SHBG in Athletes: What Your Sex Hormone-Binding Globulin Results Actually Mean
Table of Contents
Introduction: SHBG in Athletes
In my clinical work, male athletes are often especially interested in their testosterone results. This is understandable: most athletes know that testosterone is connected to strength, recovery, body composition, libido, and physical performance. At the same time, many serious athletes live highly disciplined lives. They train hard, often eat carefully, and may be studying, working, competing, and managing everyday responsibilities at the same time. These are often the same personality types who can push themselves very far — sometimes far enough to develop symptoms of exhaustion or burnout.
When a male athlete presents with persistent fatigue, stalled strength gains, low libido, poor recovery, or a general sense that something is not right, testosterone is often one of the first blood tests they ask about. But total testosterone alone does not always tell the full story. In some athletes, total testosterone may sit within the laboratory reference range while free testosterone is relatively low because a larger proportion is bound to sex hormone-binding globulin, or SHBG.
This is why I wrote this article. SHBG is not usually the first marker athletes think about, but it can strongly influence how testosterone results should be interpreted. Athletes who train hard, maintain low body fat, restrict energy intake, or use hormonal contraception may be exposed to physiological factors that alter SHBG and androgen bioavailability. Understanding these factors helps explain why a “normal” testosterone result may not always mean the hormonal picture is normal.
At the same time, it is important not to overmedicalise athletic fatigue. Sport itself is not an automatic indication to measure testosterone or SHBG. In practice, these tests are most relevant when there is a clinical reason to assess androgen status — especially when symptoms raise the question of hypogonadism or reduced free androgen availability. When testosterone is tested in this context, SHBG and calcul
For a broader overview of hormone testing in sport, the articles on testosterone in athletes and free testosterone in athletes provide essential context alongside this one.
Why SHBG in Athletes Matters More Than Total Testosterone
Sex hormone-binding globulin (SHBG) is a glycoprotein produced by the liver that binds sex steroids with high affinity and specificity [1]. Its central role in physiology is not passive transport — it is active hormonal gating. Only the free and albumin-bound fractions of sex hormones are considered biologically available; SHBG-bound testosterone is tightly held and generally unavailable for tissue uptake.
The proportions of binding differ importantly between sexes. In men, approximately 44% of testosterone is tightly bound to SHBG, roughly 50% is loosely bound to albumin, and about 2% circulates as free testosterone [1][8]. In women, a larger fraction — approximately 65% — is bound to SHBG, with the remainder split between albumin and the free fraction [1]. Women with low SHBG can have normal total testosterone levels but elevated bioavailable- and free-testosterone levels [1].
These binding ratios have enormous practical consequences for interpreting SHBG in athletes. Total testosterone — the number most standard lab panels report — reflects the sum of all fractions. An athlete with elevated SHBG can carry a total testosterone well within the laboratory reference range and still have free testosterone low enough to impair recovery, training adaptation, and body composition. SHBG and total testosterone must always be interpreted together, and a hormone panel without SHBG leaves the picture incomplete.
The article on free testosterone in athletes explains exactly how binding protein levels translate into bioavailable androgen fractions, and how to calculate the free androgen index from your results.
Primary, Secondary, and Functional Hypogonadism in Athletes
In clinical practice, it is important to distinguish between primary, secondary, and functional hypogonadism. These concepts are often mixed together, especially when testosterone results are interpreted too narrowly through total testosterone alone.
Primary hypogonadism refers to impaired testosterone production at the testicular level. Secondary (central) hypogonadism reflects insufficient hypothalamic–pituitary stimulation of the testes. Functional hypogonadism is different: it describes a potentially reversible state where androgen availability is reduced because of factors such as low energy availability, heavy training load, weight cutting, illness, chronic stress, poor sleep, medication effects, or systemic disease.
This distinction matters especially in athletes. A low total testosterone level does not automatically mean clinically relevant hypogonadism, because free testosterone may still be adequate. Conversely, total testosterone may appear normal, but if SHBG is elevated, free testosterone may be low. In that situation, the total amount of circulating testosterone may look reassuring, while the biologically available androgen signal is reduced.
A typical diagnostic pathway begins with total testosterone. If total testosterone is low or borderline, the test is usually repeated and interpreted alongside SHBG and calculated free testosterone. If low testosterone is confirmed, luteinizing hormone helps localize the problem. Elevated LH with low total and free testosterone suggests primary hypogonadism. Low or inappropriately normal LH with low total and free testosterone suggests secondary, or central, hypogonadism.
In reality, however, primary hypogonadism is relatively uncommon. I do encounter it in clinical practice, but in my experience, low testosterone values are more often related to secondary or functional causes. Excess body weight is a common contributor, but nutritional factors, chronic illness, sleep problems, heavy training load, psychological stress, and exhaustion can also be part of the picture. I have also seen patients with significant burnout-like symptoms who have low or borderline testosterone values, although this does not automatically mean that the testosterone finding is the primary cause of their symptoms.
This is why careful diagnostic work is essential before concluding that a patient has true primary hypogonadism requiring testosterone replacement therapy. When patients come to the clinic already thinking about testosterone substitution, I usually explain that this is not a small or temporary decision. Testosterone replacement is often long-term treatment, and in younger men especially it can suppress the hypothalamic–pituitary–testicular axis and impair fertility. By contrast, many secondary or functional causes of low testosterone are potentially treatable, especially when the main drivers are obesity, untreated systemic disease, poor sleep, under-recovery, or inadequate energy availability.
But elevated SHBG with normal total testosterone and reduced free testosterone does not automatically fit either classical category. In athletes, this pattern may instead point toward a functional reduction in androgen availability, where the hormonal environment is being shaped by training, nutrition, recovery, and metabolic context rather than permanent structural disease of the testes or pituitary axis.
This is the key point of this article: when I discuss SHBG in athletes, I am not mainly talking about classical primary or secondary hypogonadism. I am talking about a functional category that may be reversible if the underlying drivers are corrected. Elevated SHBG alone does not diagnose functional hypogonadism, but it can explain why total testosterone alone may miss the clinically relevant part of the picture.
How Training Affects SHBG in Athletes — A Context-Dependent Response
The relationship between exercise and SHBG in athletes is not simple or unidirectional — and this is where most generic endocrine advice breaks down.
Chronic endurance training tends to increase resting SHBG, and this has been documented in adults over 40 years of age. In a systematic review of exercise training effects in this population, small to large increases were observed for basal sex hormone-binding globulin in both male and female exercising adults, with effect sizes ranging from 0.25 to 1.68 across six studies [2]. Whether the same magnitude of response applies consistently in younger athletes requires further study, and the directional effect of exercise training on SHBG is supported in older adult training studies but may not translate uniformly to younger athletic populations.
A widely cited sports biomarker review notes that SHBG is a useful indicator of training status and performance (strength and rate of force development), and that SHBG transports hormones such as testosterone in the body and increases in response to exercise training in both male and female athletes [3]. Critically, increased SHBG and decreased testosterone may indicate insufficient recovery [3].
It is important to note, however, that SHBG does not always rise with training stress. In a study of a professional male rowing team, SHBG actually decreased from 39.50 ± 2.48 to 34.27 ± 2.33 nmol/L across the competitive season, alongside a parallel decrease in total testosterone and an increase in estradiol [4]. The direction of SHBG change in athletes depends on the interplay of training load, energy availability, and individual hormonal regulation. The pattern of elevated SHBG alongside falling free testosterone described by Lee et al. [3] represents one scenario; declining SHBG with declining testosterone, as seen in the soutajat study, represents another — both may reflect training-related endocrine adaptation or strain, and neither is conclusive without broader clinical context.
This overtraining-related hormonal pattern, and how it can be tracked over a season, is covered in detail in the companion article on cortisol in athletes, which examines the testosterone-to-cortisol ratio as a recovery marker. For a deeper look at morning cortisol and HPA axis function in overtrained athletes, see also the article on the cortisol awakening response in athletes.
At the same time, I think it is important not to overstate the practical usefulness of SHBG as a recovery marker. Although changes in SHBG have been discussed in the sports physiology literature in relation to training status and recovery, in reality SHBG is not a particularly sensitive standalone marker for monitoring recovery in athletes. Interpretation is heavily dependent on context and individual baseline variation.
In practice, meaningful interpretation would require repeated measurements over time and a well-established personal baseline obtained during a stable training state. Even then, SHBG is influenced by many factors outside recovery alone, including energy availability, body composition, thyroid status, illness, medication use, and general metabolic health. A change in SHBG therefore cannot independently diagnose overtraining or inadequate recovery.
This is also important clinically: even if testosterone or SHBG levels shift during a heavy training phase, the diagnosis of overtraining or recovery impairment remains fundamentally clinical. Laboratory markers may support the overall picture, but they cannot replace the athlete’s symptoms, performance changes, training history, recovery capacity, and broader clinical assessment.
Acute exercise drives a different, short-term response to SHBG in athletes. During a single 45-minute session at 70% VO₂max, significant increases were seen in total testosterone (+32.0%) and free testosterone (+39.6%), while SHBG binding affinity did not change significantly [5]. This suggests that the acute free testosterone rise during exercise is driven by increased testosterone production rather than reduced SHBG binding, and should not be confused with resting hormonal status [5].
Interestingly, many strength athletes intuitively notice that they “feel more anabolic” immediately after training. The acute rise in testosterone during and shortly after exercise is probably one small part of that sensation, although the classic post-workout urge to flex in front of the mirror is much more strongly explained by the muscle pump itself, increased blood flow, sympathetic nervous system activation, heightened arousal, and the psychological reward response associated with training. In other words, the feeling is real — but it is not simply a testosterone effect.
The Energy Availability Problem: When SHBG in Athletes Signals a Nutritional Crisis
For athletes in weight-category sports — combat sports, rowing, cycling — or those in body composition phases, the relationship between SHBG and energy availability is clinically essential to understand.
SHBG is a liver-synthesized glycoprotein, and hepatic production is closely regulated by nutritional and metabolic signals [6]. There is an inverse relationship between serum insulin and SHBG, with low levels of SHBG being associated with insulin resistance [6]. In athletes, chronically low energy availability and the associated drop in insulin may drive SHBG upward — a pattern directly demonstrated in male physique athletes during competition preparation [7].
In males undergoing competition dieting, testosterone (p < 0.01) and free testosterone (p < 0.05) decreased, while SHBG (p < 0.001) and cortisol (p < 0.05) increased. Insulin decreased significantly only in males (p < 0.001) [7]. Many of these hormonal changes improved during the post-competition recovery period when energy availability was restored [7], supporting a potentially reversible, energy-availability-related component rather than structural endocrine impairment. Note that this pattern was observed in male physique athletes specifically; hormonal responses to energy restriction can differ between sexes and sporting contexts.
The practical implication for interpreting SHBG in athletes: a male athlete who is lean, training hard, and eating below energy requirements may present with rising SHBG, falling free testosterone, and normal or modestly reduced total testosterone. This pattern is easily missed if only total testosterone is measured.
The practical implication, as I see it clinically, is that SHBG should not be treated as a general marker of burnout, malnutrition, RED-S, low energy availability, or recovery status. It is not a good standalone tool for assessing an athlete’s mental health, nutritional state, or training adaptation.
In clinical practice, the main reason to measure SHBG is much narrower. In Finland, at least in everyday clinical work, SHBG is mainly measured as part of hypogonadism evaluation — in other words, to help interpret testosterone results and estimate whether free androgen availability is adequate. If an athlete happens to have poor nutrition or chronically low energy availability, SHBG may change as part of the broader endocrine adaptation, but this is not usually the primary reason to order the test.
Low energy availability and RED-S are much broader clinical conditions. They can affect thyroid hormones, stress hormone signalling, reproductive hormones, bone health, immune function, mood, performance, and recovery. Testosterone may decrease as part of that wider adaptation, and SHBG may change alongside it, but SHBG does not measure the whole syndrome. The diagnosis remains clinical and must be based on symptoms, training history, nutritional intake, body composition changes, menstrual or reproductive function, performance trends, and the broader medical picture.
I also think it is important to emphasize that this is not unique to athletes. The underlying issue is not sport itself, but the balance between energy intake and energy expenditure. Athletes are simply more exposed to this problem because high training volumes, weight-category demands, body composition goals, and busy schedules can make it difficult to eat enough consistently.
This is why I would describe SHBG in low energy availability as more of a contextual finding than a diagnostic marker. It may be interesting, and it may help explain why total testosterone does not reflect free testosterone accurately, but by itself it does not diagnose under-fuelling, RED-S, burnout, or overtraining. Those diagnoses require a broader clinical assessment.
In other words, SHBG is not an energy availability test. It is a testosterone interpretation marker. Its main clinical value is in the evaluation of suspected hypogonadism or reduced free androgen availability, not in the routine assessment of nutrition, training stress, or low energy availability itself.
For that reason, I would keep the metabolic discussion separate from the clinical role of SHBG. The metabolic dimension of this picture — including how insulin sensitivity and fasting glucose interact with energy availability — is explored in the articles on fasting glucose in athletes and HbA1c in athletes.
Conclusion: SHBG in Athletes
SHBG in athletes is clinically important because it helps explain what total testosterone alone can miss. A normal total testosterone result may look reassuring, but it does not automatically mean that free androgen availability is adequate. If SHBG is elevated, a larger proportion of testosterone may be tightly bound, leaving less available as free or bioavailable testosterone. This is why SHBG can be useful when symptoms such as fatigue, poor recovery, low libido, or unexplained performance decline raise the question of hypogonadism or reduced androgen availability.
At the same time, SHBG should not be overinterpreted. It is not a standalone marker of overtraining, burnout, RED-S, malnutrition, or recovery status. In clinical practice, its main value is much narrower: it helps interpret testosterone results. Low energy availability, heavy training load, weight cutting, poor recovery, thyroid changes, hormonal contraception, and metabolic factors may all influence SHBG, but none of these can be diagnosed from SHBG alone.
For me, the key clinical point is context. SHBG should be read together with total testosterone, calculated free testosterone, symptoms, training history, nutrition, body composition changes, recovery, medications, and the wider hormonal picture. In some athletes, an abnormal SHBG pattern may point toward a potentially reversible functional reduction in androgen availability. In others, it may simply be a contextual finding without major clinical significance.
Ultimately, SHBG in athletes is best understood as a testosterone interpretation marker. It can make the hormonal picture clearer, but it does not replace clinical judgment. The goal is not to chase a single laboratory value, but to understand whether the athlete’s symptoms, training load, recovery, nutrition, and androgen profile fit together in a clinically meaningful way.
For the complete picture, pair the SHBG in athletes data with the dedicated articles on testosterone in athletes, free testosterone in athletes, cortisol in athletes, free T3 in athletes, and free T4 in athletes to build a complete hormonal profile that supports — rather than misleads — clinical decision-making in sport.
References
[1] https://pmc.ncbi.nlm.nih.gov/articles/PMC7663738/
[2] https://pmc.ncbi.nlm.nih.gov/articles/PMC9124654/
[3] https://pmc.ncbi.nlm.nih.gov/articles/PMC5640004/
[4] https://pmc.ncbi.nlm.nih.gov/articles/PMC10136069/
[5] https://pubmed.ncbi.nlm.nih.gov/9506793/
[6] https://pmc.ncbi.nlm.nih.gov/articles/PMC11471403/
