The Evidence

Numerous studies have been carried out proving the positive effect that exercise has on human growth hormone secretion and growth hormone’s effect on body composition, and there are plenty more to back up niacin’s role in increasing the growth hormone response to exercise. You’ll find full details of many of these studies on this page, as well as those relating to exercise-induced cell damage, niacin’s positive effect on cell oxidative stress and more.

Studies related to human growth hormone (HGH) response to exercise and its effects on body composition and muscle growth

  • Summary:

    Exercise stimulates the pituitary secretion of growth hormone. HGH starts to increase within approximately 15 minutes after the onset of exercise. All types of exercise potentially stimulate HGH secretion, and hundreds of investigations have been published describing the impact of different types of exercise (endurance and resistance, sprint and marathon running etc.) on HGH secretion in different types of people (young and old, lean and obese, trained and untrained).

  • Frystyk, J.: “Exercise and the growth hormone-insulin-like growth factor axis.” Medicine and Science in Sports Exercise. 2010 Jan;42(1):58-66. PMID: 20010129 DOI: 10.1249/MSS.0b013e3181b07d2d 

  • Study:

    A single 30 second sprint is a potent stimulator for growth hormone release, but this response is weakened with repeated bouts of sprinting, possibly because of elevated free fatty acids (FFS). This study used nicotinic acid (niacin) to suppress lipolysis (the breakdown of fats and lipids to release fatty acids) in order to investigate whether the growth hormone response to exercise is affected by serum FFA. Seven healthy men performed two maximal 30-second cycle sprint trials on an ergometer, with 4 hours of recovery in between. They took niacin in one trial (1g 60 minutes before, 0.5g at 60 minutes and 0.5g 180 minutes after the first sprint).

  • Results:

    Serum FFA was not significantly different before sprint 1 in both trials. In the niacin trial, FFA was significantly lower immediately before sprint 2. In the niacin trial, peak and integrated HGH were significantly greater following sprint 2 compared with sprint 1, and compared with sprint 2 in the non niacin trial.

  • Conclusion:

    Suppressing lipolysis with niacin resulted in a significantly greater HGH response to the second of two sprints. This suggests that FFAs play a role in regulating the HGH response to exercise.

  • Stokes, KA., Tyler, C., Gilbert, KL.: “The growth hormone response to repeated bouts of sprint exercise with and without suppression of lipolysis in men.”  Journal of Applied Physiology.2008 Mar;104(3):724-8. PMID: 18187617 DOI: 10.1152/japplphysiol.00534.2007

  • Study:

    8 healthy men completed 3 separate cycling ergometer sprint trials.Trial A consisted of two 30 second sprints separated by 60 minutes of recovery. Trial B consisted of two 30 second sprints separated by 240 minutes of recovery and trial C consisted of a single 30 second sprint carried out the day after trial B. Blood samples from each sprint were taken at rest and during recovery periods to determine HGH response to exercise.

  • Results:

    HGH increased immediately following trial A, just before the second sprint. There was no further increase following the second sprint. In trial B there was a trend for a smaller HGH response to the second sprint and there was no difference in HGH response to sprinting on consecutive days (trials B and C).

  • Conclusion:

    A single 30 second sprint on a cycle ergometer elicits a marked increase in HGH, which remains elevated for between 90-120 minutes following the sprint.  When two sprints are separated by 60 minutes of recovery, HGH response to the second sprint is increased.

  • Stokes, K., Nevill, M., Frystyk, J., Lakomy, H., and Hall, G.: “ Human growth hormone responses to repeated bouts of sprint exercise with different recovery periods between bouts.” Journal of Applied Physiology (1985). 2005 Oct;99(4): 1254-61. Epub 2005 May 26, PMID: 15920098  DOI: http://jap.physiology.org/content/99/4/1254

  • Study:

    11 sprint-trained (6 male and 5 female) and 12 endurance-trained (6 male and 6 female) athletes performed a maximal 30 second sprint on a nonmotorized treadmill to examine the HGH response to treadmill sprinting in both types of athletes.

  • Results:

    Serum HGH was greater in sprint trained athletes but was not statistically different between men and women. HGH was approximately 10 times higher in sprint-trained athletes after 1 hour of recovery. 82% of the variation in peak HGH response was explained by the peak power output and peak blood lactate response to the sprint.

  • Conclusion:

    The exercise-induced HGH increase could have important physiological effects in sprint-trained athletes, including increased protein synthesis and sparing of protein breakdown leading to maintained or increased muscle mass.

  • Nevill, ME., Holmyard, DJ., Hall, GM., Allsop, P., van Oosterhout, A., Burrin, JM., and Nevill, AM.: “Growth hormone responses to treadmill sprinting in sprint-and-endurance-trained athletes.” European Journal of Applied Psychology, 1996;72(5-6):460-7. PMID: 8925817 DOI: 10.1007/BF00242276 

  • Study:

    9 male subjects completed 2 cycle ergometer sprint trials, on one occasion performing a single 6 second sprint and on another a single 30 second maximal sprint. They then rested for 4 hours, during which blood samples were obtained. 3 of the participants completed a further control trial involving no exercise.

     

  • Results:

    Mean serum HGH levels were more than 450% greater after the 30 second sprint than after the 6 second sprint and remained elevated for 90-120 minutes compared to approximately 60 minutes after the 6 second sprint. HGH levels were not elevated above normal levels at any time during the control trial in which no exercise was completed.

     

  • Conclusion:

    Exercise is a potent stimulus for the release of HGH. The duration of a bout of maximal sprint exercise seems to determine the degree of the HGH response, although the mechanism for this is still unclear.

  • Stokes, KA., Nevill, ME., Hall, GM., and Lakomy, HK.: “The time course of the human growth hormone response to a 6 s and a 30 s cycle ergometer sprint.” Journal of Sports Sciences, 2002 Jun;20(6):487-94. PMID: 12137178  DOI: http://www.tandfonline.com/doi/abs/10.1080/02640410252925152

  • Study:

    10 male subjects completed two 30 second sprints separated by two 1 hour recovery periods, against a resistance equal to 7.5% (fast trial) and 10% (slow trial) of their body mass. Blood samples were taken during rest periods, between the two sprints and for 1 hour after the second sprint.

  • Results:

    The first sprint in each trial elicited an HGH response, which was still elevated 60 minutes after the first sprint. There was no HGH response to the second sprint. HGH response tended to be greater in the fast trial.

  • Conclusion:

    Repeated sprint cycling results in an attenuation of the HGH response.

  • Stokes, K., Nevill, ME., Hall, GM., and Lakomy, HK.: “Growth hormone responses to repeated maximal cycle ergometer exercise at different pedaling rates.” Journal of Applied Physiology (1985). 2002 Feb;92(2):602-8. PMID: 11796670 DOI: http://jap.physiology.org/content/92/2/602.long

  • Study:

    7 moderately trained men took part in 30 minute exercise bouts at 70% maximal O2 consumption on a cycle ergometer on a control day, a sequential exercise day (at 1000, 1130 and 1300) and a delayed exercise day (at 1000, 1400 and 1800). HGH was measured every 5-10 minutes for 24 hours.

     

  • Results:

    Daytime HGH concentrations were 150-160% greater during the sequential and delayed exercise days than during the control days. HGH increased progressively with each subsequent exercise bout, with a slightly greater increase on the delayed exercise day. There was no change in HGH release during sleep.

     

  • Conclusion:

    HGH response to acute aerobic exercise increases with repeated bouts of exercise.

  • Kanaley, JA., Weltman, JY, Veldhuis, JD., Rogol, AD., Hartman, ML., and Weltman, A.: “Human growth hormone response to repeated bouts of aerobic exercise.” Journal of Applied Physiology. 1997 Nov;83(5):1756-61. PMID: 9375348 DOI: http://jap.physiology.org/content/83/5/1756.long

  • Study:

    10 healthy male volunteers aged between 18-35 performed an progressive cycle exercise on an ergometer after an overnight fast and on subsequent mornings performed bouts of 1, 5 and 10 minute of either high or low intensity constant rate exercise. Each bout was separated by a 1 hour interval.

     

  • Results:

    Low intensity exercise did not produce any significant increase in HGH. But HGH in 9 out of 10 subjects significantly increased after 10 minutes of high intensity exercise.

     

  • Conclusion:

    A minimum duration of 10 minutes of high intensity exercise consistently increased circulating HGH in adult males.

  • Felsing, NE., Brael., JA., and Cooper, DM.: “Effect of high and low intensity exercise on circulating growth hormone in men.” Journal of Clinical Endocrinology and Metabolism. 1992 Jul;75(1):157-62 PMID: 1619005 DOI: http://press.endocrine.org/doi/abs/10.1210/jcem.75.1.1619005

  • Study:

    9 male subjects performed 6 randomly assigned heavy resistance protocols (HREPs) consisting of identically ordered exercises designed to control for load (5 vs 10 repetitions maximum) rest period (1 vs 3 minutes) and total work effects. Serum growth hormone, testosterone, somatomedin-C, glucose and blood lactate concentrations were measured before exercise, mid exercise (after 4 of 8 exercises) and at 0, 5, 15, 30, 60, 90 and 120 minutes post exercise.

  • Results:

    Although not all HREPs produced an increase in HGH, the highest levels were observed following the H10/1 exercise protocol (high total work, 1 minute rest, 10-RM load) for both temporal and time integrated responses.

     

  • Conclusion:

    Because of possible differences in hormonal and growth factor release, all HREPs may not affect muscle and tissue growth in the same manner.

  • Kraemer, WJ., Marchitelli, L., Gordon, SE., Harman, E., Dziados, JE., Mello, R., Frykman, P., McCurry, D., and Fleck, SJ.: “Hormonal and growth factor responses to heavy resistance exercise protocols.” Journal of Applied Physiology. 1990 Oct;69(4):1442-50. PMID: 2262468 DOI: http://jap.physiology.org/content/69/4/1442  

  • Study:

    A heavy resistance exercise session consisting of bench press, bilateral leg press and a sit-up exercise was performed by 8 young women and 8 young men (in the 30-year age group), 7 middle-aged women and 8 middle-aged men (in the 50-year age group) and 8 elderly women and 8 elderly men (in the 70-year age group). 5 sets of each exercise with the maximal load possible for 10 repetitions per set were performed with 3 minutes of recovery in between sets.

     

  • Results:

    While there was no change in HGH levels in either the elderly men or women, HGH increased in both young women and young men, as well as in both middle aged women and middle aged men. The increase was greater in young women and young men.

     

  • Conclusion:

    Heavy resistance exercise elicits a HGH response, but this response is lowered with increasing age both in men and women.

  • Hakkinen, K., Pakarinen, A.: “Acute hormonal responses to heavy resistance exercise in men and women at different ages.” International Journal of Sports Medicine. 1995 Nov;16(8):507-13. PMID: 8776203 DOI: 10.1055/s-2007-973045

  • Study:

    96 recreationally trained athletes (63 men and 33 women) took part in a placebo-controlled, double blind 8 week study. Men received either growth hormone, testosterone, combined treatments or a placebo. Women received either growth hormone or a placebo. Body composition and physical performance variables were measured.

     

  • Results:

    Growth hormone significantly reduced fat mass and increased lean body mass. It also significantly increased sprint capacity by 3.9%. This increase was not maintained 6 weeks after discontinuation of HGH.

     

  • Conclusion:

    Growth hormone supplementation influenced body composition and increases sprint capacity.

  • Meinhardt, U., Nelson, AE., Hansen, JL., Birzniece, V., Clifford, D., Leung, KC., Graham, K., Ho, KK.: “The effects of growth hormone on body composition and physical performance in recreational athletes: a randomized trial.” Annals of Internal Medicine, 2010 May 4;152(9):568-77 PMID: 20439575 DOI: 10.7326/0003-4819-152-9-201005040-00007

  • Study:

    7 healthy men aged between 18-23 years received HGH via intrabrachial artery infusion for 6 hours. The effects of HGH on forearm amino acid and glucose balances were measured after 3 and 6 hours.

     

  • Results:

    There was no change in glucose uptake, but HGH suppressed the forearm release of phenylalanine, leucine, total branched amino acids and essential neutral amino acids.

     

  • Conclusion:

    The results suggest that HGH stimulates skeletal muscle protein syntheses.

  • Fryburg, DA., Gelfand, RA., Barrett, EJ.: “Growth hormone acutely stimulates forearm muscle protein synthesis is normal humans.” American Journal of Physiology. 1991, Mar;260(3 Pt 1):E499-504. PMID: 2003602 DOI: http://ajpendo.physiology.org/content/260/3/E499

  • Study:

    Normal volunteers ages between 18-24 years received an infusion of 3H-phenylalanine and 14C-leucine in their forearms over a period of 8 hours. Basal samples to determine forearm and whole body amino acid kinetics were taken between 90 and 120 minutes. HGH was then added to the infusion to raise HGH concentration.

     

  • Results:

    Insulin like growth factor (IGF-1) level increased. HGH suppressed forearm phenylalanine and leucine release by increasing 3H-phenylalanine and 14C-leucine. Oxidative leucine decreased. Non oxidative leucine, whole-body proteolysis and leucine rate of appearance did not change.

     

  • Conclusion:

    Acute stimulation of muscle but not whole body protein synthesis by systematically infused HGH suggests that muscle protein is acutely and specifically regulated by HGH.

  • Fryburg, DA., Barrett, EJ.: “Growth hormone stimulates skeletal muscle but not whole-body protein synthesis in humans.” Metabolism Clinical & Experimental. 1993 Sep;42(9):1223-7. PMID: 84127802 DOI: http://www.metabolismjournal.com/article/0026-0495(93)90285-V/abstract 

  • Study:

    21 healthy men aged 61 to 81 years old took part in a 6 month study. 12 of the men received HGH 3 times per week and 9 of the men received no treatment.

     

  • Results:

    In the HGH group, mean plasma IGF-1 level rose into the youthful range, accompanied by an 8.8% increase in lean body mass, a 14.14% decrease in adipose-tissue mass, a 1.6% increase in average lumbar vertebral bone density and a 7.1% increase in skin thickness. There was no significant change in any of these things in the non-HGH group.

  • Conclusion:

    Diminished secretion of HGH is partly responsible for the decrease of lean body mass, the expansion of adipose-tissue mass and the thinning of skin that occur in old age.

  • Rudman, D., Feller, AG., Nagraj, HS., Gergans, GA., Lalitha, PY., Goldberg, AF., Schlenker, RA., Cohn, L., Rudman, IW., Mattson, DE.: “Effects of human growth hormone in men over 60 years old.” The New England Journal of Medicine. 1990 Jul 5;323(1):1-6 PMID: 2355952 DOI: 10.1056/NEJM199007053230101

  • Study:

    13 adults with growth hormone deficiency (GHD) took part in a 3 month, double blind, placebo controlled trial of HGH.

     

  • Results:

    Lean body mass decreased and fat mass significantly decreased in the group taking HGH. HGH significantly increased red cell mass, plasma volume and total blood volume, Serum IGF-1 and IGF-binding protein-3 concentrations increased. No significant changes in body composition or blood volume were recorded in the placebo group.

  • Conclusion:

    HGH stimulates the production of red blood cells (erythropoiesis) in adult GHD, as well as plasma volume and total blood volume, which may contribute to the increased exercise performance seen in the HGH group.

  • Christ, ER., Cummings, MH., Westwood, NB., Sawyer, BM., Pearson, TC., Sönksen, PH., Russell-Jones, DL.: “The importance of growth hormone in the regulation of erythropoiesis, red cell mass, and plasma volume in adults with growth hormone deficiency.” Journal of Clinical Endocrinology and Metabolism. 1997 Sep;82(9):2985-90 PMID: 9284731 DOI:  10.1210/jcem.82.9.4199

Studies relating to niacin’s effect on HGH and endothelial function

  • Study:

    8 healthy male volunteers received either nicotinic acid (niacin) or adenosine (both inhibitors of lipolysis) in order to determine what, if any, effect the presence of free fatty acids (FFAs) has on the plasma concentrations of growth hormone, cortisol and glucagon. In the second phase of the study, an infusion of fatty acids was introduced in addition to the niacin and adenosine infusions.

     

  • Results:

    Niacin elicited a significant increase in HGH. But no HGH increase occurred when additional fatty acids were introduced into the bloodstream along with the niacin.

     

  • Conclusion:

    The presence of FFAs inhibits the release of HGH. Suppressing free fatty acids stimulates the secretion of HGH.

  • Quabbe, HJ., Luyckx, AS., L’age, M., Schwarz, C.: “Growth hormone, cortisol, and glucagon concentrations during plasma free fatty acid depression: different effects of nicotinic acid and an adenosine derivative (BM 11.189).” The Journal of Clinical Endocrinology and Metabolism. 1983 Aug;57(2):410-4. PMID: 6345570 DOI: 10.1210/jcem-57-2-410 

  • Study:

    The effects of nicotinic acid on plasma HGH (human growth hormone), FFA (free fatty acids)  and glucose in normal, obese and hypopituitary patients was studied.

     

  • Results:

    In normal patients there was an acute reduction of plasma FFA followed by a marked, progressive secondary rise. There was a significant rise in HGH following the reduction of plasma FFA. There was no significant change in plasma HGH in obese and hypopituitary patients, although there was a more pronounced reduction and rapid rise of plasma FFA in obese subjects than normal subjects, and in hypopituitary patients the secondary rise of plasma FFA was slow and diminished.

     

  • Conclusion:

    It appears that the late rebound of plasma FFA following administration of nicotinic acid is at least partly related to the increase in HGH secretion.

  • Irie, M., Tsushima, T., Sakuma, M.: “Effect of nicotinic acid administration on plasma HGH, FFA and glucose in obese subjects and in hypopituitary patients.” Metabolism Clinical and Experimental. 1970 Nov;19(11):972-9. PMID: 5479511 DOI: http://dx.doi.org/10.1016/0026-0495(70)90043-0

  • Study:

    127 healthy, non-smoking men and women aged between 48-77 who were taking no medication took part in a study to test the hypothesis that higher dietary niacin intake is associated with greater brachial artery flow-mediated dilation (FMD) and lower oxidative stress. All participants refrained from taking any dietary supplements for 2 weeks before the study, which was conducted following a 12 hour food and caffeine fast and a 24 hour abstention from exercise and alcohol.

     

  • Results:

    Flow-mediated dilation was 25% greater in subjects with above-average dietary niacin intake than in subjects with below-average intake. Dietary niacin intake (above vs. below average) was an independent predictor of FMD. Plasma oxidized low-density lipoprotein, a marker of systemic oxidative stress, was inversely related to niacin intake and was lower in subjects with above- vs. below-average niacin intake. In endothelial cells sampled from the brachial artery of a subgroup, dietary niacin intake was inversely related to nitrotyrosine, a marker of peroxynitrite-mediated oxidative damage and expression of the prooxidant enzyme, NADPH oxidase. These markers were lower in subjects with above- vs. below-average niacin intake.

     

  • Conclusion:

    The findings support the hypothesis that dietary niacin intake is associated with greater vascular endothelial function related to lower systemic and vascular oxidative stress among healthy, middle-aged and older adults.

  • Kaplon, RE., Gano, LB., Seals, DR.: “Vascular endothelial function and oxidative stress are related to dietary niacin intake among healthy middle-aged and older adults.” Journal of Applied Physiology. 2014 Jan 15;116(2):156-63. PMID: 24311750 PMCID: PMC3921358 DOI: 10.1152/japplphysiol.00969.2013

  • Study:

    In a double-blind, placebo controlled trial, 63 men aged 35-60 after a myocardial infarction (heart attack) received either a daily combination of 1000mg niacin and 20mg laropiprant (a drug used in combination with niacin to reduce blood cholesterol) for 4 weeks, rising to 2000/40mg daily thereafter, or a placebo. At the beginning and after 12 weeks, flow-mediated dilation (FMD), nitroglycerin-induced (GTN) dilation of the brachial artery, total cholesterol (TC), LDL-C, HDL-C, triglycerides (TG), lipoprotein(a) [Lp(a)], and apolipoprotein (Apo) A1/B were measured.

     

  • Results:

    FDM significantly increased in the niacin/laropiprant group but not in the placebo group. GTN dilation also increased, but not in the placebo group. Niacin/laropiprant reduced TC and LDL-C and increased HDL-C without influencing TG, while there were no changes in the placebo group. Lp(a) and ApoB were significantly lower in the niacin/laropiprant group, with no difference in the placebo group. ApoA1 did not change in either of the groups.

     

  • Conclusion:

    Niacin/laropiprant improves endothelium-dependant and endothelium-independent dilation of the brachial artery.

  • Bregar, U., Jug, B., Keber, I., Cevc, M., Sebestjen, M.: “Extended-release niacin/laropiprant improves endothelial function in patients after myocardial infarction.” Heart and Vessels. 2014 May;29(3):313-9. PMID: 23712600 DOI: 10.1007/s00380-013-0367-5 

  • Study:

    A randomised controlled study was carried out to determine the short-term effects of extended release niacin (ERN) on endothelial function in 19 HIV-infected adults with low HDL-c. This was measured by flow-mediated vasodilation (FMD) of the brachial artery.  Participants on stable HAART with fasting HDL-c less than 40 mg/dl and low-density lipoprotein-cholesterol less than 130 mg/dl received either ERN (500mg per night, rising to 1500mg for 12 weeks) or control arms.

     

  • Results:

    Participants receiving ERN had an increase in HDL-c and FMD. The FMD for ERN at the end of the study was significantly different from controls after adjusting for baseline differences in FMD and HDL-c.

     

  • Conclusion:

    Short-term niacin therapy could improve endothelial function in HIV-infected patients with low HDL-c.

  • Chow, DC., Stein, JH., Seto, TB., Mitchell, C., Sriratanaviriyakul, N., Grandinetti, A., Gerschenson, M., Shiramizu, B., Souza, S., Shikuma, C.: “Short-term effects of extended-release niacin on endothelial function in HIV-infected patients on stable antiretroviral therapy.” Official Journal of the International AIDS Society. 2010 Apr 24;24(7):1019-23. PMID: 20216298 PMCID: PMC2925834 DOI: 10.1097/QAD.0b013e3283383016

Studies related to red blood cell turnover and exercise-induced oxidative stress during exercise and niacin’s effects on oxidative stress

  • Summary:

    Red blood cells (RBCs) have a lifespan of about 120 days, but intensive training may increase the rate of aging, leading to what has been termed ‘sports anaemia’. Cycling, running and swimming have all been shown to cause RBC damage. RBCs are vulnerable to oxidative damage because of their continuous exposure to oxygen and their high concentrations of polyunsaturated fatty acids and haem iron. Antioxidants in muscle and  RBCs can be depleted during exercise and oxidative damage can also impair the ability of RBCs to change shape, which can impede their passage through the smallest blood vessels and capillaries. This may reduce the amount of oxygen reaching working muscle during single episodes of exercise and possibly increased the rate of RBC destruction with long term exercise.

     

  • Smith, JA.: “Exercise, training and red blood cell turnover.” Sports Medicine. 1995 Jan;19(1):9-31 PMID: 7740249 DOI: 10.2165/00007256-199519010-00002 

  • Summary:

    The main function of red blood cells (RBCs) in exercise is the transport of O2 from the lungs to the tissues and the delivery of metabolically produced CO2 to the lungs for expiration. Trained athletes, particularly in endurance sports have a decreased hematocrit (RBC volume). This is known as ‘sports anaemia’. Exercise can decrease the RBC mass. This is caused by the rupture of RBCs when passing through capillaries in contracting muscles, and by compression of RBCs, e.g., in foot soles during running or in hand palms in weightlifters. This can all lead to a decrease in the average age of the population of circulating red blood cells in trained athletes.

  • Mairbäurl, H.: “Red blood cells in sports: effects of exercise and training on oxygen supply by red blood cells.”  Frontiers in Physiology. 2013 Nov 12;4:332. PMID: 24273518 PMCID: PMC3824146 DOI: 10.3389/fphys.2013.00332

  • Summary:

    Research evidence suggests that strenuous aerobic exercise is associated with oxidative stress and tissue damage. The cause of exercise-induced oxidative damage is thought to be caused by the generation of oxygen free radicals and other reactive oxygen species (ROS). Antioxidants play a vital role in protecting tissues from excessive oxidative damage during exercise, and depletion of the body’s natural antioxidant systems increases the vulnerability of tissues and cells to ROS. Because acute strenuous exercise and training increases antioxidant consumption, dietary supplementation of specific antioxidants would be beneficial.

  • Ji, LL.: “Oxidative stress during exercise: implication of antioxidant nutrients.” Free Radical Biology and Medicine. 1995 Jun;18(6):1079-86 PMID: 7628730 DOI: 0891584994002123  

  • Study:

    Strenuous physical activity is known to increase the production of reactive oxygen species (ROS), which is associated with the depletion of antioxidant defence. 53 healthy male volunteers aged between 22 and 26 years took part in a study in which the level of lipid peroxidation and antioxidant components in the blood of sportsmen under resting conditions was compared with those in an age-matched control.

  • Results:

    In sportsmen, there was a significant increase in thiobarbituric acid reactive substances (TBARS – a measure of the damage produced by oxidative stress) and conjugated dienes. There was a decrease in levels of the antioxidants ascorbic acid and glutathione. Superoxide dismutase (an enzyme that breaks down harmful molecules in cells) activity increased by 52% and glutathione peroxidase (which protects from oxidative damage) decreased by 42% in the red blood cells of sportsmen compared to controls.

     

  • Conclusion:

    Dietary supplementation with antioxidant vitamins has been shown to beneficial in combating oxidative stress, and supplemental glutathione has been found to enhance the endurance capacity of athletes, demonstrating the critical role of glutathione, suggesting that intervention trials should include a mixture of antioxidants rather than a single antioxidant.

     

  • Balakrishnan, SD., Anuradha, CV.: “Exercise, depletion of antioxidants and antioxidant manipulation.” Cell Biochemistry and Function. 1998 Dec;16(4):269-75. PMID: 9857489 DOI:

    10.1002/(SICI)1099-0844(1998120)16:4<269::AID-CBF797>3.0.CO;2-B

  • Study:

    6 well-trained athletes had blood samples taken before and 72 hours after taking part in the “Marathon of Sands” extreme running competition consisting of 6 long duration races in the desert, in order to determine whether extreme running might alter the blood’s enzymatic and non-enzymatic antioxidant status.

     

  • Results:

    A significant alteration of blood antioxidant defense capacity was induced by the Marathon of Sands. Significant decreases in erythrocyte superoxide dismutase activity, plasma concentrations of retinol, beta-carotene and other carotenoids were recorded 72 hours after the race, which were associated with an increase in RBC glutathione (an antioxidant) and in plasma TBARS (a measure of the damage produced by oxidative stress) levels.

     

  • Conclusion:

    Such an extreme endurance running competition induced an imbalance between oxidant and antioxidant protection, reducing the blood’s antioxidant defense capacity.

  • Machefer, G., Groussard, C., Rannou-Bekono, F., Zouha,l H., Faure, H., Vincent, S., Cillard, J., Gratas-Delamarche, A.: “Extreme running competition decreases blood antioxidant defense capacity.” Journal of the American College of Nutrition. 2004 Aug;23(4):358-64. PMID: 15310740

  • Study:

    This study looked at the effect of niacin on excessive hepatic fat accumulation, production of reactive oxygen species (ROS), inflammatory mediator IL-8 secretion caused by non-alcoholic fatty liver disease. Palmitic acid was used to treat human hepatoblastoma cell line HepG2 or human primary hepatocytes (liver cells), after which they were treated with niacin or a control for 24 hours.

     

  • Results:

    Niacin significantly inhibited palmitic acid-induced fat accumulation in human hepatocytes by 45-62%. Niacin reduced hepatocyte ROS production, palmitic acid-induced IL-8 levels and inhibited NADPH oxidase activity.

     

  • Conclusion:

    Niacin reduces hepatic fat accumulation and ROS production through inhibiting hepatocyte DGAT2 and NADPH oxidase activity. Decreased ROS production may have contributed to the inhibition of pro-inflammatory IL-8 levels.

  • Ganji, SH., Kashyap, ML., Kamanna, VS.: “Niacin inhibits fat accumulation, oxidative stress, and inflammatory cytokine IL-8 in cultured hepatocytes: impact on non-alcoholic fatty liver disease.” Metabolism Clinical and Experimental. 2015 Sep;64(9):982-90. PMID: 26024755 DOI: 10.1016/j.metabol.2015.05.002

  • Study:

    17 patients with hypercholesterolemia and low HDL-C and 8 healthy control subjects were treated with niacin for 12 weeks. Lipid profile, oxidative stress and C-reactive protein (CRP) levels were determined at the start of the study, and 2 and 12 weeks after the start of the niacin treatment.

     

  • Results:

    Niacin treatment in hypercholesterolemic patients caused a significant increase in HDL-C and apolipoprotein A1 levels, and a decrease in triglyceride levels. Niacin also significantly reduced oxidative stress levels. Serum CRP levels were not affected, but a correlation between CRP and HDL levels was found when computing the results.

     

  • Conclusion:

    Niacin treatment in hypercholesterolemic patients with low HDL levels caused a significant decrease in their oxidative stress status, indicating an additional beneficial effect of niacin beyond its ability to affect the lipid profile.

  • Hamoud, S., Kaplan, M., Meilin, E., Hassan, A., Torgovicky, R., Cohen, R., Hayek, T.: “Niacin administration significantly reduces oxidative stress in patients with hypercholesterolemia and low levels of high-density lipoprotein cholesterol.” American Journal of the Medical Sciences. 2013 Mar;345(3):195-9 PMID: 22990043 DOI: 10.1097/MAJ.0b013e3182548c28

Studies related to niacin’s effects on HDL and LDL cholesterol

  • Summary:

    Changes in modern lifestyle habits such as over nutrition and physical inactivity have led to exaggerated and prolonged states of postprandial hyperlipemia (abnormally high blood concentration of fats or lipids) following multiple fat-enriched meals throughout the day. Studies have shown that niacin may decrease fasting levels of plasma very-low-density lipoproteins (VLDL), low-density lipoprotein cholesterol (LDL-C) and lipoprotein [a] (Lp[a]), and may increase high-density lipoprotein cholesterol (HDL-C).

  • Montserrat-de la Paz, S.,  Bermudez, B., Naranjo, MC., Lopez, S., Abia, R., Muriana, FJ.: “Pharmacological effects of niacin on acute hyperlipemia.” Current Medicinal Chemistry. 2016 Apr 11 PMID: 27063258

  • Study:

    Randomised control trials and comparative cohort trials were carried out on the efficacy of Niaspan (extended release niacin) on serum lipids.

     

  • Results:

    LDL cholesterol, triglycerides and lipoprotein(a) all decreased by 13, 26 and 17% respectively and HDL cholesterol increased by 18% in four randomised control trials. An additional 22% reduction in LDL cholesterol, 7% in triglycerides and 6% in lipoprotein(a) levels were shown  in four comparative cohort trials using a combination of Niaspan and statins.

     

  • Conclusion:

    Niaspan effectively raises HDL cholesterol (with benefits on triglycerides and lipoprotein(a)) and can be combined safely with statins.

  • Birjmohun, RS., Hutten, BA., Kastelein, JJ., Stroes, ES.: “Increasing HDL cholesterol with extended-release nicotinic acid: from promise to practice.” The Netherlands Journal of Medicine. 2004 Jul-Aug;62(7):229-34. PMID: 15554597 DOI: http://www.njmonline.nl/getpdf.php?id=147

  • Study:

    12 subjects with a history of cardiovascular disease received either atorvastatin or a combination therapy of atorvastatin and niacin. The concentration of high density lipoprotein (HDL) and its 3 subclasses (small, medium and large) was measured at the beginning of the study and after 1 year of treatment.

     

  • Results:

    Atorvastatin decreased LDL (low-density lipoprotein) cholesterol by 39% and raised HDL cholesterol by 11% but did not increase HDL-PIMA or macrophage cholesterol efflux. The combination of atorvastatin and niacin raised HDL cholesterol by 39% and increased HDL-PIMA by 14%. Combination therapy increased macrophage cholesterol efflux capacity (16%, P<0.0001) but not ABCA1-specific efflux.

     

  • Conclusion:

    Adding niacin to statin therapy increased HDL cholesterol levels and macrophage efflux, but had much less effect on HDL-PIMA.

  • Ronsein, GE.,, Hutchins, PM., Isquith, D., Vaisar, T., Zhao, XQ., Heinecke, JW.: “Niacin therapy increases high-density lipoprotein particles and total cholesterol efflux capacity but not ABCA1-specific cholesterol efflux in statin-treated subjects.” Arteriosclerosis, Thrombosis, and Vascular Biology. 2016 Feb;36(2):404-11 PMID: 26681752 DOI: 10.1161/ATVBAHA.115.306268 

Studies relating to sleep and human growth hormone secretion

  • Summary:

    In adults, HGH secretion occurs shortly after the onset of sleep, in association with the first phase of slow-wave sleep. Approximately 70% of HGH pulses during sleep in men coincide with slow-wave sleep. The amount of GH secreted during these pulses correlates with the concurrent amount of slow wave sleep.

  • Van Cauter, E., Plat, L.: “Physiology of growth hormone secretion during sleep.” The Journal of Pediatrics. 1996 May;128(5 Pt 2):S32-7. PMID: 8627466

  • Study:

    HGH, insulin, cortisol and glucose levels during sleep were measured on 38 nights in 8 young adults. Blood samples were taken at 30-minute intervals and EEG and electrooculogram were recorded throughout the night.

  • Results:

    An HGH peak occurred with the onset of deep sleep in 7 subjects, lasting 1.5-3.5 hours. During subsequent deep sleep phases, smaller HGH peaks appeared. Peak HGH secretion was delayed if the onset of sleep was delayed. Subjects who were awakened for 2-3 hr and allowed to return to sleep exhibited another peak of GH secretion.

  • Conclusion:

    The initiation of sleep results in a major peak of HGH secretion.

  • Takahash,i Y., Kipnis, DM., Daughaday, WH.: “Growth hormone secretion during sleep.” The Journal of Clinical Investigation. 1968 Sep;47(9):2079-90. PMID: 5675428 PMCID: PMC297368 DOI: 10.1172/JCI105893

  • Study:

    10 male subjects took part in a 3 night study comparing the effect of delayed sleep onset and temporary slow wave sleep deprivation on HGH release.

  • Results:

    HGH secretory peaks coincided with the onset of slow-wave sleep when subjects were allowed to fall asleep normally at 2300. When the onset of sleep was delayed until 0200, HGH peaks were also substantially delayed. These peaks coincided again with the initial periods of slow-wave sleep. HGH peaks were not significantly changed on nights when slow-wave sleep was deprived between 2300 and 0200, but they occurred mostly after the onset of sleep rather than during the main slow-wave sleep time periods after 0200.

     

  • Conclusion:

    The timing of nocturnal HGH secretion is more dependant on sleep onset than on slow wave sleep.

  • Born, J., Muth, S., Fehm, HL.: “The significance of sleep onset and slow wave sleep for nocturnal release of growth hormone (GH) and cortisol.” Psychoneuroendocrinology. 1988;13(3):233-43.  PMID: 3406323

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