Does Boosting Your Testosterone Build More Muscle? In a Word, No — Here’s Why

Three different situations, not one

At sufficiently high doses testosterone can even increase muscle without resistance training, while combining high testosterone exposure with resistance training can produce much larger gains (Bhasin et al., 1996).

The evidence becomes much clearer once we separate three completely different situations:

1. Clinically low testosterone.
2. Normal physiological testosterone.
3. Testosterone pushed well above the normal physiological range.

Mixing those together is where most of the confusion begins.

Does testosterone build muscle?

Yes. There is no credible scientific argument that testosterone has no anabolic effect on skeletal muscle.

Testosterone is an androgen hormone that can influence muscle protein balance, muscle fibre size, satellite-cell activity, myonuclear accretion and the expression of genes involved in muscle growth (Bhasin et al., 2001; Sinha-Hikim et al., 2002).

” The size of the change matters enormously.

Moving somebody from genuinely deficient testosterone towards a healthy physiological concentration is very different from moving an otherwise healthy person from one normal value to another. And both are very different again from using pharmacological doses that produce testosterone concentrations several times higher than normal. That distinction matters throughout this article.

How does muscle actually grow?

Before looking at testosterone, it helps to understand what resistance training is actually doing.

Muscle hypertrophy means an increase in the size of existing skeletal muscle fibres. Those fibres contain large quantities of structural and contractile proteins, including actin and myosin. Muscle proteins are continually being created and broken down.

Two useful terms are muscle protein synthesis (MPS) — the creation of new muscle proteins — and muscle protein breakdown (MPB) — the degradation of existing muscle proteins.

Muscle growth occurs when the cumulative balance over time favours the retention of additional muscle protein and other cellular material. That does not happen because one workout instantly turns into new muscle. It is the accumulated result of repeated training and recovery periods over weeks, months and years (Roberts et al., 2023).

What resistance training does to a muscle fibre

When a muscle produces force against resistance, recruited muscle fibres experience mechanical loading. Structures inside and around the fibre detect these forces. The conversion of a mechanical stimulus into a biological signal is known as mechanotransduction (Wackerhage et al., 2019).

Those signals affect a network of cellular processes involved in adaptation, including:

• muscle protein synthesis
• mTORC1 signalling
• gene expression
• ribosomal activity
• ribosome production
• satellite-cell activity
• tissue remodelling.

Mechanical loading is therefore considered one of the strongest candidates for the initiating stimulus behind resistance-training-induced hypertrophy (Wackerhage et al., 2019; Roberts et al., 2023).

This is much more accurate than the old explanation that lifting simply “tears the muscle and it grows back bigger”. Muscle damage can happen, particularly after unfamiliar or excessive training, but substantial muscle damage is not required for hypertrophy.

Resistance exercise increases muscle protein synthesis

One of the most repeatable responses to resistance exercise is an increase in muscle protein synthesis.

A 2024 systematic review and exploratory meta-analysis analysed 79 controlled trials examining the muscle protein synthetic response to resistance exercise. Overall, resistance exercise produced a robust increase in MPS. In some studies this elevation remained measurable for up to around 48 hours after training, although the magnitude and duration varied substantially between participants, protocols and training status (Davies et al., 2024).

Protein feeding can further stimulate this response by supplying amino acids. That is one reason resistance training and adequate dietary protein work together. However, there is an important caveat.

A bigger short-term MPS response does not automatically mean more eventual muscle growth.

An acute laboratory measurement of muscle protein synthesis is not the same thing as measuring months of hypertrophy. Early in a resistance-training programme, some increased MPS appears to be associated with tissue repair and remodelling following an unfamiliar stimulus.

Damas and colleagues highlighted that the early acute MPS response in previously untrained muscle does not reliably predict the amount of hypertrophy somebody will eventually achieve (Damas et al., 2015).

Witard and colleagues reached a similar conclusion: MPS is fundamental to muscle accretion, but a single short-term measurement should not be interpreted as a direct measurement of future muscle growth (Witard, Bannock and Tipton, 2022). The repeated long-term response is what matters.

Where does mTOR fit into muscle growth?

You will often hear mTOR described as the body's “muscle-building switch”. That is an oversimplification.

mTORC1 — mechanistic target of rapamycin complex 1 — is an important regulator of muscle protein synthesis, translational processes and other aspects of skeletal muscle adaptation (Schiaffino et al., 2021; Roberts et al., 2023).

Resistance exercise can influence mTORC1 signalling. Amino acids and other signals interact with related pathways too. But muscle hypertrophy cannot be reduced to: lift weights → activate mTOR → grow muscle. The system is much more complex.

Your muscles can also build more protein-making machinery

Protein synthesis requires ribosomes. Ribosomes are essentially the cellular machinery that translates genetic instructions into proteins.

A muscle therefore has two broad ways to increase its ability to manufacture protein. It can make its existing ribosomes work more efficiently. And it can increase the amount of protein-making machinery available by producing more ribosomes. The latter process is called ribosome biogenesis (Roberts et al., 2023).

Researchers increasingly distinguish translational efficiency — how effectively existing machinery produces proteins — from translational capacity — how much protein-producing machinery is available. Long-term hypertrophy appears to involve both.

This helps explain why measuring one signalling molecule immediately after one workout does not tell us everything about long-term muscle growth.

Satellite cells and myonuclei

Skeletal muscle fibres are enormous cells containing many nuclei. These nuclei are known as myonuclei. Around muscle fibres are satellite cells, which are muscle stem/progenitor cells.

With an appropriate stimulus, satellite cells can become activated and eventually fuse with existing muscle fibres, contributing additional nuclei.

The precise role and timing of satellite-cell involvement continues to be investigated, but satellite-cell activity and myonuclear accretion are associated with substantial muscle-fibre hypertrophy (Sinha-Hikim et al., 2002. Roberts et al., 2023; Schiaffino et al., 2021).

This becomes particularly interesting when discussing testosterone, because androgen signalling can influence this biology too.

So what does testosterone actually do?

Testosterone exerts many of its effects through the androgen receptor. Testosterone can enter androgen-responsive cells and bind to this receptor.

The resulting signalling can alter gene transcription and influence numerous processes associated with skeletal muscle. These include effects on:

• muscle protein balance
• muscle fibre size
• satellite cells
• myonuclear accretion
• growth-related gene expression
• interactions with other anabolic signalling systems.

This is important because the amount of testosterone circulating in the blood is not the whole story. The ability of the target tissue to respond to androgen signalling matters too. We will return to that shortly.

What happens when scientists deliberately raise testosterone?

Some of the clearest evidence comes from controlled testosterone dose-response studies.

Bhasin and colleagues experimentally suppressed endogenous testosterone production in healthy young men and then gave them different weekly doses of testosterone for 20 weeks (Bhasin et al., 2001). The resulting circulating testosterone concentrations ranged from relatively low values to levels far above the normal physiological range.

As testosterone exposure increased, so did fat-free mass. In groups receiving 125, 300 and 600 mg of testosterone enanthate per week, average increases in fat-free mass were approximately 3.4 kg, 5.2 kg and 7.9 kg respectively (Bhasin et al., 2001).

Changes in leg strength, power, thigh muscle volume and quadriceps muscle volume were also related to testosterone exposure.

This is compelling evidence that testosterone can produce a dose-dependent anabolic response when the differences in exposure are sufficiently large.

But fat-free mass is not automatically muscle

This is an important methodological point. Fat-free mass includes more than skeletal muscle. Water and other non-fat tissue can affect measurements such as DXA. Fortunately, further research examined actual muscle tissue.

Sinha-Hikim and colleagues analysed muscle biopsies and MRI data from men exposed to graded testosterone doses (Sinha-Hikim et al., 2002). Higher testosterone exposure produced greater increases in muscle volume and muscle-fibre cross-sectional area. Both type I and type II fibres were affected. At higher doses the researchers also observed increases in myonuclear number.

So the anabolic effect of testosterone is not merely a change in body water being mislabelled as muscle. Actual muscle fibre hypertrophy occurs.

Testosterone can increase muscle even without resistance training

One of the best-known experiments was published by Bhasin and colleagues in the New England Journal of Medicine in 1996. Healthy men were allocated to four groups:

• placebo with no resistance training
• testosterone with no resistance training
• placebo plus resistance training
• testosterone plus resistance training.

The testosterone dose used was supraphysiological: 600 mg of testosterone enanthate per week. The testosterone group that did not lift weights still gained more muscle size and strength than the placebo group that did not train (Bhasin et al., 1996).

The biggest effects occurred when testosterone and resistance training were combined. Over ten weeks, the testosterone-plus-training group gained approximately 6.1 kg of fat-free mass and produced large increases in bench-press and squat strength.

This demonstrates two things very clearly. First, sufficiently high testosterone exposure has an independent anabolic effect. Second, resistance training and high androgen exposure can have additive effects.

What it does NOT demonstrate is that naturally increasing normal testosterone by a relatively small amount will reproduce the same result. That would be a completely different exposure.

Does more testosterone mean more muscle?

At sufficiently large differences in testosterone exposure, yes. This is particularly obvious when comparing physiological testosterone with supraphysiological drug exposure.

A systematic review and meta-analysis of randomised placebo-controlled anabolic-androgenic steroid studies in healthy exercising adults found that anabolic-androgenic steroid use produced a moderate increase in lean mass and a smaller but statistically significant increase in strength compared with placebo (Andrews et al., 2018).

So testosterone unquestionably matters. Where things become much less convincing is when people assume the same dose-response relationship continues neatly across ordinary natural testosterone levels.

For example: a healthy person at 700 ng/dL is not automatically going to build 40% more muscle than a healthy person at 500 ng/dL. Human physiology is not that linear.

What if testosterone is genuinely low?

Clinically low testosterone is a different situation from being somewhere towards the lower end of an otherwise healthy physiological range. Hypogonadism can negatively affect lean mass, sexual function, bone health and other systems.

Randomised trials and meta-analyses investigating testosterone replacement in men with lower testosterone generally find increases in lean body mass (Varanoske, Margolis and Pasiakos, 2020; Parahiba et al., 2020; Lee et al., 2023).

A systematic review and meta-analysis by Parahiba and colleagues reported an average increase of approximately 2.54 kg in lean body mass following testosterone supplementation in middle-aged and older men (Parahiba et al., 2020).

A 2023 systematic review and meta-analysis of older men with low or low-normal testosterone also found a statistically significant improvement in muscle strength, although the overall effect was modest. Importantly, the response tended to be greater when starting testosterone concentrations were lower (Lee et al., 2023).

That makes biological sense. Correcting a genuine deficiency is not equivalent to pushing an already normal concentration slightly higher.

Does naturally higher testosterone predict more muscle growth?

This is the part that often surprises people. If circulating testosterone inside the normal physiological range were the dominant determinant of resistance-training hypertrophy, we would expect men with higher testosterone to consistently build substantially more muscle from the same training. That relationship has not been demonstrated consistently.

Morton and colleagues studied resistance-trained young men during 12 weeks of resistance training (Morton et al., 2018b). They measured numerous circulating and intramuscular hormones, including:

• total testosterone
• free testosterone
• dihydrotestosterone
• growth hormone
• IGF-1.

None of the measured circulating hormones consistently predicted increases in muscle fibre cross-sectional area or lean body mass. However, something else did.

Androgen receptor content, however, was associated with muscle growth.

The researchers found that muscle androgen receptor content was positively associated with hypertrophy. That is an important clue.

Two people with similar testosterone concentrations may not necessarily experience identical downstream androgen signalling. The muscle's ability to respond to androgen exposure also matters.

The endocrine system is not simply: more hormone in blood = proportionally more muscle. The receptor and the target tissue matter. So do numerous other biological factors.

Your testosterone result is not a muscle-building score

This is where testosterone discussions online often become misleading. Someone with testosterone of 750 is not necessarily a dramatically better muscle builder than someone at 500. Hypertrophy differs enormously between individuals even when they perform similar training.

Potential contributors include:

• androgen receptor characteristics
• ribosome biogenesis
• satellite-cell response
• myonuclear adaptation
• genetics
• muscle architecture
• training history
• training volume
• exercise execution
• effort and proximity to failure
• protein intake
• total energy intake
• recovery
• sleep
• age
• other biological differences.

Testosterone is one component of a complicated adaptive system. It is not the sole control dial.

What about the testosterone spike after lifting weights?

Resistance exercise can temporarily increase circulating testosterone. Some types of sessions produce a larger endocrine response than others. High-volume workouts involving large muscle groups have historically been associated with larger temporary rises in testosterone and other hormones.

This observation led to the idea that training programmes should be designed to maximise the post-workout “anabolic hormone response”. The evidence has not supported that idea particularly well.

Acute systemic testosterone responses do not consistently predict subsequent muscle hypertrophy (Van Every, D'Souza and Phillips, 2024; Morton et al., 2018b).

One particularly useful experiment compared men and women after resistance exercise. Men experienced an exercise-induced testosterone response approximately 45 times larger than the women. Yet the increase in muscle protein synthesis was similar between the sexes (West et al., 2012).

That provides powerful evidence against the idea that the temporary systemic testosterone spike following resistance exercise is the principal cause of the post-workout MPS response.

But men have far more testosterone than women

Correct. Men generally have much higher circulating testosterone concentrations and substantially more absolute muscle mass. Yet men and women can respond remarkably similarly to resistance training when hypertrophy is considered relative to their starting muscle size.

A systematic review and meta-analysis by Roberts, Nuckols and Krieger found no significant difference between young and middle-aged men and women in relative resistance-training-induced muscle hypertrophy (Roberts, Nuckols and Krieger, 2020).

A newer 2025 systematic review and Bayesian meta-analysis also found that males tended to gain somewhat more absolute muscle, but relative increases in muscle size were similar between sexes.

This does not mean testosterone is irrelevant. It means differences in physiological testosterone concentrations are not a simple measure of someone's percentage capacity to hypertrophy.

Does testosterone increase muscle protein synthesis?

Testosterone can alter skeletal muscle protein balance and can contribute to an anabolic environment. However, resistance exercise itself is a very powerful stimulus for muscle protein synthesis (Davies et al., 2024).

And the similar post-exercise MPS response observed in men and women despite enormous differences in testosterone strongly suggests that resistance-exercise-induced MPS does not require a large systemic testosterone surge (West et al., 2012).

Testosterone therefore influences the biological environment in which muscle growth takes place. It should not be described as the only trigger for muscle protein synthesis.

Do squats boost testosterone enough to grow your arms?

This is one of the more persistent gym myths. A demanding lower-body exercise session may temporarily increase testosterone. That does not mean the resulting hormone response will meaningfully grow a muscle that was not appropriately trained.

Your biceps do not replace curls because you performed heavy squats beforehand. The muscles you want to grow still need an appropriate mechanical stimulus.

Choose exercises because they effectively train the target muscle, not because they supposedly create the biggest temporary testosterone spike (Morton et al., 2018b; Van Every, D'Souza and Phillips, 2024; West et al., 2012).

What about “naturally boosting” testosterone?

This is where marketing often runs far ahead of the evidence. Sleep, adequate nutrition, resistance training, maintaining a healthy body composition and looking after general health are all sensible things to do. They are worthwhile whether or not they alter testosterone.

If poor sleep, severe energy restriction, illness or another problem is suppressing testosterone, correcting that problem may help restore normal endocrine function.

But that is very different from taking an otherwise healthy man with physiologically normal testosterone and finding a natural trick that suddenly creates pharmacological levels of androgen exposure. That does not happen.

And therefore research showing large anabolic effects from supraphysiological testosterone cannot simply be used as evidence that a small natural increase will produce additional kilograms of muscle.

So what matters most if you want to build muscle naturally?

The largest controllable variable is still resistance training.

A major 2023 Bayesian network meta-analysis included 119 studies and 3,364 participants in its hypertrophy network. Virtually all sensible resistance-training prescriptions produced more hypertrophy than not training. Multiple-set programmes were particularly effective, while muscle hypertrophy could occur across a broad range of training loads (Currier et al., 2023).

An even larger American College of Sports Medicine evidence synthesis published in 2026 examined 137 systematic reviews involving more than 30,000 participants. Resistance training reliably increased muscle size (Currier et al., 2026).

Higher weekly training volumes generally enhanced hypertrophy, with approximately 10 or more sets per muscle per week emerging as a useful evidence-based benchmark rather than a rigid threshold.

For a natural lifter with normal testosterone, those training variables are far more actionable than worrying about tiny differences in blood testosterone.

Protein matters too

Resistance training provides the stimulus. Dietary protein provides amino acids needed for protein synthesis and further stimulates the anabolic response.

A major systematic review, meta-analysis and meta-regression involving 49 resistance-training studies and 1,863 participants found that additional dietary protein produced modest but significant additional gains in fat-free mass and muscle size (Morton et al., 2018a).

Its dose-response analysis found that average additional benefits became difficult to detect beyond approximately 1.6 g of protein per kilogram of bodyweight per day. Individual requirements and circumstances vary — the guide to how much protein you need covers this in detail — but this is much more practically useful than trying to optimise a temporary exercise-induced testosterone spike.

So what actually determines how much muscle you gain?

There is no single switch.

• Resistance training mechanically loads muscle.
• Muscle fibres sense that mechanical stimulus.
• Intracellular signalling changes.
• Muscle protein synthesis increases.
• Ribosomes manufacture new proteins.
• Repeated training can increase translational capacity.
• Satellite cells and myonuclei may help support substantial muscle-fibre expansion.
• Adequate protein supplies amino acids.
• Adequate energy and recovery support adaptation.
• Hormones such as testosterone influence the environment in which all of this takes place.

Over repeated training cycles, the accumulated result can be a larger muscle fibre. That is hypertrophy.

Testosterone matters. But testosterone does not replace the training stimulus, protein, recovery or the biological machinery that actually constructs new muscle tissue.

The bottom line: does testosterone build muscle?

Yes. Testosterone is anabolic. Clinically low testosterone can negatively affect lean mass, and treating genuine testosterone deficiency can increase it.

If testosterone is deliberately pushed far above its normal physiological range, muscle size and fat-free mass can increase dramatically and in a dose-dependent manner.

”

Current evidence gives us little reason to believe that small changes within the normal physiological range will reproduce the effects seen with pharmacological testosterone exposure. Nor does a bigger temporary testosterone spike after training appear to predict greater muscle growth.

For the healthy natural lifter, the priorities remain remarkably ordinary:

• Train the target muscles effectively.
• Perform enough productive training volume.
• Progress over time.
• Eat enough protein.
• Support recovery.

And stop treating a testosterone number as a muscle-building score.