Thyroid Disorders in Sport

Hypothyroidism produces fatigue, cold intolerance, weight gain, constipation, dry skin, low mood and muscle symptoms, including stiffness and a proximal (shoulder and hip girdle) myopathy that can raise the serum creatine kinase (CK). Thyrotoxicosis does the opposite: weight loss despite a good appetite, heat intolerance, palpitations, tremor, anxiety, loose stools and, in Graves disease, eye signs. In an athlete these features are easily attributed to hard training, so a low threshold for testing is sensible when they are persistent or unexplained, and a single symptom alone is not taken as evidence of thyroid disease.

Testing is led by TSH. If the TSH is above the reference range, free T4 is measured in the same sample; if the TSH is below the reference range, free T4 and free triiodothyronine (free T3) are measured. A raised TSH with a low free T4 confirms primary hypothyroidism, while a raised TSH with a normal free T4 is subclinical hypothyroidism. A suppressed TSH with a raised free T4 or free T3 confirms the thyrotoxic state but not its cause, and subclinical hyperthyroidism requires a suppressed TSH with a normal free T4 and free T3, ideally confirmed on a repeat sample. The cause is then clarified: thyroid-stimulating hormone receptor antibodies confirm Graves disease, whereas anti-thyroid peroxidase (anti-TPO) antibodies support autoimmune thyroid disease rather than independently confirming that current symptoms are due to hypothyroidism. Results are interpreted alongside the history, remembering that acute illness, pregnancy, and medicines and supplements, notably high-dose biotin, can produce falsely abnormal thyroid results.

The symptoms of hypothyroidism, fatigue, low mood, poor sleep and sluggish recovery, are almost identical to those of overtraining, so thyroid disease sits within the differential of the underperforming athlete. Equally important is the reverse trap. Low energy availability, the driver of relative energy deficiency in sport (RED-S), can disturb the hypothalamic-pituitary-thyroid axis, and a low free triiodothyronine with a non-elevated TSH may occur with low energy availability. This pattern is not specific, however: other illness, medication and nutritional causes must be excluded, and it is not sufficient on its own to diagnose RED-S.

Getting this distinction right matters, because attributing an abnormal thyroid result to low energy availability without excluding other causes, or conversely starting thyroid hormone for a pattern that actually reflects low energy availability, both lead to the wrong management. The practical approach is to interpret a low free triiodothyronine with a non-elevated TSH cautiously, to take a diet and training history, and to consider energy availability and the wider features of RED-S alongside other explanations. Where the pattern does reflect low energy availability it is addressed by restoring energy availability rather than by prescribing thyroxine, while genuine primary thyroid disease, with the classic TSH and free T4 changes and supportive antibodies, is managed on its own merits.

Hypothyroidism is treated with levothyroxine as first-line therapy, titrated against the TSH to keep it within the reference range, with symptoms often lagging behind dose changes by several weeks. Thyrotoxicosis is treated according to its cause. For hyperthyroidism such as Graves disease or toxic nodular disease, an antithyroid drug such as carbimazole is used, and a beta-blocker such as propranolol is an optional addition for symptom control where clinically appropriate; definitive options include radioiodine or surgery, while transient thyrotoxicosis from thyroiditis often needs only supportive treatment. A key safety point is that anyone taking carbimazole is advised to stop it and seek urgent assessment with a full blood count if they develop a fever or sore throat, because of the risk of agranulocytosis; a full blood count and liver function tests are also checked before starting antithyroid drugs.

Return to sport is individualised rather than tied to a fixed biochemical target. Vigorous exercise is restricted where there is uncontrolled symptomatic thyrotoxicosis, significant tachycardia, arrhythmia or cardiovascular instability, and is progressed as control improves. The anti-doping position is straightforward for thyroid hormone: levothyroxine is currently permitted and is not on the World Anti-Doping Agency (WADA) Prohibited List. Beta-blockers are a separate issue and are prohibited only in specified sports and periods, so if one is used for thyrotoxic symptoms the rules are checked and a therapeutic use exemption (TUE) obtained where required. As always, the exact product and the athlete's sport and competition level are checked before prescribing.

• •Testing is led by TSH: measure free T4 if TSH is high, and free T4 with free triiodothyronine if TSH is low; a suppressed TSH with raised free T4 or free triiodothyronine confirms thyrotoxicosis but not its cause.
• •Thyroid-stimulating hormone receptor antibodies confirm Graves disease; anti-thyroid peroxidase antibodies support autoimmune thyroid disease; high-dose biotin can cause falsely abnormal results.
• •A low free triiodothyronine with a non-elevated TSH may occur with low energy availability, but it is not specific and other illness, medication and nutritional causes must be excluded.
• •Levothyroxine treats hypothyroidism (titrated to TSH); an antithyroid drug such as carbimazole treats hyperthyroidism, with a beta-blocker as optional symptom control.
• •Warn about carbimazole and agranulocytosis: stop it and seek urgent assessment with a full blood count for fever or sore throat; restrict vigorous exercise while thyrotoxicosis is uncontrolled.
• •Levothyroxine is permitted in sport; beta-blockers are a separate issue and are prohibited only in specified sports and periods, needing a therapeutic use exemption where required.