Melatonin Growth Hormone Resistance Exercise: Acute Effects in Young Adults Original paper
Researched by:
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Giorgos Aristotelous
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Giorgos Aristotelous
Read MoreGiorgos — BSc, MSc. Giorgos is an exercise scientist whose training and professional practice sit at the intersection of human performance, clinical health, and emerging microbiome science. He holds a BSc in Sports Science & Physical Education from Aristotle University (2012) and an MSc in Exercise & Health from Democritus University (2016), where his graduate work explored physiological adaptations to training across the lifespan. Now in his 15th year of practice, Giorgos pairs evidence-based coaching (ACSM-CPT, NSCA, USA Weightlifting) with a research-driven interest in how physical activity, body composition, and musculoskeletal integrity shape—and are shaped by—host–microbiome dynamics.
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Karen Pendergrass
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Karen Pendergrass
Read MoreKaren Pendergrass is a microbiome researcher specializing in microbiome-targeted interventions (MBTIs). She systematically analyzes scientific literature to identify microbial patterns, develop hypotheses, and validate interventions. As the founder of the Microbiome Signatures Database, she bridges microbiome research with clinical practice. In 2012, based on her own investigative research, she became the first documented case of FMT for Celiac Disease—four years before the first published case study.
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Giorgos Aristotelous
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Researched by:
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Giorgos Aristotelous
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Giorgos Aristotelous
Read More
Fact-checked by:
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Karen Pendergrass
ID
Karen Pendergrass
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Microbiome Signatures identifies and validates condition-specific microbiome shifts and interventions to accelerate clinical translation. Our multidisciplinary team supports clinicians, researchers, and innovators in turning microbiome science into actionable medicine.
Giorgos Aristotelous
What was studied?
This original research article examined the acute effects of a single oral dose of melatonin (N-Acetyl-5-methoxytryptamine) on the growth hormone (GH)/insulin-like growth factor-1 (IGF-1) axis in young males and females, both at rest and following a bout of heavy resistance exercise. Specifically, the study aimed to determine how 0.5 mg or 5.0 mg melatonin (versus placebo) influenced serum levels of free GH, somatostatin (SST, a GH inhibitor), IGF-1, and the IGF binding proteins IGFBP-1 and IGFBP-3. A secondary objective was to assess the safety of acute melatonin supplementation by monitoring hemodynamic and clinical chemistry markers. Blood samples were collected at multiple time points before and after the exercise protocol to capture both baseline and dynamic hormonal responses.
Who was studied?
The study recruited 60 healthy, resistance-trained young adults—30 males (mean age 22.72 years) and 30 eumenorrheic females (mean age 21.90 years)—all of whom had participated in regular resistance training at least twice weekly for at least one year. Participants were randomized to receive either 0.5 mg or 5.0 mg melatonin, or a 1.0 mg dextrose placebo, in a double-blind fashion. All participants were cleared for exercise according to American College of Sports Medicine guidelines and excluded if they had used supplements (other than multivitamins) in the previous two months or anti-inflammatory medications in the two weeks prior. The exercise protocol involved 7 sets of 7 repetitions of leg press at 85% of their one-repetition maximum (1-RM), following a fasting period and standardized pre-testing meal.
Most important findings
Key findings centered on sex- and dose-dependent effects of melatonin on the GH/IGF-1 axis in the context of resistance exercise:
- Growth Hormone (GH): In males, 5.0 mg melatonin significantly increased serum free GH levels prior to exercise compared to placebo, with both 0.5 mg and 5.0 mg melatonin resulting in higher GH levels post-exercise. In females, the GH response was less pronounced, and the greatest increases were actually observed in the placebo group, suggesting potential sex-specific regulatory mechanisms or hormonal influences such as estradiol.
- Somatostatin (SST): In males, 5.0 mg melatonin led to a significant reduction in SST (which inhibits GH) before exercise. Both melatonin doses resulted in lower SST levels post-exercise compared to placebo. In females, reductions in SST were smaller and not as consistent.
- IGF-1: No significant changes were observed in serum free IGF-1 levels in response to melatonin or exercise in either sex, likely due to the delayed hepatic response to GH.
- IGFBP-1: Males had higher IGFBP-1 responses than females, independent of supplementation, with the lowest response observed in the 5.0 mg melatonin group.
- IGFBP-3: Both melatonin doses increased IGFBP-3 in males post-exercise, indicating a potential GH-mediated effect, but without corresponding increases in free IGF-1, suggesting that elevated IGFBP-3 was not accompanied by increased IGF-1 bioavailability.
- Safety: No adverse effects or significant changes in hemodynamic or clinical chemistry markers were observed, supporting the acute safety of these melatonin doses.
While the study did not directly address the gut microbiome, the findings are relevant for a microbiome signatures database in that they clarify how exogenous melatonin and resistance exercise modulate systemic hormonal axes that can, in turn, influence host metabolism, immune function, and potentially the intestinal microbiome via signaling molecules such as GH and IGF-1.
Key implications
This study provides evidence that acute oral melatonin supplementation, particularly at a 5.0 mg dose, can enhance GH secretion and suppress SST in young, resistance-trained males, both before and after resistance exercise. These effects are less pronounced in females, highlighting the importance of sex as a biological variable in hormonal response studies. From a clinical perspective, this suggests that melatonin could have potential as an ergogenic or anabolic adjunct in males, with implications for muscle growth, recovery, and metabolic health. The lack of effect on IGF-1 and safety data support short-term use, but further research is required to examine chronic dosing and broader metabolic outcomes, including potential downstream effects on the gut microbiome and associated microbial signatures.