Exercise-induced Growth Hormone Response Research Articles

Heart Rate Recovery, Blood Pressure Recovery, and 24-hour Heart Rate among Firefighters

The purpose of the present study was to examine the effects of 3 days isoenergetic high-fat/low-carbohydrate diet (HF-LC) relative to low-fat/high-carbohydrate diet (LF-HC) on the exercise-induced growth hormone (GH) response in healthy male subjects.Ten healthy young males participated in this study. Each subject consumed the HF-LC (18 ± 1% protein, 61 ± 2% fat, 21 ± 1% carbohydrate, 2720 kcal per day) for 3 consecutive days after consuming the LF-HC (18 ± 1% protein, 20 ± 1% fat, 62 ± 1% carbohydrate, 2755 kcal per day) for 3 consecutive days. After each dietary intervention period, the hormonal and metabolic responses to an acute exercise (30 min of continuous pedaling at 60% of V˙O2max) were compared. The intramyocellular lipid (IMCL) contents in the vastus lateralis, soleus, and tibialis anterior were evaluated by proton magnetic resonance spectroscopy.Serum GH concentrations increased significantly during the exercise after both the HF-LC and LF-HC periods (P < 0.05). However, the exercise-induced GH response was not significantly different between the two periods. Fat utilization and lipolytic responses during the exercise were enhanced significantly after the HF-LC period compared with the LF-HC period. IMCL content did not differ significantly in any portion of muscle after the dietary interventions.We could not show that short-term HF-LC consumption changed significantly exercise-induced GH response or IMCL content in healthy young males.

Growth Hormone Concentrations in Different Body Fluids Before and After Moderate Exercise.

BackgroundGrowth hormone (GH) has many direct and indirect actions and roles including substrate regulation and priming of some cells of the immune system, and the expected aspects of growth and repair. Different concentrations in human body fluids reflect the exercise-induced growth hormone response (EIGR) after exercise. In populations such as elite athletes, the invasive nature of venous sampling is poorly accepted. Thus, this study examines possible viable alternatives such as urine and saliva samples and the GH concentration.MethodsA heterogeneous group of 11 males (age 26.0 ± 5.0 years; body mass 76.5 ± 9.3 kg; VO2peak 57.0 ± 6.0 mL kg−1 min−1) ran for 40 min on a treadmill at 5 % below their individually indentified lactate threshold pace. Samples of urine, saliva and blood were collected immediately pre- and post-test and at 30 and 60 min post-test.ResultsSalivary GH was correlated with serum pre- and post-exercise (p < 0.001); urinary GH was correlated with serum (p < 0.05). However, despite being significantly correlated, it is clear from the large differences in absolute concentration in the three media that the appearance of serum GH due to exercise is different from that of the appearance of salivary and urinary GH. This aspect of compartmental exchanges is very difficult to define and to investigate. Differences in any analyte concentration in different compartments are to be expected between different media, and hence the same medium should be used where the same ‘pattern of response’ can be tracked.ConclusionsThe results suggest that urinary and saliva sampling cannot substitute for venous sampling with respect to exercise-induced changes in GH concentration. The use of the analyses in these three areas may be appropriate for further investigation.

A 3-day high-fat/low-carbohydrate diet does not alter exercise-induced growth hormone response in healthy males

ObjectiveThe purpose of the present study was to examine the effects of 3days isoenergetic high-fat/low-carbohydrate diet (HF-LC) relative to low-fat/high-carbohydrate diet (LF-HC) on the exercise-induced growth hormone (GH) response in healthy male subjects. DesignTen healthy young males participated in this study. Each subject consumed the HF-LC (18±1% protein, 61±2% fat, 21±1% carbohydrate, 2720kcal per day) for 3 consecutive days after consuming the LF-HC (18±1% protein, 20±1% fat, 62±1% carbohydrate, 2755kcal per day) for 3 consecutive days. After each dietary intervention period, the hormonal and metabolic responses to an acute exercise (30min of continuous pedaling at 60% of V˙O2max) were compared. The intramyocellular lipid (IMCL) contents in the vastus lateralis, soleus, and tibialis anterior were evaluated by proton magnetic resonance spectroscopy. ResultsSerum GH concentrations increased significantly during the exercise after both the HF-LC and LF-HC periods (P<0.05). However, the exercise-induced GH response was not significantly different between the two periods. Fat utilization and lipolytic responses during the exercise were enhanced significantly after the HF-LC period compared with the LF-HC period. IMCL content did not differ significantly in any portion of muscle after the dietary interventions. ConclusionsWe could not show that short-term HF-LC consumption changed significantly exercise-induced GH response or IMCL content in healthy young males.

Thyroid hormone and estrogen regulate exercise-induced growth hormone release.

Growth hormone (GH) regulates whole body metabolism, and physical exercise is the most potent stimulus to induce its secretion in humans. The mechanisms underlying GH secretion after exercise remain to be defined. The aim of this study was to elucidate the role of estrogen and pituitary type 1 deiodinase (D1) activation on exercise-induced GH secretion. Ten days after bilateral ovariectomy, animals were submitted to 20 min of treadmill exercise at 75% of maximum aerobic capacity and tissues were harvested immediately or 30 min after exercise. Non-exercised animals were used as controls. A significant increase in D1 activity occurred immediately after exercise (~60%) in sham-operated animals and GH was higher (~6-fold) 30 min after exercise. Estrogen deficient rats exhibited basal levels of GH and D1 activity comparable to those found in control rats. However, after exercise both D1 activity and serum GH levels were blunted compared to sedentary rats. To understand the potential cause-effect of D1 activation in exercise-induced GH release, we pharmacologically blocked D1 activity by propylthiouracil (PTU) injection into intact rats and submitted them to the acute exercise session. D1 inhibition blocked exercise-induced GH secretion, although basal levels were unaltered. In conclusion, estrogen deficiency impairs the induction of thyroid hormone activating enzyme D1 in the pituitary, and GH release by acute exercise. Also, acute D1 activation is essential for exercise-induced GH response.

Exercise-Induced growth hormone during acute sleep deprivation.

The effect of acute (24‐h) sleep deprivation on exercise‐induced growth hormone (GH) and insulin‐like growth factor‐1 (IGF‐1) was examined. Ten men (20.6 ± 1.4 years) completed two randomized 24‐h sessions including a brief, high‐intensity exercise bout following either a night of sleep (SLEEP) or (24‐h) sleep deprivation (SLD). Anaerobic performance (mean power [MP], peak power [PP], minimum power [MinP], time to peak power [TTPP], fatigue index, [FI]) and total work per sprint [TWPS]) was determined from four maximal 30‐sec Wingate sprints on a cycle ergometer. Self‐reported sleep 7 days prior to each session was similar between SLEEP and SLD sessions (7.92 ± 0.33 vs. 7.98 ± 0.39 h, P =0.656, respectively) and during the actual SLEEP session in the lab, the total amount of sleep was similar to the 7 days leading up to the lab session (7.72 ± 0.14 h vs. 7.92 ± 0.33 h, respectively) (P =0.166). No differences existed in MP, PP, MinP, TTPP, FI, TWPS, resting GH concentrations, time to reach exercise‐induced peak GH concentration (TTP), or free IGF‐1 between sessions. GH area under the curve (AUC) (825.0 ± 199.8 vs. 2212.9 ± 441.9 μg/L*min, P <0.01), exercise‐induced peak GH concentration (17.8 ± 3.7 vs. 39.6 ± 7.1 μg/L, P <0.01) and ΔGH (peak GH – resting GH) (17.2 ± 3.7 vs. 38.2 ± 7.3 μg/L, P <0.01) were significantly lower during the SLEEP versus SLD session. Our results indicate that the exercise‐induced GH response was significantly augmented in sleep‐deprived individuals.

4weeks of high-intensity interval training does not alter the exercise-induced growth hormone response in sedentary men.

SummaryThis study determined the effects of high-intensity interval training on the exercise-induced growth hormone (GH) responses, whole body and regional fat content. Twenty-four sedentary males were randomized to either a high-intensity interval training (HIT) group or a low-intensity continuous training (LT) group. The HIT group performed intermittent exercises at 85% of , whereas the LT group performed continuous exercise for 22 min at 45% of . Before and after 4 weeks of training, hormonal and metabolic responses to acute exercise were determined. Acute exercise significantly increased GH concentrations in both groups (p < 0.05). However, the responses did not change after training period in either group. Furthermore, the training did not significantly affect intramyocellular or intrahepatic lipid content in either group. The present study indicates that 4 weeks of high-intensity interval training does not alter the exercise-induced GH responses, whole body fat mass or intramyocellular and intrahepatic lipid content in sedentary males.

Effects Of 3 Days Of High Fat Diet On Exercise-induced Growth Hormone Response In Men

Effects Of 3 Days Of High Fat Diet On Exercise-induced Growth Hormone Response In Men

The role of lactate in the exercise-induced human growth hormone response: evidence from McArdle disease

Purpose:Increased blood lactate concentration has been suggested as a primary stimulus for the exercise-induced growth hormone response (EIGR). Patients with McArdle disease are unable to produce lactate in response to...

The effect of submaximal exercise on immuno- and bioassayable IGF-I activity in patients with GH-deficiency and healthy subjects

Objective Growth hormone (GH) increases during exercise, but the response of the insulin-like growth factor (IGF) system has not been as definitive. Therefore, we investigated the effect of the exercise-induced GH response on the circulating IGF-system in GH-deficient (GHD) and intact adults. Design Eight GHD adults were studied on 2 occasions, with (+GH) and without (−GH) GH administered (0.4 IU) during exercise (45 min of cycle ergometer exercise at the lactate threshold). Eight age-matched controls were only studied on one occasion. Blood samples were drawn at baseline, during and post-exercise. IGFBP-3 proteolysis was measured by an in vitro proteolytic activity assay, IGF-I bioactivity by novel IGF-I kinase receptor activation assay (KIRA) and other hormones by immunoassay. Results GH administration to GHD adults resulted in a serum GH peak similar to the exercise-stimulated GH response in GH intact controls, but exercise had only a small impact on the IGF system. IGF-I concentration was lower in controls but was only significantly lower than the +GH day. Neither IGF-I nor -II levels changed over time. IGFBP-1 demonstrated a time effect ( P < 0.01) in all groups, and a time × group interaction ( P < 0.01) with a rise at 75 min post-exercise, which was greater in the GHD subjects than controls. IGFBP-2 and -3 increased significantly ( P < 0.01) over time in the GHD subjects, but not in the controls. No change in IGFBP-3 proteolysis or IGF-I bioactivity was found during exercise or recovery in either group. Conclusion Submaximal exercise induced minor changes in IGFBP-1, -2 and -3, without affecting IGFBP-3 proteolysis and IGF-I bioavailability. Thus the metabolic status during submaximal exercise does not require a change in plasma IGF-I bioavailability. Administration of GH to GHD adults does not result in changes in proteolysis or bioavailability.

The Role Of Lactate In The Exercise-induced Growth Hormone Response

The Role Of Lactate In The Exercise-induced Growth Hormone Response

The Role Of Lactate In The Exercise-induced Growth Hormone Response

PURPOSE During the last thirty years the contention that lactate is the major stimulus for the exercise induced hGH response (EIGR) has undergone a cycle of popularity and rejection. Currently, there is a growing body of evidence of the ubiquity of roles for lactate and in this regard the EIGR is no exception. McArdles disease is a type V inherited glycogen storage disease in which moyphorylase is absent. Accordingly these individuals do not produce lactate during exercise and hence represent an ideal model to explore the role of lactate in the EIGR. The present study examined the acute hGH response to a standardised graded exercise stimulus in McArdles patients. METHODS Eleven patients entered the study. All have McArdles disease as confirmed by both DNA and muscle biopsy analysis. Participants completed an incremental exercise test on a motorised treadmill. This comprised walking, beginning at 1.5 kph and increasing by 0.5 kph with each 3-minute stage. A 60s rest interval was given between successive stages for blood sampling. The test was terminated either after completion of 3 minutes at 6.5 kph or when a CR10 pain scale rating of “4” was achieved. Capillary (earlobe) blood samples for lactate and hGH determination were taken before the test and after each stage. HR was measured continuously throughout exercise. RESULTS Six individuals demonstrated no EIGR whilst five individuals demonstrated a modest rise in growth hormone concentration during exercise with peak values ranging from 0.73 to 8.40 μg.1−1. The two groups which arose from this demonstrated a significantly higher (p<0.05) peak heart rate in those who had an EIGR (169.25 ± 10.34 bpm vs 131.83 ± 24.00, mean ± SD). Although peak heart rate as a percentage of age-predicted maximal heart rate demonstrated a non-significant difference between the two groups, calculation of effect size revealed a meaningful difference (1.36) suggesting that those who produce hGH in response to exercise have a higher relative heart rate than those who do not. CONCLUSION The dichotomous response observed in McArdles patients in the present study suggests that lactate is not the primary stimulus for the EIGR. However, by virtue of a modest response in half the participants, lactate may be a co-stimulus of the EIGR along with other factors that have yet to be fully identified.

The exercise-induced growth hormone response in athletes.

Human growth hormone (hGH) is secreted in a pulsatile fashion, generally following a circadian rhythm. A number of physiological stimuli can initiate hGH secretion, the most powerful, non-pharmacological of which are sleep and exercise. hGH has many varied roles throughout life, from growth itself, including the turnover of muscle, bone and collagen, to the regulation of selective aspects of metabolic function including increased fat metabolism and the maintenance of a healthier body composition in later life. The exercise-induced growth hormone response (EIGR) is well recognised and although the exact mechanisms remain elusive, a number of candidates have been implicated. These include neural input, direct stimulation by catecholamines, lactate and or nitric oxide, and changes in acid-base balance. Of these, the best candidates appear to be afferent stimulation, nitric oxide and lactate. Resistance training results in a significant EIGR. Evidence suggests that load and frequency are determining factors in the regulation of hGH secretion. Despite the significant EIGR induced by resistance training, much of the stimulus for protein synthesis has been attributed to insulin-like growth factor-1 with modest contributions from the hGH-GH receptor interaction on the cell membrane. The EIGR to endurance exercise is associated with the intensity, duration, frequency and mode of endurance exercise. A number of studies have suggested an intensity 'threshold' exists for EIGR. An exercise intensity above lactate threshold and for a minimum of 10 minutes appears to elicit the greatest stimulus to the secretion of hGH. Exercise training above the lactate threshold may amplify the pulsatile release of hGH at rest, increasing 24-hour hGH secretion. The impact of chronic exercise training on the EIGR remains equivocal. Recent evidence suggests that endurance training results in decreased resting hGH and a blunted EIGR, which may be linked to an increased tissue sensitivity to hGH. While the potential ergogenic effects of exogenous GH administration are attractive to some athletes, the abuse of GH has been associated with a number of pathologies. Identification of a training programme that will optimise the EIGR may present a viable alternative. Ageing is often associated with a progressive decrease in the volume and, especially, the intensity of exercise. A growing body of evidence suggests that higher intensity exercise is effective in eliciting beneficial health, well-being and training outcomes. In a great many cases, the impact of some of the deleterious effects of ageing could be reduced if exercise focused on promoting the EIGR. This review examines the current knowledge and proposed mechanisms for the EIGR, the physiological consequences of endurance, strength and power training on the EIGR and its potential effects in elderly populations, including the aged athlete.

Effect of hydration on exercise-induced growth hormone response.

Growth hormone (GH) has demonstrated water-retaining effects in subjects at rest, whereas other research has indicated that GH may stimulate sweating. Thus, the aim of this study was to investigate the effect of fluid intake on the exercise-induced GH response. Seven healthy male volunteers (age: 27.4+/-1.3 years, weight: 74.5+/-1.1 kg, height: 179.3+/-2.3 cm) performed a 40-min submaximal rectangular cycling exercise in two different sessions. The first session (Session 1) was performed without water intake, and the second (Session 2) involved the ingestion of spring water (four intakes) corresponding to the volume of water lost during the first session. In session 1, the water loss was 568+/-32 ml. In Session 2, the volume of water loss was not significantly different from the volume of fluid intake (524+/-16 versus 568+/-32 ml respectively). The decrease in plasma volume was significantly reduced in Session 2 (-6.69+/-1.59% versus -11.3+/-1.89%; P<0.05). In Session 1, the GH concentration was significantly lower than that during Session 2 after 25 min (3.04+/-1.05 versus 5.26+/-1.81; P<0.05) and after 40 min (13.7+/-3.55 versus 17.60+/-4.14 ng/ml; P<0.05) of exercise. The total GH response was significantly lower in Session 1 than in Session 2 (136.6+/-39.2 versus 202.4+/-58.9 ng/ml x min; P<0.05). We conclude that the exercise-induced GH response decreases when exercise is performed without fluid intake.

Normal stimulated growth hormone secretion but low peripheral levels of insulin‐like growth factor I in prepubertal children with insulin‐dependent diabetes mellitus

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.

Exercise-induced increases in plasma catecholamines and growth hormone are augmented by selective alpha 2-adrenoceptor blockade in man.

A specific alpha 2-adrenoceptor antagonist (idazoxan) was used in man to examine the neuroregulation of growth hormone (GH) release and the effect of alpha 2-adrenoceptors on noradrenaline release. In the first study, GH-releasing factor (GRF)-induced GH release was unaffected in 6 normal volunteers by the prior administration of idazoxan, suggesting that the alpha 2-receptors involved in GH release are not operative at pituitary level. In the second study, 6 normal volunteers performed a bicycle exercise test with and without prior treatment with idazoxan. The exercise-induced GH response (to 13 +/- 5 mU/l) was significantly augmented by idazoxan (to 20 +/- 7 mU/l) which contrasts with the current view of GH release being regulated by stimulatory hypothalamic alpha 2-adrenoceptors and suggests that these alpha 2-adrenoceptors are capable of exerting a dual effect on GH release. The exercise-induced increase in plasma noradrenaline (to 1.45 +/- 0.19 micrograms/l) and in heart rate (to 142 +/- 5 beats/min) were also augmented by idazoxan (to 2.24 +/- 0.23 micrograms/l and 152 +/- 6 beats/min). A similar augmentation of the plasma adrenaline response to exercise was also found, whereas the blood glucose, plasma insulin and potassium response to exercise was unaffected by idazoxan. These results suggest that during exercise in man, alpha 2-adrenoceptors exert a tonic inhibitory influence on noradrenaline release which also serves to limit the exercise-induced tachycardia.