Growth Hormone and metabolism
In terms of evolutionary biology,
“The effects of GH on substrate metabolism strategies in humans relatively straight forwards: for example during conditions of energy surplus, GH, in concert with IGF-I and insulin, promotes nitrogen retention, and when food is sparse, GH alters fuel consumption from the use of carbohydrates and protein to the use of lipids, thereby allowing conservation of vital protein stores…… this strategy has been used for the survival of man”
(Cited in Moller & Jorgensen 2009)
Lypolysis and exercise
To date, many studies have demonstrated that growth hormone plays and important role in the regulation of metabolism during exercise. The cycling between feast and famine is regulated by insulin building up glycogen and fat, insulin and GH building up protein, and GH with low insulin levels triggers fat mobilization and utilization (Moller & Jørgensen 2009). Brooks et al (2005) agree, the authors suggest that GH stimulates fat metabolism whilst suppressing carbohydrate metabolism. Godfrey et al (2003) suggest that Peptide hormones initiate changes in lipolysis as a result of the hormone binding to beta receptors on the outer surface of the membrane. This proves that GH is plays a major role in lypoloysis. In relation to this theme Ottosson et al (2001) studied the effects of effects of cortisol and GH on basal and stimulated lipolysis in human adipose tissue using the incubation technique, subsequently the authors found that cortisol and GH have opposite effects on the basal lipolytic activity in human adipose tissue in vitro. They discovered that the sensitivity to GH may directly repress glucose uptake or antagonize insulin signalling in the adipose tissue. The results of this study concluded that, GH lowers serum leptin levels; plus was found was found as being the lipolytic agent, whilst cortisol was found to be antilipolytic during this study.
The latest research concerning GH is alluring as it has been discovered that GH exerts a lipolytic effect predominantly in the visceral adipose tissue, furthermore the lipolytic effect is applied to a lesser extent in the sub-cutaneous adipose tissue, resulting in increased FFA flux from the adipose tissue (Vijayakumar et al, 2009), Moller & Jorgensen (2009) agree with this finding they propose that the accumulation of visceral fat rather than chronological age is the most important predictor of GH status in midlife adults. According to Vijayakumar et al (2009) the depot-specific effect of GH could be explained by the fact that GH increases lipolysis by increasing adipose tissue hormone sensitive lipase (HSL) activity. GH triggers TG lipolysis mainly in the visceral adipose tissue via the activation of Hormone sensitive lipase therefore stimulates triglyceride uptake within this region.
The physiological role for exercise-induced GH release is generally poorly understood, recent evidence suggests that one key effect is elevated adipose tissue lypolysis and mobilization of free fatty acids (FFA) for use as an energy resource during recovery (Godfrey et al 2003). Stokes et al (2008) support the concept that GH release in response to exercise, at hours highlight the importance of the role in the regulation of substrate availability in the hours after exercise and that circulating FFAs, in turn, play a role in regulating the GH response to a subsequent exercise stimulus and that elevated FFA can inhibit GH release. This further implies that a relationship exists between GH exercise and FFA.. Brooks et al (2005) have suggested that that due to the GH affect on adipose is indirect GH has a delayed effect on the release of FFA’s from adipose during exercise. Another discovery is that there are GH receptors within adipose cells and via the phosphorylation of triglyceride lipase, GH increases free fatty acid utilisation as a chosen substrate.
Two hormones that stimulate muscle growth by increasing muscle protein synthesis are testosterone and GH. (Urban 1999). This growth stimulating pathway will be discussed below in further detail. GH has been shown to have a net anabolic effect on protein metabolism, as it stimulates protein synthesis (Brooks et al 2005) whilst repressing proteolysis. This theory has been supported by studies which show that GH increases lipid oxidation in both humans and rodents whereby GH activated the mTOR signalling pathway, an established pathway involved in protein synthesis and muscular hypertrophy. Data also suggests that the effects of GH on protein metabolism may be mediated by IGF-1 It has also been hypothesized that the GH-induced increase in FFA flux from the adipose tissue could, via the provision of substrates for gluconeogenesis could reduce the need for amino acids
Exercise protocols and HGH release
It is clear that exercise induced growth hormone release is important in terms if the influence of body compositional changes and metabolic functions in the body. There are two main exercise protocols regarded as eliciting the greatest stimuli of growth hormone release which include endurance based exercise and resistance based exercise.
Upon revising the literature, it appears that intensity of exercise and duration directly relates to GH release has influence on lypolysis and protein synthesis. There are many different modes of exercise, intensities of exercise durations, and also recovery between exercise bouts however it is part of the objective to explain to the reader which exercise mode is best used for promoting lypolysis and protein synthesis via GH release so that it can be utilised in training programs for the clinical and athlete populations.
Endurance based exercise
In relation to endurance exercise, it has been found that exercise above the lactate threshold three times per week rather than 6 times per week at the same intensity aids GH release contributing to favourable body composition changes (Roemmich & Rogol et al, 1997). By review of the literature, it appears that training at a specific exercise intensity greatly influenced the release of GH and its effects,. The duration of exercise seems to be a denominating factor also here, for example According to Widdowson et al (2009) lypolysis is essentially promoted as a fuel source via an increased release of Growth Hormone post 10mins of the onset of moderate to high intensity exercise. Jenkins (2001) agrees that indeed GH levels have been shown to accentuate, after 10 mins in response to acute exercise with a threshold level of approximately 70% VO 2 max. So we can see that it is not only duration but intensity that are all major ingredients to allow GH to take effect in the body.
Weltham et al (1992) agrees with Roemmich & Rogol et al (1997). Authors investigated growth hormone (GH) in 21 eumenorrheic (normal menstruation) untrained women after 1 year of run training. During this particular investigation group training at the lactate threshold plus above the lactate threshold and a control group were devised to formulate the results for the investigation. Measurements for this investigation included the oxygen consumption (vo2) at the lactate threshold (LT); fixed blood lactate concentrations, peak VO,; maximal Vo; body composition; and pulsatile release of GH for all subjects. Whist both the lactate and above lactate threshold group increased their VO2, increases in the >LT group was greater than that in the @LT group (P < 0.05), no change was reported for the control group. Although no among- or within-group differences were observed for body weight, it is interesting to note that trends for reductions in percent body fat (P < 0.06) and fat weight (P < 0.15) were observed in the >LT group, and both training groups significantly increased fat-free weight (P < 0.05). Changes were reported for the trained above LT group exclusively for the pulsatile release of GH after 1 year of run training. Results of this study concluded that when training above the LT would influence the release of GH much greater than training at the lactate threshold.
Recovery between sprint bouts plus intermittent exercise such as sprinting which challenges non-steady state capacity appears to effect growth hormone secretion (Stokes et al 2005). Stokes et al (2008) questioned whether the new discovery that elevated adipose tissue lypolysis and mobilisation of FFA was one of the key roles of GH, GH being suggested as an energy resource for recovery. Stokes et l postulated that repeated sprint exercise could actually cause a GH auto inhibition at the level of the pituitary caused by an increased FFA concentrations in the blood preventing any further increases in GH. Authors suggested a threshold of GH, whereby if a certain level of exercise intensity was initially reached then this would prevent any further rise in GH secretion due to FFA in the blood. Seven non-obese, healthy male volunteers aged 21 to 30 yrs were investigated. One group consumed nicotinic acid (NA) to suppress lipolysis to investigate whether serum FFA could modulate the GH response to exercise, the other group was the control who performed the same series of tests as the group under investigation. The exercise testing protocol consisted of two maximal 30-s cycle ergo meter sprints separated by 4 h of recovery. Peak and integrated GH were significantly greater following sprint 2 compared with sprint 1 in the NA trial (p >0.05) compared with sprint 2 in the control group. The authors concluded that upon suppressing lipolysis significantly greater GH response resulted to the second of two sprints, suggesting a potential role for serum FFA in negative feedback control of the GH response to repeated exercise.
What this indicates is that if GH release and the physiological effects of GH release is the focus of training, we must consider that GH maximum release peaks at the initial phases of sprinting bouts and no further release is enabled. Therefore it maybe suggested that only one sprint session per day is of value when training to manipulate the physiological effects of GH. Research also highlights the fact that exercise should last for 10 mins or more to manipulate the effect of GH.
Resistance based exercise
In humans, resistance exercise is known to influence both circulating and muscle IGFI expression levels. There are countless varieties of exercise protocols for resistance training. Because our focus is trying to find the most successful concepts of training in relation to GH secretion, it is imperative that we investigate a number of studies in order to find a more precise answer on the resistance training protocols which bring about more favourable body compositional changes via GH release.
Evidence suggests that both load and frequency are determining factors in the regulation of human growth hormone secretion, and although there is a significant influence of resistance exercise on growth hormone secretion much of the stimulus for protein synthesis has been attributed to insulin like growth factor with less of a contribution from the human growth hormone receptor interaction on the cell membrane (Godfrey et al 2003)
Within a study by Bottario et al (2007) investigated resistance based exercise an the hormonal responses to different 3 rest times between sets being rest periods of 30, 60 and 120s in 12 healthy previously trained females. The subjects were assigned to 3 resistance training sessions consisting of the same protocol which was 4 sets of 10 repetitions Maximum (RM) with three sets of the four chosen lower body exercises. Interestingly the investigators found a significant rise (p=0.05) in all serum GH levels for subjects in comparison to baseline after each training session however the group with the largest increase was the group with the least rest time between sets of 30 seconds in comparison to the other two groups. GH peaks were found immediately after exercise plus 5 minutes after the exercise had ceased in comparison to any other time. This study suggests that athletes and coaches should manipulate recovery times between sets in order to achieve the highest peaks in GH release.
Sartorio et al (2006) reported the extent of GH release is not related to exercise intensity GH response to resistance exercise in women is greater during the luteal phase than during the follicular phase of the menstrual cycle. What transpires through research is women and men have different responses to resistance training protocols; the extent of these differences is interesting yet requires further research.
Interestingly, Yarrow et al (2007) investigated the Neuroendocrine Responses to an Acute Bout Of Eccentric-Enhanced Resistance Exercise. Previously untrained males (n=22) were involved, within this randomized matched-group study. 4 training sessions were carried out by all participants which were separated by 48hrs. One group was assigned to a traditional training group performing exercises with eccentric and concentric phase, whilst the other group was assigned to eccentric loading techniques for the same exercises whereby the muscle is under load for longer periods whilst it the muscle is being lengthened. Both groups had volume matched exercise protocols. The traditional exercise group in this study completed the same exercise protocol they were tested within which consisted of four sets of six repetitions on both the bench press and squat exercise at 52.5% 1RM. The eccentric training group however performed a protocol consisting of three sets of six repetitions on both the bench press and squat exercise at 40% 1RM on the concentric phase and 100% 1RM eccentric phase. Each exercise set was separated by 1 min of rest. After exercise bout 1, GH concentrations increased approximately 4800% (P <0.05) above baseline and subsequently returned to resting value within 45 min of exercise cessation. During exercise bout 2, GH concentrations increased approximately 250% in the traditional group and 3700% in the eccentric groups before returning to baseline. Authors report that no differences in GH concentrations were observed between groups at any time point . In the eccentric group lactate values were approximately 130–180% greater than exercise bout 1 and 2 traditional protocols (P <0.01).
Results from the above study suggest that acute alterations in post- exercise serum anabolic hormone concentrations may not explain the heightened muscular adaptations associated with eccentric loading. However, it could be suggested that future research is required to enable us to establish the patterns in anabolic hormone responses to eccentric and concentric loading within resistance exercise in for example a more longitudinal based study. Remembering that effects of hypertrophy are not always immediate (as this study seems to presume), although it is postulated here that eccentric loading makes no difference to the effects of GH, there is a obvious design flaw and without seeing the results of the study on the extent of muscular hypertrophy the outcomes may not be as useful as originally planned. By analysing in closer detail the behaviour of GH release in eccentric loading we can see there is more increased rises above base line however GH returns to base line levels in the same was as eccentric and concentric loading it could be suggested that this finding was taken out of context as what really appears here is there are much larger rises in GH in the eccentric group than the concentric group.
Further investigations are to required affirm these suggestions made above although it is postulated that eccentric loading does indeed induce GH release and this effects muscular hypertrophy. It must be noted that women and men may respond differently to resistance training. The evidence suggests that recovery periods between sets of exercises should be no more than 30 seconds to promote GH secretion.
Conclusion
Evidence clearly illustrates that GH plays an important role in metabolism and can enhance sports performance via initiating changes in body composition. There are a myriad of exercise protocols which can be separated in groups of endurance based protocols and resistance training methods. Because these are different in terms of their effects (i.e. endurance promotes lypolysis and resistance training promotes hypertrophy) it is difficult to compare both of the effects plus the protocols vary vastly in terms of the energy systems used. Despite these differences, both protocol types regard rest duration and intensity as important factors when attempting to accentuate the GH response. However because the nature of the industry even when addressing the type of energy systems and GH there continues to be many variations of rest, intensities and durations , now we must make gather evidence and make more specific judgments so we can acquire the desired training effect within current training programs. In order to employ a better understanding of GH release and furthermore implicate training protocols which best accentuate the secretion of growth hormone changing body compositions, additional investigations need to be performed. With the spotlight within this investigation upon current research it can be suggested that for endurance based exercise higher intensities (e.g. sprints) seem to accentuate the GH response with long recoveries between these higher intensity types of exercise sessions. Recovery time in hypertrophy protocols seems to be an indicating factor to growth hormone release, for GH release to be accentuated shorter recovery times of 30 seconds need to be considered.
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