Free Testosterone in Athletes: Why the Bound Fraction Doesn’t Tell the Whole Story
Table of Contents
Introduction
In clinical practice, testosterone assessment usually starts with total testosterone, which remains the central screening marker in most standard evaluations. However, when testosterone is low, borderline, or does not match the patient’s symptoms, it is common to look beyond the total value and assess related markers such as SHBG and free or calculated free testosterone. This helps clarify whether the apparent testosterone level reflects the amount of androgen that is actually available to tissues.
Total testosterone captures everything circulating in your bloodstream — the vast majority of which is locked away, bound tightly to sex hormone-binding globulin (SHBG) or loosely to albumin. Only the small unbound fraction — free testosterone — is considered the biologically available form under the free hormone hypothesis. This fraction can activate androgen receptors at the tissue level and is thought to better reflect androgenic exposure than total testosterone alone in situations where SHBG is altered.
In my everyday clinical work, testosterone testing is usually part of a broader laboratory assessment, or something I consider when a male patient presents with symptoms such as fatigue, erectile dysfunction, reduced libido, or other features that raise concern about androgen deficiency. In real life, I rarely see testosterone measured simply as a general marker of athletic performance.
That is why I think context matters so much. Markers such as the testosterone:cortisol ratio are often discussed in relation to overreaching or overtraining, and they can be interesting from a sports physiology perspective. But in routine clinical practice, they are not always very practical. A single ratio does not tell me whether an athlete is training well, recovering poorly, or developing overtraining syndrome.
When I assess an athlete with low or borderline testosterone, I am usually more interested in the whole clinical picture: symptoms, training history, sleep, energy availability, recent illness, medications, SHBG, and whether the finding is persistent on repeat testing. The laboratory result matters, but it is only one part of the story.
What Free Testosterone in Athletes Actually Means
Testosterone in the bloodstream is not fully available to tissues. The majority is bound to SHBG with high affinity or loosely bound to albumin, with only a small fraction circulating unbound as free testosterone — considered the biologically available form under the free hormone hypothesis.
SHBG is one of the main determinants of how total testosterone relates to free testosterone. If SHBG is elevated, total testosterone may not fully reflect androgen availability, and in that situation calculated or measured free testosterone can add useful clinical context.
One recent measurement study in professional athletes suggests this is relevant in at least some athletic populations. Measuring testosterone in 200 professional athletes (98 male athletes and 102 female athletes) using LC-MS/MS, the authors found that serum TT, FT, and FT/TT levels of professional athletes were significantly higher than the general population [1]. The authors also describe TT and FT as biochemical markers related to anabolism and as potential early screening indicators for overtraining syndrome (OTS), although they should not be treated as stand-alone OTS diagnostic tests [1]. These data suggest that athlete populations may differ from general-population reference distributions, which is worth considering when interpreting results.
In my own clinical practice, total testosterone is usually the starting point, especially if the test is being used as a basic screening or follow-up measurement. However, if there is any reason to suspect a hormonal explanation behind the patient’s symptoms, I usually want to see more than total testosterone alone. In that situation, free or calculated free testosterone and SHBG become important.
The reason is simple: total testosterone can look acceptable, but if the free fraction is low, androgen availability may still be reduced. In practical terms, the patient may have a result that appears “normal” on paper while the biologically available testosterone is lower than expected. That is why I do not like interpreting total testosterone in isolation when the symptoms, training history, or recovery pattern suggest that something hormonal may be going on.
At the same time, it is important to separate this from classical hypogonadism. If total testosterone is clearly normal but free testosterone is low, the explanation is not necessarily primary or secondary hypogonadism. In some cases, SHBG may be elevated for other reasons, which can reduce the free fraction despite an apparently adequate total testosterone level. That distinction matters clinically, because the next step is not simply to label the athlete as hypogonadal, but to understand why the relationship between total and free testosterone has changed.In my own clinical practice, total testosterone is usually the starting point, especially if the test is being used as a basic screening or follow-up measurement. However, if there is any reason to suspect a hormonal explanation behind the patient’s symptoms, I usually want to see more than total testosterone alone. In that situation, free or calculated free testosterone and SHBG become important.
The reason is simple: total testosterone can look acceptable, but if the free fraction is low, androgen availability may still be reduced. In practical terms, the patient may have a result that appears “normal” on paper while the biologically available testosterone is lower than expected. That is why I do not like interpreting total testosterone in isolation when the symptoms, training history, or recovery pattern suggest that something hormonal may be going on.
At the same time, it is important to separate this from classical hypogonadism. If total testosterone is clearly normal but free testosterone is low, the explanation is not necessarily primary or secondary hypogonadism. In some cases, SHBG may be elevated for other reasons, which can reduce the free fraction despite an apparently adequate total testosterone level. That distinction matters clinically, because the next step is not simply to label the athlete as hypogonadal, but to understand why the relationship between total and free testosterone has changed.
How Exercise Acutely Changes Free Testosterone in Athletes
Understanding the acute response to exercise is essential for correct blood draw timing and result interpretation.
In cited endurance-exercise studies, free testosterone rose acutely after exercise. Research examining intensive, prolonged endurance exercise in women running to exhaustion (75.1 ± 7.0 min) found that total (56%), free (36%), and bioavailable testosterone (50%) were increased from pre-exercise values (p < 0.05) [2]. Critically, at 24 h post-exercise, these measures were decreased from pre-exercise values (−21%, −31%, −18%, respectively; p < 0.05) [2]. This biphasic pattern — acute rise, followed by a post-recovery dip below baseline — suggests that recent exhaustive exercise should be considered when interpreting testosterone measurements.
A similar immediate post-exercise rise has been documented in trained men. Research examining moderately prolonged endurance exercise (45 min at 70% VO₂max) in ten trained men found significant (p<0.01) increases in total testosterone (+32.0%) and free testosterone (+39.6%) immediately post-exercise [3]. The same study found that norepinephrine was the only variable significantly associated with the changes observed in free testosterone (r = +0.92, p < 0.05), and that the free testosterone rise was not explained by altered SHBG binding affinity — findings that suggest sympathetic stimulation may be involved, though the mechanism was not fully established [3].
A 2026 systematic review of randomized controlled trials concluded that testosterone levels demonstrate a greater increase following resistance training, with a delayed return to baseline levels; in contrast, testosterone levels typically recover within 1 h after aerobic exercise [4]. The same review concluded that moderate-to-high intensity exercise may transiently stimulate testosterone via the HPG axis, whereas prolonged high-intensity exercise may be followed by suppressed testosterone during recovery, possibly involving cortisol-related mechanisms [4].
In practice, however, this acute testosterone response is rarely the most clinically relevant issue. Testosterone is not usually measured immediately after a training session. In routine clinical work, I try to keep the testing conditions as standardized as possible: the sample is usually taken in the morning, ideally early in the day, and interpreted with attention to recent exercise, sleep, illness, and other factors that could distort the result.
For that reason, the acute post-exercise testosterone rise is mostly a physiological curiosity rather than the main clinical question. It matters because it explains why timing and context can influence the result, but it is not usually the pattern I am trying to assess when ordering testosterone tests. Clinically, the more important question is whether resting testosterone — especially free or calculated free testosterone in the right context — is persistently low, and why.
Chronic Training Load and Low Resting Testosterone in Endurance Athletes
The acute rise seen during exercise is not the clinical concern for most athletes. The concern is the chronic suppression of resting testosterone that develops over months and years of high-volume training.
Research studies on men show the existence of a select group who, through their exposure to chronic endurance exercise training, have developed alterations in their reproductive hormonal profile — principally, low resting testosterone levels. The prevalence of the problems seems low (~15 to 25% of men doing chronic endurance training) [5]. These athletes display clinically “normal” levels of testosterone, but the levels are at the very low end of normal, and in some cases reach a sub-clinical status [5].
The relationship between training years and resting testosterone is telling. Research on male endurance runners found that the longer an endurance runner is engaged in consistent and chronic endurance training, the lower their resting testosterone becomes (p < 0.01), with the level of reductions observed plateauing at approximately −30% (after 5 years training) [6]. This association is clinically relevant and is consistent with the hypothesis that long-term endurance training may alter hypothalamic-pituitary-testicular regulation, though the mechanism remains postulated rather than fully established.
Reduced testosterone in this condition may have implications for androgen-dependent processes including reproductive function; available evidence on the clinical consequences remains limited [5]. This is one reason why serial monitoring may be more informative than a single snapshot in athletes with multi-year high training volumes.
It is also important to remember that low free testosterone is not always caused by training itself. For that reason, the differential assessment starts with a careful history. Before interpreting the result as a training-related hormonal change, I want to understand the athlete’s broader context: eating patterns, recent dieting or weight loss, energy availability, medication use, underlying medical conditions, sleep, recovery, and recent illness.
This matters because the same laboratory pattern can have different explanations. In one athlete, low free testosterone may fit with a broader picture of high training load and insufficient recovery. In another, it may point more toward low energy availability, medication effects, an endocrine issue, or another medical condition unrelated to sport.
RED-S and Free Testosterone in Athletes: Why Energy Availability Matters
Chronic low testosterone in athletes cannot always be attributed to training volume alone. Energy availability is frequently the missing variable — and it suppresses testosterone through a distinct, well-characterized pathway.
Relative energy deficiency in sport (RED-S) results from low-energy diets (intentional or unintentional) and/or excessive exercise. Energy deficiency reduces hypothalamic pulsatile release of gonadotropin-releasing hormone, this impairing anterior pituitary release of gonadotropins. In men, it reduces testosterone and negatively affects bone health [10].
The quantitative impact of low energy availability (LEA) on testosterone in male endurance athletes is striking. A review of studies on male endurance athletes reported that runners who covered 81±14 km per week showed lower levels of total testosterone (9.2±2.3 vs 16.2±3.4 nmol/L) as well as lower energy availability (27.2±12.7 vs 45.4±18.2 kcal/kg/FFM/day) compared to their inactive counterparts [8]. This association is consistent with the concept that low energy availability can suppress reproductive hormone function as part of an energy-conservation response.
Male athletes developing this suppression — the Exercise Hypogonadal Male Condition (EHMC) — may be harder to recognize clinically because there is no menstrual marker analogous to menstrual disruption in female athletes. In male athletes at risk of RED-S, testosterone testing may provide one objective piece of information, but it should be interpreted alongside dietary, training, clinical, and bone-health data. Energy availability can also be relevant when interpreting other athlete blood markers; for a separate discussion of iron markers, see the guide to serum iron vs ferritin in athletes.
RED-S is also important because it does not affect testosterone in isolation. Low energy availability can disturb the broader hormonal environment, including reproductive, thyroid, stress, and metabolic signalling. In that sense, testosterone is only one part of a wider endocrine response.
I often explain this to patients in practical terms: when the body is under-fuelled, reproduction is not an immediate physiological priority. From an evolutionary perspective, it makes sense that prolonged energy deficiency would suppress reproductive signalling and shift the body toward conservation rather than growth, recovery, and reproductive function. This can be a helpful way to understand why libido may decrease during periods of heavy stress, under-fuelling, or poor recovery.
The same clinical pattern is not unique to sport. In my clinical work, I also see reduced libido or a sense of hormonal “shutdown” in people who are under prolonged strain for reasons that have little to do with training. Long-term psychological stress, depression, burnout, chronic illness, poor sleep, and general under-recovery can all create a similar clinical picture.
That is why I try not to interpret low testosterone or low libido in an athlete only through the lens of training. Training load is important, but it is rarely the whole story. I want to understand the person behind the result: their energy availability, mood, sleep, stress level, recovery, recent illnesses, medications, and overall endocrine health. In many cases, the testosterone result is not the final answer — it is one clue in a broader clinical picture.
Free Testosterone in Athletes and the Anabolic/Catabolic Balance
Free testosterone in athletes does not work in isolation. Its clinical significance is often best understood in the context of its ratio to cortisol — the primary catabolic stress hormone.
The testosterone/cortisol ratio is used as an indication of the anabolic/catabolic balance. This ratio decreases in relation to the intensity and duration of physical exercise, as well as during periods of intense training or repetitive competition, and can be reversed by regenerative measures [9]. Using the free testosterone:cortisol ratio (FTCR) specifically, older athlete-monitoring literature has proposed a FTCR lower than 0.35 × 10⁻³ (calculated using free testosterone in nmol/L and cortisol in mmol/L) or a decline in TCR by ≥30% from a previous value as possible markers of insufficient recovery or impaired performance, although these thresholds are not universally validated [7]. Serial monitoring may be more informative than relying on a single absolute value, especially when changes are compared with the athlete’s own baseline [7].
Some sports-endocrinology literature describes higher or more stable TCR values as consistent with better adaptation to training stress, but this should be interpreted cautiously and in context [7]. Athletes undergoing excessive training loads with insufficient time to recover may experience a reduced TCR, signalling a shift towards a more catabolic state that could impair performance and increase the risk of injury [7]. A low or falling T:C ratio may support concern for high training stress or incomplete recovery, especially when symptoms are present, and should prompt broader clinical and training-load assessment.
Overtraining affects multiple systems simultaneously, and free testosterone in athletes rarely falls in isolation. For broader context on how blood markers shift with high exercise load, the guides on liver enzymes in athletes and hemoglobin levels in runners are worth reading alongside this one.
In practical clinical work, however, the free testosterone:cortisol ratio is still quite far from routine use. At this stage, I see it mostly as a research-based and intellectually interesting concept rather than a truly established clinical tool. It appears in sports endocrinology and overtraining research, but it remains far from everyday clinical decision-making.
In reality, very few patients or athletes have this ratio measured in a structured way. There are several reasons for that. It is not usually included as a standard laboratory panel, it often has to be calculated or ordered separately, and its interpretation is not well standardized.
Another practical limitation is that the ratio is most useful only if there is a reliable baseline for comparison. Without knowing the athlete’s previous values under similar conditions, a single free testosterone:cortisol ratio is difficult to interpret. Most athletes simply do not have repeated, standardized hormone measurements available across a season.
This is why I think the ratio should be treated as a possible monitoring tool, not as a diagnostic test. Even if the result looks abnormal, it does not prove overtraining by itself. Overtraining syndrome remains a clinical diagnosis, based mainly on the athlete’s history, symptoms, performance changes, recovery pattern, sleep, mood, training load, and exclusion of other causes. At the moment, there is no single objective blood marker that can diagnose it reliably.
In that context, the free testosterone:cortisol ratio may provide some additional information, but it remains highly dependent on timing, baseline data, assay method, and clinical interpretation. I would not use it alone to decide whether an athlete is overtrained. I would use it, at most, as one small piece of a much larger clinical picture.
Conclusion: Free Testosterone in Athletes Is a Context Marker, Not a Stand-Alone Answer
Free testosterone in athletes is useful because it helps explain what total testosterone alone may miss, especially when SHBG, energy availability, training load, recovery, or illness change the relationship between total and biologically available testosterone. However, it should never be interpreted as an isolated performance marker or a simple diagnostic shortcut. Acute post-exercise changes are interesting from a physiological perspective, but in clinical practice the more important question is whether resting testosterone is persistently low, whether the free fraction is reduced, and what broader context explains the finding.
In my clinical work, I see testosterone as one clue in a larger picture. Low or borderline values may reflect chronic high training load, under-recovery, RED-S, low energy availability, medication effects, psychological stress, depression, burnout, sleep problems, endocrine disease, or other medical conditions unrelated to sport. The same laboratory pattern can therefore mean very different things in different athletes. That is why careful history-taking, standardized testing conditions, SHBG interpretation, repeat measurements, and clinical judgment matter more than any single number.
Free testosterone can add real value when used correctly, but it does not replace the need to understand the athlete behind the result. For athletes who are training hard, recovering poorly, losing libido, or feeling persistently fatigued, the goal is not simply to “optimize” a hormone value. The goal is to understand whether the body is adapting well, under-fuelled, over-stressed, or signalling that something deeper needs attention. In that sense, free testosterone in athletes is best viewed as a context-sensitive marker of androgen availability and recovery physiology — useful, but only when interpreted as part of the whole clinical picture.
References
[1] https://pmc.ncbi.nlm.nih.gov/articles/PMC11547523/
[2] https://pmc.ncbi.nlm.nih.gov/articles/PMC7695234/
[3] https://pubmed.ncbi.nlm.nih.gov/9506793/
[4] https://pmc.ncbi.nlm.nih.gov/articles/PMC12790781/
[5] https://pmc.ncbi.nlm.nih.gov/articles/PMC5988228/
[6] https://link.springer.com/article/10.1007/s42000-018-0010-z
[7] https://pmc.ncbi.nlm.nih.gov/articles/PMC12604835/
[8] https://pmc.ncbi.nlm.nih.gov/articles/PMC10388605/
