We examined associations between the acute exercise-induced elevations of growth hormone, testosterone, IGF-1 and cortisol, measured at the midpoint of a 12 week training program, and training adaptation measures: LBM, muscle fibre CSA, and leg press strength. We found no association between the acute response of any hormone and increase in leg press strength. There was no association between GH or testosterone and the increase in LBM, whereas GH and cortisol were correlated to increases in type II area and explained ~8% and 12% of the variance in this outcome. It should be noted that this data assesses correlations between post-exercise hormone increments and training adaptations, and does not address the possibility of between-subject differences in hormone flux (i.e., secretion, clearance and uptake) and how this relates to individual differences in the propensity to increase strength or hypertrophy with training.
Data points in the correlation analyses were generally dispersed but resulted in positive Pearson correlation coefficients that were the result of net positive ratios of hormone AUC to strength or hypertrophy markers. Given that the correlation is the sum result of all data points, it is possible that there were hormone-adaptation associations in some individuals that were masked by no association in others. The factors that account for individual versus population gains continues to warrant further investigation; the possibility that the combinations of factors underpinning individual adaptation could vary across individuals adds another layer of complexity to our understanding of adaptation to exercise biology.
We extended our correlation analyses by performing an ANOVA on hormone responses that were stratified into standardized scores using the nutritional group means and standard deviations as defined in the original protocol. We found that the hormone responses of individuals who were responders (defined in “Statistical analyses
”) for gains in LBM, fibre area and leg press strength were no different from the hormone responses of non-responders. Phrased simply, subjects at the top ~16% in terms of resistance exercise phenotypic responses were no different from those at the bottom ~16% in terms of the acute response of testosterone, GH, IGF-1 and cortisol.
Our hormone analysis is limited to the acute 120 min period after the exercise bout and does not offer insight into potential later (e.g., 24 h) changes in hormone secretion/pulsatility, although it has been shown that acute resistance exercise does not affect the circadian rhythm of testosterone (Kraemer et al. 2001
). Our analysis was conducted on blood samples that were collected at the midpoint of the training period and thus does not address how the acute hormone response may have changed over the course of the training period. However, we have recently reported similar acute hormone responses, and resting hormone concentrations, at the beginning and end of 15 weeks of training (West et al. 2009
) and thus believe the measurements made at the midpoint represent a reasonable characterization of the acute hormonal milieu, an assumption shared by others (Ahtiainen et al. 2003a
; Ronnestad et al. 2011
). Our measures did not account for the various aggregate and splice variant isoforms of GH that are reported to be >100 in number (Kraemer et al. 2010
Previously, associations between the acute increase in GH and fibre hypertrophy (McCall et al. 1999
), and between pre- and post-training changes in acute testosterone responses and percentage of increase in quadriceps femoris CSA (Ahtiainen et al. 2003a
), have been reported using small sample sizes (n
= 11 and 7, respectively). In our view, it is difficult to interpret the correlations reported in these small data sets and their bearing on the importance of acute physiological growth hormone and testosterone responses to hypertrophy. Here we examined associations between the acute increases in GH, IGF-1, free testosterone, and cortisol, with adaptations to resistance training in 56 young men. Our sample had resistance training-induced gains in strength, LBM and muscle fibre CSA that represented a substantial range and that were normally distributed and therefore less prone to correlative bias due to outlying data points.
Acute changes in ostensibly anabolic hormones are frequently measured after resistance exercise with the assumption that they promote skeletal muscle anabolism (Ahtiainen et al. 2003b
; Crewther et al. 2008
; Gotshalk et al. 1997
; Hakkinen and Pakarinen 1993
; Kraemer et al. 1995
; Migiano et al. 2009
; Ronnestad et al. 2011
). Because the biological roles of exercise-induced hormone changes are presently altogether uncertain, making concomitant measures of muscle (Spiering et al. 2009
) or other tissues will provide insight into how the complex dynamic post-exercise hormonal milieu, which is a product of simultaneous secretion and clearance processes, might affect adaptation to exercise. Indeed, methods that measure hormone flux, in addition to characterizing the blood profile, will permit a clearer understanding of the actions of each hormone in producing a phenotypic change in response to training. For example, measurement of exercise-induced cortisol often presents a conundrum based on its equivocal physiological role. That is, cortisol is frequently elevated after resistance exercise protocols designed to elicit hypertrophy (Kraemer et al. 1993
; Kraemer and Ratamess 2005
) and yet is generally considered to be catabolic and as such counteractive to hypertrophy (Kraemer and Ratamess 2005
; Spiering et al. 2008
; Tarpenning et al. 2001
). The findings of the present study are no different; that is, cortisol was significantly, albeit weakly, related to gains in type II fibre area. Likewise, GH was associated with changes in type I fibre hypertrophy and yet is reported to have no effect on myofibrillar protein accretion (Meinhardt et al. 2010
; Rennie 2003
; Yarasheski et al. 1993
). As the regulation of GH becomes clearer (Inagaki et al. 2011
), it is possible that a shared mechanism, such as neural drive/muscle activation and/or metabolic stress, that could affect both GH and muscle adaptation may explain the association of GH with hypertrophy. Collectively, GH and cortisol are known to have gluconeogenic action as well as liberate substrates such as free fatty acids (Sakharova et al. 2008
) and amino acids (Simmons et al. 1984
), respectively; it remains unknown whether exercise-induced changes in these hormones could also be modulating these energy-releasing and tissue-remodelling processes leading to an improved phenotype with training.
In contrast to GH, testosterone is known to have potent effects on contractile tissue accretion when administered pharmacologically (Bhasin et al. 1996
). Due to the potency of exogenous testosterone for hypertrophy, physiological exercise-induced changes in testosterone have also garnered significant interest (Crewther et al. 2011
; Hayes et al. 2010
; Vingren et al. 2010
). However, we did not observe any significant relationships between the exercise-induced increase in testosterone concentration and the degree of LBM, hypertrophy or strength. This observation is in agreement with our previous findings (West et al. 2009
; Wilkinson et al. 2006
) but is in contrast to a recent study (Ronnestad et al. 2011
). The latter study (Ronnestad et al. 2011
) reported that subjects who trained their elbow flexors after lower-body exercise, which elevated testosterone concentrations ~1.2-fold, achieved greater increases in strength and muscle CSA (at two of four scanned locations in the muscle mid-belly), despite equivalent progression in training load and equivalent increases in calculated muscle volume to elbow flexors trained alone. In the present study, free testosterone concentrations were elevated ~2-fold for ~15–30 min after lower-body exercise. In our view, the lack of association to adaptation was not surprising and is likely the result of the fact that exercise-induced testosterone elevations are small and transient compared to the sixfold increases that can be imposed by pharmacological intervention which are chronically sustained and which have potent effects on hypertrophy (Bhasin et al. 1996
). Thus, our finding that the magnitude of the exercise-induced testosterone elevation was not associated with training adaptations may underscore differences between physiological and pharmacological interventions that affect muscle hypertrophy. Pharmacological administration of testosterone results in a different pattern (chronically elevated basal concentrations vs. transitory increases) and greater persistent increases in the concentration of the hormone (supraphysiological vs. physiological concentrations that are of comparable magnitude to the spread of normal diurnal variation).
In summary, differences in the post-exercise response free testosterone and IGF-1 showed no association with increases in adaptations to resistance training. While responses of GH and cortisol were positively correlated with changes in fibre area, the association was relatively weak and the relevance to hypertrophy is presently unclear due to evidence that GH is not anabolic to contractile tissue and that cortisol, which is catabolic in nature, is elevated after exercise programs that induce hypertrophy. A more detailed study of hormonal mechanisms is clearly required. Whereas increments in post-exercise GH and cortisol concentration were weakly associated with resistance training-induced phenotypes, other previously measured acute intramuscular markers, such as p70S6K1 phosphorylation, microRNA expression and satellite cell activation, can yield relatively robust associations with hypertrophy. Overall, because the regulation and biological actions of the post-exercise hormonal milieu are largely undefined, measuring systemic hormone profiles as well as local hormone and receptor concentrations, together with markers of hypertrophy or the phenotype itself, will enhance our understanding of their role in tissue remodelling with exercise.