and exocrine secretions, investigations into their mechanism of action have led to the discovery of five separate SS receptor genes encoding a family of G protein-coupled SS receptors, which are widely expressed in the pituitary, brain, and the periphery, and to the synthesis of analogs with subtype specificity. Better understanding of the function of GHRH, SS, and their receptors and, hence, of neural regulation of GH secretion in health and disease has been achieved with the discovery of a new class of fairly specific, orally active, small peptides and their congeners, the GH-releasing peptides, acting on specific, ubiquitous seven-transmembrane domain receptors, whose natural ligands are not yet known.
Eight healthy young men were studied during three periods of heat exposure in a Finnish sauna bath: at 80 degrees C dry bulb (80 D) and 100 degrees C dry bulb (100 D) temperatures until subjective discomfort, and in 80 degrees C dry heat, becoming humid (80 DH) until subjective exhaustion. Oral temperature increased 1.1 degrees C at 80 D, 1.9 degrees C at 100 D and 3.2 degrees C at 80 DH. Heart rate increased about 60% at 80 D, 90% at 100 D and 130% at 80 DH. Plasma noradrenaline increased about 100% at 80 D, 160% at 100 D and 310% at 80 DH. Adrenaline did not change. Plasma prolactin increased 2-fold at 80 D, 7-fold at 100 D and 10-fold at 80 DH. Blood concentrations of the beta-endorphin immunoreactivity at 100 D, adrenocorticotropic hormone (ACTH) at 100 D and 80 DH, growth hormone at 100 D and testosterone at 80 DH also increased, but cortisol at 80 D and 100 D decreased. The plasma prostaglandin E2 and serum thromboxane B2 levels did not change. Patterns related to heat exposure were observed for heart rate, plasma noradrenaline, ACTH and prolactin in the three study periods.
To identify factors that regulate the tempo of growth and puberty, the present study examined how the environment influenced the timing of menarche and first ovulation in rhesus monkeys and how these events were related to differential rates of growth. Spring-born females were raised from 12 months of age under natural outdoor conditions (OH; n = 6) or indoors (IH; n = 9) under a controlled photoperiod (12h of light, 12h of darkness) and temperature (20-23 C). Ages at the initial increases in serum bioactive LH levels (27.7 +/- 0.7 vs. 31.4 +/- 1.0 months), menarche (26.0 +/- 0.7 vs. 32.5 +/- 0.9 months), and first ovulation (33.9 +/- 1.4 vs. 43.5 +/- 0.3 months) were significantly advanced in IH compared to OH females. First ovulation for the OH females occurred exclusively in October and November of the fourth year, whereas the distribution of first ovulation of IH females was biomodal, with seven of nine occurring in November or December at 31.8 +/- 0.5 months, and two of nine ovulating in September or October at 41.2 +/- 0.5 months. Serum levels of PRL varied seasonally in OH females throughout development, with peaks in July and nadirs in October. A similar rhythm was observed for IH females during the first 12 months of indoor housing, after which point the period decreased from 11.9 +/- 0.5 to 9.3 +/- 0.6 months. Overall increments in body weight did not differ between groups. An acceleration of growth in both crown-rump and tibial lengths occurred just before menarche in both groups, and this occurred at about 26 months for IH and about 32 months for OH females. Skeletal maturity was significantly advanced at 27 months in IH females and at every chronological age thereafter. Serum concentrations of somatomedin-C and GH paralleled group differences in bone maturation. Both hormones were significantly elevated by 16-18 months of age in IH animals compared to OH females and remained so until 34-36 months of age. Although a distinct seasonal rhythm in both GH and somatomedin-C was evident in OH animals, no such pattern was observed in IH females. These data suggest that exposure to an outdoor environment moderates the tempo of both sexual and skeletal maturation. The acceleration in reproductive development in animals exposed to a constant environment was associated with an acceleration in bone maturation, suggesting that common factors may be responsible for the initiation of both events.
The hypothalamo-pituitary-insulin-like growth factor I (IGF-I) axis was studied in 24 prepubertal children with insulin-dependent diabetes mellitus (IDDM) and 12 non-diabetic children. There were no significant differences between the diabetic and control subjects in basal concentrations of immunoreactive growth hormone releasing hormone (ir-GHRH), growth hormone (GH) or stimulated GH levels, but after exercise ir-GHRH concentrations were higher in the diabetic children. Peripheral IGF-I levels were significantly lower in the diabetic children, and even lower in those with poor metabolic control. A positive correlation was found between IGF-I levels and circulating free insulin concentrations in the diabetic subjects (r = 0.49, p < 0.05). These observations suggest that the GH response to physiological stimulation is normal in prepubertal diabetic children. Exercise-induced GH response may not be mediated by GHRH. IGF-I levels were reduced in prepubertal children with IDDM and even more so in subjects with poor metabolic control. This may be a consequence of transitory hypoinsulineamia, emphasizing the importance of adequate insulinization to facilitate optimal growth in children and adolescents with IDDM.
To study the role of peripheral immunoreactive growth hormone releasing hormone (ir-GHRH) concentrations and the GHRH test in the evaluation of growth hormone (GH) secretion in short stature, 46 children with a mean age of 9.4 years (range 1.6-16.3 years) and a mean relative height score of -3.2 SD (range -5.0-2.1 SD) were investigated. The children were divided into prepubertal (n = 35) and pubertal (n = 11) and the prepubertal children further into three groups based on their maximal GH responses to insulin-induced hypoglycaemia (IIH) and clonidine: (1) GH deficient subjects (maximal GH < 10 micrograms/l in both tests); (2) discordant responders (maximal GH < 10 micrograms/l in one test and > or = 10 micrograms/l in the other); and (3) normal responders (maximal GH > or = 10 micrograms/l in both tests). Peripheral ir-GHRH concentrations were measured during the IIH test by radioimmunoassay after purification of plasma samples on Sep-pak cartridges. Among the prepubertal children 10 fell into group 1, 16 into group 2 and 9 into group 3. Children in group 1 were older than those in group 3. There were no significant differences in relative heights and weights or absolute and relative growth velocities between the groups. Subjects in groups 1 and 2 had lower maximal GH responses to GHRH than those in group 3. There were no significant differences in the basal plasma ir-GHRH concentrations between the groups. Nine children (19.6%) had somatotrophs with a poor response to a single dose of exogenous GHRH (maximal GH < 10 micrograms/l).(ABSTRACT TRUNCATED AT 250 WORDS)
Previous studies on the effects of ethanol on circulating pituitary hormones have been carried out mostly during daytime when the secretion of these hormones is generally at a nadir. Therefore, we studied the effects of ethanol on the nocturnal secretion of GH, PRL, TSH, and thyroid hormones (protocol I, nine healthy subjects, five women) and on the TSH and PRL responses to synthetic TRH (protocol II, healthy subjects, four women). Ethanol was given in doses of 0, 0.5 or 1.0 g/kg of BW(protocol I) and 0 or 1.0 g/kg (protocol II) and ingested po at 1900-1945 h. In protocol I, plasma GH rose from 0.6 +/- 0.2 microgram/L (mean +/- SE) at 2200 h to 25.0 +/- 4.3 micrograms/L at 0100 h in control subjects and was almost completely inhibited at 4.5 +/- 1.7 micrograms/L at 0100 h in subjects receiving 1.0 g/kg ethanol (P < 0.01). In subjects receiving 0.5 g/kg ethanol, the inhibition was also significant (P < 0.01), plasma GH being 8.2 +/- 2.5 micrograms/L at 0100 h. Plasma GHRH was measured after solid phase separation in RIA, but it did not show any ethanol-related changes. Plasma PRL exhibited a clear diurnal rhythm in control subjects and rose from 77 +/- 16 at 1800 h to 248 +/- 62 micrograms/L at 0700 h (P < 0.01). The plasma PRL profile was not affected by ethanol. Plasma TSH was 1.4 +/- 0.2 mU/L at 1800-2200 h and rose to 2.3-2.4 mU/L for 0100-0700 h (P < 0.001) in the control subjects. Ethanol 1.0 g/kg suppressed plasma TSH to 1.4 +/- 0.2 mU/L (P < 0.05 at 0100 h and P < 0.01 at 0200 h). According to the area under the curve analyses, the suppression in the nocturnal TSH was 32% in the 0.5 g/kg group and 45% in the 1.0 g/kg group (P < 0.05 for both cases). Circulating free or total T3 and T4 did not show any statistically significant changes that could explain the ethanol-induced inhibition in the nocturnal TSH peak. In protocol II, synthetic TRH (1 microgram/kg BW) was given intravenously, and blood samples were collected before, at 20 and 60 min. TRH significantly stimulated plasma TSH and PRL, but ethanol (1.0 g/kg BW) had no effect on these responses. In conclusion, small amounts of ethanol have unexpectedly great effects on nocturnal surges of TSH, and especially on those of GH, that are apparently mediated by suprapituitary mechanisms. On the other hand, ethanol did not affect the nocturnal PRL surge. These inhibitory effects of ethanol may have unfavorable effects on growth and metabolism in adolescent drinkers.
In the attempt to define a GH stimulation test with high specificity and reproductibility, few studies have addressed the influence of potential interfering external factors on the test result. We therefore tested the influence of physical activity (admission to hospital on test morning) and mild heat exposure on the GH response to L-arginine stimulation test (Arg) and insulin-tolerance test (ITT).
One Arg stimulation test and one ITT were performed in all subjects during standard conditions (overnight hospital stay, 10 hours fasting). In addition, each subject was randomized to undergo either two additional Arg tests, or two ITTs, performed under two different conditions: admission to hospital on the morning of the test and during standard conditions except for heat exposure before testing. The four tests were performed in random order.
Twenty-two patients (six women, 16 men) (mean age +/- SEM, 38.3 +/- 5.3 years and 36.1 +/- 2.7 years, respectively) presenting with pituitary disease and a group of healthy age and gender-matched normal subjects (six women, 13 men) (age 38.3 +/- 4.8 years and 35.7 +/- 2.4 years, respectively) participated.
During the GH-stimulation tests serum GH, cortisol, blood glucose, and plasma glucagon were measured and compared in the three different test conditions.
During standard conditions, peak GH response was higher in the ITT compared to the Arg test in the control group (23.4 +/- 3.6 mU/l vs 11.6 +/- 2.0 mU/l, P = 0.004), and the specificity of the ITT was higher (18/19 versus 13/19, P = 0.047). Minor heat exposure before the ITT (temperature rise 0.24 +/- 0.05 degrees C, range 0.0-0.5 degrees C) did not change the GH response in the healthy adults whereas admission to hospital on the morning of the test reduced the GH response significantly (P < 0.05). The lowest blood glucose did not change in the three situations and did not correlate with peak GH during the ITT. In the patients there were no significant differences between the GH response during different conditions. Plasma glucagon did not significantly differ between the different test conditions in the control group (P = 0.88), but there was a significant decrease in the glucagon response to the test performed after hospital admission on the test morning in the patients (P < 0.025). Serum cortisol response in the control group did not differ in the three situations.
Since provocative GH responses are influenced by external factors, conditions should be standardized to optimize the reproductibility and specificity of the tests. Furthermore the higher specificity of the insulin-tolerance test as compared to the arginine stimulation test was confirmed.
This review focuses on the response of "stress" hormones to heat, exercise (single or repeated bouts), and combinations of these stimuli, with particular reference to their impact upon immune function. Very hot conditions induce a typical stress response, with secretion of catecholamines and cortisol. The catecholamines induce a demargination of leukocytes, and cortisol subsequently causes cells to migrate to lymphoid tissue. Sustained exercise, even in a thermally comfortable environment, induces a larger hormonal response than moderate thermal stress. With moderate exercise, increases in leukocyte numbers are related mainly to plasma norepinephrine concentrations, but with more intense exercise epinephrine concentrations assume a major importance. As exercise continues, plasma cortisol levels also rise, inducing an influx of neutrophils from bone marrow and an efflux of other leukocyte subsets. A combination of exercise and heat stress augments both hormonal and leukocyte responses. But these changes seem to be reversed if temperatures are clamped by exercising in cold water. If a second bout of exercise is performed with an inter-test interval of 30-45 min, neither hormone concentrations nor immune responses show any great cumulative effect under temperate conditions. However, in a hot environment the second exercise bout induces a larger and more persistent neutrophilia. Training influences these various responses mainly by decreasing the stress imposed when exercising at a given absolute work-rate.
Heat exposure has been shown to stimulate GH release, but the specificity and the reproducibility have not been determined, and the test has not been compared with validated GH stimulation tests in adulthood. We therefore tested the specificity and the reproducibility of the heat exposure test in healthy subjects and compared the results with those obtained with the insulin-tolerance test (ITT).
Ten healthy non-obese men, aged 31.3+/-4.80 years, underwent four GH stimulation tests in random order: two ITTs and two heat exposure tests. In the heat test, subjects were placed in a hot bath with water temperature at 40.3+/-0.11 degrees C for 45 min, resulting in an identical (P = 0.477) significant increase in tympanic temperature of 1.26+/-0.05 and 1.41+/-0.07 degrees C in the two tests.
Peak GH response to the heat exposure test was less than the peak GH response to ITT (5.25+/-1.72 vs 15.5+/-3.17 microg/l, P = 0.006). Furthermore the specificity (arbitrary cut-off level = 3 microg/l) of the heat test was lower than of the ITT (8/17 vs 18/20, P = 0.006). The coefficient of variation did not differ between the two tests (heat test 0.31, ITT 0.36, P = 0.77). Peak GH values in the individual tests were highly correlated (heat, r = 0.908, P = 0.002; ITT, r = 0.815, P = 0.004). Reproducible increments in the circulating levels of stress hormones were observed during ITT. but these hormones remained largely unchanged during heat exposure.
The heat exposure test is not a reliable GH stimulation test compared with the ITT in adults. This study documents that the ITT has a high specificity and reproducibility in the diagnosis of GH deficiency in adulthood. We propose that the heat exposure test is not used in the diagnosis of this condition in adulthood.
We describe a 12-y-old boy with excessive growth hormone and prolactin secretion presumably due to diffuse somatotroph hyperplasia. Until mid-puberty, his growth rate was under reasonable control, with high-dose octreotide injections every 8 h combined with a dopamine agonist. As his growth velocity started to increase, the efficacy of continuous s.c. octreotide infusion on GH secretion was tested. Similar total daily doses (600 microg) of octreotide were administered either by incremental s.c. injections at 8 h intervals, or by continuous s.c. infusion, two-thirds of the amount during night-time to control the presumed high nocturnal growth hormone (GH) peaks of the pubertal growth spurt. An overnight GH profile showed inadequate suppression of GH levels by incremental injections, while continuous s.c. infusion efficiently brought down the GH secretion. Another somatostatin analogue, lanreotide as a single depot injection was not effective. A 6-mo trial on the s.c. infusion regimen significantly reduced growth hormone secretion (as judged by IGF-I and IGFBP3 concentrations), and normalized growth velocity overcoming the pubertal growth spurt. It also caused a decrease in the pituitary size in magnetic resonance images. We conclude that the efficacy of octreotide infusion in suppressing GH secretion is superior to incremental injections with the same dose.
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