muscle, is required to determine the response of muscle, over short periods of time, such as hours or days (Rennie 2003). This technique was not available to early researchers and is still not freely available. RhGH administration did not enhance the muscle anabo- lism associated with heavy-resistance exercise in 16 males with a mean age of 27 years and a weight of 70.6 kg. Resistance training, plus rhGH group (0.04 mg.kg−1.day−1 [~8.4 IU.day−1]) did not differ from 9 resistance train- ing males, compared with 9 placebo males for 12 weeks (Yarasheki et al 1992). The fractional rate of skeletal muscle protein synthesis and the whole body rate of protein breakdown did not increase during a constant intravenous infusion of [13C] leucine in 7 young healthy experienced male weightlift- ers with a mean age of 23 years and a mean weight of 86.2 kg before and at the end of 14 days of subcutaneous rhGH administration (0.04 mg.kg−1.day−1 [~10.5 IU.day−1]) (Yarasheki et al 1993). RhGH administration in 8–10 healthy, nonobese males with a mean age of 23 years, body weight of 122 kg, and body fat of 10.1% (0.03 mg.kg−1.day−1 [~11 IU.day−1]) for a period of 6 weeks, had no effect on maximal strength during concentric contraction of the biceps and quadriceps muscles (Deyssig et al 1993). In such highly trained athletes with such a low fat mass there were no effects of rhGH treatment on strength or body composition. The administration of rhGH to 8 healthy, sedentary males (0.0125–0.024 mg.kg−1.day−1; [2.9–5.6 IU.day−1]) versus placebo administration to15 healthy, sedentary males, with low serum IGF-I levels, with a mean age of 67 years and a body mass of 78.5 kg, for 16-weeks, did not increase muscle strength over resistance exercise training (Yarasheki et al 1995). These results may be as a consequence of the differ- ent dosages of rhGH used, because of adverse side effects incurred dosages ranged from 0.013–0.024 mg.kg−1.day−1 (0.04–0.072 IU.kg−1.day−1). The dosages for the ﬁrst two subjects were equivalent to 5 IU.day−1 but the second two subjects had 4 IU.day−1 and the last four subjects had the equivalent of 3 IU.day−1. RhGH administration (0.03 mg.kg−1of body weight [7.2 IU × 3.week−1]), for 6 months in 52 healthy males with a mean age of 75 years and a body mass of 80 kg, with well-preserved functional ability, but low baseline IGF-I levels, signiﬁcantly increased LBM, by 4.3%. There were no statistically or clinically signiﬁcant differences seen between the groups in knee or hand grip strength, nor in aerobic performance (Papadakis et al 1996). Therapeutics and Clinical Risk Management 2008:4(3) AAS, growth hormone, and insulin abuse Wallace and colleagues (1999) demonstrated that there was no improvement in morphological or performance characteristics, assessed by cycle ergometry and V˙O2 peak assessment, following rhGH administration to 8 males (0.05 mg.kg−1.day−1 [0.15 IU.kg−1.day−1]) versus placebo administration to 8 males, for 7 days. The combined effects of testosterone and rhGH, administration for 1 month, signiﬁcantly improved aerobic performance in “stair climb time” in 10 healthy older males (Brill et al 2002). A single rhGH dose (2.5 mg [7.5 IU]) in 7 highly trained males with a mean age of 26 years, body mass of 77 kg, and a V˙O2 peak of 65 ml.min−1.kg−1, who performed 90 min of cycling 4 hours after taking the rhGH, prevented two sub- jects from completing the exercise protocol. It signiﬁcantly increased plasma lactate and glycerol as well as serum NEFA. This may compromise exercise performance. V˙O2 peak remained unaltered by drug effect until exhaustion (Lange et al 2002a). Plasma glucose was, on average, 9% higher during exercise after rhGH administration compared with placebo. Any beneﬁt of exercise in terms of increased glucose tolerance appeared to be negated by rhGH in the subjects. Myosin heavy chain (MHC) 2X isoforms, were signiﬁ- cantly increased by rhGH administration in healthy elderly males (Lange et al 2002b). This has been regarded as a change into a more youthful MHC composition, possibly induced by the rejuvenation of systemic IGF-I levels. There was no effect on isokinetic quadriceps muscle strength, power, cross-sectional area (CSA), or ﬁbre size. Resistance training (RT) and placebo caused substantial increases in quadriceps isokinetic strength, power, and CSA; but these RT-induced improvements were not further augmented by additional rhGH administration. In the RT and rhGH group, there was a signiﬁcant decrease in MHC 1 and 2X isoforms, whereas MHC 2A increased. Resistance training, therefore, seems to overrule the changes in MHC composition induced by rhGH administration alone. Blackman and colleagues (2002) administered rhGH (0.03–0.02 mg.kg−1.day−1) and gender related sex steroids to healthy aged males and females, aged 65–88, for 26 weeks. LBM increased and fat mass decreased. Testosterone and rhGH increased V˙O2 peak in males, but transdermal oes- tradiol, 100 µ g.d−1, plus oral medroxyprogesterone acetate, 10 mg.d−1 and rhGH did not increase female V˙O2 peak. The effect on strength and endurance exercise could not entirely be attributed to the administration of rhGH. The administration of rhGH in a dosage of 0.067 mg.kg −1. day−1 (~15.3 IU.day−1) exerts an anabolic effect both at rest 591