Does Lifting Weights Increase Testosterone? Yes, Briefly — and That Spike Builds Nothing

There’s a specific belief that shapes how a lot of people train: that the point of a hard leg day is the hormone surge afterward, and that squats “build arms” because of what they do to your bloodstream.

It’s a satisfying idea. It’s also one of the few questions in exercise science with a genuinely clean answer, because somebody ran the exact experiment needed to settle it.

Here’s the short version. Heavy resistance exercise does raise testosterone — transiently, in a window measured in tens of minutes. That part is real and well documented.¹ But when researchers deliberately trained one arm in a low-hormone state and the other arm in a high-hormone state in the same men, both arms grew the same amount.²

So the honest answer splits in two, and most of the internet only tells you the first half.

Question	Short answer
Does lifting raise testosterone?	Yes, acutely — elevated right after heavy, high-volume sessions in men1
How long does the spike last?	Elevated immediately and at 15 and 30 minutes post-exercise2
Does that spike build muscle?	No. Same arm, same man, high vs low hormones: 12% vs 10% growth, no difference2
Does it predict strength gains?	No correlation across 56 men over 12 weeks3
Does training raise resting testosterone?	Not in healthy trained men — no change over 6 months4
Who does gain resting testosterone?	Men with obesity or type 2 diabetes — aerobic training, g = 0.575
Biggest natural lever?	Sleep. One week at 5 hours a night cut daytime testosterone 10-15%6
Can training lower it?	Yes — chronic high volume plus underfueling7
Normal range?	264-916 ng/dL in healthy non-obese men 19-398

Does lifting weights increase testosterone?

Yes — for about as long as it takes to shower and drive home.

Jakob Vingren of the University of North Texas, with William Kraemer and colleagues, reviewed the acute endocrine response to resistance exercise and found the pattern is consistent in men: testosterone concentration is elevated directly following heavy resistance exercise.¹ The response isn’t automatic, though. It depends on how the session is built. To get a meaningful acute rise, the session needs high volume and high metabolic demand — big muscle groups, multiple sets, short-ish rest.¹

That’s the physiological basis for the folk wisdom about squats and deadlifts. A set of heavy leg press moves more tissue and generates more metabolic stress than a set of lateral raises, and the hormonal response follows.

The response also varies by who you are. Vingren’s review notes that before puberty, children show no acute testosterone rise from resistance exercise at all. After puberty, boys do and girls generally don’t. And from roughly age 35-40 onward, circulating testosterone in men declines about 1-3% per year, with a correspondingly blunted acute response to training.¹ That age curve is one reason strength training after 40 needs a different set of expectations than the same program at 25.

Then there’s a wrinkle that turns out to matter: what gets defined as a “testosterone-optimized” workout usually isn’t.

Juha Ahtiainen’s group at the University of Jyväskylä ran 13 resistance-trained men through six months of hypertrophy training in a crossover design — three months with two-minute rest periods, three months with five-minute rest periods, matched for total work.⁴ The short-rest protocol is the one that’s supposed to maximize the hormonal response.

Both protocols produced large acute rises in testosterone, free testosterone, cortisol, and growth hormone. There was no significant difference between them.⁴ Rest interval didn’t change the hormone response, and it didn’t change the outcomes either — both blocks produced similar gains in muscle size and strength. If you’ve been cutting your rest between sets to chase a hormone spike, the trade you’re making is worse set quality for a response that doesn’t differ.

Does the testosterone spike actually build muscle?

No. This is the part where the research is unusually decisive, because the design is unusually clever.

In 2010, Daniel West and Stuart Phillips at McMaster University published a study that put the question to a within-subject test.² Twelve young men trained their elbow flexors — biceps curls — for 15 weeks. Each man trained both arms, on separate days, under deliberately different hormonal conditions:

• Low-hormone arm: isolated arm curls only. No measurable rise in testosterone, growth hormone, or IGF-1.
• High-hormone arm: identical arm curls, immediately followed by a high volume of leg resistance exercise, producing large, significant elevations in all three hormones at 0, 15, and 30 minutes post-exercise.

Same man. Same arm exercise. Same training volume for the arm. The only difference was the hormonal bath that arm’s muscle was sitting in afterward.

The result: muscle cross-sectional area increased 12% in the low-hormone arm and 10% in the high-hormone arm. No significant difference (interaction P = 0.25). Type I and type II fiber areas both grew, with no effect of the hormone elevation. Strength increased in both arms, and the increase was not different between conditions.²

The authors’ conclusion is about as blunt as journal language gets: exposure of loaded muscle to acute exercise-induced elevations in endogenous anabolic hormones “enhances neither muscle hypertrophy nor strength with resistance training in young men.”²

It held up twice more

That’s one study with twelve men, so the natural response is to want replication. There is some.

West and Phillips, 2012, n = 56. They measured post-exercise free testosterone, growth hormone, IGF-1, and cortisol in 56 young men at the midpoint of a 12-week training study, then correlated each hormone’s response with gains in lean body mass, fiber cross-sectional area, and leg press strength.³

There were no significant correlations between exercise-induced elevations in growth hormone, free testosterone, or IGF-1 and gains in lean mass or leg press strength. The associations that did reach significance were, if anything, an argument against the whole framework: cortisol — the hormone the same folklore casts as the villain — correlated with the change in lean body mass (r = 0.29) and type II fiber area (r = 0.35).³ No hormone correlated with strength.

Morton and colleagues, 2016, n = 49. Forty-nine resistance-trained men did 12 weeks of whole-body training, randomized to higher-repetition (30-50% 1RM, 20-25 reps) or lower-repetition (75-90% 1RM, 8-12 reps) sets, all to volitional failure.⁹ Lean mass and both fiber types increased with no significant difference between groups. And again: no significant correlations between the acute post-exercise rise in any purported anabolic hormone and the change in strength or hypertrophy.⁹

Three studies, three designs, one answer. This is why SensAI programs around load, volume, and recovery rather than around exercise selection theory — the variables that survived these trials are the ones worth writing a program from. Stuart Phillips — Professor of Kinesiology at McMaster and one of the most-cited researchers in muscle protein metabolism — has spent a decade making the same point: acute post-exercise systemic hormonal rises “are not related to or in any way indicative of” training-mediated gains in muscle mass or strength.⁹

Then why does testosterone obviously build muscle?

Because it does — at doses your body will never produce.

This is the distinction that resolves the apparent contradiction, and it’s worth being precise about. A normal male physiological range is roughly 264 to 916 ng/dL.⁸ The acute post-workout bump moves you around inside that range for under an hour. Anabolic steroid protocols move you far outside it, for months.

Shalender Bhasin, now Professor of Medicine at Harvard Medical School and Director of the Research Program in Men’s Health at Brigham and Women’s Hospital, ran the definitive experiment in 1996.¹⁰ Forty-three normal men were randomized to four groups: placebo without exercise, testosterone without exercise, placebo plus exercise, and testosterone plus exercise. The testosterone dose was 600 mg of testosterone enanthate weekly for 10 weeks — several times the body’s natural output.

Group	Fat-free mass	Squat 1RM	Bench 1RM
Placebo, no exercise	no significant change	no significant change	no significant change
Testosterone, no exercise	+3.2 kg	+19%	+10%
Placebo + exercise	+1.9 kg	+21%	+11%
Testosterone + exercise	+6.1 kg	+38%	+22%

Read the middle two rows again. Men who took testosterone and never touched a weight gained more fat-free mass (3.2 kg) than men who took placebo and trained three times a week for ten weeks (1.9 kg) — and got almost identically stronger, 19% vs 21% on the squat.¹⁰ The combination was greater than any other group on every measure.

The effect is dose-dependent, not binary. Thomas Storer and Bhasin later gave 44 healthy men aged 60-75 graded doses — 25, 50, 125, or 300 mg/week — after suppressing their natural production, and found dose-dependent increases in skeletal muscle mass, leg press strength, and leg power.¹¹ More testosterone, more muscle, in an orderly line.

So the correct summary isn’t “testosterone doesn’t build muscle.” It’s:

Testosterone builds muscle across a pharmacological dose range. Movement within your natural range, for under an hour, does not.

Those are two different biological questions that share a word. Almost every supplement marketed as a “testosterone booster” trades on the ambiguity — citing the pharmacology, selling you something that at best nudges the physiology. Most recovery and performance supplements have thinner evidence than their labels imply, and this category is among the worst offenders.

Does training raise your resting testosterone long-term?

Mostly no, if you’re a healthy man who already trains. Meaningfully yes, if you’re not.

Ahtiainen’s six-month crossover found no statistically significant changes in basal hormone concentrations across the entire experimental training period, despite real gains in strength (+16% on right-leg 1RM) and quadriceps cross-sectional area (+4%).⁴ The men got substantially stronger and bigger. Their resting testosterone stayed where it was.

Ruba Riachy and colleagues at the University of Texas Medical Branch reviewed the broader literature and found the variability across studies is mostly explained by four factors: exercise type, intensity and rest structure, study population (young vs elderly, lean vs obese, sedentary vs athlete), and — often decisive — the time point at which testosterone was measured.¹² That third factor is the one that separates the null results from the positive ones.

Where exercise genuinely raises testosterone

In men carrying excess fat, exercise raises testosterone reliably, and the mechanism isn’t mysterious. Adipose tissue converts testosterone to estradiol and suppresses the upstream signal; reduce the fat and the axis recovers.

A 2024 systematic review and meta-analysis by Rhiannon Healy and colleagues at Victoria University pooled seven trials of aerobic training in people with obesity or type 2 diabetes. In the 62 men, aerobic exercise moderately increased testosterone concentrations (Hedges’ g = 0.565, 95% CI 0.307-0.822, p < 0.001). In the 41 women, no significant effect.⁵

The weight-loss literature points the same direction and quantifies the dose-response. Giovanni Corona’s meta-analysis of 24 trials found both low-calorie dieting and bariatric surgery significantly increased total testosterone, with surgery producing a larger rise (8.73 nmol/L) than dieting (2.87 nmol/L) — and multiple regression showed the degree of weight loss was the single best determinant of the testosterone increase.¹³ A 2026 umbrella review of systematic reviews reached the same conclusion, with bariatric surgery raising total testosterone by up to 8.73 nmol/L and dietary interventions helping to a lesser extent.¹⁴

Read those two findings together and the practical implication is uncomfortable but clear: if your testosterone is low and your body fat is high, the training that raises it is the training that changes your body composition — not the training that maximizes your post-workout hormone curve. What matters is total weekly work you can recover from and repeat, which is a body composition problem, not an endocrine one. SensAI plans against that: weekly volume you can actually complete, adjusted by what your last week’s sessions and recovery data showed.

What actually moves your testosterone

Ranked by effect size and how much control you have over it.

Lever	Evidence	Realistic effect
Sleep	1 week at 5 h/night in 10 young men	−10 to −15% daytime testosterone6
Losing body fat (if overweight)	24-trial meta-analysis	Rises with weight lost; diet +2.87 nmol/L13
Aerobic training (obesity/T2D)	7 trials, 62 men	g = 0.565, moderate increase5
Eating enough	Endurance athletes, low energy availability	Prevents the drop rather than causing a rise7
Not over-restricting carbs at high protein	27 studies, 309 men	High-protein low-carb: −5.23 nmol/L15
Post-workout hormone spike	3 trials, 117 men total	No measurable effect on outcomes239

Sleep is the big one

Rachel Leproult and Eve Van Cauter at the University of Chicago put 10 healthy men, mean age 24.3, through a controlled laboratory protocol: three nights of 10-hour bedtimes, then eight nights restricted to 5 hours.⁶

Daytime testosterone fell 10-15%. Measured across waking hours, levels dropped from 18.4 nmol/L rested to 16.5 nmol/L after restriction (P = .049). Self-reported vigor declined progressively across the week, from 28 after the first restricted night to 19 after the seventh.⁶

One week. Ten to fifteen percent. No supplement in the “test booster” aisle has that kind of effect size behind it, and the intervention is free.

There’s a mechanistic reason sleep sits at the top of the list rather than in the middle: testosterone secretion is tightly coupled to sleep architecture. Gary Wittert of the University of Adelaide, reviewing the sleep-testosterone relationship, notes that the overnight testosterone rise is sleep-dependent rather than circadian-dependent, and requires at least three hours of sleep with normal architecture — and that abnormalities of sleep quality, duration, or circadian timing can all reduce testosterone. Wittert is also careful to say the evidence for a direct effect independent of SHBG and comorbidities is “equivocal and on balance seems tenuous.”¹⁶ Take that as a reason to protect sleep for the whole package of reasons, not as a promise about one lab value. Sleep is upstream of far more than one hormone, which is why SensAI reads its duration and quality from HealthKit before deciding whether today’s session should be heavy — and why sleep quality shows up in training readiness long before it shows up in your performance.

Eating too little is the fast way down

Anthony Hackney of the University of North Carolina at Chapel Hill has spent years documenting what the group calls the Exercise-Hypogonadal Male Condition — low serum testosterone with associated symptoms in men doing high training volumes.⁷ It’s most described in endurance athletes, but Daniel Hooper, Adam Tenforde, and Hackney note similar changes appear in power sports like American football and in weight-class sports like wrestling.⁷

Their recommended treatment is instructive, because it isn’t hormonal. It’s nutritional intervention and modification of training — pharmacological options being unavailable to athletes under World Anti-Doping Agency rules anyway.⁷ In other words: eat more, train less. The line between underfueling and overtraining is genuinely hard to see from the inside, and low testosterone is often the lab value that finally makes it visible.

Diet composition matters at the extremes too. Joseph Whittaker and Miranda Harris pooled 27 studies covering 309 men and found that moderate-protein low-carbohydrate diets had no consistent effect on resting testosterone — but high-protein (≥35% of calories) low-carbohydrate diets produced a large decrease, roughly 5.23 nmol/L.¹⁵ They also found short-term low-carb dieting raised resting cortisol, with post-exercise cortisol staying elevated even after three weeks. If you’re simultaneously cutting carbs hard, pushing protein very high, and training heavy, you’ve assembled the exact combination that suppresses the hormone you’re trying to protect. Worth checking against how much protein you actually need, which is lower than most cutting diets assume.

What is a normal testosterone level?

264 to 916 ng/dL for healthy non-obese men aged 19-39, with a median of 531 ng/dL.

That range comes from the most careful work available on the question: Thomas Travison, Shalender Bhasin, and colleagues harmonized testosterone measurements across four large cohort studies — the Framingham Heart Study, the European Male Aging Study, the Osteoporotic Fractures in Men Study, and the Male Sibling Study of Osteoporosis — covering 9,054 community-dwelling men, cross-calibrated against a CDC reference method.⁸

Percentile	Total testosterone
2.5th	264 ng/dL
5th	303 ng/dL
50th (median)	531 ng/dL
95th	852 ng/dL
97.5th	916 ng/dL

An important caveat buried in that paper: a substantial proportion of the variation between cohorts was due to assay differences, not real biological differences between the men.⁸ Two labs can hand you meaningfully different numbers from the same blood. Treat a single result from an unharmonized assay as a rough estimate, not a verdict.

The 2018 Endocrine Society clinical practice guideline, which Bhasin chaired, is also explicit that a diagnosis of hypogonadism requires symptoms plus unequivocally and consistently low morning testosterone on more than one occasion — not a single number, and not a number in isolation.¹⁷ If you’re in that territory, that’s a conversation with a physician, not a training-app question.

What this means for how you train

Strip out the hormone theory and the training implications get simpler, not more complicated.

Stop selecting exercises for their hormonal response. Squat and deadlift because they load a lot of muscle through a long range and give you a productive amount of work per unit of time — not because of what they do to your bloodstream in the following half hour. The bloodstream effect is real and it does nothing for you.²³⁹

Stop compressing rest periods to chase a spike. Ahtiainen’s crossover found two- and five-minute rests produced the same hormonal response and the same six-month outcome.⁴ Rest long enough to make the next set count.

Do protect sleep like it’s part of the program, because on this specific metric it demonstrably is — a 10-15% swing from one bad week.⁶

Do eat enough to support the training you’re doing. The fastest route to genuinely low testosterone in an active man isn’t insufficient squatting; it’s chronic high volume on chronic low intake.⁷

This is where an honest read of the evidence changes what’s worth measuring. The variables that actually decide whether a training block works — how much you’re lifting, whether load is climbing at a rate you can absorb, whether you slept, whether you’re recovering between sessions — move week to week and are visible in data you already generate. Your hormone profile mostly isn’t, and the part of it you can move on a given afternoon turns out not to matter.

That’s the gap SensAI was built to close. It reads your recovery data, your sleep, and your actual completed sessions, then decides whether today should be heavy — rather than asking you to infer that from a rule of thumb about which exercises “boost testosterone.” When the honest answer to a popular training question is “that mechanism isn’t doing what you think,” what’s left is the training itself: load, progression, recovery, consistency. Those are measurable, and SensAI measures them continuously.

It also means SensAI won’t tell you a workout raised your testosterone, because that claim wouldn’t survive the literature. What it will tell you is whether your ramp rate is outrunning your recovery — which is the version of this question with an actionable answer.

The mechanism people wanted testosterone to be — a lever you pull each session — was never there. The mechanism that is there is slower and less exciting: sleep enough, eat enough, add load you can recover from, repeat for months. Which happens to be the same advice that builds muscle for reasons that have nothing to do with hormones at all.

Frequently asked questions

Does lifting weights increase testosterone?

Yes, acutely. Heavy, high-volume resistance exercise elevates circulating testosterone in men — measurably immediately after the session and still at 15 and 30 minutes.¹² It does not raise your resting testosterone in healthy trained men — six months of hypertrophy training produced no significant change in basal concentrations.⁴

Does the post-workout testosterone spike build muscle?

No. Twelve men trained one arm in a low-hormone state and the other in a high-hormone state for 15 weeks: muscle cross-sectional area rose 12% and 10% respectively, with no significant difference.² Two larger studies (n = 56 and n = 49) found no correlation between any acute anabolic hormone response and gains in size or strength.³⁹

What is the best workout to increase testosterone?

For the acute spike, high-volume compound lifting with large muscle groups.¹ But since that spike doesn’t affect your results,²³⁹ the better question is what raises resting testosterone — and for men with excess body fat, that’s aerobic training and weight loss (g = 0.565 in men with obesity or type 2 diabetes).⁵ For lean, already-trained men, no workout design reliably raises resting testosterone.

Does cardio lower testosterone?

Not by itself. Chronic high-volume endurance training combined with insufficient energy intake can produce the Exercise-Hypogonadal Male Condition — low testosterone with hypogonadal symptoms.⁷ In men with obesity or type 2 diabetes, aerobic training increases testosterone.⁵ The variable that determines which way it goes is energy availability, not the cardio itself.

How can I increase my testosterone naturally?

In order of evidence strength: sleep more (one week at 5 hours a night cut daytime testosterone 10-15%),⁶ lose excess body fat if you have it (the degree of weight loss is the best predictor of the rise),¹³ eat enough total calories to support your training,⁷ and avoid very-high-protein, very-low-carbohydrate diets, which reduced resting total testosterone by about 5.23 nmol/L across 27 studies.¹⁵

What is a normal testosterone level for men?

264-916 ng/dL for healthy non-obese men aged 19-39, median 531 ng/dL, based on harmonized data from 9,054 men across four cohorts.⁸ Assay differences between labs account for a substantial share of apparent variation, so one number from one lab is an estimate.⁸ A hypogonadism diagnosis requires symptoms plus consistently low morning levels on more than one occasion.¹⁷

Do testosterone booster supplements work?

The category trades on a real finding applied to the wrong dose range. Testosterone at pharmacological doses clearly builds muscle — 600 mg/week for 10 weeks produced a 6.1 kg fat-free mass gain when combined with training.¹⁰ Movement within the natural range, which is the most any supplement could plausibly achieve, has never been shown to produce the corresponding benefit.²³⁹

Does testosterone actually build muscle?

At pharmacological doses, unambiguously. Men given 600 mg/week of testosterone enanthate for 10 weeks while doing no exercise gained 3.2 kg of fat-free mass — more than the men who took placebo and trained three times a week (1.9 kg) — with near-identical strength gains.¹⁰ The effect is dose-dependent in older men across 25-300 mg/week.¹¹ That is a completely different question from whether your own post-workout fluctuation matters — it doesn’t.²

The bottom line

Lifting raises your testosterone for less than an hour, and that hour is not where your results come from. The three best-designed tests of the idea — including one where the same man’s two arms trained under different hormone conditions — all found the spike predicts nothing.²³⁹

Testosterone genuinely builds muscle at doses your body doesn’t make. Inside your natural range, the levers that move the number are sleep, body fat, and eating enough.⁶¹³⁷ None of them is a workout variable.

Which is oddly freeing. It means you can stop optimizing your session for an endocrine response and start optimizing it for the thing that actually drives adaptation: load you can recover from, applied consistently, for a long time.

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References

Footnotes

1. Vingren, J.L., Kraemer, W.J., Ratamess, N.A., Anderson, J.M., Volek, J.S., & Maresh, C.M. “Testosterone physiology in resistance exercise and training: the up-stream regulatory elements.” Sports Medicine, 2010, 40(12), 1037-1053. https://pubmed.ncbi.nlm.nih.gov/21058750/ ↩ ↩² ↩³ ↩⁴ ↩⁵ ↩⁶ ↩⁷

2. West, D.W., Burd, N.A., Tang, J.E., Moore, D.R., Staples, A.W., Holwerda, A.M., Baker, S.K., & Phillips, S.M. “Elevations in ostensibly anabolic hormones with resistance exercise enhance neither training-induced muscle hypertrophy nor strength of the elbow flexors.” Journal of Applied Physiology, 2010, 108(1), 60-67. https://pubmed.ncbi.nlm.nih.gov/19910330/ ↩ ↩² ↩³ ↩⁴ ↩⁵ ↩⁶ ↩⁷ ↩⁸ ↩⁹ ↩¹⁰ ↩¹¹ ↩¹² ↩¹³ ↩¹⁴

3. West, D.W. & Phillips, S.M. “Associations of exercise-induced hormone profiles and gains in strength and hypertrophy in a large cohort after weight training.” European Journal of Applied Physiology, 2012, 112(7), 2693-2702. https://pubmed.ncbi.nlm.nih.gov/22105707/ ↩ ↩² ↩³ ↩⁴ ↩⁵ ↩⁶ ↩⁷ ↩⁸ ↩⁹

4. Ahtiainen, J.P., Pakarinen, A., Alen, M., Kraemer, W.J., & Häkkinen, K. “Short vs. long rest period between the sets in hypertrophic resistance training: influence on muscle strength, size, and hormonal adaptations in trained men.” Journal of Strength and Conditioning Research, 2005, 19(3), 572-582. https://pubmed.ncbi.nlm.nih.gov/16095405/ ↩ ↩² ↩³ ↩⁴ ↩⁵ ↩⁶

5. Healy, R., Patten, R., Bauer, C., Woessner, M.N., Bourke, M., Grossmann, M., & Levinger, I. “The Effects of Aerobic Exercise Training on Testosterone Concentration in Individuals Who are Obese or Have Type 2 Diabetes: A Systematic Review and Meta-Analysis.” Sports Medicine - Open, 2024, 10(1), 117. https://pubmed.ncbi.nlm.nih.gov/39467940/ ↩ ↩² ↩³ ↩⁴ ↩⁵

6. Leproult, R. & Van Cauter, E. “Effect of 1 week of sleep restriction on testosterone levels in young healthy men.” JAMA, 2011, 305(21), 2173-2174. https://pubmed.ncbi.nlm.nih.gov/21632481/ ↩ ↩² ↩³ ↩⁴ ↩⁵ ↩⁶ ↩⁷

7. Hooper, D.R., Tenforde, A.S., & Hackney, A.C. “Treating exercise-associated low testosterone and its related symptoms.” The Physician and Sportsmedicine, 2018, 46(4), 427-434. https://pubmed.ncbi.nlm.nih.gov/30063407/ ↩ ↩² ↩³ ↩⁴ ↩⁵ ↩⁶ ↩⁷ ↩⁸ ↩⁹

8. Travison, T.G., Vesper, H.W., Orwoll, E., Wu, F., Kaufman, J.M., Wang, Y., Lapauw, B., Fiers, T., Matsumoto, A.M., & Bhasin, S. “Harmonized Reference Ranges for Circulating Testosterone Levels in Men of Four Cohort Studies in the United States and Europe.” Journal of Clinical Endocrinology & Metabolism, 2017, 102(4), 1161-1173. https://pubmed.ncbi.nlm.nih.gov/28324103/ ↩ ↩² ↩³ ↩⁴ ↩⁵ ↩⁶

9. Morton, R.W., Oikawa, S.Y., Wavell, C.G., Mazara, N., McGlory, C., Quadrilatero, J., Baechler, B.L., Baker, S.K., & Phillips, S.M. “Neither load nor systemic hormones determine resistance training-mediated hypertrophy or strength gains in resistance-trained young men.” Journal of Applied Physiology, 2016, 121(1), 129-138. https://pubmed.ncbi.nlm.nih.gov/27174923/ ↩ ↩² ↩³ ↩⁴ ↩⁵ ↩⁶ ↩⁷ ↩⁸ ↩⁹

10. Bhasin, S., Storer, T.W., Berman, N., Callegari, C., Clevenger, B., Phillips, J., Bunnell, T.J., Tricker, R., Shirazi, A., & Casaburi, R. “The effects of supraphysiologic doses of testosterone on muscle size and strength in normal men.” New England Journal of Medicine, 1996, 335(1), 1-7. https://pubmed.ncbi.nlm.nih.gov/8637535/ ↩ ↩² ↩³ ↩⁴

11. Storer, T.W., Woodhouse, L., Magliano, L., Singh, A.B., Dzekov, C., Dzekov, J., & Bhasin, S. “Changes in muscle mass, muscle strength, and power but not physical function are related to testosterone dose in healthy older men.” Journal of the American Geriatrics Society, 2008, 56(11), 1991-1999. https://pubmed.ncbi.nlm.nih.gov/18795988/ ↩ ↩²

12. Riachy, R., McKinney, K., & Tuvdendorj, D.R. “Various Factors May Modulate the Effect of Exercise on Testosterone Levels in Men.” Journal of Functional Morphology and Kinesiology, 2020, 5(4), 81. https://pubmed.ncbi.nlm.nih.gov/33467296/ ↩

13. Corona, G., Rastrelli, G., Monami, M., Saad, F., Luconi, M., Lucchese, M., Facchiano, E., Sforza, A., Forti, G., Mannucci, E., & Maggi, M. “Body weight loss reverts obesity-associated hypogonadotropic hypogonadism: a systematic review and meta-analysis.” European Journal of Endocrinology, 2013, 168(6), 829-843. https://pubmed.ncbi.nlm.nih.gov/23482592/ ↩ ↩² ↩³ ↩⁴

14. Nayak, S.S., Partheepan, K., Mantena, S., Misra, M., De Leon, G., Perali, T., Chen, J., Islam, M.A., Sedaliu, T., & Polisetty, L. “The Effect of Weight Loss and Weight Loss Interventions on Sex Hormones: An Umbrella Review of Systematic Reviews and Meta-Analyses.” Endocrine Practice, 2026, 32(2), 246-257. https://pubmed.ncbi.nlm.nih.gov/41167564/ ↩

15. Whittaker, J. & Harris, M. “Low-carbohydrate diets and men’s cortisol and testosterone: Systematic review and meta-analysis.” Nutrition and Health, 2022, 28(4), 543-554. https://pubmed.ncbi.nlm.nih.gov/35254136/ ↩ ↩² ↩³

16. Wittert, G. “The relationship between sleep disorders and testosterone in men.” Asian Journal of Andrology, 2014, 16(2), 262-265. https://pubmed.ncbi.nlm.nih.gov/24435056/ ↩

17. Bhasin, S., Brito, J.P., Cunningham, G.R., Hayes, F.J., Hodis, H.N., Matsumoto, A.M., Snyder, P.J., Swerdloff, R.S., Wu, F.C., & Yialamas, M.A. “Testosterone Therapy in Men With Hypogonadism: An Endocrine Society Clinical Practice Guideline.” Journal of Clinical Endocrinology & Metabolism, 2018, 103(5), 1715-1744. https://pubmed.ncbi.nlm.nih.gov/29562364/ ↩ ↩²