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Introduction

    Growth hormone (GH) is a peptide hormone produced by the anterior lobe of the pituitary gland. Its concentration is regulated by the hypothalamus via secretion of growth hormone releasing factor hormone (GHRH) and somatotropin release inhibiting factor hormone (SRIH), which stimulate and inhibit GH release, respectively. GH may act through two different ways: directly on tissues via a GH receptor (GHR) (3; 32) or indirectly, inducing the production and secretion of somatomedins (17; 39).

    Until the mid 1980's treatment with GH was carried out with hormones directly extracted from the pituitary glands of human cadavers. However, this practice exposed patients to transmissible brain diseases such as Creutzfedkt-Jakob Disease (13; 14; 33; 41; 46; 56), which is fatal and could develop years after the cessation of the treatment (41). In 1985, human growth hormone recombined from DNA became available, augmenting its supply and decreasing the risk of the treatment (1). However, the accessibility of GH combined with the enthusiasm of scientists and retailers had stimulated its use in several situations where its efficacy and safety had not been proven.

    Among other promises, there are anectodus claims that GH promotes increases in lean body mass, muscle mass, body fat and physical performance. Since the landmark investigation by Rudman et al (48), recombinant human growth hormone has been prescribed to elderly people in order to promote changes in body composition and functionality. Lately, its anabolic properties have been confirmed in animals (11; 47) and humans (31; 48).

    Various studies reported that resistance training of different intensities and duration markedly stimulate GH release (34; 35; 42; 51), this response along with the supposed physiological actions of GH brought the suggestion that this hormone may mediate some adaptations to resistance exercise and raised the theory that treatment with exogenous GH might enhance this response. Based on this hypothesis, many athletes and fitness enthusiasts started using GH with the purpose of increasing muscle hypertrophy and strength. Hence, the purpose of this review is to explore the effects of GH utilization in physiological and ergogenic responses to resistance training. The responses will be divided in seven groups: bone mass, fat free mass (FFM), body fat, muscle strength and power, muscle hypertrophy, insulin-like growth factor-1 (IGF-1) concentrations and adverse reactions.

Methods

    Computerized literature searches were performed using Medline (January 1965 to October 2004). The following keywords were used: "GH", "growth hormone" or "somatotropin" in combination with "resistance exercise", "resistance training", "strength training", "strength exercise", "weight lifting" or "weight training". In addition to computer searches, cross-referencing from retrieved articles and original investigations were performed.

    Inclusion criteria were: controlled trials (randomized or nonrandomized); resistance training as the only exercise intervention; adults (> 18 years) as subjects; studies published in English language journals.

    The following abbreviation will be widely used: GH (growth hormone); RT (resistance training); RT+GH (resistance training plus growth hormone), RT+PLA (resistance training plus placebo).

Physiological and ergogenic effects

    The studies reviewed are summarized in table 1.

Table 1: summary of the studies reviewed (RT+PLA - resistance training plus placebo; RT+GH - resistance training plus growth hormone; FFM - fat free mass; FM - fat mass; NMRI - nuclear magnetic resonance imaging; BMD - bone mineral density; DEXA - dual X-ray absorptiometry; CSA - cross sectional area)

Bone mass

    GH has an important influence in regulation of longitudinal growth and several studies have demonstrated that this hormone is important in regulation of bone formation and resorption (45). GH may increase bone formation in two ways: directly, via interaction with GH receptors on osteoblasts (44; 50) or indirectly, via an induction of IGF-1 production and excretion by the liver (25). Also, GH can control osteoclast formation, but both stimulatory and inhibitory mechanisms have been presented (45).

    Some authors suggested that GH treatment has positive effects on bone mineral density (7; 53), however controversy exists (5; 6). Specifically with resistance training (RT), Yarasheski et al (62) conducted an experiment to determine if GH treatment plus RT would increase whole body and regional bone mineral density (BMD) in elderly men more than RT alone. After 16 weeks, osteocalcin concentration in RT+GH was greater than in RT+PLA, however there were no differences in the magnitude of the changes in BMD between groups, indicating an increase in bone turnover without bone mineral accretion. In other studies, bone mineral content, as measured by DEXA, were not changed after 10-12 weeks of RT+GH or RT+PLA in elderly males (36; 55).

    The literature reviewed does not bring irrefutable data to support GH use in order to increase bone changes with RT. However the short duration of the studies and the evaluation methods possibly bias the results, additional studies with longer periods of intervention and/or more accurate methods, such as biochemical markers of bone formation and resorption are needed to clarify this issue.

Fat free mass (FFM)

    In most studies reviewed, increases in FFM produced by RT+GH were significantly greater than those produced by RT+PLA (15; 19; 36; 55; 63; 64) with a concomitant elevation in whole body protein synthesis (63; 64).

    In elderly men, 12 weeks of RT+GH increased FFM by 2.52 + 0.54 kg, as measured by DEXA, while there were no significant changes in RT+PLA. Regional analysis also revealed an increase in FFM in all three body compartments for RT+GH, with no change in RT+PLA (36). In earlier studies, only RT+GH significantly increase FFM in older men, with no significant changes in RT+PLA (55; 57).

    Previously, Crist et al (15) evaluated the effects of RT+PLA or RT+GH on body composition of well-trained young subjects and found superior increases in FFM (2,7 vs. 1 kg) and FFM/FM (1,8 vs. -0,9 kg) in RT+GH vs. RT+PLA. Yarahseski et al also assessed body composition with hydrodensitometry and found greater increases in FFM in RT+GH than RT+PLA in older (4.8 + 0.6% vs. 2.1 + 0.6%) (64) and young men (4.5 + 0.6% vs. 1.6 + 0.7%) (63).

    The controversy appears in a study by Deyssig et al (19), where GH administration had no effect on body composition of well-trained male athletes.

Body fat

    Reduction in fat mass is frequently desirable for health, athletic and aesthetical purposes. Fat accumulation is characteristic of growth hormone deficiency and GH treatment is usually prescribed as a way of reducing body fat (4; 29). In agreement with this practice, most of the reviewed studies showed an additive effect of GH in body fat reduction promoted by RT.

    In a study by Lange et al (36) fat mass (FM), as determined by DEXA, significantly decreased in RT+GH group (-3.16 + 1 kg), but not in RT+PLA. Also using DEXA in elderly men, Taafe et al (55) found that only RT+GH promoted a significant reduction in FM (-12.3%), with no difference in RT+PLA (55). The same seems to happen in well trained young subjects, where RT+GH promoted more expressive reductions in %fat compared to RT+PLA (1,5% vs. 0,4%) (15).

    However the controversy exists, since hydrostatic weighting showed no difference in body fat loss between RT+GH and RT+PLA in older (57; 64) and young subjects (63). Additionally, using skin fold measures, Deyssig et al (19) found that GH treatment had no influence in body composition changes during resistance training in highly trained males, who apparently had no excessive fat stores to be metabolized.

Muscle strength and power

     Although of some intrinsic interest, changes in body composition achieve clinical or athletic importance only when accompanied by altered body function. However, the literature reviewed lends no support to the view that GH administration exerts a synergistic effect with resistance training on the muscle strength improvements observed in elderly (30; 55; 57; 64) and younger subjects (15; 19; 63).

     As assessed by 1RM test, there were no differences after 10-12 weeks (36; 55) or 6 months (30) of RT+GH and RT+PLA in elderly people. Also, isokinetic quadriceps torque and power increase significantly and equally in RT+GH and RT+PLA (36; 57). Interestingly, one study has found that leg extensor power increased from baseline to 12 week in RT+PLA but did not change in RT+GH in elderly men (36).

     In young (63) and older (64) males, relative percent strength improvement in each exercise tested and average improvement for all exercises were similar between RT+GH and RT+PLA. Also, Deyssig et al (19) treated highly trained athletes with GH in a double-blind placebo controlled study and found that muscle strength, measured by 1 RM test, is not affected by GH administration. Thus, based on current evidence we cannot conclude that GH confers any additional benefit on muscle strength compared to exercise alone.

Muscle hypertrophy

     The increase in FFM without concomitant changes in muscle strength is strong evidence that GH treatment does not augment contractile protein content. In fact, besides positive changes in fat free mass, most of the studies reviewed did not show any additive effects of GH on muscle hypertrophy in exercising adults, either measured by nuclear magnetic ressonance imaging (NMRI) (36), muscle biopsies (30; 36; 54) or rates of muscle protein synthesis (63; 64; 65).

    Taafe et al (54) took biopsies of the vastus lateralis muscle from 18 healthy elderly men engaged in RT+GH or RT+PLA for 10 weeks and found that fiber CSA increased in both groups, with no difference between them. Also using biopsies, Hennessey et al (30) found no difference in muscle hypertrophy of type I and type II fibers in elderly people submitted to six months of RT+GH or RT+PLA (3,9% vs 5,8% type I fiber and 4,5% vs. 15,9% for type II fiber).

    Similarly, in a recent study, muscle biopsies did not reveal any changes in muscle fiber size between RT+GH and RT+PLA (36). Additionally, Lange et al (36) found that quadriceps cross-sectional area (CSA) measured by NMRI increased significantly in RT+GH (10.4 + 2.7%) and RT+PLA (6.3 + 2.5%) after 12 weeks of treatment, with no difference between groups.

    Two similar experiments were conducted to determine whether GH administration enhances muscle anabolism associated with heavy-resistance training in young (63) and older (64) men. The results showed that the increases in whole-body protein synthesis and protein balance were more evident in RT+GH. However, fractional quadriceps muscle protein synthesis rate were not different between groups, suggesting no muscle protein accretion with GH treatment (63; 64). In a similar work, Yarasheski et al (65) examined the effects of 14 days GH administration in protein metabolism of experienced weight lifters and found no difference in fractional rate of vastus lateralis muscle protein synthesis and whole body protein breakdown rate before and after GH administration, raising doubts if prolonged GH administration would result in additional muscle hypertrophy.

    Later, Welle et al (57) found that GH administration has no acute (4 hours) effect on myofibrilar protein synthesis compared to placebo. Additionally, after 3 months of treatment, mean whole body leucine appearance, leucine oxidation and leucine incorporation into proteins were similar in RT+GH and RT+PLA. There were also no significant differences in the mean fractional rate of myofibrilar protein breakdown or mean postabsorptive fractional rate of myofibrilar synthesis between groups. Contrary to others, Welle et al (57) found that muscle mass, as measured by creatinine excretion, significantly increased in RT+GH (3.3 + 1.1 kg) but not in RT+PLA (1.3 + 3.3 kg). However the author themselves admitted that the results raised question of how there could be an increase in muscle mass without alterations in protein metabolism.

     One of the possible causes of the increase in FFM without muscle hypertrophy or gains in strength and power seen in most studies is that GH did not increase contractile protein. Thus, the increase in FFM could be due to the known water retention caused by GH (38). This hypothesis is supported by some studies (10; 12; 63; 64), but not others (15). Another possible explanation is soft-tissue overgrowth induced by GH treatment (15; 63; 64).

     Although the lack of effect of GH in muscle hypertrophy might seem surprising, it is in accordance with the early work of Goldberg (26), who demonstrated that work-induced muscle growth is independent of systemic GH. Similarly, posterior studies in rats showed that skeletal muscle adaptation to mechanical stimulus occur independently of GH status (18; 66).

Insulin-lige growth factor-1 (IGF-1) concentration

    In all studies reviewed, IGF-1 significantly increased from baseline in RT+GH groups but not in RT+PLA groups in sedentary young (64), elderly (30; 36; 55; 54; 63) and highly trained adults (15; 19; 65).

     In spite of the increase in serum IGF-1 of more than 100% in many cases (19; 28; 63; 64), GH treatment did not change IGF-1 mRNA expression in muscle (54). This could explain the lack of effect in muscle hypertrophy and strength, since literature is consistent in showing no correlation between systemic IGF-1 and muscle adaptations to overload (18; 23; 22; 24), thus being proposed that adaptations are mediated by the autocrine/paracrine form of IGF-1 (16; 40; 60; 61). For example, Eliakim et al (24) found significant correlations between muscle leg volume and serum concentration of IGF-1 at baseline in young girls, however, in response to training, there were an increase in muscle volume without alterations in IGF-1 levels for the training group, while in control group, serum IGF-1 were elevated without an increase in muscle volume.

    It is important to note that there is relative independence between the two forms of IGF-1 (2; 18; 28). Regardless of systemic GH been a precursor of hepatic IGF-1, the same is not true for the autocrine/paracrine form. Studies in hypophysectomized animals revealed that even with low concentrations of GH and IGF-1 in blood, rat muscles still revealed hypertrophy in response to overload due to autocrino/paracrine IGF-1 (2; 18; 59). The local effects of IGF-1 were clearly demonstrated either through localized infusion of small quantities of IGF-1 (3) or through induction of increased IGF-1 response in specific tissues (8; 9; 37), demonstrating that increases in muscle hypertrophy and strength occur with muscle-specific elevations in IGF-1, even in the absence of alterations in the level of the hormone in serum.

Side effects

    In the literature reviewed the most commom side effects acompaning RT+GH were: fluid retention, cabohydrate intolerance, carpal tuunel syndrome, artrhalgia, edema atrial fibrilation.

    Crist et al (15) found two main adverse reactions associated with GH treatment: cabohydrate intolerance and soft-tissue overgrowth. In a study conducted by Taafe et al (55) several participants experienced fluid retention, which was sufficient to cause three subjects to withdraw from the study and two others to require diuretic medication.

     Two subjects in the study conduced by Yarasheski et al (63) developed carpal tunnel syndrome symptoms compression and were withdrawn from the experiment. Lately, GH treatment had to be discontinued in several subjects due to adverse reactions such as carpal tunnel syndrome compression, artrhalgia and fluid retention in hands and feet (64). Because of side effects, GH dosage had to be reduced in many subjects in both studies (64; 63). Symptoms of carpal tunnel syndrome and fluid retention were also seen by Deyssig et al (19) and Welle et al (57).

     Hennessey et al (30) had to drop GH dose from 0.015 to 0.005 mg/kg/d due to side effects such as arthralgia and edema and eventually, because of long-term side effects such as carpal tunnel syndrome, the final dose dropped to 0.0025 mg/kg/d. In a recent study (36), one subject in GH group abandoned the experiment because of intolerable side effects attributable to GH administration (pitting leg edema)., Of the 15 subjects receiving GH who completed the study and, 12 experienced side effects (pitting leg edema, n = 10; carpal tunnel syndrome, n = 1; so-called triggerfingers, n = 1; transient atrial fibrillation, n = 1; weight gain, n = 1), and the GH dose had to be reduced in 10 individuals.

Conclusions

    Although it would be difficult do make comparisons among studies because of differences in methodology and subjects selection, it is notable that none of the studies reviewed support the use of GH as a mean to improve gains in muscle strength and hypertrophy in response to resistance training.

    It is important to stress that the use of growth hormone as a performance aid is illicit. This, along with the large evidence of side effects without a significant ergogenic effect, reinforces the orientations that this hormone should be used only in the cases suggested by FDA. Moreover, GH use by athletes is often accompanied by other dangerous practices making it difficult to assess its side effects in these cases. However, the literature submits some reports of GH abuse by bodybuilders presenting diverse pathological conditions (20; 21; 58).

    The exact mechanisms of muscle adaptation to overload are still not completely understood; however, there is much evidence that systemic GH does not play a major role in this process (2; 18; 26). Furthermore, in acromegaly, muscles appear hypertrophied but are often functionally impaired (43). Besides some speculative hypothesis for the augmentation in FFM without correspondent increases in contractile structures and function, it is not clear what changes occur during GH treatment. Thus, requirements for future studies in this area should include expression of non-contractile protein and precise measurements of water retention.

    This study does not question the potential benefit of GH to specific groups and we are not able to determine if GH have a synergistic effect with resistance training in cases such as GH deficiency, HIV, burn-induced wasting or sarcopenia as the literature reviewed only addressed the effects in apparently healthy persons.

    Although GH does seem to have no synergistic effect on muscle anabolism promoted by resistance training, it is possible that GH response to training is statistically correlated to muscle hypertrophy, since training protocols frequently used for this purpose also induce expressive elevations in GH levels (27; 34; 35, 42; 51). This, however, could be attributed to a relation between GH and metabolic stress, instead of a direct relation between GH and muscle anabolism, since protocols that induced higher elevations in GH also produced higher elevations in lactate (27; 35), and according to some authors metabolic stress is an important stimulus to muscle hypertrophy (49; 52).

Pratical implications

    Based on the literature reviewed we conclude that GH treatment have no additive effect to resistance training for healthy people looking towards improvements in muscle strength and hypertrophy. The increase in FFM without a concomitant improvement in muscle performance and hypertrophy in conjunction with a wide variety of side effects and the high cost of treatment make GH an unviable alternative as an ergogenic aid to resistance training for healthy subjects. Despite some positive results observed in fat mass, the magnitude of the results are not enough to justify the high incidence of side effects and the elevate cost, making GH treatment not recommended in this cases too. It is important to note that FDA had approved GH as a treatment for several conditions, but not as a therapy for ageing or as an ergogenic aid for sports. Thus, athletes, coaches and trainees involved with resistance training are recommended not to use and/or recommend GH, unless there is strong clinical evidence to support this practice.

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