In Part I of this article, we looked at the impact training intensity has on GH, as well as when one should supplement with BCAAs to maximize their impact. Now let’s turn our attention to how GH affects adipose tissue, fat loss and obesity.
GH Preferentially Burns Abdominal Adipose Tissue
Interestingly GH stimulates adipose tissue mobilization after a delay of approximately 2 hours (3). During sleep, the peaks in GH result in maximal levels of free fatty acids about 120 minutes later (9). Additionally, GH increases circulating levels of glycerol and free fatty acids in GH deficient men after a lag time of 2-3 hours (12).
So if you are trying to get ripped, is one little peak in GH during your workout going to make that big of a difference in your physique? Your damn right it does! Researchers took subjects and gave them a dose of GH but kept it in the physiological range; a single GH spike increased fat mobilization in femoral (thigh) and abdominal adipose tissue, the greatest increases being more prominent in the abdomen. The more pronounced effect of fat mobilization in abdominal adipose tissue may be the reason why GH deficient men look like they are pregnant and hold most of their fat in their stomach. The lipolytic response is two to threefold more pronounced in the abdomen; the effects of GH will lead to preferential loss of abdominal subcutaneous fat10. When obese men are administered GH the fat seems to just melt off. For example, thirty men, with abdominal/visceral obesity were treated with recombinant human GH in a 9-month randomized, double-blind, placebo-controlled trial. The mean total bodyfat dropped by 9%, moreover, the volume of visceral adipose tissue (stomach) decreased by 17%, whereas no changes were seen in the placebo group.
No Increase in Post Exercise Fat Utilization without Acute Exercise Increases in GH
Since there is a delay in GH’s effect on fat metabolism, back in 2005 researchers wanted to see exactly what acute increases in GH did to fat metabolism after exercise. They gathered test subjects and had them cycle @ 70% of their peak exercise capacity. Post exercise fat metabolism was directly related to the acute rises in GH that occurred during the exercise protocol (6). Based on the study, the best way to increase your fat metabolism post exercise is to increase your GH levels. It is well established that prolonged rest periods (3-5 minutes) result in very small rises in GH compared to taking short rest periods which leads to large increases in GH. Is there any metabolic advantage of the large increases in GH that occur with short rest periods for increasing fat metabolism? According to a new study, the acute increases in GH are essential for increasing post exercise fat utilization. Here was the study design. Researchers had subjects exercise for 1 hour. One group served as a control group while one group of subjects received an infusion of Octreotide (a potent inhibitor of growth hormone) which as an injectable formulation for the treatment of acromegaly (GH excess). The control group had a fourfold rise in GH while the group receiving Octreotide had a blunted GH response during exercise. Researchers found that post exercise fat utilization in subcutaneous adipose tissue was increased due to GH while it remained unchanged in the group receiving the drug that blunted GH responses during exercise (4). Researchers suspect the reason GH peaks about 2 hours after an intense bout of exercise is that glycogen needs to be replenished during that time. As a result, high levels of GH increase fat mobilization to spare glucose which is being incorporated into glycogen. So if you are looking to get lean, in addition to diet, large increases in GH from high intensity exercise may facilitate this process.
GH has Direct and Indirect Actions on Fat Burning
The fat burning properties of GH are well documented. Studies in fat cells and in human and animal models have shown that in addition to its direct lipolytic (fat burning) effect on adipose tissue (demonstrated by stimulation of basal fat lipolysis) (17,18,19). GH can also increase fat loss by blocking fat storage. 11ß-HSD1 converts the inactive glucocorticoid, cortisone, to active cortisol in adipose tissue; 11ß-HSD1 is highly expressed in human adipose tissue (31), and over expression in adipocytes in a rodent model leads to a centrally obese. It has shown that exogenous GH is able to inhibit 11ß-HSD1 activity in patients with simple obesity which means GH blocks cortisol from binding to the adipose tissue receptor limiting fat storage (32).
Small pulses of GH designed to mimic physiologic pulses, have been shown to induce a dose-dependent stimulation of fat oxidation and increase circulating levels of FFA and glycerol10. In normal subjects, the onset of exercise leads to a 3-fold increase in the rate of fat oxidation and a rapid increase in uptake of free fatty acids into skeletal muscle where fat is burned as a fuel source (13). It seems GH’s biggest impact on fat metabolism is during the post- exercise period. For example, fat oxidation was studied in GH deficient subjects during and following discontinuation of long-term GH replacement. Discontinuation of GH was not associated with any change in fat oxidation at rest, but resulted in a marked reduction in fat oxidation and fatty acid release into the circulation during and following exhaustive exercise (14). In a similar study, GH deficient adults were receiving long-term GH replacement on 2 separate days, once with and once without a bolus of GH administered intravenously at the start of exercise. The protocol resulted in an increment in circulating GH levels during exercise that was indistinguishable from that seen in healthy normal subjects. Under resting conditions there was no effect of GH, while during and following 45 minutes of exercise at lactate threshold there was a greater fat oxidation following GH administration (15).
GH and Catecholamines: The Fat Burning Combo
Adipose tissue lipolysis increases during exercise. The major stimulus for the enhanced lipolysis seems to be circulating catecholamines in combination with a low insulin concentration. Just all about all the major fat burners and thermogenics increase catecholamines for fat loss. These supplements essentially mimic the actions of norepinephrine and epinephrine in a direct and indirect manner. Directly, agonists activate beta adrenoreceptors (?-AR) and indirectly, they facilitate the release of epinephrine and/or norepinephrine (catecholamines). Catecholamines activate cAMP production and stimulate fat metabolism through ?-AR stimulation and inhibit the process through ?2-AR activation (8). Fat cell responsiveness to catecholamines depends on the ratio and functional balance between ? – and ? 2- receptors located on fat cells, which are influenced by sex, anatomical location of the fat depot, and obesity9. GH enhances the actions of catecholamines. One study reported that when GH is added to fat cells, the addition of GH increased the fat cells response to epinephrine ( a powerful fat burning hormone) (18). Further studies have reported that GH results in an up-regulation of ß-adrenergic receptor density on fat cells (29,30). Although both catecholamines and GH work together, GH still outperforms catecholamines in terms of post-exercise fat utilization. In 2000 researchers studied the response of GH and catecholamines during and following exercise of varying intensity and related these responses to changes in fat oxidation. During exercise, neither glucose utilization, which was directly proportional to exercise intensity, nor fat oxidation, which remained constant, was influenced by either GH or catecholamines. Fat oxidation following exercise was related to exercise intensity and it correlated to both the peak GH and peak epinephrine response. After further analysis only the peak GH response was found to be the greatest predictor of post exercise fat utilization (16). There is evidence, therefore, that endogenous GH secretion exerts an immediate as well as a delayed effect to increase fatty acid availability following exercise.
What Influences Resting GH?
At rest, GH secretion is characterized by episodic bursts over a 24-hour period and is influenced by age, gender, nutrition, sleep, body composition, regional distribution of bodyfat, stress, fitness level, sex hormones (testosterone and estrogen), insulin, and IGF-1 levels. Of the factors listed above that influence GH secretion, if you had to choose the two most important predictors of your 24-hour GH release which would they be?
Researchers examined the 10 physiological factors regulating GH secretion at rest during men and found that the 2 physiological factors that had the greatest impact on resting GH secretion are: abdominal visceral fat and fasting insulin levels. In the study, abdominal fat was the strongest predictor of 24-hr GH release among the ten variables studied, followed closely by fasting insulin levels. An inverse relationship between abdominal fat and 24-h GH release (the bigger your stomach, the lower GH secretion you have) was demonstrated in both young and old men. It’s interesting that although with age there is a reduction in GH secretion, having a big gut suppresses GH greater than the aging process. Having a big stomach not only suppresses GH secretion but also serum IGF-I concentrations which is a powerful muscle builder (22, 23, 24). It seems that adhering to diets that are low in carbs or generally low glycemic would result in greater insulin control which would enhance the actions of GH.
Excess Fat Blunts the GH Response to Exercise
Some researchers have found that obese individuals have lower resting GH and higher cortisol levels than normal weight subjects, and that obese subjects have a blunted GH response to exercise compared to normal subjects (26, 27). What better excuse to lose the gut than to realize that with increased weight gain there is a lowered GH response not only at rest but also in response to exercise? In the J. Clin. Endocrinology and Metabolism it was reported that not only do obese men have a blunted GH response to exercise but also have a blunted respiratory quotient (RQ) (RQ is a measure of fat oxidation), increased cortisol production, and a smaller post-exercise rate of metabolism compared to lean individuals (28). In contrast to obese men, lean individuals demonstrated significant increase in GH during exercise and a clear shift toward enhanced fat utilization after intense exercise accompanied by a 28% higher rate of oxygen consumption post exercise (higher metabolic rate). Bottom line: Getting too fat in the offseason makes it all the harder to get back in competition shape.
1. Pritzlaff CJ, Wideman L, Weltman JY, Abbott RD, Gutgesell ME, Hartman ML, Veldhuis JD, Weltman A. Impact of acute exercise intensity on pulsatile growth hormone release in men. J Appl Physiol. 1999 Aug;87(2):498-504. 2. Nevill ME, Holmyard DJ, Hall GM, Allsop P, van Oosterhout A, Burrin JM, Nevill AM. Growth hormone responses to treadmill sprinting in sprint- and endurance-trained athletes. Eur J Appl Physiol Occup Physiol. 1996;72(5-6):460-7. 3. Moller N, Gjedsted J, Gormsen L, Fuglsang J, Djurhuus C. Effects of growth hormone on lipid metabolism in humans. Growth Horm IGF Res. 2003 Aug;13 Suppl A:S18-21. Review. 4. Enevoldsen LH, Polak J, Simonsen L, Hammer T, Macdonald I, Crampes F, de Glisezinski I, Stich V, Bulow J. Post-exercise abdominal, subcutaneous adipose tissue lipolysis in fasting subjects is inhibited by infusion of the somatostatin analogue octreotide. Clin Physiol Funct Imaging. 2007 Sep;27(5):320-6. 5. N.A. Mulla, L. Simonsen, J. Bulow, Post-exercise adipose tissue and skeletal muscle lipid metabolism in humans: the effects of exercise intensity, J. Physiol. 524 (2000) 919–928. 6. Wee J, Charlton C, Simpson H, Jackson NC, Shojaee-Moradie F, Stolinski M, Pentecost C, Umpleby AM. GH secretion in acute exercise may result in post-exercise lipolysis. Growth Horm IGF Res. 2005 Dec;15(6):397-404. 7. Berlan M, Lafontan M. The alpha 2-adrenergic receptor of human fat cells: comparative study of alpha 2-adrenergic radioligand binding and biological response. J Physiol. 1982; 78:279–87. 8. Mauriege P, Galitzky J, Berlan M, Lafontan M. Heterogeneous distribution of beta and alpha-2 adrenoceptor binding sites in human fat cells from various fat deposits: functional consequences. Eur J Clin Invest. 1987;17:156–65. 9. Rosenthal, M. J., andW. F.Woodside. Nocturnal regulation of free fatty acids in healthy young and elderly men. Metabolism 37: 645–648, 1988. 10. Gravholt CH, Schmitz O, Simonsen L, Bulow J, Christiansen JS, Moller N. Effects of a physiological GH pulse on interstitial glycerol in abdominal and femoral adipose tissue. Am J Physiol. 1999 Nov;277(5 Pt 1):E848-54. 11. Tremblay A, Simoneau JA, Bouchard C. Impact of exercise intensity on body fatness and skeletal muscle metabolism. Metabolism. 1994 Jul;43(7):814-8. 12. Laursen T, Jørgensen JOL, Christiansen JS 1994 Metabolic effects of growth hormone administered subcutaneously once or twice daily to growth hormone deficient adults. Clin Endocrinol 41:337-343. 13. Wolfe RR, Klein S, Carraro F, Weber JM 1990 Role of triglyceride-fatty acid cycle in controlling fat metabolism in humans during and after exercise. Am J Physiol 258:E382-9. 14. Gibney J, Healy ML, Stolinski M, et al. 2003 Effect of growth hormone (GH) on glycerol and free fatty acid metabolism during exhaustive exercise in GHdeficient adults. J Clin Endocrinol Metab 88:1792-7. 15. Kanaley JA, Dall R, Moller N, et al. 2004 Acute exposure to GH during exercise stimulates the turnover of free fatty acids in GH-deficient men. J Appl Physiol 96:747-53. 16. Pritzlaff CJ, Wideman L, Blumer J, et al. 2000 Catecholamine release, growth hormone secretion, and energy expenditure during exercise vs. recovery in men. J Appl Physiol 89:937-46. 17. Marcus C, Bolme P, Micha-Johansson G, Margery V, Bronnegard M 1994 Growth hormone increases the lipolytic sensitivity for catecholamines in adipocytes from healthy adults. Life Sci 54:1335-41 18. Beauville M, Harant I, Crampes F, et al. 1992 Effect of long-term rhGH administration in GH-deficient adults on fat cell epinephrine response. Am J Physiol 263:E467-72. 19. Harant I, Beauville M, Crampes F, et al. 1994 Response of fat cells to growth hormone (GH): effect of long term treatment with recombinant human GH in GH deficient adults. J Clin Endocrinol Metab 78:1392-5. 20. Kraemer WJ, Hatfield DL, Spiering BA, Vingren JL, Fragala MS, Ho JY, Volek JS, Anderson JM, Maresh CM. Effects of a multi-nutrient supplement on exercise performance and hormonal responses to resistance exercise. Eur J Appl Physiol. 2007 Nov;101(5):637-46. 21. Poehlman ET, Melby C. Resistance training and energy balance. Int J Sport Nutr. 1998 Jun;8(2):143-59. Review. 22. Ferrando AA, Wolfe RR. Restoration of hormonal action and muscle protein. Crit Care Med. 2007 Sep;35(9 Suppl):S630-4. 23. Reeves GV, Kraemer RR, Hollander DB, Clavier J, Thomas C, Francois M, Castracane VD. Comparison of hormone responses following light resistance exercise with partial vascular occlusion and moderately difficult resistance exercise without occlusion. J Appl Physiol. 2006 Dec;101(6):1616-22. 24. M.S. Vigas, S. Nemeth, L. Jurcoricora, J. Mikula, L. Komadel, The importance of lactate in exercise-induced growth hormone release in man. Radioimmunoassays: methodology and applications in physiology and clinical studies, Horm. Metab. Res. 5 (Suppl) (1974) 166–169. 25. J.R. Sutton, N.L. Jones, C.J. Toews, Growth hormone secretion and acid–base alteration at rest and during exercise, Clin. Sci. Mol. Med. 50 (1976) 241–247. 26. Holt RI, Webb E, Pentecost C, Sonksen PH. Aging and physical fitness are more important than obesity in determining exercise-induced generation of GH. J Clin Endocrinol Metab. 2001 Dec;86(12):5715-20. 27. Vettor R, Macor C, Rossi E, Piemonte G, Federspil G. Impaired counterregulatory hormonal and metabolic response to exhaustive exercise in obese subjects. Acta Diabetol. 1997 Aug;34(2):61-6. 28. Wong T, Harber V. Lower excess postexercise oxygen consumption and altered growth hormone and cortisol responses to exercise in obese men. J Clin Endocrinol Metab. 2006 Feb;91(2):678-86. Epub 2005. 29. Watt, PW, Finley, E, Cork, S, Legg, RA, Vernon, RG. (1991) Chronic control of the ß- and 2-adrenergic systems of sheep adipose tissue by growth hormone and insulin Biochem J 273,39-42 30. Yang, S, Xu, X, Björntorp, P, Edén, S. (1995) Additive effects of growth hormone and testosterone on lipolysis in adipocytes of hypophysectomized rats J Endocrinol 147,147-152. 31. Ricketts ML, Verhaeg JM, Bujalska I, Howie AJ, Rainey WE, Stewart PM 1998 Immunohistochemical localization of type 1 11ß-hydroxysteroid dehydrogenase in human tissues. J Clin Endocrinol Metab 83:1325–1335. 32. Tomlinson JW, Crabtree N, Clark PM, Holder G, Toogood AA, Shackleton CH, Stewart PM. Low-dose growth hormone inhibits 11 beta-hydroxysteroid dehydrogenase type 1 but has no effect upon fat mass in patients with simple obesity. J Clin Endocrinol Metab. 2003 May;88(5):2113-8. 33. Kraemer WJ, Volek JS, Bush JA, Putukian M, Sebastianelli WJ. Hormonal responses to consecutive days of heavy-resistance exercise with or without nutritional supplementation. J Appl Physiol. 1998 Oct;85(4):1544-55.
No Increases in Post-Exercise Fat Utilization without Acute Increases in GH – Part II