The thyroid is an endocrine gland, located in the anterior base of the neck, responsible for numerous systemic metabolic processes. Its implications are far-reaching, including energy expenditure, cardiac function, muscle physiology, protein synthesis, and bone and other body substrate turnover. Disturbances in its normal function can lead to a range of symptoms with excess (hyperthyroidism) and diminished (hypothyroidism) hormone levels. For athletes, these symptoms can negatively impact the ability to effectively train, compete, and/or recover. Manifestations may present as decreases in performance. Once the level of concern for such decreases becomes apparent, it is important for providers to remain suspicious of possible hormonal or endocrine causes so as to reveal any potentially reversible conditions (1). The signs may not be as overt as in other populations, thus the physician must exercise his or her clinical judgment in pursuing a laboratory work-up. In this review, we aim to discuss the current guidelines for diagnosis and management of thyroid disease, studies and case reports concerning thyroid disorders in athletes, and potential return to play strategies.
Thyroid hormone production and secretion is part of a neuroendocrine cascade involving the hypothalamus and anterior pituitary gland. The hypothalamus releases thyrotropin-releasing hormone (TRH), which triggers the thyrotropic cells of the anterior pituitary gland to secrete thyroid-stimulating hormone (TSH), also called thyrotropin. The TSH binds to the epithelial membrane of the follicular cells of the thyroid gland, stimulating the production and secretion of T3 and T4. This cascade is regulated by a negative feedback loop. When circulating levels of thyroid hormone are high, the hypothalamus decreases its production of TRH, which in turn decreases the pituitary production of TSH, and thus inhibits glandular production of T3 and T4. When circulating levels are low, the opposite effect takes place in which the hypothalamus signals the pituitary to further stimulate thyroid hormone production. The follicular cells of the thyroid normally secrete roughly 20% of the body’s T3, as well as all of the endogenous T4, which is converted to the more metabolically active T3 in peripheral tissues throughout the body via a series of deiodinase enzymes (2). Additionally, there are parafollicular cells (or C cells) that secrete calcitonin, which is responsible for helping to maintain calcium homeostasis.
Abnormal thyroid function can manifest as oversecreting (hyperthyroidism) or undersecreting (hypothyroidism). While these can be their own distinct entities, they also can represent various points along a spectrum. In the setting of thyroiditis, there is a period of increased activity, followed by a period of decreased activity, with most returning to a euthyroid state. In the setting of Graves disease, there is a period of hyperthyroidism that transitions to hypothyroidism over time as the gland burns out. Hypothyroidism causes decreased caloric utilization while hyperthyroidism causes increased metabolism. Both entities have widespread, systemic effects, and may or may not be associated with an enlarged gland. Dysfunction of the thyroid gland can impact the ability to exercise, in terms of duration and intensity.
A small study of eight elite male weight lifters looked at the effects of 1 wk of very intense strength training on pituitary-thyroid function, measuring maximal isometric leg extension, TSH, T4, and T3 levels. They learned that while there was no significant change in the maximal isometric leg extension force, there was a decrease in the serum concentrations of TSH, T4, and T3. This suggests that the stress of intense training affects thyroid function by acting at the hypophyseal and/or hypothalamic level (3). Another study performed by the same authors looked at 11 elite male weight lifters over the course of 1 yr, after their training levels and relating those to serum levels of TSH, free and total T4, T3, and TBG. They found that in periods of decreased volume of training, there were increases in free and total T4 and T3. In periods of increased intensity and volume, those changes returned to their initial levels. Over the course of the year, there was no net change in TSH, free and total T4, T3, or TBG. It was concluded that in elite strength athletes, intensive training leads to changes in pituitary-thyroid function, but these changes are minor and physiologic with the potential for adaptation (4). Intense, interval exercise (IE), when compared with steady-state endurance exercise (SSE), results in suppressed T4 to T3 conversion, meaning a longer time to recover is needed after IE as compared with SSE. This finding may help guide implementation of training regimens so as to ensure adequate recovery and prevent overtraining (5).
One of the known effects of overtraining in female athletes is secondary amenorrhea. This can lead to, among other things, thyroid dysfunction (1). One study looked at the effects of chronic high volume athletic training on hypothalamic-pituitary-thyroidal function in female athletes who were both eumenorrheic and amenorrheic. Both groups had significantly decreased total T4 levels, while the amenorrheic group also had significantly reduced levels of free T4, free and total T3, and reverse T3. While both had comparable TSH levels, the amenorrheic group had a blunted response as compared with the eumenorrheic group. The results of this study demonstrated two clinically relevant points: 1) regular menstrual cycles in female athletes who engage in high-volume athletic training is accompanied by decreased levels of total T4; 2) impairments of the hypothalamic-pituitary-thyroidal axis occur selectively in female athletes who engage in high-volume athletic training who also have disturbances in their hypothalamic-pituitary-ovarian axis, which manifests as amenorrhea (6).
Hypothyroidism is estimated to affect 1 in 300 Americans (7). The disorder results from reduced effects of thyroid hormone on bodily tissues. This is most commonly due to primary gland failure, but also may be secondary to insufficient thyroid gland stimulation by the hypothalamus or pituitary gland (8). In either case, there is an insufficient amount of hormone to meet the metabolic demands. Primary gland failure is due to congenital abnormalities, iodine deficiency, infiltrative processes (such as amyloidosis or lymphoma), and autoimmune destruction (Hashimoto thyroiditis), which is the most common etiology in the United States (8). There also are iatrogenic causes, such as thyroidectomy, radioactive I-131 ablation therapy and head and neck radiation for other pathology (9). Medications implicated in causing hypothyroidism include amiodarone, lithium, and interferon-alpha (10). In children, the most common cause worldwide is iodine deficiency, a problem not commonly encountered in developed countries, but a cause to consider in the care of athletes who are originally from areas where iodine supplementation is not readily available.
The clinical presentation can vary, with patients complaining of nonspecific symptoms of weight gain, fatigue, diffuse myalgias, and feeling depressed (10). Other common presenting symptoms that are more sensitive for hypothyroidism include cold intolerance, constipation, dry skin, hair loss, and proximal muscle weakness (10). Female athletes with hypothyroidism may present with menstrual irregularities which can lead to, or be a component of, the female athlete triad. This includes disordered eating, amenorrhea, and decreased bone mineral density (BMD) driven by chronically poor energy status (10–12).
Laboratory testing should begin with TSH. If this demonstrates an elevated level (greater than 5.5 mIU/L), then the test is to be repeated along with free T4 below normal range (13).
With regard to treatment, most patients will require lifelong thyroid hormone therapy, usually with synthetic thyroxine, like endogenous thyroxine, it will be metabolized to the more active T3 by deiodinase enzymes throughout the body (10).
Effects on the Athlete
Hypothyroidism can have negative effects on cardiac, neuromuscular, and musculoskeletal function if left untreated. From a cardiovascular standpoint, hypothyroidism can present with bradycardia, demonstrate flat T waves and low voltage on electrocardiography, progress to pleural or pericardial effusions, or hemodynamic instability. Bradycardia also can be seen in well-conditioned athletes as a physiologic response to exercise, resulting in increased vagal tone. The bradycardia seen in hypothyroidism can, in theory, be distinguished by an accompanying clinical history of decreased exercise tolerance or athletic performance (2,10). Low levels of active thyroid hormone can lead to decreased myocardial contractility, diastolic dysfunction, and a premature stiffening of blood vessels (2).
In bone, hypothyroidism can lead to increased fracture risk due to poor bone turnover and decreased competence. There is decreased turnover in trabecular and cortical bone. Once treated, there is enhanced remodeling to renew accumulated old bone, increase turnover and improved BMD. However, bone biomechanical competence may still be abnormal due to persistent, underlying changes in bone architecture (14). It is thought that compounding stress on accumulated old bone elevates the fracture risk in patients who have primary hypothyroidism, especially those who are postmenopausal (14,15). On plain radiographs, manifestations of hypothyroidism can be seen as delayed skeletal maturation (in neonates and children) as well as a disorganized ossification pattern, arising from multiple centers, that presents as irregular or striped epiphyses, commonly at the femoral and humeral heads. These radiographic changes will quickly normalize with initiation of replacement therapy (16).
Muscle weakness, especially proximally, also is seen in hypothyroidism and can present with pseudohypertrophy and increased creatine kinase levels (10,17). Hypothyroidism causes decreased protein turnover and impaired carbohydrate metabolism. This leads to slowed muscle contraction and relaxation, which causes a change in muscle fibers from fast-twitch (Type II) to slow-twitch (Type I) (18). There also have been case reports to suggest an association between hypothyroidism and rhabdomyolysis, as well as elevated levels of CK and myoglobin in up to 90% of asymptomatic patients (17,19). Other additional neuromuscular and musculoskeletal manifestations include slowed deep tendon reflexes, chondrocalcinosis and pseudogout flares in calcium pyrophosphate deposition disease, and carpal tunnel syndrome (19).
Subclinical Hypothyroid Disease
Subclinical hypothyroidism is a serologic diagnosis. Biochemically, a patient will demonstrate greater than normal TSH (4.500-10 mIU/L), with normal range free T4. It is believed that symptoms are representative of a relative lack of T4, with an overall total body decrease, which still lies within the laboratory normal range (2). There is an approximately 5% risk of progression to overt hypothyroidism, particularly in patients with an initial TSH level greater than 10 to 15 mIU/L, or elevated thyroid peroxidase antibody titers (2,10). The American Association of Clinical Endocrinologists (AACE) and the American Thyroid Association (ATA) recommend that treatment be considered in these patients (13). A 2017 review examined the relationship between iron deficiency and impairments in thyroid function; particularly how iron deficiency can progress subclinical hypothyroidism to clinical, or overt, hypothyroidism (20). Iron deficiency and hypothyroidism are frequent comorbidities and the association is such that those with iron deficiency have a twofold to fivefold increase in likelihood of hypothyroidism (21–23). This is thought to be due to iron being used as a cofactor in T4 synthesis by thyroid peroxidase and the suppression of hepatic T4 deiodinase activity (24,25). While there are no guidelines as such, Petkus et al. (20) recommend screening for iron deficiency and monitoring serum ferritin in female athletes, even without signs of overt anemia because of the possible implications of iron deficiency. Decreased athletic performance and exercise capacity can sometimes be seen, indicating a progression to overt hypothyroidism. There also are associations with hypercoagulability, impaired vascular function, atherosclerotic cardiovascular disease, and reduced submaximal exercise capacity (2). The treatment of choice is the same as overt hypothyroidism, daily levothyroxine monotherapy. A retrospective cohort study found that levothyroxine use in patients with subclinical hypothyroidism was associated with a decreased risk of ischemic heart disease and overall mortality, but no trials have been identified that show levothyroxine therapy can prevent future cardiac events (26).
Hyperthyroidism and Thyrotoxicosis
Thyrotoxicosis is a clinical state resulting from inappropriately high thyroid hormone action in tissues (27). Hyperthyroidism is a form of thyrotoxicosis due to inappropriately high production and secretion of thyroid hormones from the thyroid. The overall prevalence of hyperthyroidism is estimated to be 1.2% in the United States, with a 0.5% prevalence of overt hyperthyroidism (28). The most common etiologies of hyperthyroidism are a toxic multinodular goiter, in which the thyroid gland has multiple hyperfunctioning nodules; Graves disease, an autoimmune condition, in which preformed antibodies to TSH receptors lead to continuous stimulation and subsequent secretion; and a hyperfunctioning thyroid adenoma (16,28).
Thyrotoxicosis presents with a wide range of symptom types and severities. Patients can be entirely asymptomatic, have aspects of hypermetabolism (such as weight loss despite having increased appetite), increased adrenergic symptoms (palpitations, diaphoresis, heat intolerance, tremor, lid lag, hyperdefecation) and proximal muscle weakness. Additionally, initial presentation can be as seemingly innocuous as mild symptoms or can manifest as severely as a thyroid storm, involving tachycardia, dysrhythmias and/or hyperpyrexia, which requires immediate treatment (28).
Serologic testing will demonstrate decreased TSH less than the lower limit of normal (0.4 mIU/L), with elevation of T4 levels (27). Diagnosis is not quite as simple as hypothyroidism, because laboratory findings such as these would then need to be followed up with radioactive uptake and a scan of the thyroid (28). Low uptake would indicate thyroiditis, ectopic hormone, or exogenous hormone. High uptake would be indicative of Graves disease, toxic multinodular goiter, or toxic adenoma (28).
In 2016, AACE and ATA published updated treatment guidelines for the management of hyperthyroidism and other forms of thyrotoxicosis. The treatment of hyperthyroidism consists mainly of symptom control. This is often achieved with beta-adrenergic blockade (27). Additionally, there are options for treatment including antithyroid medications (methimazole, propylthiouracil), radioactive thyroid ablation, and thyroidectomy (28).
Effects on the Athlete
Among athletes, hyperthyroidism may be associated with medical complications unique to this population. Athletes with hyperthyroidism experience increased basal metabolic rate caused by elevated levels of thyroid hormone. As a result, these athletes are more vulnerable to heat-related illness due to increased oxygen consumption and heat production (2). While rare, this same process may lead to rhabdomyolysis resulting from depleted muscle energy stores (29). Another concern is change in heart rate, including arrhythmias, such as atrial fibrillation and atrial flutter (30). Many well-conditioned athletes have resting bradycardia, a normal physiologic phenomenon. However, this condition may be concerning in cases where bradycardia masks one of the common signs of hyperthyroidism, resting tachycardia. Among this group, patients may not present as tachycardic despite increased adrenergic stimulation from excess thyroid hormone. While beta-blockers are commonly used to treat the symptoms of hyperthyroidism, they are not recommended in athletes. Beta-blockers decrease exercise endurance, likely occurring due to decreased heart rate, cardiac output, and mean arterial and central venous pressures (2). It also should be noted that beta-blockers are on the NCAA Banned Drug List for Rifle and beta-blockers also are prohibited in certain sports by the World Anti-Doping Agency (31,32).
From a musculoskeletal standpoint, hyperthyroidism can have negative consequences, especially for athletes. There are reports of proximal muscle weakness in up to 67% of patients, with an overall loss of muscle mass as muscle fibers atrophy and adipose tissue infiltrates (16,19). With regard to soft tissue structures, there is an increased prevalence of adhesive capsulitis in patients with hyperthyroidism (33).
Hyperthyroidism also has negative effects on bony architecture and physiology. Thyroid hormone increases bone turnover via increases in osteoclast-mediated bone resorption by increasing resorptive time, decreasing mineralization time, and decreasing the amount of both cortical and trabecular bone, with the effects more pronounced in trabecular bone. Clinically, this leads to decreased BMD (16,19). Radiographically, this appears as increased lucency in the vertebral bodies on plain radiographs and CT scans, with a lattice like appearance of the long bones. It also is possible to see acropachy on radiographs, which is pathognomonic of hyperthyroidism. It is a lacy, periosteal new bone formation in the diaphysis of short trabecular bones of the hands and feet, distributed asymmetrically and favoring the upper over the lower extremities. Clinically, this results in clubbing, swelling of the digits, and joint pain, and is seen in the treated and healing phase of hyperthyroidism, almost always in conjunction with thyroid ophthalmopathy (16,19). This distorted architecture and altered physiology contributes to low BMD, which places patients at a higher risk for insufficiency fractures (14,19). In athletes, this can lead to an increased risk of stress fractures, particularly in those athletes who over train, have poor biomechanics, or who have an ongoing endocrine, hormonal, or metabolic disorder, such as the female athlete triad (11). This risk can change throughout the season for the athlete (34). Treatment of hyperthyroidism may reverse these negative effects. One study showed that hyperthyroid patients who achieved a euthyroid state had increased lumbar spine BMD after 5 yr (19). Another study demonstrated that patients with hyperthyroidism were at an increased risk of femur fractures, which comes into play for athletes in contact or collision sports (14). The same study also demonstrated that controlling the hyperthyroid state might reduce fracture risk, with surgical treatment resulting in prompt control, as compared to radioactive iodine therapy, which takes longer and is associated with an increased risk of fractures (14).
Subclinical Hyperthyroid Disease
Subclinical hyperthyroidism is defined by a lower than normal TSH level (usually under 0.4 mIU/L) and normal range T4 and T3 levels. In the United States, the prevalence is estimated to be 0.7% of the population, and more common in females than in males (28). It may be due to several endogenous or exogenous causes. Patients with TSH between 0.1 and 0.4 mIU/L are unlikely to develop overt hyperthyroidism. There also is a relatively low (1% to 2%) probability that patients with TSH level less than 0.1 mIU/L will develop overt disease (28). Subclinical hyperthyroidism can have deleterious effects on the musculoskeletal and cardiac systems. From a bone standpoint, there may be an accelerated development of osteoporosis, increased vulnerability to trauma, and an increased incidence of stress fractures in athletes (2). From a cardiac standpoint, subclinical hyperthyroidism may present with resting tachycardia, increased potential for arrhythmias, ventricular hypertrophy, reduced exertional systolic function and decreased exercise tolerance (35). In 2009, a study looked at cardiovascular pre-participation screening in untrained female athletes with known subclinical hyperthyroidism and multi-nodular goiter being treated with levothyroxine. The treatment group had higher resting heart rates, thicker left ventricular posterior walls, higher mean heart rate during the 24-h Holter ECG, and a lower achieved maximum workload as compared to the untreated group and a healthy control group. However, there were no differences in the prevalence of cardiac arrhythmias. The authors concluded that while there were some anatomic and physiologic alterations in those athletes with subclinical hyperthyroidism on levothyroxine, these were likely not of clinical significance, and did not contraindicate sport participation (36).
Thyroiditis is a general term describing acute or chronic inflammation of the gland. Its presentation is variable, but patients can experience a range of symptoms, from hyperthyroidism to hypothyroidism, and sometimes return to a euthyroid state (37). When evaluating an athlete with suspected thyroiditis, it is important to check their serologies, interpret laboratory results within the context of the overall medical status, correlate those values with symptoms, and differentiate between possible causes. Identifying the underlying etiology is critical as it guides decision-making with regard to potential treatment options. Providers need to be wary of patients who present with an enlarged, painful thyroid gland, and especially in those with signs or symptoms of thyrotoxicosis. These include fever, tachycardia, tremor, and increased warmth of the skin (37,38). Hashimoto’s thyroiditis is the most common cause of hypothyroidism, especially in the United States (10,37). Treatment in this case involves replacement therapy with levothyroxine as the gland is destroyed via an autoimmune mediated process. Other etiologies include infectious (suppurative thyroiditis), postviral (subacute thyroiditis), postpartum, and after exposure to, or treatment with, radiation. In these cases, treatment involves intravenous antibiotics (for suppurative thyroiditis), acetylsalicylic acid, nonsteroidal anti-inflammatory drugs (NSAID), and possibly corticosteroids (37).
Special Considerations in the Athlete
Due to its capacity for increasing metabolism, exogenous thyroid hormone has some appeal to athletes. The ability to increase caloric expenditure is useful for athletes in sports where controlling weight becomes important. Factitious hyperthyroidism should be considered in athletes who have signs and symptoms of excess thyroid hormone, but may not have the history or physical exam findings to corroborate a true thyroid disorder. This can be confirmed with a low 24-h thyroid radioiodine uptake scan, and a low serum thyroglobulin concentration (2). While excess exogenous thyroid hormone can produce a range of symptoms and signs, it also can precipitate thyrotoxicosis, with increased tissue oxygen consumption and heat production, tachycardia, arrhythmia, and possibly even myocardial infarction (2). Despite its potentially life-threatening consequences when used surreptitiously, the World Anti-Doping Agency (WADA) does not list levothyroxine as a banned substance (32). However, authorities at the United States Anti-Doping Agency (USADA) and United Kingdom Anti-Doping (UKAD) have recently lobbied WADA to include levothyroxine on the banned list. The USADA feels that the medication is being used for performance enhancing effects while UKAD argues that liberal prescribing is detrimental to the health of athletes who do not actually have a medical need for it (39). Additionally, in collegiate athletes, the National Collegiate Athletic Association (NCAA) does not consider levothyroxine a banned substance (31).
Anabolic steroids are another group of agents that may be utilized by athletes to improve performance, as well as aesthetics. It is believed that their primary effect on circulating thyroid hormone levels is due to inhibition of thyroid-binding globulin (TBG) (2,40). In a study of power athletes who underwent a 12-wk strength training period while taking high doses of androgenic-anabolic steroids, there were significant decreases in their serum concentrations of TSH, T4, T3, free T4 and TBG, and a significant increase in their T3 uptake (40). Another study looked at the effects of recombinant growth hormone (GH) on body composition, strength and various hormonal parameters. While there were no significant differences in strength or body composition in those athletes taking GH and those who were not, there was a significantly decreased level of serum thyroxine in the GH group (41).
Determining when an athlete can return to play can be difficult because there is no consensus return to play guideline at this time of which the authors are aware. As providers, we need to manage symptoms, look for root causes, and monitor for overt signs of hyperthyroid and hypothyroid states, as well as thyroiditis. Serial monitoring of laboratory markers left to the discretion of the treating physician should be followed if replacement or suppression is initiated. In 2009, Duhig and McKeag (30) advocated for a graded incremental increase in intensity and frequency of athletic activity after a hyperthyroid state. In 2013, Eken and Smoot published a case of a 20-yr-old collegiate football athlete who had subacute thyroiditis. They recommended a graded return to play with periodic heart rate monitoring, consideration for cardiac stress evaluation in athletes returning to high-level competition, and surveillance of thyroid hormone levels (38). While not every athlete will have potentially life-threatening manifestations of thyroid disease, it is important to monitor for recurrent or persistent symptoms in athletes with a known history of thyroid disease, or in those athletes in whom a thyroid disorder might be suspected. It is the opinion of the authors that athletes displaying abnormalities of thyroid function may benefit from endocrinology evaluation for more extensive testing and/or definitive treatment in the setting of persistent or recalcitrant signs and symptoms.
Thyroid gland disorders are among some of the most common endocrine conditions evaluated and treated by clinicians (27). Abnormalities of normal thyroid function can have deleterious effects on athletes, from a training, competition, and recovery standpoint. These abnormalities can be varied in their presentation, and should be considered in the context of other external factors, such as age, activity level, medical history, and other concurrent medical conditions. As a sports medicine provider, it is not uncommon to care for athletes of all ages and skill levels. Therefore, it is imperative that clinicians remain vigilant in considering underlying endocrine disorders, especially those of the thyroid, in patients who present with related complaints. Physicians should use judgment in ordering laboratory studies, because these may not necessarily correlate with patient symptomatology. However, serum markers may be used to follow response to treatment and to monitor control of the underlying etiology as part of a comprehensive process guiding return to play decisions. It also is important to recognize scenarios in which more specialized evaluation and management is indicated, leading to endocrinology consultation.
The authors declare no conflict of interest and do not have any financial disclosures.
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