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Original Article |
Sports Medicine Research Unit (K.H.W.L., M.K.) and Denmark Team Danmark Test Center (B.L., M.B.), Bispebjerg Hospital, DK-2400 Copenhagen NV; Denmark Medical Research Laboratories (A.F., R.D., H.Ø.), Aarhus University Hospital, DK-8000, Aarhus C; and Denmark Clinical Development, Novo Nordisk A/S, DK-2880 Bagsvaerd, Denmark
Address all correspondence and requests for reprints to: Kai H. W. Lange, M.D., Sports Medicine Research Unit, Building 8, Bispebjerg Hospital, Bispebjerg Bakke 23, DK-2400 Copenhagen NV, Denmark. E-mail: klange{at}dadlnet.dk.
Abstract
We studied the acute effects of a single, sc GH dose on exercise performance and metabolism during bicycling. Seven highly trained men [age, 26 ± 1 yr (mean ± SEM); weight, 77 ± 3 kg; maximal oxygen uptake, 65 ± 1 ml O2·min-1·kg-1] performed 90 min of bicycling 4 h after receiving 7.5 IU (2.5 mg) GH or placebo in a randomized, double-blinded, cross-over design trial. A standardized pre-exercise meal was given 2 h before exercise. Blood was sampled at rest and during exercise and analyzed for GH, IGF-I, glucose, lactate, insulin, glycerol, and nonesterified fatty acids (NEFA). In the placebo trial, all subjects completed the exercise protocol without any difficulties. In contrast, two subjects were not able to complete the exercise protocol in the GH trial, and one subject barely managed to complete the protocol. In addition, GH administration resulted in exaggerated increases in plasma lactate concentrations during exercise (P < 0.0001). The combined lipolytic effect of GH and exercise, evidenced by increased plasma glycerol and serum NEFA concentrations, was 3-fold greater than the effect of exercise alone (P < 0.0001), but this increased substrate availability did not result in increased whole body fat oxidation (indirect calorimetry). Plasma glucose was, on average, 9% higher during exercise after GH administration compared with placebo (P < 0.0001).
We conclude that a single, relevant GH dose causes exaggerated increases in plasma lactate and glycerol as well as serum NEFA during 90 min of subsequent bicycling at moderate to high intensity. The exaggerated increase in plasma lactate may be associated with substantially decreased exercise performance.
MANY ATHLETES BELIEVE that GH administration enhances athletic performance. The most common belief is that GH administration increases muscle mass and strength, which seems logical based on the well documented nitrogen-retaining effects of GH administration (1, 2, 3). However, there is no scientific evidence that GH administration either alone or combined with different resistance exercise training regimens should augment muscle strength in healthy humans (4, 5, 6, 7, 8, 9, 10). On the other hand, there is ample evidence that GH administration reduces fat mass (6, 8, 11, 12, 13), and the mechanism is likely to be increased resting energy expenditure combined with increased fractional fat oxidation (14). Obviously, this latter effect on body composition may be of potential benefit for different indications.
GH abuse in sports is believed to be widespread (15, 16, 17, 18) and is not only confined to power sports. In the past decade, GH abuse has also found its way to endurance sports like swimming and bicycling. However, the performance effects of using GH in endurance sports are unknown, and the metabolic effects of GH administration on subsequent endurance exercise have, to our knowledge, never been reported.
In the present study, we report the acute effects of a single, moderate sc GH dose on carbohydrate and lipid metabolism during 90 min of subsequent bicycling at moderate to high intensity. The subjects were highly trained, healthy, young men, and the GH dose, intensity, and duration of exercise were chosen to imitate physiological conditions encountered in training as well as in competitive bicycling. To further imitate these conditions, a standardized pre-exercise meal was provided 2 h before the exercise protocols. It was hypothesized that, during exercise, prior GH administration would enhance the exercise-induced increase in both lipolysis and fat oxidation.
Subjects and Methods
Subjects
Seven healthy, well trained young male subjects were enrolled in the study protocol, and their individual baseline characteristics are presented in Table 1
. Before inclusion, each subject underwent a medical evaluation, including medical history, physical examination, and routine blood tests. Exclusion criteria were any kind of medication, metabolic, cardiac, or malignant disease or anemia. Only subjects training regularly on a bicycle were recruited.
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Informed written and oral consent was obtained according to the Helsinki 2 Declaration, and the study protocol was approved by the Ethics Committee for Medical Research in Copenhagen (KF 01–004/01) and by the Danish National Board of Health (journal no. 2612–1592).
Study design and experimental protocol
The study was a randomized, placebo-controlled, double-blinded, cross-over trial comparing the effects of a single GH or placebo dose on carbohydrate and fat metabolism during 90 min of bicycling exercise. A standardized pre-exercise meal was provided 2 h before the exercise protocol to imitate the physiological conditions encountered during training and competition. The study design is presented in Fig. 1, A and B. After inclusion, maximal oxygen uptake (VO2max) was determined as described below, and, on a separate day, the subjects performed an exercise protocol consisting of 45 min of cycling at a load eliciting 65% of VO2max followed by 30 min of bicycling at a load eliciting 75% of VO2max (customization). This customization procedure ensured that the subjects were able to complete the exercise protocol on experimental d 1 and 2. The subjects were then assigned to perform the 2 experimental days in random order and separated by 7 d.
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Whole body oxygen uptake (VO2) and carbon dioxide production (VCO2) were measured in 5-min periods from 0–5, 10–15, 25–30, 40–45, 55–60, 70–75, and 85–90 min through a mouthpiece connected to an AMIS 2001 automated metabolic cart (INNOVISION, Odense, Denmark). Respiratory variables were averaged for each 15-sec period, and values between 2:45 and 4:30 min in each 5-min period were further averaged to estimate VO2 and VCO2 in the respective periods. Appropriate calibrations of the O2 and CO2 sensors and the volume transducer were performed twice before exercise start and after 45 min of exercise. Heart rate (HR) was registered continuously during exercise through a wireless HR monitor (Polar Sport Tester, Polar Electro OY, Kempele, Finland).
Each subject was allowed to drink water freely during exercise on the first experimental day, and on the second experimental day the subject was given the same amount of water at the same time points. A fan placed in front of the subject was started immediately after exercise started to ensure adequate cooling, and the room temperature was kept between 21 and 22 C.
To further standardize the measurements, only light training (<2 h and no interval training) was allowed 2 d before the experimental day, and no physical training was allowed on the day preceding the experimental day. Each exercise protocol was performed on the subject’s own racing bike. In addition, the subjects were instructed to continue their habitual training programs and dietary habits. Dietary intake was recorded during 7-d periods in six of the seven subjects.
One subject repeated the 2 experimental days, each separated by 7 d from the preceding experimental day. He received GH/placebo from the same vial on experimental d 1 and 4 and on experimental d 2 and 3, respectively.
Submaximal and VO2max test
On a separate day after inclusion, the subjects performed an incremental exercise test (using the same bicycle ergometer and metabolic cart as described above). The stationary magnetic brake replaced the rear wheel of the racing bicycle (19). The basic principle in the braking of the rotation is a compact magnetic power unit. The subject has to increase cadence or change gear to generate increased speed at a fixed resistance (workload in watts = 9.93 x cycling speed (km·h-1) - 96.34). After a 10- to 15-min warm-up with a workload between 150 and 190 W, four submaximal workloads of 5-min duration were performed. The initial workload was 210 W (31 km·h-1) for subjects with a body weight less than 72 kg and 240 W (34 km·h-1) for subjects with a body weight above 72 kg and corresponded to approximately 50% of VO2max. The load was increased by 30 W per step, and the final workload corresponded to approximately 80% of VO2max (300 or 330 W; 40 or 43 km·h-1). When the workload increased, the subject had to find the correct speed within 15 sec either by an increase in cadence or by changing gear. The cadence, gear, and thus the workload remained fixed for the remainder of the 5-min period. After a 10-min rest, a 5-min "all-out" test was performed to determine VO2max. During the 5-min all-out test, the subject was allowed to change gear and increase/decrease cadence. The distance covered was measured, and the workload was calculated. Respiratory variables were measured continuously through a mouthpiece and averaged for each 15-sec period. The mean of the three highest 15-sec values was recorded as VO2max. HR was measured continuously by a HR monitor as described above. To ensure that a true VO2max was attained, at least two of the following three criteria had to be met: VO2 plateau reached, a HR within ±5 beats/min of the age-adjusted maximal HR, and VCO2/VO2 greater than 1.0.
The velocities eliciting 65% and 75% of VO2max were calculated by linear regression and used in the exercise protocol during the customization procedure and on the experimental days. On the customization day, the subjects found the cadence and gear corresponding to 65% and 75% of VO2max. The same cadence, gear, and thus workloads were used on the experimental days.
Analytical methods
GH, IGF-I, and insulin. After separation by centrifugation, serum was stored at -80 C until analysis. Serum GH was determined by a commercial time-resolved immunofluorometric assay (TR-IFMA; Wallac, Inc., Turku, Finland). Serum IGF-I was measured in acid ethanol serum extracts using an in-house monoclonal antibody-based TR-IFMA as previously described (20). The within-assay coefficient of variation (CV) was less than 5% for both assays. Serum insulin was determined by a commercial TR-IFMA (Wallac, Inc.). The within-assay CV for this assay was less than 5%.
Glucose and lactate. Whole blood (500 µl) was immediately transferred to a vial containing 25 IU heparin. Plasma was separated by centrifugation at 4 C and analyzed immediately, on site, for L-lactate and D-glucose in duplicate using a YSI 2300 STAT PLUS analyzer (YSI, Inc., Yellow Springs, OH).
Nonesterified fatty acids (NEFA) and glycerol. Serum NEFA were determined by a colorimetric method using a commercial kit (Wako Chemicals, Neuss, Germany). The within-assay CV was less than 5%. Plasma (EDTA-plasma) glycerol was measured spectrophotometrically using a glycerol kinase method (Cobas Fara II; Hoffmann-La Roche, Diagnostics Division, Basel, Switzerland).
Hematocrit. Blood hematocrit was determined by the microhematocrit method.
Statistical analysis
Data are presented as individual data and as means ± SEM and range. The effects of time and drug (GH or placebo) on plasma metabolites, serum and plasma hormones, and physiological variables were analyzed using a two-way ANOVA repeated measures test with Bonferroni post tests (GraphPad Prism version 3.00 for Windows 95; GraphPad Software, Inc., San Diego, CA). P value less than 0.05 (two-tailed) was considered statistically significant. Missing values (two subjects were not able to complete the exercise protocol when GH was administered, generating three missing values for every variable) were estimated by extrapolation. The extrapolation procedure was performed by maintaining the last measured value. The analyses were also performed with n = 6 (one missing value) and n = 5 (complete data set), and this did not change the statistical inference in the study.
Results
Order of experimental days
Four subjects completed the main experimental days in the medication order placebo-GH, and three subjects completed the main experimental days in the order GH-placebo.
Bicycling speed and trial completion
The bicycling speeds on the experimental days were calculated from the actual distances covered during the first 45 min and the last 45 min of exercise, until completion of the experimental protocol or until exhaustion or any drop of pace (Table 2). There was no difference in bicycling speed at either 65% or 75% of VO2max between the placebo trial and the GH trial (P = 0.39 and P = 0.44, respectively; paired t test), and the mean bicycling speed at both intensities differed by less than 0.3% between the two trials.
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Serum GH and IGF-I
Serum GH was low at rest (-4 h) in both trials (placebo, 0.9 ± 0.3 µg·liter-1; GH, 0.5 ± 0.1 µg·liter-1) and increased significantly over time (P < 0.0001; Fig. 2A). There was a significant effect of drug, and the drug-time interaction was also highly significant (both P < 0.0001). Post hoc Bonferroni tests revealed that serum GH was significantly higher in the GH trial than in the placebo trial at all time points from -2 h to 90 min (all P < 0.001, except 75 min and 90 min were both P < 0.01).
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). The drug effect on serum IGF-I was not due to methodological errors in the analytical procedures. On average, serum IGF-I was approximately 17% higher in the GH trial than in the placebo trial. Plasma lactate, glucose, and serum insulin
The effects of drug and time on plasma lactate during exercise were highly significant (both P < 0.0001), and the drug-time interaction was also significant (P = 0.011). This analysis was performed on seven subjects by extrapolating the three missing values in the GH trial as described in the statistics section. However, the same results were obtained when analyzing data from six subjects (subject 3 excluded, one missing value) and five subjects (subjects 1 and 3 excluded, no missing values). In the GH trial, plasma lactate increased to levels well above the anaerobic threshold (onset of blood lactate accumulation; Ref. 21) during exercise at 75% of VO2max (Fig. 3, A and B). This exaggerated lactate response was heterogeneous, i.e. large in subjects 1, 3, and 7; intermediate in subjects 4 and 5; low in subject 6; and nonexistent in subject 2 (Fig. 3, A and B). However, the effect was highly reproducible in the subject who repeated the two trials in reverse order (Fig. 3C).
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). Plasma glucose was, on average, approximately 9% higher in the GH trial than in the placebo trial.
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). At the onset of exercise (0 min), serum insulin was 44 pmol·liter-1 higher in the GH trial than in the placebo trial (P < 0.001), most likely reflecting a GH-pre-exercise meal interaction, but this difference was already reduced to 15 pmol·liter-1 after 15 min of exercise and remained at this level throughout the rest of the exercise period. Plasma glycerol, serum NEFA, and respiratory exchange ratio (RER)
The effects of drug and time on plasma glycerol were highly significant, as was the drug-time interaction (all P < 0.0001; Fig. 5A). In the placebo trial, plasma glycerol increased by approximately 250% as opposed to approximately 750% in the GH trial from rest (-4 h) to the termination of exercise (90 min). Both drug and time significantly influenced serum NEFA, as did the drug-time interaction (all P < 0.0001; Fig. 5B). In both trials, serum NEFA was slightly above 200 µmol·liter-1 after an overnight fast (-4 h), and this value was only marginally higher at the end of exercise (90 min) in the placebo trial (
250 µmol·liter-1) but was substantially higher in the GH trial (650 µmol·liter-1). Post hoc Bonferroni tests comparing all means identified glycerol and NEFA concentrations to be higher after GH administration compared with placebo after 30 min of exercise and onward. The GH-induced increase in plasma glycerol and NEFA concentrations was small during resting conditions but very large from the onset of exercise and onward, suggesting a synergistic interaction between GH and exercise on lipolysis.
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). RER was not affected by either time (P > 0.11) or drug (P > 0.76). Because lactate accumulated during the last 45 min of exercise, the assumptions of pulmonary steady-state gas exchange may have been violated during this time period. However, the statistical inference remained the same when the analysis was confined to include only data from 15–45 min of exercise. The 3-fold higher plasma NEFA concentration after GH administration did therefore not result in increased fat oxidation during exercise compared with placebo. VO2 and HR
There was a significant effect of time on VO2 during exercise (P = 0.014), but no drug effect or drug-time interaction (P = 0.94 and P = 0.85, respectively; Fig. 6A). Corresponding VO2 values were almost identical in the two trials. In the subject who repeated the two trials in reverse order, VO2 was also almost identical in all four trials until the time of exhaustion in the two GH trials (63 min; Fig. 6B).
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). Post hoc Bonferroni tests identified values after 30 and 45 min to be significantly different (both P < 0.05). On average, HR was approximately 5 beats·min-1 higher in the GH trial than in the placebo trial. Hematocrit
There was no effect of either drug or time on blood hematocrit during exercise (drug, P = 0.083; time, P = 0.62). However, a paired t test on data from 0 and 5 min in both trials showed that the hematocrit was significantly elevated after 5 min of exercise (placebo trial, P = 0.0031; GH trial, P = 0.0004).
Discussion
The data from the present study demonstrate that a single GH dose leads to exaggerated increases in plasma lactate levels during subsequent moderate to intense endurance exercise. This increase in lactate may be associated with severely reduced exercise performance, although we did not perform such a test. These findings are very unexpected, but, nonetheless, highly reproducible as evidenced by the data obtained in the subject who repeated the experimental days in reverse order. Moreover, plasma glycerol and NEFA concentrations were 3-fold higher during exercise after GH administration compared with placebo. This exaggerated increase in lipolytic markers was quantitatively confined to the exercise period, suggesting a synergistic interaction between GH administration and exercise on lipolysis. However, the substantial increase in NEFA availability did not increase whole body fat oxidation during exercise. To our knowledge, these acute effects of GH administration on exercise metabolism are novel and have not been reported before.
We designed the current study to investigate acute effects of a single GH dose on lipid and carbohydrate metabolism during endurance exercise, and the subjects, GH dose, type of exercise, and exercise intensities were all selected to increase the pertinence of possible effects with respect to GH abuse. The subjects were thus very fit young men (VO2max, 65 ml O2·min-1·kg-1) who performed bicycle training on a regular basis, and the GH dose (2.5 mg, 7.5 IU) was similar to doses that, unofficially, are reported to be used in doping. Moreover, a load eliciting 65% to 75% of VO2max is likely to be encountered during prolonged periods of both training and competitive bicycling. To further imitate the physiological conditions encountered during training/competition, a standardized pre-exercise meal was provided 2 h before the initiation of exercise. However, it is possible that this latter procedure, by introducing an interaction between GH and feeding on the insulin response, may have influenced some of the exercise differences. More research is needed to clarify these issues.
Obviously, we do not know the duration of these acute effects of GH administration. It is possible that no effect would have been observed if GH had been administered more than 4 h before the initiation of exercise. Moreover, it is not likely that GH doping is performed by taking just a single shot of GH, but rather as daily injections over prolonged periods. Our subjects were not habituated to GH administration, and it is unknown whether the observed acute effects may persist or disappear with chronic GH administration.
In the absence of more sophisticated measurements and kinetic data, we can only speculate on mechanisms involved in the exaggerated blood lactate concentrations and the possible association with reduced exercise performance. The reported uniform feeling of fatigued leg muscles in the GH trial was accompanied by a marked increase in blood lactate. However, this does not prove that lactate is causally related. Certainly, im lactate accumulation has been shown to play a role in the development of muscle fatigue encountered in short-term, high-intensity exercise, possibly by lowering intracellular pH, but multiple factors are likely to be involved (22).
Although lactate was measured in the blood only, we are inclined to believe that the lactate originated from the working muscles (22, 23), and the increase must be a result of either increased production, decreased clearance (intramuscular and/or extramuscular), or a combination of the two. Exercise is likely to be a prerequisite, because previous studies have shown that blood lactate concentrations and forearm lactate release do not change during resting conditions both during and after 5-h GH infusion (24). Exercise intensity is also likely to be important, as evidenced by the highly significant drug-time interaction. Because serum IGF-I did not increase in the GH trial, the effect is probably not mediated through IGF-I signaling, and baseline IGF-I could not be identified as a covariate (data not given).
GH has been reported to increase the activity of mitochondrial uncoupling proteins in skeletal muscle (25, 26), and this may lead to increased lactate formation to sustain sufficient ATP production to supply the metabolic demands during exercise. However, one would expect oxygen consumption to increase if this mechanism were to play a role, and this is not supported by the almost identical VO2 data in the two trials.
Although puzzling at first glance, the substantial increase in NEFA availability with GH administration may lead to increased lactate concentration. The classical Randle hypothesis holds that increased fat oxidation leads to inhibition of glycogen and glucose metabolism (27) due to inhibition of pyruvate dehydrogenase (PDH), phosphofructokinase, and hexokinase (28). Controversy still exists regarding the validity of the hypothesis both at rest (29, 30) and during exercise (31, 32, 33). It is clear, however, that only a selective inhibition of PDH may result in increased lactate formation, and Odland et al. (34) actually demonstrated that artificially increased NEFA availability and fat oxidation reduced muscle PDH activity. This was accompanied by increased muscle pyruvate as well as muscle lactate concentrations during exercise, but blood lactate concentrations remained unchanged (33, 34). However, blood lactate did not increase in any of the studies in which NEFA availability during exercise was increased artificially by lipid infusion and despite the fact that NEFA concentrations were substantially higher compared with the present study (31, 35). Thus, it is not clear whether the increased NEFA availability induced by GH administration in the present study is causally related to the increased plasma lactate concentrations.
Short-term GH administration is known to induce insulin resistance reflected by exaggerated increases in plasma insulin and glucose to an oral glucose load (36, 37). GH- induced insulin resistance may therefore explain the elevated glucose levels during exercise and confirm previously reported effects of GH administration on blood glucose during exercise (38). However, we do not know whether this quantitatively affects muscle glucose uptake during exercise, and it is hard to understand how this should lead to an increase in lactate.
Insulin is the main inhibitory hormone of lipolysis; the decrease in circulating insulin during exercise and increased circulating catecholamine levels are believed to be the main factors in exercise-induced lipolysis. From the present data, it is impossible to assess the roles of the GH-insulin- catecholamine interactions on the increased lipolytic response observed with GH administration. In the present study, we could not demonstrate increased fat oxidation, despite substantially increased NEFA availability induced by GH administration. Obviously, methodological errors introduced by pulmonary non-steady-state gas exchange may have influenced the measurements to some extent, but we still believe that the data obtained during the initial 45 min of exercise are valid. The influence of NEFA availability on substrate oxidation during exercise has been subject to intense research. The results are diverging, but in general only small increases in fat oxidation have been observed despite substantial increases in NEFA availability (39), which is in agreement with the results obtained in the present study.
Plasma lactate levels are very sensitive to minor changes in workloads in the vicinity of the anaerobic threshold (40), and it is therefore important that the performed work is controlled carefully in exercise trials. It is equally important that VO2max and anaerobic threshold do not change between measurements due to training effects or long time periods between measurements. The possibility that these factors had any significant influence on the results in the present study is remote. First, the amount of work performed in the two trials was almost identical as evidenced from the calculated cycling speeds. Second, training effects were eliminated by including only highly trained subjects, by performing measurements with only 7-d interval, and by the random order of the placebo and GH trials.
A minor, but novel, finding in the present study is that HR was increased during exercise after GH administration. It is known that GH increases resting HR (41, 42), and the current observations extend these findings to also include exercise, although mechanisms involved remain unknown.
In conclusion, the present study demonstrates that acute GH administration results in exaggerated increases in plasma lactate, glycerol, and serum NEFA concentrations 90 min subsequent to bicycling at moderate to high intensity. The exaggerated increase in lipolytic markers suggests additive effects of acute GH administration and exercise on lipolysis, but the increased NEFA availability does not increase whole body fat oxidation. The exaggerated increase in plasma lactate may be associated with substantially decreased exercise performance, but this remains to be proven.
Acknowledgments
We thank Annie Høj, Kirsten Nyborg, and Inga Bisgaard for excellent technical assistance and clinical dietitian Kirsten Sonne Pedersen for valuable advice and assistance. Novo Nordisk A/S kindly provided GH and placebo.
Footnotes
This study was supported by the IMK Foundation, the Danish National Research Foundation (Grant 504-14), the Danish Medical Research Council (Grant 9802636), and the Aarhus University–Novo Nordisk Centre for Research in Growth and Regeneration (Danish Health Research Council Grants 9600822 and 9700592).
Abbreviations: CV, Coefficient of variation; HR, heart rate; NEFA, nonesterified fatty acids; PDH, pyruvate dehydrogenase; RER, respiratory exchange ratio; TR-IFMA, time-resolved immunofluorometric assay; VCO2, carbon dioxide production; VO2, oxygen uptake; VO2max, maximal oxygen uptake.
Received November 12, 2001.
Accepted July 30, 2002.
References
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