Cortisol and growth hormone responses to exercise at different times of day.

Exercise of appropriate intensity is a potent stimulus for GH and cortisol secretion. Circadian and diurnal rhythms may modulate the GH and cortisol responses to exercise, but nutrition, sleep, prior exercise patterns, and body composition are potentially confounding factors. To determine the influence of the time of day on the GH and cortisol response to acute exercise, we studied 10 moderately trained young men (24.1 +/- 1.1 yr old; maximal oxygen consumption, 47.9 +/- 1.4 mL/kg.min; percent body fat, 13.2 +/- 0.6%). After a supervised night of sleep and a standard meal 12 h before exercise, subjects exercised at a constant velocity (to elicit an initial blood lactate concentration of approximately 2.5 mmol/L) on a treadmill for 30 min on 3 separate occasions, starting at 0700, 1900, and 2400 h. Blood samples were obtained at 5-min intervals for 1 h before and 5 h after the start of exercise; subjects were not allowed to sleep during this period. Subjects were also studied on 3 control days under identical conditions without exercise. There were no significant differences with time of day in the mean blood lactate and submaximal oxygen consumption values during exercise. The differences over time in serum GH and cortisol concentrations between the exercise day and the control day were determined with 95% confidence limits for each time of day. Exercise stimulated a significant increase in serum GH concentrations over control day values for approximately 105--145 min (P < 0.05) with no significant difference in the magnitude of this response by time of day. The increase in serum GH concentrations with exercise was followed by a transient suppression of GH release (for approximately 55--90 min; P < 0.05) after exercise at 0700 and 1900 h, but not at 2400 h. Although the duration of the increase in serum cortisol concentrations after exercise was similar (approximately 150--155 min; P < 0.05) at 0700, 1900, and 2400 h, the magnitude of this increase over control day levels was greatest at 2400 h. This difference was significant for approximately 130 min and approximately 40 min compared to exercise at 1900 and 0700 h, respectively (P < 0.05). The cortisol response to exercise at 0700 h was significantly greater than that at 1900 h for about 55 min (P < 0.05). A rebound suppression of cortisol release for about 50 min (P < 0.05) was observed after exercise at 2400 h, but not 0700 or 1900 h. Both baseline (before exercise) and peak cortisol concentrations were significantly higher at 0700 h than at 1900 or 2400 h (P < 0.01). We conclude that time of day does not alter the GH response to exercise; however, the exercise-induced cortisol response is modulated by time of day.

Alterations in luteinizing hormone secretory activity in women with insulin-dependent diabetes mellitus and secondary amenorrhea.

To investigate hypothalamic and/or pituitary abnormalities in women with poorly controlled insulin-dependent diabetes mellitus (IDDM) and secondary amenorrhea, we measured serum LH every 10 min for 24 h and for 2 additional h after the administration of exogenous GnRH in 8 women with IDDM and amenorrhea and compared these to data from 15 eumenorrheic nondiabetic women. LH pulses were characterized by the pulse detection algorithm Cluster, and secretory episodes were evaluated using the multiple parameter deconvolution procedure Deconv. Cluster analysis revealed fewer LH pulses per 24 h (14.3 +/- 1.2 vs. 19.9 +/- 0.6; P < 0.001; mean +/- SEM), a greater peak width (63 +/- 4.9 vs. 44 +/- 2.2 min; P < 0.01), and greater peak area (136 +/- 17 vs. 89 +/- 13 IU/L.min; P < 0.01) in the diabetic women. Analysis with Deconv revealed fewer LH secretory episodes per 24 h in the diabetic women (14.4 +/- 0.9 vs. 20.4 +/- 0.5; P < 0.001) and no statistical difference in LH half-lives. The IDDM women responded to a 10-micrograms GnRH bolus with LH pulses of larger total (51 +/- 15.9 vs. 15 +/- 1.4 IU/L; P < 0.01) and incremental (29 +/- 7.6 vs. 9 +/- 1.2; P < 0.001) amplitude. In summary, we observed that amenorrheic diabetic women have fewer LH pulses/secretory episodes than normal women. However, they respond well to exogenous GnRH, suggesting that compromise of the GnRH pulse generator, rather than pituitary dysfunction, is responsible for their menstrual dysfunction.

Short-term modulation of the androgen milieu alters pulsatile, but not exercise- or growth hormone (GH)-releasing hormone-stimulated GH secretion in healthy men: impact of gonadal steroid and GH secretory changes on metabolic outcomes.

Gonadal steroids are known to alter GH secretion as well as tissue metabolism. The present study was designed to examine the effects of short term (2- to 3-week) alterations in gonadal steroids on basal pulsatile (nonstimulated) and exercise- and GH-releasing hormone-stimulated GH secretion, urinary nitrogen excretion, and basal and exercise-stimulated oxygen consumption. Two protocols were conducted, which reflect a total of 18 separate studies. In the first paradigm, 5 healthy young men were each studied in a double blind, randomized manner during 3 different gonadal hormone manipulations, in which serum testosterone was varied from hypogonadal (induced by leuprolide) to eugonadal (saline injections) to high levels (testosterone enanthate, 3 mg/kg.week, i.m.). There was a washout period of 8 weeks between treatments. In the second protocol, 3 of the original subjects were studied after 2 weeks of treatment with stanozolol (0.1 mg/kg.day). Two to 3 weeks after the desired changes in serum testosterone, each subject was admitted to the General Clinical Research Center for study. The hypogonadal state (serum testosterone, 33 ng/dL) increased urinary nitrogen loss (by 34%; P < 0.005) and decreased basal metabolic rate (by 12%; P < 0.02) compared with the eugonadal state (testosterone, 796 ng/dL). High dose testosterone (1609 ng/dL) further decreased urinary nitrogen loss over the eugonadal state (by 16%; P < 0.05). Stanozolol yielded the lowest urinary nitrogen excretion of all (P < 0.03). Like urinary nitrogen, the basal metabolic rate showed the greatest change between the hypogonadal and eugonadal states (12%; P < 0.02), with a lesser change during high dose testosterone treatment (4%). Analogously, end-exercise oxygen consumption rose by 11% between the hypogonadal and eugonadal states (P < 0.05). Between the hypogonadal and eugonadal states, no significant changes in pulsatile (nonstimulated), exercise-stimulated, or GRF-stimulated GH secretion or serum insulin-like growth factor I concentrations were observed. Raising testosterone to supraphysiological levels increased pulsatile GH secretion by 62% over that with leuprolide and by 22% over that with saline (P < 0.05). High dose testosterone treatment also increased serum insulin-like growth factor I concentrations by 21% and 34% over those during the eugonadal and hypogonadal states, respectively (P < 0.01). Testosterone did not affect either exercise- or GRF-stimulated GH secretion. In protocol 2, stanozolol did not affect any parameter of GH secretion. To examine the interaction between GH secretion and testosterone on urinary nitrogen excretion and basal metabolic rate, a one-way analysis of covariance was undertaken. Statistical examination of GH production as the covariate and testosterone (by tertile) as the interactive factor demonstrated significant relationships between serum testosterone levels and either urinary nitrogen (P < 0.02) or basal metabolic rate (P < 0.01), but not GH secretion (P = NS). In summary, these results demonstrate that short term modulation of the androgen milieu affects metabolic outcome without necessitating changes in GH secretion. These results have significance for both normal physiology and for the treatment of hypogonadal GH-deficient patients.

Reliability of estimates of pulsatile characteristics of luteinizing hormone and growth hormone release in women.

The test-retest reliability of estimates of pulsatile LH and GH release was evaluated in 23 eumenorrheic women during the early follicular phase of the menstrual cycle. Each subject was studied during two successive or near-successive menstrual cycles by repetitive blood sampling every 10 min for 24 h. Pulsatile parameters for LH and GH release were identified and characterized using the Cluster pulse detection algorithm. For LH, no significant differences existed in any parameter mean between the two 24-h admissions. Correlation coefficients for consecutive 24-h studies ranged from r = 0.22 (P less than 0.32) for number of LH peaks to r = 0.79 (P less than 0.0001) for 24-h integrated LH values (area under the concentration vs. time curve). No significant mean differences in any parameter were observed for consecutive 24-h GH evaluations. Correlation coefficients for 24-h GH ranged from r = 0.25 (P less than 0.34) for nadir to r = 0.71 (P less than 0.002) for incremental peak increase. Cosinor analysis was used to determine significant 24-h variations in LH and GH concentrations. Statistically significant differences existed between admissions for the amplitude of the nyctohemeral LH rhythm and its acrophase (time at which maximal hormone value was attained), but no mean differences were found for mesor (mean concentration). Correlation coefficients for LH were r = 0.10 (P less than 0.65), r = 0.43 (P less than 0.08), and r = 0.78 (P less than 0.0001) for phase, amplitude, and mesor, respectively. No significant mean differences existed for any parameter of nyctohemeral GH rhythms. Correlation coefficients were r = -0.18 (P less than 0.52), r = 0.49 (P less than 0.72), and r = 0.14 (P less than 0.80) for 24-h GH amplitude, phase, and mesor, respectively. We conclude that comparisons of mean and integrated LH and GH concentrations over a 24-h interval in the early follicular phase of the menstrual cycle are reliable; however, certain pulsatile properties responsible for the achievement of the mean daily concentrations of LH and GH may be nonuniform from menstrual cycle to menstrual cycle. In addition, nonuniformities may exist in the nyctohemeral rhythms of serum concentrations of LH and GH in the adult woman between cycles when a single 24-h time series is the basis for the analysis.

Abdominal visceral fat and fasting insulin are important predictors of 24-hour GH release independent of age, gender, and other physiological factors.

Numerous physiological factors modulate GH secretion, but these variables are not independent of one another. We studied 40 younger (20-29 yr.; 21 men and 19 women) and 62 older (57-80 yr.; 35 men and 27 women) adults to determine the contributions of several demographic and physiological factors to the variability in integrated 24-h GH concentrations. Serum GH was measured every 10 min for 24 h in an enhanced sensitivity chemiluminescence assay. The predictor variables included: age group (young or old), gender, abdominal visceral fat (by computed tomography), total body fat mass and percentage body fat by dual-energy x-ray absorptiometry, serum IGF-I, fasting serum insulin, 24-h mean estradiol and testosterone, and peak oxygen uptake by graded exercise (treadmill) testing. Multiple ordinary least squares regression analysis was used to quantitatively assess the individual contribution that each predictive measure made to explain the variability among values of integrated 24-h GH concentrations while in the presence of the remaining predictors. The model explained 65% of the variance in integrated 24-h GH concentrations. Abdominal visceral fat (P < 0.002) and fasting insulin (P < 0.008) were consistently important predictors of integrated 24-h GH concentrations independent of age group, gender, and all other predictor variables. Although serum IGF-I was an important overall predictor of integrated 24-h GH concentrations (P = 0.002), this relationship was present only in the young subjects and was modulated by gender. The remaining variables failed to contribute significantly to the model. We conclude that abdominal visceral fat and fasting insulin are important predictors of integrated 24-h GH concentrations in healthy adults, independent of age and gender. Serum IGF-I is an important predictor of integrated 24-h GH concentrations in young but not older subjects. Bidirectional feedback between each of these three factors and GH secretion may account for the strong relationships observed.

Relationship between age, percentage body fat, fitness, and 24-hour growth hormone release in healthy young adults: effects of gender.

We investigated whether gender affects the physiological relationships between the release of GH and age, body composition, and levels of physical fitness in humans. We studied 32 eumenorrheic females (age = 31 +/- 5 yr) and 12 males (age = 27 +/- 5 yr). Significant gender differences were found for peak oxygen consumption [VO2 peak = 40.5 +/- 6.9 (females) vs. 50.1 +/- 11.6 (males) ml/kg.min-1, P < 0.05] and body composition [hydrostatic weighing, percentage body fat = 28.7 +/- 5.4 (females) vs. 18.1 +/- 9.8 (males), P < 0.05] but not for body mass index [BMI = 23.7 +/- 3.1 (females) vs. 24.0 +/- 3.3 (males)]. Blood samples were drawn every 10 min for 24 h from 0800 h to determine integrated serum GH concentration [2350 +/- 1260 (females) vs. 3110 +/- 1760 (males) microgram/L x min]; females were studied during the early follicular phase (days 4-5) of the menstrual cycle. In females, a significant relationship existed between 24-h integrated serum GH concentration and age (r = -0.35, P = 0.05) but not BMI (r = -0.19, P = 0.29); the relationship between 24-h integrated serum GH concentration and VO2 peak (r = 0.31, P = 0.08) and percentage body fat (r = 0.29, P = 0.11) approached significance. In males, significant relationships existed between 24-h integrated serum GH concentration and age (r = -0.79, P = 0.002), percentage body fat (r = -0.75, P = 0.005), and VO2 peak (r = 0.58, P = 0.05) but not between 24-h integrated serum GH concentration and BMI (r = -0.53, P = 0.08). Standardized regression coefficients revealed that for each SD change in age, BMI, percentage body fat, or VO2 peak the associated change in 24-h integrated serum GH concentration was 1.9-2.6 times greater in males than in females. We conclude that age, percentage body fat (but not BMI), and fitness are related to 24-h GH release in young adults and that these relationships are considerably stronger in males than females.

Mode of pulsatile follicle-stimulating hormone secretion in gonadal hormone-sufficient and -deficient women--a clinical research center study.

To test the hypothesis that FSH is secreted at least in part within discrete secretory bursts in women and that the characteristics of episodic FSH secretion are altered within differing gonadal hormone environments, we measured FSH by immunoradiometric assay every 10 min for 24 h in premenopausal women during the early follicular (EF), late follicular (LF), and midluteal (ML) phases of the menstrual cycle and in postmenopausal (PM) women (n = 8 in each group). Secretory events were evaluated using multiparameter deconvolution. FSH was secreted in an episodic manner, with the number of secretory bursts (per 24 h; mean +/- SEM) detected in LF (20 +/- 0.79) and PM (20 +/- 0.90) women being greater than that in EF (16 +/- 0.88) and ML (14 +/- 0.93) women. FSH secretory burst mass (milliinternational units per mL) was significantly higher in PM (12 +/- 1.6) than in EF (1.8 +/- 0.21), LF (3.1 +/- 1.3), or ML (0.8 +/- 0.11) women and primarily reflected a relative increase in the maximal secretory rate rather than increased burst half-duration. The estimated half-life (minutes) of endogenous FSH in LF women (155 +/- 18) was shorter than those calculated in EF (251 +/- 24), ML (277 +/- 38), and PM (231 +/- 18) women. Cross-correlation analysis showed strongly positive associations between successively paired serum FSH and LH concentrations in all four groups of women. Deconvolution of simultaneously obtained LH concentration-time series revealed statistically significant concordance (13-25%) between FSH and LH secretory episodes at a lag time of 0 min in EF, LF, and PM women and when LH secretory bursts led FSH secretory bursts by 10 min in ML phase women. However, as 75-87% of FSH and LH secretory pulses were discordant, we infer the operation of distinct control mechanisms in the generation of FSH and LH release episodes. In summary, these results suggest that FSH is secreted within discrete secretory bursts in women, that the mass and frequency of FSH secretory bursts differ in women exhibiting various gonadal hormone environments, and that FSH and LH secretory bursts occur coincidentally at a higher rate than expected on the basis of chance alone, but at such a low overall rate of concordance that distinct mechanisms probably operate to direct episodic FSH and LH secretory activity.

Dietary patterns, eating behaviors, and bone mineral density in women runners.

Although reduced gonadal steroid hormone concentrations appear to play a major role in lower trabecular bone mineral density (BMD) in women with athletic amenorrhea, dietary deficiencies and eating behaviors may also affect BMD in women runners. To investigate this possibility, dietary patterns (7-d records), eating-disorders inventory (EDI), and BMD were examined in nine nonrunning eumenorrheic control (Contl) and 32 women runners classified as eumenorrheic (n = 19, Eumen) and oligo/amenorrheic (a group in which some were oligomenorrheic and some were amenorrheic; Ol/Am, n = 13). Runner groups had similar cardiorespiratory fitness, body composition, and training characteristics. Lumbar spine BMD was lower in the Ol/Am runners (-12%, P less than 0.05) but proximal femur BMD did not differ. Dietary intake and EDI subscale scores were similar among the groups. However, there was an inverse trend between EDI subscale scores for bulimia and ineffectiveness and femoral BMD in the Ol/Am runners (r = -0.62 to -0.71, P less than 0.05). These results suggest that self-reported dietary intake and/or eating behaviors do not predict reproductive-function alterations in women runners, but eating behaviors may be associated with lower BMD in Ol/Am runners.

Long-term endurance training alters the hypothalamic-pituitary axes for gonadotropins and growth hormone.

In a prospective fashion we have studied the impact of chronic exercise of two intensities on the hypothalamic-pituitary-end organ axes for gonadotropins and GH in gynecologically mature, previously sedentary women. Physiologic alterations are evident in both axes with a doubling of 24-hour mean serum GH concentrations at 1 year and smaller, transient changes in pulsatile LH release during the first four menstrual cycles. The latter period of physiologic adaptation should be studied more intensively with more frequent exercise evaluation. Perhaps more significant "adaptation to stress" would be quantitated. We also emphasize that gynecologically less mature women were not studied and only the early follicular phase was evaluated. Adaptive changes of greater magnitude (including amenorrhea) might have been produced if a different group of women, a markedly different training regimen, or a different phase of the menstrual cycle were studied. Finally, whether or not they participate in physical training, younger amenorrheic women are at increased risk for diminished lumbar spine bone mineral content and skeletal fractures.

Endurance training amplifies the pulsatile release of growth hormone: effects of training intensity.

The effects of intensity of run training on the pulsatile release of growth hormone (GH) were investigated in 21 eumenorrheic untrained women. The O2 consumption (VO2) at the lactate threshold (LT); fixed blood lactate concentrations (FBLC) of 2.0, 2.5, and 4.0 mM; peak VO2; maximal VO2; body composition; and pulsatile release of GH were measured. Subjects in both the at-lactate threshold (/LT, n = 9) and above-lactate threshold (greater than LT, n = 7) training groups increased VO2 at LT and FBLC of 2.0, 2.5, and 4.0 mM and VO2max after 1 yr of run training. However, the increase observed in the greater than LT group was greater than that in the /LT group (P less than 0.05). No change was observed for the control group (n = 5). No among- or within-group differences were observed for body weight, although trends for reductions in percent body fat (P less than 0.06) and fat weight (P less than 0.15) were observed in the greater than LT group, and both training groups significantly increased fat-free weight (P less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

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 microg/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 microg x l(-1) x 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 microg x l(-1) x min, Ex vs. R, respectively; 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 microg x l(-1) x 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 microg/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 (Delta) GH was proportionate to both DeltaNE (P = 0.002) and DeltaEpi (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.

Cholinergic and opioid involvement in release of growth hormone during exercise and recovery.

Cholinergic and opioid pathways have been implicated as mediators of the increased growth hormone (GH) release observed during exercise. This study compared the GH responses induced by a moderate-intensity exercise bout during treatment with placebo (Plac), the opioid receptor antagonist naltrexone (Nalt), the indirect cholinergic agonist pyridostigmine (PD), or a combination of the two drugs (P + N). Ten active males served as subjects (age, 25.1 +/- 0.6 yr; wt, 79.7 +/- 2.5 kg; % body fat, 14.9 +/- 1.4; peak oxygen consumption, 46.2 +/- 2.7 ml.kg-1 x min-1). Blood samples were drawn at 5-min intervals during the 4.5-h testing period to determine the GH concentration. The testing period was divided as follows: 0600-700 h = baseline, 0700-0800 h = preexercise, 0800-0830 h = exercise, and 0830-1030 h = recovery. Drugs were administered 1 h before exercise (at 0700 h). Exercise consisted of 30 min of cycling at an individualized work load previously found to elicit a blood lactate concentration of 2.5 mM. Heart rate, oxygen consumption, blood lactate, and blood glucose were measured throughout the exercise period. Results indicated that neither the resting GH concentration nor the metabolic parameters during exercise were altered by the treatments. Peak serum GH concentration was not significantly altered by the treatments (range 7.3 +/- 2.0 to 12.6 +/- 4.4 micrograms/l).(ABSTRACT TRUNCATED AT 250 WORDS)

Human growth hormone response to repeated bouts of aerobic exercise.

We examined whether repeated bouts of exercise could override growth hormone (GH) auto-negative feedback. Seven moderately trained men were studied on three occasions: a control day (C), a sequential exercise day (SEB; at 1000, 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 (VO2max) on a cycle ergometer. Standard meals were provided at 0600 and 2200. GH was measured every 5-10 min for 24 h (0800-0800). Daytime (0800-2200) integrated GH concentrations were approximately 150-160% greater during SEB and DEB than during C: 1,282 +/- 345, 3,192 +/- 669, and 3,389 +/- 991 min.microgram.l-1 for C, SEB, and DEB, respectively [SEB > C (P < 0.06), DEB > C (P < 0.03)]. There were no differences in GH release during sleep (2300-0700). Deconvolution analysis revealed that the increase in 14-h integrated GH concentration on DEB was accounted for by an increase in the mass of GH secreted per pulse (per liter of distribution volume, lv): 7.0 +/- 2.9 and 15.9 +/- 2.6 micrograms/lv for C and DEB, respectively (P < 0.01). Comparison of 1.5-h integrated GH concentrations on the SEB and DEB days (30 min exercise + 60 min recovery) revealed that, with each subsequent exercise bout, GH release apparently increased progressively, with a slightly greater increase on the DEB day [SEB vs. DEB: 497 +/- 162 vs. 407 +/- 166 (bout 1), 566 +/- 152 vs. 854 +/- 184 (bout 2), and 633 +/- 149 vs. 1,030 +/- 352 min.microgram.l-1 (bout 3), P < 0.05]. We conclude that the GH response to acute aerobic exercise is augmented with repeated bouts of exercise.

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 microg x l(-1) x 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 microg x distribution volume(-1) x 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.

Release of luteinizing hormone and growth hormone after recovery from maximal exercise.

Pulsatile properties of luteinizing hormone (LH) and growth hormone (GH) release were evaluated in 19 eumenorrheic untrained females [mean age 31.1 +/- 1.1 yr, height 165.2 +/- 1.4 cm, weight 64.8 +/- 2.1 kg, peak oxygen uptake (Vo2) 41.6 +/- 1.4 (SE) ml.kg-1.min-1] during the early follicular phase of the menstrual cycle (days 3-4 after the onset of menses). Each subject was studied during two consecutive menstrual cycles under each of two conditions in random order: 1) no formal exercise for 72 h (C) and 2) 12-24 h after two maximal exercise bouts (peak Vo2/lactate threshold treadmill evaluation and a 3,200-m time-trial run or a maximal Vo2 inclined treadmill test) performed on consecutive days (EX). Blood sampling was performed every 10 min for 12 h. LH and GH pulsatile parameters were identified and characterized by the Cluster pulse detection algorithm. No significant differences were noted in the number of peaks, peak amplitude, interpeak interval, peak increment, or 12-h integrated concentrations between C and EX for LH or GH. We conclude that maximal exercise protocols typically used for exercise evaluation do not have an effect on the pulsatile characteristics of LH or GH release in untrained women during the early follicular phase of the menstrual cycle if 12-24 h of recovery are allowed before evaluation of the pulsatile secretion of gonadotropins or GH.

Reproductive hormones and bone mineral density in women runners.

We examined the relationships among reproductive hormone concentrations and bone mineral density (BMD) in 43 women runners classified as eumenorrheic (n = 24), oligomenorrheic (n = 8), or amenorrheic (n = 11). Results were compared with a eumenorrheic nonrunner control group (n = 11). Serum 17 beta-estradiol, progesterone, and dehydroepiandrosterone sulfate concentrations were determined in daily blood samples for 21 days, and integrated concentrations (areas under the curve) were calculated. BMD was assessed at the lumbar spine and proximal femur by dual-photon absorptiometry. As expected, 17 beta-estradiol, progesterone, and lumbar spine BMD were higher in the control and eumenorrheic runner groups than in the oligomenorrheic and amenorrheic runner groups (P less than 0.05). Progesterone concentration was significantly correlated with lumbar spine BMD in the eumenorrheic runners (r = 0.61). None of the steroid hormones was significantly related to BMD in the oligomenorrheic/amenorrheic group. The present data suggest that circulating levels of gonadal steroid hormones affect axial BMD in eumenorrheic runners.

Durability of the reproductive axis in eumenorrheic women during 1 yr of endurance training.

Menstrual cycle (MC) alterations occur in some endurance-training women. We hypothesized that a prospective running program would evoke alterations in MC phase lengths and in the physiological frequency of pulses of luteinizing hormone (LH) and/or diminish 24-h integrated serum LH concentrations in some women. In addition, we postulated that women who train more intensively (above the lactate threshold) would show alterations in gonadotropin release earlier in the training program or to a greater degree. To test these hypotheses, we examined the effects of different exercise intensities on physiological and endocrine responses. Twenty-three healthy eumenorrheic gynecologically mature (postmenarchal age 17.8 +/- 0.9 yr) untrained women undertook a 1-yr training program at one of two exercise intensities, one at a velocity corresponding to the lactate threshold (LT) and the other halfway between that of LT and peak running velocity, or served as controls. Training distance was the same in each exercise group. Physiological measurements were repeated every four MC to track changes in fitness and readjust training velocities. The lengths of the MC and the follicular and luteal phases were determined from hormonal concentrations. Body composition, nutritional intake, and pulsatile release of LH were determined. The women ran approximately 790 miles. Each group improved physiologically, with the greater than LT group improving to a greater degree. A less than 2-day decrease in the luteal phase length was observed only in the greater than LT group. No significant changes for any parameter of pulsatile LH release were noted between exercise groups. No significant changes in nutritional intake and only small changes in body composition were noted in either exercise group despite the added energy expenditure of exercise. We conclude that a progressive exercise program of moderate distance and intensity does not adversely affect the robust reproductive system of gynecologically mature eumenorrheic women.

Effects of a functional knee brace for ACL insufficiency during treadmill running.

PURPOSE: To assess the effects of a functional knee brace (FKB) for anterior cruciate ligament insufficiency (ACLI) on physiological and perceptual parameters during treadmill running. METHODS: Thirteen ACLI subjects (time since injury, 5.8 +/- 5.3 yr), performed an incremental test to exhaustion and two constant load 20-min tests, one at an intensity below lactate threshold (bLT), and the other at an intensity above LT (aLT) each with and without their FKB. RESULTS: Bracing had no effect on peak variables except for higher ratings of perceived exertion at the legs (RPE-L) at the velocities associated with a blood lactate concentration [HLa] of 4.0 mM and at peak. Bracing had no effect when exercising at bLT but did significantly alter the metabolic profile developed during the performance of the aLT tests (83 +/- 0.03% VO2peak). In particular, FKB resulted in elevated blood [HLa] (23%), VO2 (4%), VE (12%), VCO2 [corrected] (7%), and VE/VO2 (7%). HR and slow component VO2 did not differ between the brace and no brace aLT tests. RPE-L and RPE-knee were significantly elevated during aLT when the brace was worn. Suspected mechanisms include alterations in muscle recruitment patterns and/or occlusion. CONCLUSIONS: When ACLI individuals wear a FKB during high intensity straight-ahead running exercise of long duration, physiological parameters are affected.

Repeated bouts of exercise alter the blood lactate-RPE relation.

PURPOSE: To examine the effects of repeated bouts of exercise on the blood lactate [HLa]-ratings of perceived exertion (RPE) relation. METHODS: Six moderately trained males were studied on two occasions: a sequential exercise bouts day (SEB: 1000 h, 1130 h, and 1300 h) and a delayed exercise bouts day (DEB: 1000 h, 1400 h, and 1800 h). Each of the three exercise bouts within a given condition were 30 min in duration at the power output (PO) associated with 70% of VO2peak on a cycle ergometer. A standardized meal was provided at 0600 h. VO2, PO, HR, and RER were recorded every min during exercise and blood [HLa] and RPE were measured every 5 min during exercise. RESULTS: A 2 x 3 analysis of variance with repeated measures revealed that blood [HLa] decreased significantly with each repeated exercise bout (X +/- SEM: bout 1: SEB = 3.5 (0.3), DEB = 3.8 (0.4); bout 2: SEB = 2.6 (0.3), DEB = 2.8 (0.3); bout 3: SEB = 2.0 (0.2), DEB = 2.1 (0.4); mM). No differences were observed in the blood [HLa] response to repeated bouts of exercise between SEB and DEB. RPE-peripheral (legs, RPE-L) was higher during bout 3 compared with bout 1 (P <0.05) (bout 1: SEB = 11.8 (0.8), DEB = 12.3 (0.2); bout 2: SEB = 12.3 (0.5), DEB = 13.3 (0.4); bout 3: SEB = 13.5 (0.8), DEB = 14.0 (0.7); RPE-central (chest and breathing, RPE-C) was not affected by repeated bouts of exercise, whereas RPE-Overall (RPE-O) was higher during bout 3 compared with bouts 1 and 2 (P < 0.05) (bout 1: SEB = 12.5 (0.2), DEB = 12.3 (0.4); bout 2: SEB = 12.8 (0.4), DEB = 12.7 (0.4); bout 3: SEB = 13.7 (0.7), DEB = 13.2 (0.3)). No interaction for RPE x condition was observed. HR increased with repeated bouts of exercise with HR during exercise bout 3 being higher than HR during exercise bout 1 (164 vs. 156 bpm, P < 0.05). There was also a strong trend for HR during exercise bout 3 to be higher than HR during exercise bout 2 (P < 0.06). A trend for a reduction in VO2 with repeated exercise was observed (P < 0.07), with the reduction apparently related to the SEB condition (P < 0.12 for VO2 x condition). PO and kcal.min-1 were not affected by repeated bouts of exercise. RER decreased significantly with each repeated bout of exercise (from RER = 0.96 to RER = 0.89, P < 0.05) with no difference observed between SEB and DEB. CONCLUSIONS: We conclude that the blood [HLa]-RPE relation is altered by repeated bouts of exercise and that this alteration does not appear to be affected by recovery time between exercise bouts (up to 3.5 h of recovery). These data suggest that, after the first exercise bout, RPE should not be used to produce a specific blood [HLa] on subsequent exercise bouts.