Impact of acute exercise intensity on pulsatile growth hormone release in men

To investigate the effects of exercise intensity on growth hormone (GH) release, 10 male subjects were tested on 6 randomly ordered occasions [1 control condition (C), 5 exercise conditions (Ex)]. Serum GH concentrations were measured in samples obtained at 10-min intervals between 0700 and 0900 (baseline) and 0900 and 1300 (exercise+ recovery). Integrated GH concentrations (IGHC) were calculated by trapezoidal reconstruction. During Ex subjects exercised for 30 min (0900–0930) at one of the following intensities [normalized to the lactate threshold (LT)]: 25 and 75% of the difference between LT and rest (0.25LT and 0.75LT, respectively), at LT, and at 25 and 75% of the difference between LT and peak (1.25LT and 1.75LT, respectively). No differences were observed among conditions for baseline IGHC. Exercise+recovery IGHC (mean ± SE: C = 250 ± 60; 0.25LT = 203 ± 69; 0.75LT = 448 ± 125; LT = 452 ± 119; 1.25LT = 512 ± 121; 1.75LT = 713 ± 115 µg · l-1 · min-1) increased linearly with increasing exercise intensity (P < 0.05). Deconvolution analysis revealed that increasing exercise intensity resulted in a linear increase in the mass of GH secreted per pulse and GH production rate [production rate increased from 16.5 ± 4.5 (C) to 32.1 ± 5.2 µg · distribution volume-1 · min-1(1.75LT), P < 0.05], with no changes in GH pulse frequency or half-life of elimination. We conclude that the GH secretory response to exercise is related to exercise intensity in a linear dose-response pattern in young men

Growth hormone (GH) release during acute and chronic aerobic and resistance exercise: Recent Findings.

Exercise is a potent physiological stimulus for growth hormone (GH) secretion, and both aerobic and resistance exercise result in significant, acute increases in GH secretion. Contrary to previous suggestions that exercise-induced GH release requires that a ‘threshold’ intensity be attained, recent research from our laboratory has shown that regardless of age or gender, there is a linear relationship between the magnitude of the acute increase in GH release and exercise intensity. The magnitude of GH release is greater in young women than in young men and is reduced by 4–7-fold in older individuals compared with younger individuals. Following the increase in GH secretion associated with a bout of aerobic exercise, GH release transiently decreases. As a result, 24-hour integrated GH concentrations are not usually elevated by a single bout of exercise. However, repeated bouts of aerobic exercise within a 24-hour period result in increased 24-hour integrated GH concentrations. Because the GH response to acute resistance exercise is dependent on the work-rest interval and the load and frequency of the resistance exercise used, the ability to equate intensity across different resistance exercise protocols is desirable. This has proved to be a difficult task. Problems with maintaining patent intravenous catheters have resulted in a lack of studies investigating alterations in acute and 24-hour GH pulsatile secretion in response to resistance exercise. However, research using varied resistance protocols and sampling techniques has reported acute increases in GH release similar to those observed with aerobic exercise. In young women, chronic aerobic training at an intensity greater than the lactate threshold resulted in a 2-fold increase in 24-hour GH release. The time line of adaptation and the mechanism(s) by which this training effect occurs are still elusive. Unfortunately, there are few studies investigating the effects of chronic resistance training on 24-hour GH release. The decrease in GH secretion observed in individuals who are older or have obesity is associated with many deleterious health effects, although a cause and effect relationship has not been established. While exercise interventions may not restore GH secretion to levels observed in young, healthy individuals, exercise is a robust stimulus of GH secretion. The combination of exercise and administration of oral GH secretagogues may result in greater GH secretion than exercise alone in individuals who are older or have obesity. Whether such interventions would result in favourable clinical outcomes remains to be established

Contrasting negative-feedback control of endogenously driven and exercise-stimulated pulsatile growth hormone secretion in women and men

GH represses its own secretion via rapid and reversible feedback exerted at key hypothalamic loci. The primary mechanisms include stimulation of somatostatin release and inhibition of GHRH outflow. Autoinhibition is prominent in the adult male rat but diminutive in the female animal. The sex contrast reflects important differences in central neuropeptide signaling in this species. No comparable insights into gender-specific control of GH autofeedback are available in the human. To examine this issue, we quantitated acute recombinant human (rh)GH-induced inhibition of baseline (resting) and aerobic exercise-stimulated GH secretion in healthy young men (n = 8) and early follicular-phase women (n = 6). Each subject underwent four fasting, morning inpatient infusion studies in a prospectively randomized, placebo-controlled, double-blind, within-subject cross-over design. The feedback paradigm comprised 6-min bolus iv infusion of saline or rhGH (10 µg/kg) followed in 120 min by rest or submaximal aerobic (individually calibrated) bicycle ergometry for 30 min. Concomitantly, blood was sampled every 10 min for 6 h, and sera were submitted to immunochemiluminometric GH assay (sensitivity 0.005 µg/liter). Biexponential deconvolution analysis was applied to estimate stimulated GH secretory-burst mass (µg/liter per 90 min after onset of exercise or rest). Women and men had statistically comparable serum estradiol but unequal testosterone concentrations. Repeated-measures ANOVA documented a significant three-way interaction among gender, stimulus type (rest or exercise), and feedback status (saline or rhGH injection) in determining GH secretory-burst mass (P = 0.008). There were prominent two-factor interactions among gender and exercise (P In summary, the present clinical investigation unmasks: 1) markedly greater fractional feedback inhibition of pulsatile GH secretion by rhGH in young women than men; and 2) partial resistance of the aerobic-exercise stimulus to GH autofeedback in both women and men. We postulate that sex-steroid-specific control of somatostatin and GHRH outflow may mediate the former gender contrasts, whereas unknown (gender-independent) factors may determine the capability of exercise to significantly antagonize GH autoinhibition

Growth hormone response to graded exercise intensities is attenuated and the gender difference abolished in older adults

We investigated the joint impact of age, gender, and exercise intensity on growth hormone (GH) secretion. At a university center, nine young men, eight young women, seven older men, and six older women were each tested on six randomly ordered occasions [control (C) and 5 exercise conditions (Ex)]. Serum GH concentrations were measured by immunochemiluminometry [10-min samples: 0700–0900 (baseline); 0900–1300 (C or Ex + recovery)]. Integrated GH concentrations (IGHC) were calculated by trapezoidal reconstruction, and GH secretion was modeled by deconvolution analyses. Subjects exercised from 0900 to 0930 at graded intensities [standardized to individual lactate threshold (LT)] of 25 and 75% of the difference between rest and LT, LT, and 25 and 75% of the difference between LT and peak oxygen consumption. Data were analyzed via mixed-effects ANOVA for repeated measures with post hoc contrasts. We found that 1) Ex elevated IGHC above C in all four cohorts, 2) 1.75 LT Ex resulted in maximal IGHC, 3) IGHC differed by gender in young (women > men) but not older adults, 4) older adults secreted 50% less GH during graded exercise, 5) Ex selectively augmented the mass of GH secreted per burst, and 6) higher Ex + recovery IGHC in young women was due to higher baseline IGHC, rather than greater stimulated GH secretion. We conclude that young women manifest a greater absolute and incremental IGHC response to exercise than postmenopausal women and men of any age. Age diminishes the GH response to exercise and abolishes the young-adult gender difference. Attenuation of GH responses to all exercise intensities in older adults has implications for exercise prescription because higher exercise intensities may be required to stimulate GH release in older adults

Effect of sleep deprivation on exercise-induced growth hormone release

Growth hormone (GH) is released in a pulsatile fashion from the anterior pituitary gland, with the greatest release occurring during sleep and exercise. Under normal conditions, nocturnal GH release is attenuated during sleep deprivation. Acute sleep deprivation can also impair exercise performance and cognitive function. Therefore, the primary purpose of this study was to assess the impact of acute sleep deprivation on exercise-induced GH release. Secondary aims were to investigate alterations in exercise performance and cognitive function during acute sleep deprivation. Ten male subjects (20.6 ± 1.4 years) were screened for normal sleeping patterns before completing two randomized 24-hour laboratory sessions. They completed a brief, high-intensity exercise bout following either a night of adequate sleep (SLEEP) or acute (24-hour) sleep deprivation (SLD). Anaerobic performance (mean power [MP], peak power [PP], time to peak power [TTPP], minimum power [MinP], fatigue index [FI] and total work per sprint [TWPS]) was determined from four maximal 30-sec Wingate sprints on a cycle ergometer followed by four minutes of active recovery between each sprint. Subjects also performed psychomotor vigilance tasks (PVT) and Paced Auditory Serial Addition Tests (PASAT) during each 24-hr session (0800h, 2000h, 0600h and 0730h) with the latter two taken immediately pre- and post-exercise. The average amount of sleep in the 7 days prior to each session was similar between the SLEEP and SLD sessions (7.92 ± 0.33 vs. 7.98 ± 0.39 hr, 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 hours vs. 7.92 ± 0.33 hours, respectively) (p = 0.166). Repeated measures analysis of variance (ANOVA) revealed a significant interaction effect of sprint x session on PP (p < 0.05). Only the peak power output during sprint 1 of the SLEEP vs. SLD session was significantly greater (1207 ± 177 vs. 1150 ± 137 W, respectively, p < 0.01). MP, PP, MinP and TWPS decreased significantly within each session (p < 0.01), but there were no significant main effects of session. Respiratory rate (RR) was significantly elevated at rest during the SLD vs. SLEEP session (14.8 ± 2.2 vs. 13.7 ± 3.2 breaths/min, p < 0.05) while heart rate (HR) was significantly depressed at rest (60 ± 8 vs. 64 ± 8 bpm, p < 0.05) and during exercise (176 ± 9 vs. 182 ± 9 bpm, p < 0.05). Average oxygen consumption (VO2), metablic equivalent (METS), expired carbon dioxide (VCO2), ventilation (VE), respiratory exchange ratio (RER), respiratory rate (RR), tidal volume (VT), peak VO2 and peak METS were all similar between sessions. Resting GH concentration and time to reach exercise-induced peak GH concentration were similar between the SLEEP and SLD sessions (0.57 ± 0.13 vs. 1.35 ± 0.55 µg/L, p = 0.575; 29.5 ± 2.2 vs. 27.0 ± 1.5 min, p = 0.257, respectively). However, GH AUC (exercise + recovery), peak GH concentration and ?GH (peak GH – resting GH) were significantly lower during the SLEEP session (p < 0.01). PVT scores post-exercise were significantly poorer during the SLD session (326.2 ± 36.6 vs. 298.8 ± 21.1 msec, p < 0.05). In conclusion, acute sleep deprivation influenced exercise-induced peak HR and GH but had minimal effects on exercise performance. Furthermore, sleep deprivation had no effect on cognitive measures at rest, but did impair sensory sensitivity following exercise

Gender governs the relationship between exercise intensity and growth hormone release in young adults

We previously reported that in young adult males growth hormone (GH) release is related to exercise intensity in a linear dose-response manner (Pritzlaff et al. J Appl Physiol 87: 498–504, 1999). To investigate the effects of gender and exercise intensity on GH release, eight women (24.3 ± 1.3 yr, 171 ± 3.2 cm height, 63.6 ± 8.7 kg weight) were each tested on six randomly ordered occasions [1 control condition (C), 5 exercise conditions (Ex)]. Serum GH concentrations were measured in samples obtained at 10-min intervals between 0700 and 0900 (baseline) and 0900 and 1300 (Ex + recovery or C). Integrated GH concentrations (IGHC) were calculated by trapezoidal reconstruction. During Ex, subjects exercised for 30 min (0900–0930) at one of the following intensities [normalized to the lactate threshold (LT)]: 25 and 75% of the difference between LT and rest, at LT, and at 25 and 75% of the difference between LT and peak O2 uptake. No differences were observed among conditions for baseline IGHC. To determine whether total (Ex + recovery) IGHC changed with increasing exercise intensity, slopes associated with individual linear regression models were subjected to a Wilcoxon signed-rank test. To test for gender differences, data in women were compared with the previously published data in men. A Wilcoxon ranked-sums two-tailed test was used to analyze the slopes and intercepts from the regression models. Total IGHC increased linearly with increasing exercise intensity. The slope and intercept values for the relationship between total IGHC and exercise intensity were greater in women than in men. Deconvolution analysis (0700–1300 h) revealed that, regardless of gender, increasing exercise intensity resulted in a linear increase in the mass of GH secreted per pulse and summed GH production rate, with no changes in GH secretory pulse frequency or apparent half-life of elimination. Exercise reduced the half-duration of GH secretory burst in men but not in women. Gender comparisons revealed that women had greater basal (nonpulsatile) GH secretion across all conditions, more frequent GH secretory pulses, a greater GH secretory pulse amplitude, a greater production rate, and a trend for a greater mass of GH secreted per pulse than men. We conclude that, in young adults, the GH secretory response to exercise is related to exercise intensity in a linear dose-response pattern. For each incremental increase in exercise intensity, the fractional stimulation of GH secretion is greater in women than in men

Effects of gender on exercise-induced growth hormone release

We examined gender differences in growth hormone (GH) secretion during rest and exercise. Eighteen subjects (9 women and 9 men) were tested on two occasions each [resting condition (R) and exercise condition (Ex)]. Blood was sampled at 10-min intervals from 0600 to 1200 and was assayed for GH by chemiluminescence. At R, women had a 3.69-fold greater mean calculated mass of GH secreted per burst compared with men (5.4 ± 1.0 vs. 1.7 ± 0.4 µg/l, respectively) and higher basal (interpulse) GH secretion rates, which resulted in greater GH production rates and serum GH area under the curve (AUC; 1,107 ± 194 vs. 595 ± 146 µg · l-1 · min, women vs. men; P = 0.04). Compared with R, Ex resulted in greater mean mass of GH secreted per burst, greater mean GH secretory burst amplitude, and greater GH AUC (1,196 ± 211 vs. 506 ± 90 µg · l-1 · min, Ex vs. R, respectivley; P < 0.001). During Ex, women attained maximal serum GH concentrations significantly earlier than men (24 vs. 32 min after initiation of Ex, respectively; P = 0.004). Despite this temporal disparity, both genders had similar maximal serum GH concentrations. The change in AUC (adjusted for unequal baselines) was similar for men and women (593 ± 201 vs. 811 ± 268 µg · l-1 · min), but there were significant gender-by-condition interactive effects on GH secretory burst mass, pulsatile GH production rate, and maximal serum GH concentration. We conclude that, although women exhibit greater absolute GH secretion rates than men both at rest and during exercise, exercise evokes a similar incremental GH response in men and women. Thus the magnitude of the incremental secretory GH response is not gender dependent

Exercise-dependent growth hormone release is linked to markers of heightened central adrenergic outflow

To test the hypothesis that heightened sympathetic outflow precedes and predicts the magnitude of the growth hormone (GH) response to acute exercise (Ex), we studied 10 men [age 26.1 ± 1.7 (SE) yr] six times in randomly assigned order (control and 5 Ex intensities). During exercise, subjects exercised for 30 min (0900–0930) on each occasion at a single intensity: 25 and 75% of the difference between lactate threshold (LT) and rest (0.25LT, 0.75LT), at LT, and at 25 and 75% of the difference between LT and peak (1.25LT, 1.75LT). Mean values for peak plasma epinephrine (Epi), plasma norepinephrine (NE), and serum GH concentrations were determined [Epi: 328 ± 93 (SE), 513 ± 76, 584 ± 109, 660 ± 72, and 2,614 ± 579 pmol/l; NE: 2.3 ± 0.2, 3.9 ± 0.4, 6.9 ± 1.0, 10.7 ± 1.6, and 23.9 ± 3.9 nmol/l; GH: 3.6 ± 1.5, 6.6 ± 2.0, 7.0 ± 2.0, 10.7 ± 2.4, and 13.7 ± 2.2 µg/l for 0.25, 0.75, 1.0, 1.25, and 1.75LT, respectively]. In all instances, the time of peak plasma Epi and NE preceded peak GH release. Plasma concentrations of Epi and NE always peaked at 20 min after the onset of Ex, whereas times to peak for GH were 54 ± 6 (SE), 44 ± 5, 38 ± 4, 38 ± 4, and 37 ± 2 min after the onset of Ex for 0.25–1.75LT, respectively. ANOVA revealed that intensity of exercise did not affect the foregoing time delay between peak NE or Epi and peak GH (range 17–24 min), with the exception of 0.25LT (P < 0.05). Within-subject linear regression analysis disclosed that, with increasing exercise intensity, change in (?) GH was proportionate to both ?NE (P = 0.002) and ?Epi (P = 0.014). Furthermore, within-subject multiple-regression analysis indicated that the significant GH increment associated with an antecedent rise in NE (P = 0.02) could not be explained by changes in Epi alone (P = 0.77). Our results suggest that exercise intensity and GH release in the human may be coupled mechanistically by central adrenergic activation

Thyroxine-binding globulin: investigation of microheterogeneity

Preparations of T4-binding globulin (TBG) from human serum was performed using only two affinity chromatography steps. Purity of the protein was demonstrated by a single band in overloaded disc and sodium dodecyl sulfate electrophoresis, equimolar binding to T4, and linearity in sedimentation velocity run. The molecular weight was calculated to be 60,000 +/- 3,000 daltons (n = 3), the sedimentation coefficient was 3.95S, and the Stokes' radius was 37 A. The amino acid composition was found to be in good agreement with the calculations of other authors. By isoelectric focussing (IEF), pure TBG showed four main bands at pH 4.25, 4.35, 4.45, and 4.55 together with several fainter bands. The N- acetylneuraminic acid (NANA) content of the four TBG bands isolated by preparative IEF was found to decrease from 10.2 mol NANA/mol TBG in the band at pH 4.25 to 4.8 mol NANA/mol TBG in the band at pH 4.55. No significant difference in the affinity constants of the TBG bands to T4 was found. The affinity constants for TBG ranged from 3.1 x 10(9) to 7.2 x 10(9) M-1. Sequential kinetic desialylation of pure TBG resulted in a progressive tendency toward one major band at pH 6.0. In native sera, microheterogeneity of TBG was detected after IEF on polyacrylamide gel plates by immunofixation. The typical TBG patterns shown by pure TBG were also found in normal subjects. Characteristic deviations from this pattern were found in the sera of females during estrogen therapy or pregnancy, where there was a gradual increase in density of the band at pH 4.25 and the appearance of an additional band at pH 4.15. In sera from patients with liver disease and elevated TBG levels, there was a fading of the acidic bands, whereas the more alkaline band at pH 4.55 was intensified. It is therefore proposed that microheterogeneity of TBG is caused by differences in NANA content and that variations of TBG patterns in native sera may reflect altered TBG synthesis or degradation. A genetically related microheterogeneity of TBG could not be demonstrated after examination of 800 sera, including 2 families with quantitative TBG deficiency

The impact of sex and exercise duration on growth hormone secretion

Previous research clearly indicates a linear relationship between exercise intensity and growth hormone (GH) release and that this relationship is influenced by sex. The present study examined the GH response to increasing exercise duration in young men and women. Fifteen healthy subjects (8 men and 7 women) completed three randomly assigned exercise sessions (30, 60, and 120 min) at 70% of peak oxygen consumption. Blood samples were collected every 10 min beginning 30 min before exercise, for a total of 240 min. Total integrated GH concentration (IGHC) increased with increasing exercise duration for men and women (601, 1,394, and 2,360 µg/l·4 h; 659, 1,009 and 1,243 µg/l·4 h for 30, 60, and 120 min of exercise, respectively). Regression analysis revealed that IGHC (logarithmically transformed) was significantly influenced by exercise duration (logarithmically transformed) (120 min > 60 min > 30 min) and that a significant sex-dependent effect was present even after adjustments for fitness level and percent body fat (men > women). The slope of the regression line was greater for men than for women (1.003 vs. 0.612; P = 0.013), but the average height of the regression line was greater for women (7.287 vs. 6.595; P < 0.001). Although GH secretory pulse half-duration was greater in women (P = 0.001), and GH half-life was greater in men (P = 0.001), they were not affected by exercise duration. The total mass of GH secreted during exercise increased with exercise duration (P < 0.001) but was not affected by sex (P = 0.137). Results from the present investigation indicate that when exercise intensity is constant, exercise duration significantly increases IGHC and that this relationship is sex dependent