Testosterone in Athletes: What Your Blood Work Is Actually Telling You
Table of Contents
Introduction
When I work with athletes or review their blood work, I find that the conversation around hormones almost always gravitates toward testosterone. It is widely viewed as the key hormone for performance and physical adaptation, particularly when it comes to muscle mass and strength. At the same time, this strong focus has led to a considerable amount of misinformation and oversimplified thinking—especially in online fitness spaces, where “bro science” often replaces a more nuanced, evidence-based understanding
Testosterone in athletes is a highly dynamic, context-dependent biomarker that shifts with training load, sleep, nutrition, and recovery status — sometimes within the same day. Understanding what drives those shifts, what a “normal” range actually means for a training athlete, and when a low result genuinely warrants attention can change how you interpret your blood work entirely.
Many of my patients request testosterone testing—not just athletes, but also people from the general population who are either interested in sports or simply trying to find an explanation for their fatigue. There is also a lot of confusion surrounding testosterone, which is why I wrote this guide.
Why testosterone in athletes matters for performance
Testosterone is a steroid hormone produced primarily in the Leydig cells of the testes in men, in the ovaries in women, and in the adrenal and peripheral tissues in both sexes [1]. It acts through androgen receptors in multiple tissues and plays roles in androgenic, anabolic, and psychological functions — including muscle growth, bone formation, erythropoiesis, risk-taking, and aggression [1].
In skeletal muscle specifically, testosterone simultaneously stimulates protein synthesis and inhibits protein degradation — this dual anabolic and anti-catabolic effect accounts for the well-established link between higher testosterone and greater muscle hypertrophy [2]. Testosterone is considered the major promoter of muscle growth and the increase in muscle strength that follows resistance training in men [2]. But the acute endocrine response to a single resistance training session, the chronic adaptation across months of training, and the baseline resting level are three distinct phenomena that should not be conflated [2].
Testosterone also has a psychological dimension relevant to competitive athletes: pre-competition testosterone spikes are associated with enhanced motivation and physical readiness, and winning a contest increases testosterone levels — reinforcing positive behaviors, motivation, and reactivity [1].
In clinical practice, I see a related pattern in a different context. Some patients report subjective improvements in motivation after starting testosterone replacement therapy, which may partly explain why word-of-mouth discussions around testosterone treatment have become more common.
This, in turn, is reflected in patient expectations. I often see individuals hoping that testosterone might improve their overall motivation, including in work and everyday life. Patients presenting with fatigue or burnout frequently look to their testosterone levels as a possible explanation.
At the same time, true hypogonadism is relatively uncommon in my experience, and I believe testosterone therapy should be prescribed only with clear clinical indications. It should not be initiated lightly, as exogenous testosterone—particularly in younger men—can suppress the hypothalamic–pituitary–testicular axis and impair fertility.
In my view, athletes should not be prescribed testosterone replacement therapy based on different medical criteria than those used for the general population. In Finland, these criteria are generally the same, although competitive athletes are subject to additional antidoping regulations.
What reference ranges mean — and why they fall short for testosterone in athletes
Interpreting testosterone on a standard blood report is one of the most commonly mishandled aspects of athlete blood work. The NORIP reference interval for total testosterone in men at age 30 is 10.4–32.6 nmol/L, with values declining modestly through subsequent decades [3]. The Framingham Heart Study reported a 2.5th percentile of 12.1 nmol/L (348.3 ng/dL) in a community-based sample of healthy, non-obese young men measured under controlled conditions [4].
There is also a practical measurement issue that physicians rarely explain to their patients. Testosterone follows a pronounced diurnal rhythm — levels are higher in the morning and lower later in the day, with a roughly 20–25% decline observed in younger men by afternoon [5]. This diurnal swing tends to be larger in younger men than in older men [5], and the recommendation to restrict sampling to morning hours applies across all age groups [5]. An afternoon sample may misclassify a normal result as low. For a full breakdown of how training, fasting, and timing affect blood test results, see preparing for blood test athletes.
For this reason, low testosterone values are typically confirmed with repeat testing in clinical practice. In contrast, elevated testosterone levels are less commonly a concern unless they are clearly above the reference range, in which case underlying causes should be considered. If a low testosterone level is detected, it should be rechecked—ideally using a morning sample, when testosterone concentrations are highest.
In clinical practice, the same reference ranges for testosterone are generally applied to both athletes and sedentary individuals. While training and energy availability can influence testosterone levels, there is no separate set of performance-based reference ranges used for athletes.
How training affects testosterone in athletes: the acute response
Heavy resistance exercise can acutely elevate circulating testosterone in men in the short-term post-exercise window. According to the Sports Medicine review by Vingren and colleagues, this acute response is predominantly determined by the nature of the session: high volume and high metabolic demand are the session characteristics most consistently linked to an acute testosterone response [6]. In women, the findings are more equivocal, with some studies finding small increases and others finding no significant acute response [6].
The acute response is not a cause for concern — it is a normal physiological event. The key clinical point is that this transient elevation should not be conflated with resting testosterone status.
Many people believe that training—especially bodybuilding—increases testosterone levels. I also see that many patients are actively looking for “natural” ways to boost their testosterone and often assume that going to the gym is an effective way to achieve this. While there is a grain of truth to this in the short term, it does not necessarily translate into higher baseline levels over time.
Although testosterone levels may rise temporarily in response to exercise, athletes do not consistently have higher baseline testosterone levels than sedentary individuals. In some cases—particularly with prolonged high training loads or low energy availability—baseline levels may even decrease over time, as we shall see in the next section.
The chronic training paradox: when high-volume exercise lowers testosterone in athletes
Here is where the picture becomes more nuanced — and more relevant for endurance athletes in particular. While short-term exercise acutely elevates testosterone, sustained high-volume training — especially endurance-based work — can produce the opposite effect chronically.
This phenomenon has a formal name: the Exercise-Hypogonadal Male Condition (EHMC). First described by Hackney and colleagues, the EHMC refers to a state in which male endurance athletes exhibit persistently reduced resting testosterone levels, both free and total, compared to sedentary matched controls [7]. Evidence in this area reports testosterone levels in EHMC men to be only 50–85% of the levels found in comparable age-matched, non-exercising men [8]. The condition is described as limited to men with prolonged chronic endurance training exposure, typically measured in years [7].
The exact mechanism is postulated to be a dysfunction or readjustment within the hypothalamic-pituitary-testicular regulatory axis, though this remains incompletely understood [7]. A key parallel to the female athlete picture: energy availability is a critical mediating variable. A 2026 narrative review from Mayo Clinic researchers confirmed that Relative Energy Deficiency in Sport (RED-S blood work) is now recognized as affecting male athletes across multiple disciplines — including combat sports and jockeying — not just female endurance athletes [1]. Severe energy imbalance can lower testosterone levels and affect performance, recovery, and health — and even subtle energy imbalances may impair performance [1].
A clinically important distinction: a reduced testosterone concentration alone does not warrant pharmacological treatment — particularly in athletes competing under WADA regulations, for whom exogenous testosterone is a banned substance. Treatment of exercise-associated low testosterone should first prioritize nutritional intervention and training modification [9].
In practice, testosterone is a highly responsive hormone influenced by multiple factors. Over the long term, maintaining healthy testosterone levels is closely linked to fundamental lifestyle factors—adequate nutrition, sufficient sleep, proper recovery, and effective stress management.
In clinical practice, testosterone is most commonly measured to evaluate or exclude hypogonadism. In athletes, a low testosterone level does not necessarily indicate clinical dysfunction. In most cases, it does not reflect primary hypogonadism but rather a context-dependent physiological adaptation. While true hypogonadism does occur, low testosterone in athletes is often not indicative of underlying pathology.
Testosterone can also be interpreted in relation to cortisol, and the testosterone-to-cortisol ratio has been used as a marker of training stress and possible overreaching, as we will discuss in the next section. However, this interpretation is nuanced, and testosterone measurements alone do not confirm or exclude conditions such as overtraining.
The testosterone-to-cortisol ratio as a training load biomarker
No discussion of testosterone in athletes is complete without addressing cortisol. Testosterone is predominantly anabolic; cortisol is the body’s primary catabolic stress hormone. The testosterone-to-cortisol ratio (T/C) has been studied as an indirect marker of anabolic-catabolic balance in athletes [10].
The T/C ratio decreases in response to both the intensity and duration of exercise, and during periods of accumulated training load or inadequate recovery [10]. Urhausen and colleagues described the T/C ratio as a more useful indicator of actual physiological training strain than of overtraining syndrome per se — a distinction worth holding onto [10]. The ratio reflects the burden of stress currently being placed on the organism, not a diagnosis. The full clinical picture of how the T:C ratio in overtraining is interpreted and applied in practice is covered in detail in a separate article.
In a 4-year longitudinal study of professional basketball players, the most catabolic hormonal state — reflected by the lowest T/C ratio values — was observed during March and April, the most congested period of the competition calendar [11]. This kind of serial monitoring over a full season carries substantially more clinical weight than a single cross-sectional measurement. For a deeper look at how cortisol and overtraining interact at the clinical level, see the dedicated article on this site.
In clinical practice, however, assessing the testosterone-to-cortisol (T/C) ratio is challenging. Meaningful interpretation would require knowledge of an individual’s baseline levels for both hormones. For this reason, the T/C ratio is used primarily in research settings rather than routine clinical practice.
Importantly, the T/C ratio is not part of formal clinical guidelines or standard care pathways, and it is not a predefined laboratory test. In practice, testosterone and cortisol must be measured separately and the ratio calculated manually. As a result, it is rarely used in routine clinical work, and most clinicians—at least in Finland—do not rely on it in day-to-day practice.
In practice, only a small number of athletes have the resources to measure this consistently. Ideally, baseline values should be established before significant training loads begin, and measurements should be taken under standardized conditions—at the same time of day, typically in the morning.
Even then, interpretation is not straightforward. The T/C ratio alone cannot be used to diagnose overtraining; it can only serve as a supportive marker within a broader clinical context.
Over the longer term, changes in the T/C ratio are often driven more by reductions in testosterone than by consistent increases in cortisol. While cortisol contributes to the balance, variation in the ratio is frequently influenced by changes in testosterone levels.
What depletes testosterone in athletes: the modifiable factors
Several factors outside of training volume directly influence testosterone in athletes and are important for education:
Sleep. Testosterone secretion is linked to the rapid eye movement (REM) phase of sleep [1]. A systematic review and meta-analysis of 18 studies including 252 men found that total sleep deprivation (≥24 hours) significantly reduces testosterone levels in men (SMD −0.64; 95% CI −0.87 to −0.42, p < 0.001) [12]. In two studies of U.S. Army Rangers undergoing sleep deprivation during military training, testosterone decreased by 28% in Study 1 (from 105.91 ± 35.35 to 79.87 ± 35.65 pg/mL) and by 25.4% in Study 2 (from 115.31 ± 28.44 to 89.29 ± 29.00 pg/mL) [13]. For athletes who routinely compress sleep, this is a meaningful and modifiable variable.
None of this should come as a surprise to patients. However, in practice, sleep remains one of the most consistently overlooked factors—particularly among athletes, who often compromise sleep due to training schedules, competition demands, or lifestyle factors. As a result, sleep is one of the most important, yet underutilized, levers for optimizing hormonal health and recovery.
Nutrition. Low-fat diets appear to reduce testosterone in men, while saturated and monounsaturated dietary fats predict higher levels. Excessive protein intake above 3.4 g/kg/day combined with low carbohydrate intake may reduce basal testosterone, and low-carbohydrate diets increase the risk of energy deficiency, RED-S, and associated hormonal suppression [1]. Caloric restriction is associated with reduced testosterone [1].
In practice, this can be particularly challenging for weight-class athletes or those undergoing aggressive weight cuts before competition. I also see similar patterns in athletes following highly restrictive or imbalanced diets, where efforts to optimize body composition may unintentionally compromise hormonal health.
Zinc. Zinc is involved in steroidogenic pathways relevant to testosterone production. A systematic review including 38 studies (8 clinical, 30 animal) concluded that zinc deficiency reduces testosterone levels and that zinc supplementation improves testosterone — though the magnitude of effect depends on baseline zinc and testosterone status, dosage form, and duration [14]. Athletes in caloric restriction or following narrowly patterned diets may warrant dietary zinc assessment.
In clinical practice, however, true zinc deficiency appears to be relatively uncommon. Many patients are already supplementing zinc, so deficiency is often a less likely explanation for low testosterone than is sometimes assumed.
Vitamin D. A 2024 meta-analysis of RCTs in adult men found that vitamin D supplementation significantly increased total testosterone levels (WMD 0.38 nmol/L; 95% CI 0.06–0.70; n = 15 testosterone endpoints) [15]. The subgroup analysis indicated this effect was significant for supplementation durations longer than 12 weeks and doses above 4,000 IU/day [15]. Vitamin D status is worth monitoring in athletic populations, particularly those training indoors or at northern latitudes. The role of vitamin B12 and folate in athletes — two other micronutrients frequently suboptimal in training populations — is covered in a related article.
Vitamin D deficiency can occur periodically, especially in countries such as Finland or other high-latitude regions, and is more common among indoor athletes. In clinical practice, supplementation is often appropriate when deficiency is identified or risk is high.
NSAIDs and acetaminophen. Some evidence suggests that commonly used over-the-counter analgesics, including NSAIDs and acetaminophen, may influence testosterone levels. However, in clinical practice, this effect is rarely of major significance and typically does not lead to specific interventions. It is therefore best viewed as a “nice to know” consideration rather than a primary driver of hormonal changes [1].
Conclusion
Testosterone in athletes is neither a simple performance dial nor a number that can be interpreted in isolation. It is a highly dynamic biomarker that reflects the interaction between training load, recovery, energy availability, sleep, and overall health.
A key takeaway is that acute increases in testosterone do not necessarily translate into higher baseline levels, and in some cases—particularly with sustained high training loads or insufficient recovery—baseline levels may even decline over time. At the same time, a low testosterone value in an athlete does not automatically indicate pathology or require treatment. In most cases, it represents a physiological adaptation rather than primary hypogonadism.
From a clinical perspective, testosterone measurement is primarily useful for evaluating or excluding true hypogonadism. Beyond that, its interpretation becomes increasingly context-dependent. Factors such as timing of the sample, recent training load, nutritional status, and sleep all play a critical role in shaping the result.
Importantly, most of the meaningful ways to support healthy testosterone levels are not found in supplements or isolated interventions, but in the fundamentals: adequate nutrition, sufficient sleep, proper recovery, and balanced training. These are often the least exciting variables—but consistently the most impactful.
Finally, while hormonal markers such as the testosterone-to-cortisol ratio may provide additional insight in controlled or longitudinal settings, they are not diagnostic tools on their own and are rarely used in routine clinical practice.
In the end, the most useful way to approach testosterone in athletes is not as a single value to optimize, but as part of a broader physiological picture—one that requires context, clinical judgment, and, above all, restraint in interpretation.
References
[1] https://pmc.ncbi.nlm.nih.gov/articles/PMC12867729/
[2] https://link.springer.com/article/10.2165/11536910-000000000-00000
[3] https://pubmed.ncbi.nlm.nih.gov/19929279/
[4] https://pmc.ncbi.nlm.nih.gov/articles/PMC3146796/
[5] https://pmc.ncbi.nlm.nih.gov/articles/PMC2681273/
[6] https://link.springer.com/article/10.2165/11536910-000000000-00000
[7] https://pmc.ncbi.nlm.nih.gov/articles/PMC6853631/
[8] https://pmc.ncbi.nlm.nih.gov/articles/PMC5897104/
[9] https://pubmed.ncbi.nlm.nih.gov/30063407/
[10] https://pubmed.ncbi.nlm.nih.gov/8584849/
[11] https://pubmed.ncbi.nlm.nih.gov/25144130/
[12] https://pubmed.ncbi.nlm.nih.gov/34801825/
