Human growth hormone response to repeated bouts of aerobic exercise

Kanaley, J. A., J. Y. Weltman, J. D. Veldhuis, A. D. Rogol,M. L. Hartman, and A. Weltman. Human growth hormone response torepeated bouts of aerobic exercise. J. Appl.Physiol. 83(5): 1756-1761, 1997.We examinedwhether repeated bouts of exercise could override growth hormone (GH)auto-negative feedback. Seven moderately trained men were studied onthree occasions: a control day (C), a sequential exercise day (SEB; at1000, 1130, and 1300), and a delayed exercise day (DEB; at 1000, 1400, and 1800). The duration of each exercise bout was 30 min at 70%maximal O₂ consumption (O_{2 max}) on a cycleergometer. Standard meals were provided at 0600 and 2200. GH wasmeasured every 5-10 min for 24 h (0800-0800). Daytime(0800-2200) integrated GH concentrations were ~150-160% greater during SEB and DEB than during C: 1,282 ± 345, 3,192 ± 669, and 3,389 ± 991 min · µg · l¹for C, SEB, and DEB, respectively [SEB > C(P < 0.06), DEB > C(P < 0.03)]. There were nodifferences in GH release during sleep (2300-0700). Deconvolutionanalysis revealed that the increase in 14-h integrated GH concentrationon DEB was accounted for by an increase in the mass of GH secreted perpulse (per liter of distribution volume,l_v): 7.0 ± 2.9 and 15.9 ± 2.6 µg/l_v for C and DEB,respectively (P < 0.01). Comparisonof 1.5-h integrated GH concentrations on the SEB and DEB days (30 minexercise + 60 min recovery) revealed that, with each subsequentexercise bout, GH release apparently increased progressively, with aslightly greater increase on the DEB day [SEB vs. DEB: 497 ± 162 vs. 407 ± 166 (bout 1), 566 ± 152 vs. 854 ± 184 (bout2), and 633 ± 149 vs. 1,030 ± 352 min · µg · l¹(bout 3),P < 0.05]. We conclude thatthe GH response to acute aerobic exercise is augmented with repeatedbouts of exercise.

     

Physical fitness attenuates leukocyte-endothelial adhesion in response to acute exercise.

Studies suggest that physical fitness promotes cardiovascular health, including improved endothelial function and possibly reduced inflammatory responses to stressors. This study examined the effects of fitness on leukocyte-endothelial adhesion in response to an acute exercise challenge. Peripheral blood mononuclear cell (PBMC) adhesion to human umbilical venous endothelial cells (HUVEC) was examined in 18 more-fit and 19 less-fit individuals [mean age 39 yr (SD 11)] before and after a 20-min treadmill exercise at 65-70% peak oxygen consumption. PBMC were isolated from whole blood (Ficoll-Paque) at rest and immediately after exercise. HUVEC were incubated for 4 h in the presence of cytokines IL-1 and IL-8 to activate endothelial adhesion molecule expression. Fit subjects showed a significant reduction in PBMC-HUVEC adhesion after exercise (P < 0.01) compared with less-fit subjects, who showed no significant change. Regardless of fitness levels, both at rest and in response to exercise, soluble ICAM-1 in the incubation media attenuated PBMC-HUVEC adhesion by approximately 81% (P < 0.001). The findings indicate that immune cells that demarginate in response to exercise have reduced ability to adhere in individuals who are physically fit, an effect apparently independent of ICAM-1 binding. The findings provide evidence of how physical fitness might protect individuals from inflammatory responses to exercise.     

Bioassayable growth hormone release in rats in response to a single bout of treadmill exercise.

Plasma growth hormone (GH) measured by immunoassay [immunoassayable GH (IGH)] and by tibial bioassay [bioassayable GH (BGH)] increases in humans in response to exercise. In rats, however, IGH does not change in response to exercise. The objective of this study was to determine the BGH response to an acute exercise bout in rats. The rats ran on a treadmill at a rate of 27 m/min for 15 min, after which plasma and pituitary hormones, including IGH and BGH, and plasma metabolites were measured. Plasma and pituitary IGH were unchanged from control groups after the acute exercise bout, whereas plasma BGH was increased by 300% and pituitary BGH was decreased by 50%. Plasma thyroxine and corticosterone levels were significantly increased after a single exercise bout, but plasma testosterone, 3,5, 3'-triiodothyronine, glucose, lactate, and triglyceride concentrations were unchanged. Given previous results from in situ nerve stimulation studies (Gosselink KL, Grindeland RE, Roy RR, Zhong H, Bigbee AJ, Grossman EJ, and Edgerton VR. J Appl Physiol 84: 1425-1430, 1998), these in vivo results are consistent with the rapid BGH response during exercise being induced by the activation of muscle afferents.     

Effect of metergoline, a specific serotonin antagonist, on human growth hormone response to arginine and L-dopa.

In seven normal subjects the repeated oral administration of metergoline, a specific antiserotonin agent, has enhanced HGH response to arginine infusion. Following placebo administration, arginine-induced HGH release was slightly but not significantly reduced; similarly, in eight metergoline treated subjects, HGH response to oral L-Dopa was slightly but not significantly reduced. HGH response to i.v. L-Dopa was not modified by the drug. These results suggest that serotonin controls HGH response only in response to arginine, not to L-Dopa.     

Rapid increase in plasma growth hormone after low-intensity resistance exercise with vascular occlusion.

Hormonal and inflammatory responses to low-intensity resistance exercise with vascular occlusion were studied. Subjects (n = 6) performed bilateral leg extension exercise in the seated position, with the proximal end of their thigh compressed at 214 +/- 7.7 (SE) mmHg throughout the session of exercise by means of a pressure tourniquet. Mean intensity and quantity of the exercise were 20% of 1 repetition maximum and 14 repetitions x 5 sets, respectively. In each set, the subjects repeated the movement until exhaustion. Plasma concentrations of growth hormone (GH), norepinephrine (NE), lacate (La), lipid peroxide (LP), interleukin-6 (IL-6), and activity of creatine phosphokinase (CPK) were measured before and after the exercise was finished and the tourniquet was released. Concentrations of GH, NE, and La consistently showed marked, transient increases after the exercise with occlusion, whereas they did not change a great deal after the exercise without occlusion (control) done at the same intensity and quantity. Notably, concentration of GH reached a level approximately 290 times as high as that of the resting level 15 min after the exercise. IL-6 concentration showed a much more gradual increase and was maintained at a slightly higher level than in the control even 24 h after exercise. Concentrations of LP and CPK showed no significant change. The results suggest that extremely light resistance exercise combined with occlusion greatly stimulates the secretion of GH through regional accumulation of metabolites without considerable tissue damage.     

The growth hormone secretory response to growth hormone releasing factor in the developing rhesus monkey.

We studied the development of the GH response to growth hormone releasing hormone (GHRH) using two doses of GHRH. The newborns demonstrated higher baseline GH and responses to GHRH than animals of any older age. There was no difference noted between the rise in GH in male and female subjects with 10 mcg/kg vs 1 mcg/kg. Serum cortisol concentrations did not correlate with serum GH concentrations. These developmental patterns of serum GH are similar to those known in the human being.     

Factors influencing the growth hormone response to growth hormone-releasing hormone in children with idiopathic growth hormone deficiency

OBJECTIVE: To evaluate the factors influencing the growth hormone (GH) response to GH-releasing hormone (GHRH) test in idiopathic GH deficiency. METHODS: 28 patients aged 4.9 +/- 0.7 years with certain GH deficiency were given GHRH (2 microg/kg). RESULTS: The GH peak after GHRH was correlated negatively with age at evaluation (r = -0.37, p < 0.05) and body mass index (r = -0.44, p = 0.02), and positively with anterior pituitary height (r = 0.47, p = 0.02), GH peak after non-GHRH stimulation (r = 0.78, p < 0.0001) and spontaneous GH peak (r = 0.82, p = 0.007). It was lower in the patients aged >5 years than in the youngest (p = 0.04), but it was similar in the patients with and without features suggesting a hypothalamic origin. CONCLUSION: The GH response to GHRH test cannot be used to differentiate between hypothalamic and pituitary forms of idiopathic GH deficiency, probably because the GH response decreases after the first 5 years of life, whatever the origin of the deficiency.     

Characteristics of circulating growth hormone in women after acute heavy resistance exercise

The effects of exercise on the molecular nature of secreted human growth hormone (GH) or its biological activity are not well understood. Plasma from women (average age 23.6 yr, n = 35), drawn before and after an acute heavy resistance exercise test, was fractionated by size exclusion chromatography into three size classes, namely, > 60 kDa (fraction A), 30-60 kDa (fraction B), and < 30 kDa (fraction C), before GH assay. Concentrations of GH in these fractions, as well as in unfractioned plasma, were measured by the Nichols immunoradiometric assay, National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) polyclonal competitive RIA, Diagnostic Systems Laboratory's immunofunctional assay (measures dimerization-capable species), and the rat tibial bioassay. Significantly increased circulating GH concentrations of two- to fourfold were observed when immunoassays in unfractionated plasma samples were used, but they showed no significant change with use of the rat tibial bioassay. Significant exercise-induced increases in GH were found in fractions B and C but not in fraction A. Because chemical reduction of the samples before GH immunoassay significantly increased GH concentrations in fractions B and C (Nichols and NIDDK kits) after exercise, it is concluded that exercise may specifically increase release of disulfide-linked hormone molecules and/or fragments. Finally, because most of the GH released after exercise was able to dimerize the GH receptor in vitro, it is also concluded that these forms have the two intact binding sites required to initiate signal transduction in target cells.     

Synergistic effect of obesity and lipid ingestion in suppressing the growth hormone response to exercise in children

Diet plays an important role in modulating exercise responses, including activation of the growth hormone (GH)/insulin-like growth factor-I (IGF-1) axis. Obesity and fat ingestion were separately shown to reduce exercise GH responses, but their combined effect, especially important in children, has not been studied. We therefore measured the GH response to exercise [30-min intermittent cycling, ten 2-min bouts at ~80% maximal aerobic capacity (Vo(2max)), separated by 1-min rest], started 45 min after ingestion of a high-fat meal (HFM) in 16 healthy [controls; body mass index percentile (BMI%ile) 51 ± 7], and 19 obese (Ob, BMI%ile 97 ± 0.4) children. Samples were drawn at baseline (premeal), and at start, peak, and 30 min postexercise. In the Ob group, a marked ~75% suppression of the GH response (ng/ml) to exercise was observed (2.4 ± 0.6 vs. 10.6 ± 2.1, P < 0.001). This level of suppression was also significantly greater compared with age-, fitness-, and BMI-matched historical controls that had performed identical exercise in fasting conditions. Our data indicate that the reduction in the GH response to exercise, already present in obese children vs. healthy controls, is considerably amplified by ingestion of fat nutrients shortly before exercise, implying a potentially downstream negative impact on growth factor homeostasis and long-term modulation of physiological growth.     

Age is an important determinant of the growth hormone response to sprint exercise in non-obese young men

BACKGROUND: The factors that regulate the growth hormone (GH) response to physiological stimuli, such as exercise, are not fully understood. The aim of the present study is to determine whether age, body composition, measures of sprint performance or the metabolic response to a sprint are predictors of the GH response to sprint exercise in non-obese young men. METHODS: Twenty-seven healthy, non-obese males aged 18-32 years performed an all-out 30-second sprint on a cycle ergometer. Univariate linear regression analysis was employed to evaluate age-, BMI-, performance- and metabolic-dependent changes from pre-exercise to peak GH and integrated GH for 60 min after the sprint. RESULTS: GH was elevated following the sprint (change in GH: 17.0 +/- 14.2 microg l(-1); integrated GH: 662 +/- 582 min microg l(-1)). Performance characteristics, the metabolic response to exercise and BMI were not significant predictors of the GH response to exercise. However, age emerged as a significant predictor of both integrated GH (beta = -0.547, p = 0.003) and change in GH (beta = -0.448, p = 0.019) after the sprint. CONCLUSION: In non-obese young men, age is a more important predictor of GH following sprint exercise than BMI, sprint performance or the metabolic response to sprint exercise.     

Arterial blood pressure response to heavy resistance exercise

The purpose of this study was to record the blood pressure response to heavy weight-lifting exercise in five experienced body builders. Blood pressure was directly recorded by means of a capacitance transducer connected to a catheter in the brachial artery. Intrathoracic pressure with the Valsalva maneuver was recorded as mouth pressure by having the subject maintain an open glottis while expiring against a column of Hg during the lifts. Exercises included single-arm curls, overhead presses, and both double- and single-leg presses performed to failure at 80, 90, 95, and 100% of maximum. Systolic and diastolic blood pressures rose rapidly to extremely high values during the concentric contraction phase for each lift and declined with the eccentric contraction. The greatest peak pressures occurred during the double-leg press where the mean value for the group was 320/250 mmHg, with pressures in one subject exceeding 480/350 mmHg. Peak pressures with the single-arm curl exercise reached a mean group value of 255/190 mmHg when repetitions were continued to failure. Mouth pressures of 30-50 Torr during a single maximum lift, or as subjects approached failure with a submaximal weight, indicate that a portion of the observed increase in blood pressure was caused by a Valsalva maneuver. It was concluded that when healthy young subjects perform weight-lifting exercises the mechanical compression of blood vessels combines with a potent pressor response and a Valsalva response to produce extreme elevations in blood pressure. Pressures are extreme even when exercise is performed with a relatively small muscle mass.     

Concurrent aerobic exercise interferes with the satellite cell response to acute resistance exercise

The addition of aerobic exercise (AE) to a resistance exercise (RE) program (concurrent exercise, CE) can interfere with maximum muscle fiber growth achieved with RE. Further, CE appears to markedly affect the growth of myosin heavy chain (MHC) I, but not MHC IIa fibers. The mechanism responsible for this "interference" is unclear. Satellite cell (SC) responsiveness to exercise appears to influence muscle adaptation but has not yet been examined following acute concurrent exercise. Thus, we assessed the fiber-type-specific SC response to RE, AE, and CE exercise. Eight college-aged males completed the following two exercise trials: the RE trial, which consisted of unilateral leg extensions and presses (4 sets ≥ 10 repetitions: 75% 1 repetition maximum, RM); and the AE/CE trial, which included an identical RE protocol with the opposite leg, immediately followed by subjects cycling for 90 min (60% W(max)). Muscle biopsies were obtained from the vastus lateralis before and 4 days after each session. Samples were cross-sectioned, stained with antibodies against NCAM, Ki-67, and MHC I, counterstained with DAPI, and analyzed for SC density (SC per fiber), SC activation, and fiber type. SC density increased to a greater extent following RE (38 ± 10%), compared with CE (-6 ± 8%). Similarly, MHC I muscle fiber SC density displayed a greater increase following RE (46 ± 14%), compared with AE (-7 ± 17%) and CE (-8 ± 8%). Our data indicate that the SC response to RE is blunted when immediately followed by AE, at least in MHC I muscle fibers, and possibly MHC II fibers. This suggests that the physiological environment evoked by AE might attenuate the eventual addition of myonuclei important for maximum muscle fiber growth and consequent force-producing capacity.     

The growth hormone response to repeated bouts of sprint exercise with and without suppression of lipolysis in men.

A single 30-s sprint is a potent physiological stimulus for growth hormone (GH) release. However, repeated bouts of sprinting attenuate the GH response, possibly due to negative feedback via elevated systemic free fatty acids (FFA). The aim of the study was to use nicotinic acid (NA) to suppress lipolysis to investigate whether serum FFA can modulate the GH response to exercise. Seven nonobese, healthy men performed two trials, consisting of two maximal 30-s cycle ergometer sprints separated by 4 h of recovery. In one trial (NA), participants ingested NA (1 g 60 min before, and 0.5 g 60 and 180 min after sprint 1); the other was a control (Con) trial. Serum FFA was not significantly different between trials before sprint 1 but was significantly lower in the NA trial immediately before sprint 2 [NA vs. Con: mean (SD); 0.08 (0.05) vs. 0.75 (0.34) mmol/l, P < 0.05]. Peak and integrated GH were significantly greater following sprint 2 compared with sprint 1 in the NA trial [peak GH: 23.3 (7.0) vs. 7.7 (11.9) microg/l, P < 0.05; integrated GH: 1,076 (350) vs. 316 (527) microg.l(-1).60 min(-1), P < 0.05] and compared with sprint 2 in the Con trial [peak GH: 23.3 (7.0) vs. 5.2 (2.3) microg/l, P < 0.05; integrated GH: 1,076 (350) vs. 206 (118) microg.l(-1).60 min(-1), P < 0.05]. In conclusion, suppressing lipolysis resulted in a significantly greater GH response to the second of two sprints, suggesting a potential role for serum FFA in negative feedback control of the GH response to repeated exercise.     

Influence of training on the response to exercise of adrenocorticotropin and growth hormone plasma concentrations in human swimmers

The aim of the present study was to evaluate the response of adrenocorticotropin ([ACTH]) and growth hormone ([GH]) concentrations to a typical aerobic swimming set during a training season. Nine top-level male endurance swimmers (age range 17–23 years) were tested during three training sessions occurring 6, 12 and 18 weeks after the beginning of the season. During each session, after a standard warm-up, the swimmers performed a training set of 15 × 200-m freestyle, with 20 s of rest between repetitions, at a predetermined individual speed. Blood samples were collected before warm-up and at the end of the training set. A few days before each session, the individual swimming velocity corresponding to the 4 mmol · l⁻¹ blood lactate concentration (v ₄) was assessed as a standard of aerobic performance. Aerobic training affected v ₄ levels, which were highest 18 weeks after the beginning of the season; at the same time, while [ACTH] response was attenuated, [GH] response was enhanced. These results could be considered as adaptations to the exercise intensity. In our training programme, these adaptations seemed to have occurred between the 12th and 18th weeks of the training season. Accepted: 21 April 1998     

Effect of acute postexercise ethanol intoxication on the neuroendocrine response to resistance exercise.

This investigation was conducted to determine the effect of postexercise ethanol intoxication (21.97 +/- 1.09 mmol/l blood) on the response of selected aspects of the neuroendocrine system to a resistance exercise (Ex) session. Nine resistance-trained men (25.0 +/- 1.4 yr, 179.4 +/- 3.4 cm, 79.7 +/- 3.3 kg) were used to compare three 3-day treatments: control, Ex, and ethanol after exercise (ExEt). Blood was collected serially from an antecubital vein before exercise, immediately after exercise, and for pooled analysis at 20-40 (2 samples), 60-120 (4 samples), and 140-300 (9 samples) min after exercise on day 1 and in the morning (2 samples each) on days 2 and 3. Ethanol did not increase circulating epinephrine, norepinephrine, or cortisol concentration (Cort) above Ex elevations. At 60-120 min, only ExEt Cort was greater than control Cort. Concentrations of testosterone, luteinizing hormone, and corticotropin were not affected by either treatment. It is concluded that, although this blood ethanol concentration is insufficient to acutely increase Cort above that caused by Ex alone, it appears that ethanol may have a prolonged effect beyond the Ex response. This blood ethanol concentration does not further stimulate the sympathoadrenal system during the postexercise response.