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The Journal of Clinical Endocrinology & Metabolism Vol. 89, No. 9 4298-4305
Copyright © 2004 by The Endocrine Society

The Effects of Time following Acute Growth Hormone Administration on Metabolic and Power Output Measures during Acute Exercise

Brian A. Irving, James T. Patrie, Stacey M. Anderson, Deidre D. Watson-Winfield, Kirsten I. Frick, William S. Evans, Johannes D. Veldhuis and Arthur Weltman

Center for the Study of Complementary and Alternative Therapies (B.A.I.), Departments of Human Services (B.A.I., A.W.), Health Evaluation Sciences (J.T.P.), Internal Medicine (S.M.A., W.S.E., A.W.), Obstetrics and Gynecology (W.S.E.), and General Clinical Research Center (B.A.I., J.T.P., D.D.W.-W., K.I.F., A.W.), University of Virginia, Charlottesville, Virginia 22908; and Endocrine Research Unit (J.D.V.) and General Clinical Research Center (J.D.V.), Mayo Clinic and Foundation, Rochester, Minnesota 55905

Address all correspondence and requests for reprints to: Arthur Weltman, Ph.D., Exercise Physiology Laboratory/Memorial Gymnasium, University of Virginia, Charlottesville, Virginia 22904. E-mail: alw2v{at}virginia.edu.


   Abstract
Top
 Abstract
Introduction
 Subjects and Methods
 Results
 Discussion
 References
 
We examined the effects of GH infusion on metabolism and performance measures during acute exercise. Nine males [(X ± SEM): age 23.7 ± 1.9 yr, height 182.6 ± 1.6 cm, weight 77.3 ± 2.6 kg, percent fat 17.7 ± 1.9%, peak oxygen consumption 37.9 ± 2.9 ml/kg·min] completed six 30-min randomly assigned bicycle ergometer exercise trials at a power output midway between the lactate threshold and peak oxygen consumption. In five of the six trials, the subjects received a recombinant human GH infusion (10 µg/kg, 6-min square wave pulse) at 0800 h, followed by a 30-min exercise trial initiated at one of the following times: 0845, 0930, 1015, 1100, or 1145 h. During one of the six trials, the subject received a saline infusion followed by a 30-min exercise trial initiated at 0845 h. Mixed-effect, repeated-measures ANOVA analyses corrected for multiple comparisons revealed that there were no significant condition effects for total work, caloric expenditure, heart rate response, the blood lactate response, or ratings of perceived exertion response. However, acute GH administration resulted in a lower exercise oxygen consumption without a drop-off in power output. We conclude that the time of exercise initiation after GH infusion does not affect total work, caloric expenditure, heart rate response, blood lactate response, or ratings of perceived exertion but reduces oxygen consumption in response to 30 min of constant load exercise at an intensity above the lactate threshold. The last outcome may suggest that GH administration can improve exercise economy.


   Introduction
Top
 Abstract
 Introduction
Subjects and Methods
 Results
 Discussion
 References
 
GH ADMINISTRATION HAS become a prevalent doping technique used in athletics (1). Experimentally, GH administration has been shown to enhance protein synthesis (2, 3). As a result, some athletes believe that GH administration can augment strength training and improve performance (1). It has also been suggested that GH abuse is widespread and that it is not just confined to power sports (1, 4). Endurance athletes (e.g. swimmers, cyclists, and long-distance runners) may also be abusing GH despite the fact that the metabolic and performance effects of using GH in endurance sports are not well established (4). Part of this pattern of abuse may stem from the athlete’s belief that GH not only possesses performance-enhancing properties but that it is also currently undetectable by today’s testing standards.

Although GH administration has been recognized as an effective mechanism to enhance nitrogen retention and exercise performance among GH-deficient adults and (5, 6) healthy older men (3, 7), there are limited data in the literature that examine GH administration in healthy adult athletes (4). Moreover, few data exist with regard to the acute effects of GH administration on metabolic and performance responses during subsequent exercise. A recent study that examined acute GH administration reported increased blood lactate concentrations (HLa) and a concomitant decrease in exercise performance in some highly trained cyclists (4). However, Lange et al. (4) examined performance 4 h after acute administration of GH, and their results may have been influenced by the administration of a meal 2 h before exercise. In the present investigation, we examined the effects of acute GH administration on metabolic and performance measures during a 30-min constant load power output (CLPO) exercise at five time frames post GH infusion: 0.75, 1.50, 2.25, 3.00, and 3.75 h. We hypothesized that acute administration of GH would not impact metabolic or performance measures during 30 min of moderate- to high-intensity exercise.


   Subjects and Methods
Top
 Abstract
 Introduction
 Subjects and Methods
Results
 Discussion
 References
 
Clinical protocol

Volunteers provided a detailed medical history and underwent a complete physical examination, after providing written informed consent as approved by the Institutional Review Board, Human Investigation Committee of the University of Virginia Health System. Inclusion criterion comprised healthy young adults of age less than 35 yr. Exclusion criteria included substance abuse, acute or chronic systemic illness, endocrinopathy, hepatorenal disease, metabolic disorders, anemia (hematocrit < 38%), or exposure to psychoactive medications within five biological half-lives, recent transmeridian travel, shift work, weight gain or loss (exceeding 3 kg in the preceding 6 wk), and failure to provide informed consent. All subjects were nonsmokers and were asked to refrain from caffeine and alcohol for 24 h before each exercise condition. Nine recreationally active men participated in the present study. None were competitive cyclists. Table 1Go presents the descriptive characteristics of the subjects.


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  		TABLE 1. Descriptive data (age, height, weight) BMI, percentage of body fat, VO2 peak, VO2 at LT, peak PO, PO at LT, and CLPO

 
Subjects completed a peak oxygen consumption (VO2)/lactate threshold (LT) test on an electronically braked cycle ergometer (Ergo Metrics 800S; Sensor Medics, Yorba Linda, CA). Initial power output (PO) was 20 W, and the PO was increased 15 W every 3 min until volitional fatigue. An indwelling venous cannula was inserted in a forearm vein, and blood samples were taken at rest and during the last 15 sec of each exercise stage for the measurement of blood lactate concentration (model 2700, YSI Instruments, Yellow Springs, OH). The LT was determined from the lactate-PO relationship (8) and was defined as the highest PO attained before the curvilinear increase in blood lactate concentration above baseline. A lactate elevation of at least 0.2 mM (the error associated with the lactate analyzer) was required for LT determination (9, 10). Individual plots of VO2 vs. PO allowed for the determination of the VO2 associated with the LT.

The PO for the 30-min constant load (CL) aerobic exercise sessions (CLPO) (see below) was calculated as follows:

Each individual self-selected their seat height and the fore-aft option during each CLPO exercise session. For each CLPO session, the first 2 min of the 30-min session was used as a warm-up phase with each subject pedaling at approximately 25% of the CLPO during min 1 and at approximately 75% of the CLPO during min 2. Subjects were required to pedal between 60 and 100 rpm. If pedaling cadence dropped less than 60 rpm. the PO was reduced.

Metabolic data were collected during the VO2peak/LT protocol and the CLPO sessions, using standard open-circuit spirometric techniques (Vmax; Sensor Medics). Ratings of perceived exertion (RPE) were assessed at the end of each stage during the VO2peak/LT protocol and every 10 min during the CLPO protocol using the Borg Scale (11), and heart rate was determined electrocardiographically (Marquette Max-1 electrocardiograph, Marquette, WI). Total work was measured by summing minute-by-minute PO, and kilocalorie expenditure [total, and kilocalorie carbohydrate (CHO) and kilocalories fat] was calculated (using minute-by-minute VO2 and respiratory exchange ratio values) for each 30-min CLPO exercise session. Heart rate and blood lactate concentrations were assessed every 10 min during exercise during the CLPO session.

Body composition

Body density was measured using air displacement plethysmography (Bod-Pod, Life Measurement Instruments, Concord, CA) corrected for thoracic gas volume as described previously (12). The computational procedure of Brozek et al. (13) was used to determine percent fat from body density measurements.

To examine the effects of GH infusion on CLPO exercise, subjects were admitted to the General Clinical Research Center (GCRC) on six separate occasions [1 saline (S)/exercise, 5 GH/exercise]. To avoid an order or training effect, a prospectively randomized ordered within-subject design was employed. All tests were completed within 12–28 d, with approximately 2–4 d separating each exercise session. To obviate nutritional confounds, volunteers ingested a constant snack at 1800 h the evening before, comprising 500 kcal (60% CHO, 20% protein, and 20% fat), and then remained fasting overnight. To allow simultaneous blood sampling and GH infusion, bilateral forearm venous catheters were inserted at 0600 h the next morning. The paradigm scheduled is shown schematically in Fig. 1Go. A single dose of recombinant human GH (rhGH) (10 µg/kg) or S was infused iv as a 6-min square-wave pulse beginning at 0800 h. Exercise was initiated 0.75 h later (0845–0915 h) for the S condition, and for the GH conditions, the exercise sessions were staggered by 0.75 h (0845, 0930, 1015, 1100, and 1145 h). These time intervals were chosen so the time course after GH administration on metabolism (e.g. fat oxidation) during exercise could be examined. The five time intervals roughly reflect extensive known physiology about rapid direct effects of GH on hypothalamic peptide release in gene expression (over an interval of 0.5–3 h); the intermediate time delay induces feedback by unknown effects, which may include systemic metabolites of different putative kinds; and the delayed time course of greater than 4 h inconsistent with data in the 1980s demonstrating that GH induces central nervous system IGF-I gene expression after that much delay. No one knows otherwise the time course of feedback action in humans. These different time renditions are reviewed in detail by Giustina and Veldhuis (14) and Muller et al. (15).



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  		FIG. 1. Overall study design. Subjects were admitted to the GCRC on six occasions on the evening before each exercise bout. A standardized snack was provided at 1800 h, and subjects were asked to sleep at 2300 h. Two iv cannulas were inserted at 0600 h the following morning. GH or S infusion was administered at 0800 h, and subjects completed 30 min of CL exercise at one of six times post infusion (0845 h in S, 0845, 0930, 1015, 1100, or 1145 h in GH). The study was terminated at 1400 h; subjects were then provided a meal and discharged from the GCRC.

 
Statistical methods

Total work and energy expenditure (total kilocalories, total CHO kilocalories, total fat kilocalories) as well as end exercise VO2 (EE VO2), end exercise heart rate (EE HR), peak blood lactate concentration (peak HLa), and peak RPE data were analyzed on the natural logarithmic scale. The natural logarithmic transformation functioned both as a variance stabilizing transformation to reduce heterogeneous variance and as a remedial measure to reduce the impact that single extreme observations had on the statistical analysis.

The values of each response variable were analyzed by mixed effect repeated-measures ANOVA (16). The ANOVA procedure was used to compare the distribution of the response under the control condition (30-min CLPO exercise session initiated at 0.75 h post S infusion) to the distribution of the response under the five experimental conditions (five 30-min CLPO exercise sessions initiated at 0.75, 1.50, 2.25, 3.0, and 3.75 h post GH infusion, respectively).

The model specification included a single independent variable with six levels that identified the response to a 30-min CLPO exercise session initiated 0.75 h post S infusion and the responses to 30-min CLPO exercise initiated at 0.75, 1.50, 2.25, 3.00, and 3.75 h after GH infusion. The ANOVA model parameters were estimated by restricted-maximum likelihood, and the variance-covariance matrix was modeled in the compound symmetry form (17). Statistical tests were formulated as a 1 degree of freedom contrast, where under the null hypothesis, it was assumed that the mean change in the value of the response from the response under the S condition was equal to zero. Multiple-comparison type I error rate adjustment was based on a two-sided Bonferroni criterion, in which the experimental type I error rate was 0.05 or less. Linear and nonlinear trends, with respect to the change in the response, were evaluated by way of a set of orthogonal contrasts of the mean response at 0.75, 1.50, 2.25, 3.00, and 3.75 h post GH infusion. Model goodness of fit was evaluated by standard residual diagnostic procedures.

Because the response data were analyzed on the natural logarithmic scale, the ANOVA estimates for the postinfusion change in the response will be presented as a ratio of geometric means (18). The ratio of geometric means is a measure of the shift in the central location of two distributions and is equivalent in value to the antilogarithm of the difference between the two sample means computed from logarithmically transformed data. Often the ratio of geometric means is simply interpreted as the fold change in the response.


   Results
Top
 Abstract
 Introduction
 Subjects and Methods
 Results
Discussion
 References
 
Figure 2Go presents the mean GH profiles plus the nonparametric, bootstrapped 95% confidence intervals under each exercise condition. As can be seen, GH levels were elevated by this relatively large GH infusion. The effects of exercise can also be seen in each panel as either an alteration in the disappearance of GH (0845 and 0930 h) or an increase in GH concentration from baseline (1015, 1100, and 1145 h).



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  		FIG. 2. Mean (and nonparametric, bootstrapped 95% CIs) GH concentrations (y-axis) monitored every 10 min during and after iv infusion of S or rhGH (time 0.00 h, x-axis) followed by 30 min of CLPO exercise. Exercise was initiated 0.75 h post infusion (arrow) for the S condition, and for the GH conditions, the exercise sessions were staggered by 0.75 h (0.75, 1.50, 2.25, 3.00, and 3.75 h, arrow).

 
Table 2Go presents the means ± SEM (with the geometric mean shown in parentheses) for total work (kilojoules), total kilocalories, CHO kilocalories, fat kilocalories, EE VO2 (liters per minute), EE HR (beats per minute), peak HLa (millimoles), and peak RPE during the six 30-min CLPO exercise sessions.


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  		TABLE 2. Summary data for total work, caloric expenditure (total, CHO, fat), EE VO2, EE HR, peak HLa, and peak RPE during the six 30-min CLPO exercise sessions

 
One degree of freedom contrasts, adjusted for multiple comparisons using the two-sided Bonferroni criterion, based on the underlying mixed-effects repeated-measures ANOVA models, revealed that regardless of the time of exercise initiation after GH infusion (0.75, 1.50, 2.25, 3.00, and/or 3.75 h), there were no significant differences observed among the five GH infusion conditions and the S condition for total work. Eight of the nine subjects were able to complete all exercise sessions without a reduction in individually determined CLPO. The ninth subject reduced PO in an identical manner during each test. The reduction in total kilocalories observed after GH infusion approached statistical significance during the 30-min CLPO session that was initiated 2.25 h post GH infusion (P = 0.057). No significant differences were observed for CHO kilocalories and fat kilocalories measured in response to the 30-min CLPO.

Statistically significant reductions in EE VO2 were observed in response to the 30-min CLPO exercise sessions that were initiated at 1.50, 2.25, 3.00, and 3.75 h post GH infusion, compared with the S condition, with geometric mean ratios of 0.88 [95% confidence interval (CI) (0.80, 0.98), P = 0.011], 0.89 [CI (0.80, 0.980, P = 0.013], 0.90[CI (0.81, 1.00), P = 0.042], 0.89[CI (0.80, 0.98), P = 0.016], respectively. The decrease in EE VO2 observed over the 3.75 h of post-GH infusion was determined to be linear (P = 0.039). The average EE VO2 corresponded to approximately 75% of VO2 peak and the average CLPO corresponded to approximately 73% of peak PO.

Marginal elevations in EE HR were observed during the CLPO sessions that were initiated at 2.25, 3.0, and 3.75 h post GH infusion. However, after adjusting for multiple comparisons, there were no statistically significant differences observed between any of the GH infusion conditions and the S condition for EE HR, with the adjusted P values ranging from 0.120 to 1.0.

A marginally significant elevation in the HLa concentration was observed during the CLPO session that was initiated 3.0 h post GH infusion, compared with the S condition with a geometric mean ratio of 1.20 [CI (0.99, 1.463), P = 0.069]. There were no statistically significant differences observed among the four other GH infusion conditions and the S condition for peak HLa concentrations, with the adjusted P values ranging from 0.703 to 1.00.

Similarly, after adjusting for multiple comparisons, there were no statistically significant differences observed among the five GH infusion conditions and the condition for peak RPE concentrations, with adjusted p-values equal to 1.00.

A graphic representation of the data is shown in Figs. 3–6GoGoGoGo, with each figure showing the fold change for each GH condition vs. the S condition (solid dot), the unadjusted (least significant difference) 95% CI (solid lines), the Bonferroni-adjusted 95% CI (dotted lines), and the 1.0-fold change reference line (dashed line). The fold change under each condition was deemed statistically significant at P ≤ 0.05 if the 95% CI does not include 1.0.



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  		FIG. 3. Fold change (ratio of the geometric mean) in use of total kilocalories for each GH condition vs. S control. During each of the five GH conditions, the subject received a rhGH (10 µg/kg, 6-min square-wave pulse) infusion at 0800 h, followed by a 30-min exercise trial initiated 0.75, 1.50, 2.25, 3.00, or 3.75 h later. In control sessions, subjects received S by a 30-min exercise trial initiated 0.75 h. The values are the fold change (solid dot), unadjusted (least significant difference) 95% CIs (solid line), the Bonferroni-adjusted 95% CI (dotted line), and the control (1.0-fold) change (dashed line). Conversion factors (metric units to SI units): energy expenditure, kilocalories x 4.184 = kilojoules.

 


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  		FIG. 4. Fold change (ratio of the geometric mean) in use of total fat kilocalories (A) and CHO kilocalories (B) for each GH condition vs. control. See Fig. 3Go for data representation. Conversion factors (metric units to SI units): energy expenditure, kilocalories x 4.184 = kilojoules.

 


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  		FIG. 5. Fold change (ratio of the geometric mean) in EE VO2 for each GH condition vs. S control. See Fig. 3Go for data representation.

 


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  		FIG. 6. Fold change (ratio of the geometric mean) in EE HR (A), peak HLa concentration (B), and peak RPE for each GH condition vs. S control. See Fig. 3Go for data representation.

 
The fold change in the total kilocalories, fat kilocalories, and CHO kilocalories for comparing the five GH conditions to the S condition in response to 30-min CLPO exercise are presented in Figs. 3Go and 4Go, A and B. No significant differences were observed among the five GH conditions, compared with S because all adjusted 95% CIs include 1.0. Total work data are not presented because no drop-off was observed under any condition.

Figure 5Go presents the fold change in EE VO2 for the five GH conditions minus the S condition in response to the 30-min CLPO exercise. There were significant reductions in EE VO2 observed in response to each 30-min CLPO exercise session that was initiated 1.5 h post GH infusion or later, compared with the S condition.

Significant elevations in the unadjusted EE HR were observed (Fig. 6AGo) during the 30-min CLPO exercise session that were initiated at 2.25 and 3.0 h post GH infusion, compared with S. However, after adjusting for multiple comparisons, the elevations in EE HR were no longer significant.

The fold changes in peak HLa in response to the 30-min CLPO exercise sessions among the five GH conditions, compared with S, are presented in Fig. 6BGo. An unadjusted significant elevation in HLa was observed in response to the 30-min CLPO exercise session initiated at 3.0 h post GH infusion. However, after adjusting for multiple comparisons, this elevation in peak HLa was no longer significant.

No statistically significant differences were observed in the fold change in peak RPE (Fig. 6CGo).


   Discussion
Top
 Abstract
 Introduction
 Subjects and Methods
 Results
 Discussion
References
 
Although many clinical studies have been conducted to examine the effects of long-term GH administration on body composition, muscle hypertrophy, and strength and performance measures in hyposomatotrophic individuals (1, 3, 19, 20, 21), there are relatively few investigations of the acute effects of GH administration on metabolic and performance measures in healthy adults. Our study examined the impact of timed prior GH administration on total work (kilojoules), energy expenditure [total, total CHO, and total fat (kilocalories)], EE VO2, EE HR, peak HLa, and peak RPE in response to a uniform 30-min CLPO exercise.

The current data indicate that the acute administration of GH does not alter exercise performance initiated 45 min to 3.75 h later. Specifically, all nine subjects in the present study completed each exercise session without a detectable decrease or increase in their individual power output across conditions. This outcome does not support recent observations of Lange et al. (4), who suggested that acute GH administration may inhibit cycling performance in some subjects because two of the seven participants failed to complete the exercise protocol. Several factors may account for the foregoing difference. First, the route of GH administration may have had an impact on serum GH concentrations before and during exercise. Lange et al. (4) administered GH using a sc injection at the midthigh. This resulted in serum GH concentrations of approximately 20 µg/liter, just before and during exercise (see their Fig. 2AGo). In the present study, a 6-min iv infusion was employed. This resulted in peak GH concentrations of approximately 95 µg/liter before exercise (Fig. 2Go). Whereas in the 0845 h GH condition serum GH concentration was approximately 20 µg/liter during the other five exercise conditions, the GH response to exercise was approximately 4–8 µg/liter. In addition, in the present study, a 30-min CLPO protocol was used (~75% of VO2 peak), whereas in the study of Lange et al. (4), cyclists exercised for 90 min (45 min at 65% of VO2 peak followed by 45 min at 75% of VO2 peak). It is possible that we would have observed drop-off in the present study had a longer exercise duration been chosen. It is also possible that the reduction in exercise performance observed in the analysis of Lang et al. (4) may be related to ingestion of a meal 2 h after GH infusion and 2 h before exercise. The timing of the meal resulted in a significantly elevated serum insulin concentration at the onset of exercise in the GH condition (see their Fig. 4BGo). Whereas under most circumstances, initiation of exercise during postprandial hyperinsulinemia will be associated with an exercise-induced hypoglycemia and impaired exercise performance in some individuals (22), Lange et al.(4) actually report elevated blood glucose (9%) in the GH condition (see their Fig. 4AGo). As the author suggests short-term GH administration likely induced insulin resistance as a result of an oral glucose load (e.g. the preexercise meal). The observed elevation in blood glucose during exercise in the GH condition might be reflective of impaired muscle glucose uptake, which in turn may have resulted in impaired exercise performance.

The graded time delay between GH infusion and a consistent exercise stimulus allowed examination of the combined metabolic effect of the two interventions. This analysis is significant, given that GH is a strong lipolytic hormone (14). Statistical comparisons disclosed a marginal reduction in total caloric expenditure (Fig. 3Go) during exercise that was initiated at 2.25 h after GH, compared with S infusion. This may be explained in part by a concomitant reduction in EE VO2 (Fig. 5Go). On the other hand, CHO and fat oxidation did not differ (Fig. 4Go, A and B).

The detection of subtle differences may be limited by our use of minute-by-minute VO2 and respiratory exchange ratio values to estimate total caloric and the total CHO and fat expenditures. Nonetheless, whereas non-steady-state gas exchange can influence outcomes to some extent, all measurements were made at steady-state lactate concentrations and therefore stable tissue energy use. Our results support those of Lange et al. (4), wherein the 3-fold elevation in plasma glycerol and nonesterified fatty acid concentrations during exercise after acute GH administration did not increase whole-body fat oxidation. Analogously, we reported that GH output in response to exercise primarily stimulates fat oxidation during the recovery interval thereafter (23).

A novel finding is that GH administration 90 min or more before exercise reduced EE VO2 without lowering PO (Fig. 5Go). Moreover, the decrease in EE VO2 observed over the 3.75 h of post-GH infusion was determined to be linear (P = 0.039). The precise basis for this effect is not known but plausibly could reflect enhanced cycling economy and could translate to improved cycling performance with longer duration exercise. An alternative consideration is that the duration of (overnight) caloric restriction modulated EE VO2 after GH infusion. Nutrient withdrawal reduces the resting metabolic rate (24, 25, 26). The observation that EE VO2 did not decline when S was injected 45 min before exercise does not exclude this testable hypothesis. It should be noted that the CLPO sessions were performed on an electronically braked cycle ergometer in which PO is maintained as long as pedaling rates fall within 60–100 rpm. Although pedaling cadence was not controlled in the present study (which could potentially affect economy), none of the subjects were competitive cyclists, and all subjects pedaled at approximately 70 rpm.

EE HR rose in response to exercise that began at 2.25, 3.00, and 3.75 h after GH infusion. Lange et al. (27) also noted increased resting and exercising heart rate (4) after acute GH administration. The nitric oxide-dependent arterial dilating action of GH could contribute to this effect (14).

Exercise and GH combined did not influence RPE over exercise alone. RPE reflects comparable HLa concentrations during moderate- to high-intensity exercise (28, 29, 30). Thus, RPE values are consistent with stable HLa measures (see above).

In conclusion, preexercise timed GH administration does not affect total work, caloric expenditure, HLa concentrations, or RPE during 30 min of CL exercise at an intensity above the lactate threshold. In contradiction, preinfusion of GH reduced exercise VO2 at fixed PO, potentially denoting enhanced exercise economy in the fasting state. Although a marginal increase in heart rate was observed, this response was not statistically significant. The finding that GH administration resulted in lower exercise VO2 without a drop-off in power output may suggest that GH administration can improve exercise economy. Further studies will be required to appraise how this adaptation impacts sustained exercise performance.


   Footnotes
 
This work was supported by Grant 5T32AT00052 from the National Center for Complementary and Alternative Medicine (NCCAM), National Institutes of Health (NIH) Grants AG14799 and AG19695, and GCRC Grant RR00847.

The contents of this publication are solely the responsibility of the authors and do not necessarily represent the official views of the NCCAM or NIH.

First Published Online August 24, 2004

Abbreviations: CHO, Carbohydrate; CL, constant load; CLPO, constant load power output; EE HR, end exercise heart rate; EE VO2, end exercise VO2; HLa, blood lactate concentration; LT, lactate threshold; PO, power output; rhGH, recombinant human GH; RPE, ratings of perceived exertion; VO2, oxygen consumption.

Received January 14, 2004.

Accepted May 26, 2004.


   References
Top
 Abstract
 Introduction
 Subjects and Methods
 Results
 Discussion
 References
 

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