Skip to main content

Medical and physiological complications of exercise for individuals with an eating disorder: A narrative review


Individuals with eating disorders (ED) experience prolonged malnutrition, binge episodes, and compensatory behaviours that affect every organ system. Psychological and physiological symptoms are worsened with comorbid dysfunctional exercise, seen in up to 80% of those with an ED. Although return to exercise is an important component of treatment and recovery, little is known about the contraindications and risks of exercise engagement specific to those with an ED. This paper provides a comprehensive narrative review of the medical and physiological complications of engaging in exercise during ED treatment and outlines when exercise may be contraindicated or used in modified or cautionary ways. We conducted a literature search on MEDLINE, PubMed, and PsychArticles to identify relevant articles, which yielded six categories of medical and physiological complications of ED that may be exacerbated by exercise: energy availability, cardiovascular health, electrolyte abnormalities, biomedical function markers, sex hormones, and body composition. We summarize the evidence for these complications for readers and offer an initial set of recommendations for incorporating exercise during ED treatment based on our findings. This review may serve as a resource for members of ED treatment teams to help evaluate more readily and confidently whether exercise is safe for individual patients and when modifications and caution may be warranted.

Plain English summary

Dysfunctional exercise (DEX) is a symptom of eating disorders (ED) that precedes, maintains and exacerbates ED pathology. Health professionals struggle to clinically address and manage DEX as little information is available about its assessment and safe management. The current review provides a comprehensive summary of the medical and physiological complications of ED that may be exacerbated by exercise and outlines when exercise may be contraindicated or used in a modified or cautionary way. The literature review yielded six categories of complications: energy availability, cardiovascular health, electrolyte abnormalities, biomedical function markers, sex hormones, and body composition. We summarize the evidence for these complications for readers and offer an initial set of recommendations for incorporating exercise during ED treatment based on our findings. This review may serve as a resource for members of ED treatment teams to help evaluate more readily and confidently whether exercise is safe for individual patients and when modifications and caution may be warranted.


Eating disorders (ED) are serious psychiatric illnesses with a lifetime prevalence of 10% [1]. Prolonged malnutrition, binge episodes, and purging in EDs affect every organ system [2]. Beyond physiological complications, individuals with ED exhibit high rates of comorbid disorders, suicidality, and decreased quality of life [3,4,5,6,7]. Although many medical complications resolve with adequate nutrition and treatment, mortality rates in ED populations remain high and relapse is unfortunately common [1, 8]. Those with an ED who also engage in dysfunctional exercise are more likely to experience poor physical and psychological health outcomes [9, 10]. We define dysfunctional exercise as a pathological relationship with exercise resulting in negative physical and/or psychological health impairment; an umbrella term encompassing compulsive exercise, exercise addiction, obligatory exercise, and exercise dependence [11,12,13]. Dysfunctional exercise is present in 22–80% of individuals with an ED [9]. Acutely, these individuals may experience more severe psychological distress, worsened ED psychopathology, and poorer health-related quality of life; and chronically, greater rates of depression, less satisfaction with life, greater risk of relapse, require a longer treatment duration, and exhibit an enduring course of illness [10, 14,15,16,17,18].

Given the potential for dysfunctional exercise to exacerbate ED pathology and undermine recovery efforts, many practitioners recommend abstinence from exercise during ED treatment [19]. However, this practice has been increasingly questioned [20,21,22,23,24], bringing with it a shift toward incorporating physical activity during ED treatment [17, 25, 26]. Similar to the importance of restoring normative eating behaviors and cognitions during treatment, restoring a normative relationship with physical activity may also be vital to recovery, whether through formalized exercise (e.g., strength training, cycling, yoga), incidental activity (e.g. folding laundry, grocery shopping), or a combination of the two [12]. Despite initial concerns about the impact of exercise on weight restoration outcomes, data have not revealed any differences between those who engage in supervised exercise during ED treatment and those who do not [10, 23, 27, 28]. Conversely, supervised and therapeutic exercise including yoga [29, 30], strength training [31,32,33,34,35] endurance activities, [36], outdoor games/sports [37, 38] during ED treatment appears to predict improved physical and mental health outcomes for individuals living with an ED [10, 11, 18, 25, 26, 28, 31, 35, 39]. Benefits of exercise interventions reportedly include improvements in clients’ body composition [31, 32], fitness markers such as VO2max [36], DEX markers [26, 39] quality of life [33, 37], therapeutic alliance [40] and drive for thinness [29] amongst other benefits. Considering exercise compulsion at discharge from treatment predicts a shorter time to relapse and poorer overall outcomes [16], there is a critical need to promote safe, therapeutic, evidence-based, and nutritionally supported exercise during ED treatment, as it accounts for an important part of treatment.

Despite the promising outcomes of safe exercise interventions during ED treatment, EDs are associated with serious medical comorbidities that may contraindicate specific exercise modalities, intensities, or amounts. Thus, prior to initiating an exercise program with an individual with an ED, we must understand the contraindications and risks of exercise engagement specific to this population. This paper provides a comprehensive narrative review of the medical and physiological complications of engaging in exercise and outlines when exercise may be contraindicated.


To identify relevant empirical articles for this review, we conducted a literature search on MEDLINE, PubMed, and PsychArticles using the following keywords as our search terms: “eating disorder* OR anorexi* OR bulimi*” AND “exercise OR physical therapy OR physical activity” AND “cardiorespiratory OR mental OR metabolic OR neurological OR musculoskeletal OR mortality OR adverse events OR injury.” All articles were published articles or dissertations of which the samples included individuals with eating disorders or disordered eating behaviors. We did not define inclusion and exclusion criteria, although we did exclude studies with youth (< 18 years) and athlete only populations, as we considered the unique needs of these groups as beyond the scope of this review. Based on review, we categorized content into different themes.


Physiological complications of exercise with an eating disorder

Table 1 summarizes the medical and physiological complications of exercise with ED. We organized the complications under six categories: Energy Availability, Cardiovascular Health, Electrolyte Abnormalities, Biomedical Function Markers, Sex Hormones, and Body Composition. For each complication included in Table 1, we provide a definition, the values of concern related to it, and the bodily systems (e.g., cardiovascular, endocrine) affected by it with ongoing exercise engagement. Given that an additional purpose of this review was to identify risks and recommendations related to exercise engagement for individuals living with EDs, we excluded complications and conditions related to ED (e.g., hyperlipidaemia, polycystic ovary syndrome, and nonalcoholic fatty liver disease) that appear to be linked to positive benefits of exercise without necessary modifications [41,42,43]. Further, we have not included details on common comorbid diagnoses of ED (e.g., Type 1 and 2 diabetes, chronic pain, and asthma) [43,44,45,46,47] as reviews and clear guidance exist for exercising with these conditions [48,49,50,51]

Table 1 Summary of complications of an eating disorder exacerbated by exercise and their impact on the overarching systems of the body

Energy availability

Energy deficiency

Optimal energy availability (OEA) is defined as adequate energy intake given an individual’s typical metabolic functioning and level of exercise engagement. OEA is commonly estimated as at least 45 kilocalories (kcal) (188 kilojoules; kj) per kilogram (kg) of fat free mass (FFM) per day (45 kcal/kg of FFM/day) [52, 53]. This intake provides adequate energy availability for the human body and its systems to thrive, after subtracting the energy needed and used for regular exercise and recovery. Increased energy demands due to physical activity will likely require more than this standard amount. Low energy availabity (LEA) occurs when: 1) energy intake is insufficient to support vital bodily functions (after removing the energy cost of exercise relative to metabolically active FFM) or 2) exercise engagement increases without an adequate increase in energy to meet heightened energy output needs [54]. Importantly, the numerous and detrimental effects of LEA can occur irrespective of an individual’s body size, shape or weight and does not solely occur in those with ED [55].

Initially, LEA impacts the body’s ability to engage in, and recover from, physical activity by hindering the adequacy of glycogen stores and protein synthesis [56]. If LEA persists, the body is forced to adapt and conserve energy wherever possible by no longer performing non-essential functions such as regular menses, hair growth, mood regulation, or executive thinking, as well as reducing cellular metabolism, weakening the potency of the immune system, and decreasing cardiovascular capacity [57] This conservation process reduces both absolute and relative resting metabolic rates (RMR) to protect the unfavourable breakdown of FFM (metabolically active protein tissue including muscles, bones and organs; [58]. This reduction in RMR can negatively impact both health and performance outcomes [59]. If energy availability falls below optimal levels, metabolically active tissue can breakdown to provide the vital body systems with sufficient energy for survival, leading to even greater decreases in RMR [59]. Even the cardiac muscle may be used to produce this energy, with muscle mass and visceral adipose tissue also beginning to atrophy. Other negative consequences, such as psychological distress [60] can also occur during this LEA state.

Despite the serious consequences of LEA, there is not yet a standardised, reliable and valid assessment protocol for measuring energy availability [59]. Current measurement approaches require specialised equipment and expertise and are burdensome, requiring individuals to keep an excessively accurate food and execise log [59]. Adding to this complexity, exercise output often changes during different levels of activity engagement [59]. Despite these measurement difficulties, LEA contributes to additional conditions described in subsequent sections of the article that may either contradict exercise, worsen performance, and/or endanger health.


Starvation occurs when there is a severe deficiency in caloric intake below the level needed to maintain an organism. Starvation can result in a loss of cardiac mass (particularly ventricular mass) along with glycogen depletion, and BMD causing a premature reduction in physical and physiological capacity [61]. Exercising in a starved state encourages circulatory lactate producing widespread muscular pain [61] and, with dehydration, may trigger muscular cramps due to lack of sodium and potential magnesium. Individuals who are undernourished while engaging in intense exercise programs may trigger loss of FFM (including cardiac mass), provoking a reduction in muscle strength and aerobic performance [lower maximal oxygen uptake (VO2max), decreased work capacity] and EKG changes with exercise testing [61]. Starvation is not necessarily a direct contraindication for exercise engagement; however, for those with an ED, exercise may be contraindicated on days when they have intentionally skipped a meal [62]. Additionally, continuous difficulty in meeting one’s nutritional plan may necessitate modifying exercise, due to the self-reinforcing cycle of restriction and exercise[63]


Purging is a compensatory behaviour (e.g., self-induced vomiting, laxative or diuretic abuse) to “get rid” of food or calories [64]. All methods of purging detrimentally affect health and exercise performance and are associated with serious medical risks. Mehler and Andersen [65] describe three mechanisms through which purging can influence exercise engagement: 1) the generation of a negative caloric balance (through vomiting); 2) the facilitation of dehydration (vomiting and laxative use); and 3) the contribution to hypokalemia (vomiting and laxative use) [66]. Purging (vomiting and laxative use) contributes to critical electrolyte disturbances and water loss, which are both exacerbated by exercise due to the natural loss of electrolytes and water in sweat [65, 67, 68]. Purging may also lead to hypovolemia (decreased blood plasma volume), which can contraindicate exercise [65]. Medical risk and complications differ across modes of purging and compensatory behaviors (e.g., exercise) and starvation. This can be attributed to the concentration of acid and electrolytes in the relevant location and impact of volume loss; for example, vomitus contains a high concentration of acid and potassium [69]. We also observe differences in the mechanisms of action among common laxative classes, resulting in side effects ranging from bicarbonate resorption, expulsion of sodium, or potassium loss [70]. These differences are observed in different rates of electrolyte imbalances across patients with ED, e.g., combined low BMI, laxative use, and vomiting yields the highest likelihood of developing hypokalemia, vomiting related to hypomagnesemia, and fasting or exercise relatively unrelated to potassium levels [71, 72].

Cardiovascular health

LEA contributes to many cardiovascular complications in individuals with an ED including arrhythmias, bradycardia, tachycardia, EKG abnormalities, and orthostatic vitals. Additionally, several cardiac risk markers including mean R and T wave amplitude may be abnormal in those with an ED [73,74,75]. The following section provides an overview of cardiovascular impacts of unmodified exercise for individuals with an ED.


Hypotension is defined as a low blood pressure (< 90/60 mmHg), where blood does not exert necessary pressure on the artery walls [65, 76]. This pressure is required to supply vital organs with adequate oxygen and energy to function; thus, low blood pressure contributes to inadequate oxygen and nutrient availability, compromising vital organ functioning [77]. Low blood pressure in individuals with an ED may occur due to purging or insufficient food/fluid intake, resulting in circulating blood volume depletion [78] or autonomic dysfunction related to disturbances in key hormones and/or other mechanisms regulated by the central nervous system [79]. Even mild cases of dehydration (1–2% of body weight) can cause an individual to become symptomatic [76]. Lastly, hypotension can result from low electrolyte concentration, resulting in low concentration gradient and subsequent loss of circulating blood volume [68]. In the case of hypotension, its recommended for exercise engagement to be modified to mitigate dehydration [78].


Hypertension, also known as high blood pressure (> 140/90 mmHg) is a condition in which the blood vessels experience persistently raised pressure against them [80]. Over time, hypertension can damage arteries, prevent blood and oxygen supply to the brain, heart, and body, result in heart enlargement, prevent kidneys from filtering blood effectively, or arterial function (including the small vessels inside the eyes) [81]. Bulimia nervosa and BED have higher rates of hypertension compared to other EDs [82]. Although exercise can be protective against progression of hypertension and cardiovascular mortality risk, exercise for individuals with hypertension may require modification, medical supervision, or at times may be contrinadicated.

Additionally, rates of idiopathic intracranical hypertension in BED are also elevated [83], which can lead to intracranial pressure and increased risk of stroke. When these individuals engage in exercise it may lead to headaches [84]. Despite this, contraindications to any type of exercise have not been proposed [80]. However, the incidence of hypertension onset has been experienced by those who engage in high volumes of exercise, which could be exacerbated by a lack of energy and nutrition [85]. Although exercise is often recommended for those with high blood pressure (140/90 mm/Hg), individuals with very high blood pressure (> 200 mm/Hg) may require pharmacological intervention and medical clearance prior to exercise.


Arrhythmias refer to any change from the normal sequence of electrical impulses within the heart resulting in an abnormal heartbeat rhythm [86]. For an individual with an ED, arrhythmias may result from LEA [87], malnutrition, and/or hypokalemia [88]. Arrythmias occur when dietary intake is inadequate to support both vital function and exercise engagement, relative to metabolically active FFM [59]. Arrhythmias can present, and persist, irrespective of weight status [87]. Symptoms of arrhythmia may include fatigue, weakness, dizziness, light-headedness, fainting or near fainting, rapid heartbeat, shortness of breath, anxiety, chest pain or pressure, and in extreme cases, collapse, syncope and cardiac arrest [86]. These symptoms may require close monitoring for those with ED including both EKG and Holter monitoring. The results of exercise testing by a professional can determine the safe duration, type, and intensity of exercise.


Bradycardia is a low resting heart rate (< 60 bpm) and is a subtype of arrhythmia [89], often seen in AN [78]. The specific physiological cause of bradycardia is unclear [65] However, hypothesized causes of bradycardia include increased parasympathetic tone and loss of cardiac mass, [90, 91], vagal hyperactivity, [92], and LEA [87], in an effort to decrease strain on the heart by reducing cardiac output. Bradycardia can present, and persist, irrespective of weight status [87] and symptom severity is associated with greater frequency of exercise engagement and team sport engagement [90, 91].

Gibbons et al. [93] warn that sustained arrhythmia can interfere with cardiac output responses during exercising and, in particular, that bradyarrhythmias (with the potential to become more complex or to impede hemodynamic stability) may contraindicate exercise [93]. Fletcher et al. [94] add that uncontrolled cardiac arrhythmias with hemodynamic compromise may contraindicate exercise engagement [94]. The American College of Sports Medicine [95] recommends any noticeable change in heart rhythm by palpitation or auscultation may contraindicate exercise [95]. Likewise, McCallum et al. [78] suggest individuals experiencing an ED with bradycardia and purging should only engage in supervised exercise, and only when nutritional intake and electrolyte and fluid levels are adequate, particularly when under 80% of target body weight.


Tachycardia, a second subtype of arrhythmia, is a high resting heart rate of > 100 bpm [96]. Tachycardia in AN may indicate more severe autonomic nervous dysfunction than bradycardia and suggests a greater likelihood of poor long-term outcomes [97]. Tachycardia comprises several subtypes, ranging from a natural stress response, to abnormal, dangerous responses indicating a fault in the heart’s electrical system [96]. The latter may involve the heart beating faster than chambers can refill with blood, ultimately compromising vital blood flow to the rest of the body and potentially causing death [96]. In those with an ED, tachycardia must be carefully investigated prior to any exercise engagement.

Postural tachycardia

Orthostatic changes, as in postural tachycardia and orthostatic hypotension, represent the change between vital sign readings during the initial minutes of standing or upright tilt from the original lying position [78, 98]. Postural tachycardia is when a heart rate increases of ≥ 30 bpm (≥ 40 bpm in those aged 12–19 years old) persists for more than 30s [99, 100]. In a typical response to an upright posture change, the peripheral veins constrict and an increase in heart contractility occurs [101]; however, when these changes do not occur, blood pools in the peripheral parts of the body, causing the heart to beat abnormally fast in an effort to return sufficient blood to the brain [99]. This compensatory effort is crucial to ensure constant oxygen supply to the brain [99]. Central nervous system symptoms, a complete loss of consciousness, or even sudden cardiac death can ultimately occur if too much blood remains pooled in the extremities, as the brain becomes starved of oxygen and nutrients [100]. Postural tachycardia may result from LEA, [60], autonomic nervous dysfunction [102] and give way to weakness or postural dizziness [78], decreased heart muscle mass (particularly the left ventricle), decreased stroke volume, decreased blood volume [103] and emotional stress [104]. Postural tachycardia mimics the cardiac symptoms of Postural Orthostatic Tachycardic Syndrome; however, this syndrome should not be diagnosed in the presence of malnourishment [60]. Typically, postural tachycardia resolves as weight and nutritional status improve, suggesting that exercise may be gradually modified with symptom improvement[78].

Orthostatic hypotension

Orthostatic hypotension is defined as a sustained drop in systolic blood pressure of ≥ 20 mmHg or diastolic pressure of ≥ 10 mmHg following orthostatic (postural) change [105, 106]. A sustained drop in blood pressure means blood is not exerting sufficient pressure on artery walls, preventing the brain and other organs from receiving adequate oxygen and nutrients [101]. Symptoms of OH may include fainting, palpitations, dizziness, lightheadedness, blurred vision, weakness, fatigue, nausea, headaches, shortness of breath, and pain in the chest, shoulder or neck [101]. Orthostatic hypotension often presents similarly to postural tachycardia, however, the former only occurs in the presence of orthostatic stress, whereas the latter can be attributed to both orthostatic and emotional stress [104].

Prolonged QTc interval

The QT interval denotes an important component of the heart’s electrical activity on an electrocardiogram and represents part of the vital contraction and relaxation process of the cardiac muscle [107]. The QTc interval, more specifically, is a measure of the same time interval as the QT, however, has been corrected to account for the heart rate [108]. QTc prolongation can occur during an ED but may also suggest independent and reversible causes such as low potassium, calcium, glucose, or magnesium, or the use of psychotropic medications [109, 110]. A prolonged QTc interval can cause a life-threatening ventricular arrhythmia called torsade de pointes, ultimately resulting in ventricular fibrillation, which prevents the heart from pumping vital blood supply to the body [111].

Electrolyte abnormalities


Electrolytes, or electrically charged particles or ions, are key regulators of the exchange of fluids, nutrients and waste products inside the body [68]. Electrolytes are lost in sweat during exercise and are negatively affected by purging behaviors, even at subclinical levels [65] [67, 112]. Common electrolytes affected in EDs are potassium, sodium and bicarbonate, with common symptoms including dizziness, weakness, fatigue, constipation, muscle pain, abnormal skin sensations and depression [65]. Electrolyte imbalances often underlie cardic abnormalities [113] and can result in rhabdomyolysis (the breakdown of muscle from strenuous exercise) and sudden death [65]. That said, many of the biochemical markers rectify with improved nutrition, meaning that exercise can gradually be modified with their improvement.


Hypokalemia is a common electrolyte imbalance in ED, defined as low serum potassium. Potassium is a key electrolyte involved in normal cellular function, particularly in muscles and nerves [114]. Hypokalemia commonly presents in individuals with an ED engaging in purging behavior (BN or AN-P) and is prevalent in approximately 14% of individuals with BN [65]. Hypokalemia can also be triggered by malnutrition or the refeeding process [115]. Symptoms of hypokalemia may include muscle weakness, cramping, abnormal skin sensations, constipation, heart palpitations, fatigue, respiratory difficulty, and paralysis [65, 116]. Severe hypokalemia (< 2.5 mmol/L) can cause rhabdomyolysis, significant cardiac arrhythmias, and sudden death [65]. EKG changes due to hypokalemia can include “flat or inverted T waves, ST segment depression, and prominent U waves, which can exceed the amplitude of the T waves” [65]


Hypophosphatemia occurs mainly in AN and is defined as low serum phosphate, often as a result of refeeding, malnutrition, chronic diarrhea, or overuse of diuretics or alcohol [113, 117]. Phosphate is a core component of the energy (adenosine triphosphate) used to produce muscular work [68]. Symptoms of low phosphate relevant to exercise include muscle dysfunction and weakness, abnormal blood oxygen levels, and irregular heartbeats [117]. Hypophosphatemia may also induce a state of confusion and delirium, anaemia, an increased severity of infections, rhabdomyolysis, coma, and even death [117]. Given the core role of phosphates in energy production, an individual experiencing these symptoms may warrant  restriction of high intensity activity and long durations of exercise engagement as these can result in an even greater drop in phosphate


Hypomagnesemia, or low serum levels of magnesium, can result from diarrhea, diuretic use, hormone dysfunction, alcohol intake and some medications [116]. In the context of exercise, magnesium is involved in several processes, including oxygen uptake, energy production and the balance of electrolytes. Low magnesium can lead to muscle tremors and fasciculations, tetany, vertigo, eye problems, altered mental state, respiratory compromise, cardiac arrhythmias, ataxia, seizures, dysphagia, hormone and electrolyte disturbances, and sudden cardiac death [116]. Strenuous Exercise can induce a redistribution of magnesium in the body to accommodate metabolic needs, thus increasing the body's demand for magnesium 10-20%, may aggravate a current deficiency and increase risk of oxidative stress [118].


Hypercarbia, also known as metabolic alkalosis, is a common clinical imbalance in people with ED [65] Similar to other electrolyte disturbances, hypercarbia can occur as a result of purging. Metabolic alkalosis is often asymptomatic; however, extreme cases may result in short and shallow breathing and respiratory complications [65]. Indicators of abnormal respiration, such as shortness of breath and signs of poor perfusion, including light-headedness, cyanosis, confusion, nausea, ataxia, pallor or cold and clammy skin [95]. During this state a break from resistance training and strenuous aerobic activity may be warranted until metabolic alkalosis has been resolved [119].


Hyponatremia, a low concentration of serum sodium, may present with low blood volume status (a state where the body is left with lower than required levels of salt and water). Hyponatremia may occur due to purging or excessive sweating and is one of the most common electrolyte imbalances to occur in both AN and BN [65] Hyponatremia may also result from malnutrition (i.e., kidneys cannot excrete excess water into the urine, so excess water remains in the body), or it can present as a result of excessive water intake (most common in endurance sport activities) [60, 65]. Symptoms of hyponatremia include nausea, confusion, headaches, vomiting, delirium, impaired consciousness, seizures, and, in some cases, cardiorespiratory arrest [120]. For non-ED individuals, hyponatremia often occurs during or following a long or intense bout of activity, thus if currently in a hyponatrimic state due to an ED,  exercise should be stopped until rectified to reduced the risk of aggravating the condition [121].

Biomedical function markers

Temperature: hypothermia and hyperthermia

Hypothermia can occur as a direct result of malnutrition and hypoglycaemia [122], yet it can also persist beyond weight restoration [123]. Onset of hypothermia is related to decreased psychological and cardiac functioning, muscle rigidity, unconsciousness and death, and consequently, may warrant exercise modification until rectified [123].

Conversely, hyperthermia can result from failed thermoregulation, whereby the body produces or absorbs more heat than it can dispel through sweat. A serious medical complication of hyperthermia is heat stroke, which occurs due to excessive metabolic heat from intense exercise, excessive environmental heat, high humidity, some medications, and severe reactions to prescription medications [68]. Exercising in a hyperthermic state, especially if heat stroke presents, is a medical emergency as it can result in organ damage and ultimately mortality; thus, exercise in this state is contraindicated.

Blood urea nitrogen and urine specific gravity

Blood Urea Nitrogen (BUN) and Urine Specific Gravity (USG) are markers of bodily functioning which may indicate diabetes, renal abnormalities, or overhydration, while high urine specific gravity can suggest adrenal, liver, heart or dehydration issues in individuals who are excessively sweating, vomiting, or who have diarrhea [124]. Exercise does not directly affect USG, however, both exercise and ED can impact hydration levels, and kidney and adrenal function, which are reflected in USG and BUN levels [124]. A negative balance in BUN indicates protein breakdown, which is harmful when it arises from muscle catabolism. Subsequently, it is recommended individuals only engage in strength training once a negative nitrogen balance is reversed, accompanied by consistent weight gain [78].


Transaminase, a type of enzyme, is released into the bloodstream when the liver is damaged due to low weight, refeeding, alcohol intake, infection of the liver, or as a side effect of some medications [60, 113, 125, 126]. For indivdiuals with an ED, high levels of transaminase may result from the breakdown of bodily tissue (such as the liver) during severe low weight (BMI < 12) before refeeding [125] or due to the reduction of blood flow through the organs due to myocardial dysfunction [127], and can indicate vital organ failure [128]. During exercise, a significant increase in the rate of amino acid catabolism occurs, placing higher functional demands on the already compromised liver [129]. Thus, exercising with elevated transaminase levels (most often seen in AN) may cause additional harm and exercise intensity and type should be modified accordingly.


Hypoglycaemia is a state of low blood glucose and occurs commonly in individuals with AN [113, 130]. The presence of hypoglycemia can trigger a breakdown of both fat mass and FFM (i.e. muscle, bone, organs, etc.) in attempts to provide the brain with vital energy [60]. Exercising while hypoglycaemic harms the delivery of energy to the organs including the brain and working muscles [68]. Exercise can also worsen hypoglycaemia and its’ effects due to the high metabolic demand for glucose as energy during exercise [68]. The exacerbation of hypoglycaemia through exercise can result in coma and death, due to hepatic failure and the consecutive impairment in the process needed to increase glucose availability, gluconeogenesis [131, 132]. Thus, exercise may be contraindicated for individuals in a hypoglycaemic state until it has been resolved [68]. Individuals with BED may be at increased risk of hyperglycaemia or elevated blood glucose [133] Exercise engagement, especially high intensity or anaerobic exercise, can exacerbate hyperglycaemia, increase the risk of ketosis, or cause insulin dysregulation [134]. Indications for how to manage exercise prescriptions based on glucose levels in individuals with DM type 1 and 2 are available [134], however, there is a lack of research examining hyperglycaemia in individuals with ED.

Dehydration (hypohydration)

Moderate exercise engagement over a one-hour period can produce a sweat loss of 0.5–1L [68]. Individuals who experience > 10% dehydration demonstrate a higher risk of developing tachypnoea or tachycardia, while those with 5–10% dehydration are at risk of developing peripheral edema [135]. Being severely dehydrated and unable to rehydrate contraindicates exercise as it may contribute to increased risk of heat illness, and negatively affect blood volume and exercise capacity [61, 65]. Mountjoy et al. (2014) note that dehydration-induced haemodynamic instability can contraindicate any sport engagement [57].

Sex hormones

The following section relates to conditions of hormonal imbalances in EDs. The most effective method of preventing or reversing abnormal hormonal profiles is to increase energy availability above 30 kcal/kg of FFM/day, via either reducing exercise expenditure and/or increasing energy intake [136]. Adolescent females require greater energy availability than non-adolescent females to be able to continue normal menstrual function [137].


Amenorrhea is the absence of a menstrual cycle for more than 90 days [138]. Functional hypothalamic amenorrhea (FHA), a subtype of amenorrhea, results from metabolic stress, including LEA or psychological distress [139]. Importantly, FHA can occur in the absence of weight loss [137]. Normal menstrual function may return with 6–12 months of weight stabilization; however, longer durations of amenorrhea may take longer to reverse [137]. Women with BED are also at elevated risk for both amenorrhea and oligomenorrhea, even when controlling for the occurrence of polycystic ovary syndrome [140]. Engaging in unmodified exercise while amenorrhoeic may detrimentally impact bone health and fertility [68, 141]. High impact exercise, such as jumping or running, without return to normalised sex hormones or resumption of menses, is contraindicated due to effects on long term bone health [142, 143]. Failing to modify exercise while amenorrhoeic may worsen existing hormonal and energy disruptions, further contributing to menstrual dysfunction and its’ consequences [137].

Female sex hormones

Inadequate sex hormone concentrations, such as growth hormone-releasing hormone, luteinizing hormone, oestrogen and follicle-stimulating hormone, amongst others, can cause menstrual dysfunction, poor bone health, stunting of pubertal growth, infertility, and suboptimal muscular performance [137, 139, 144, 145]. Increasing energy availability and consistent weight gain can improve metabolic hormone profiles rapidly; however, exercise engagement must proceed cautiously while hormone profiles normalize [57].

Male sex hormones

Sex hormones in males can be negatively affected in ED due to starvation-induced central hypothalamic hypogonadism [127]. Decreased concentrations of sex hormones, including testosterone, luteinizing hormone, follicle-stimulating hormone, and gonadotrophin-releasing hormone, as well as abnormal luteinizing pulsatility, can impair reproductive function, decrease immunity, and impact bone health [57, 127]. Similar to women, men with abnormal sex hormone profiles require increased energy availability and accompanying weight gain to normalize concentrations, and exercise engagement must occur cautiously to prevent further damage to bone, the stunting of pubertal growth, infertility, and suboptimal muscular performance [57].

Body composition

Body mass index

Body mass index (BMI) is a measure of body mass as a ratio of body weight to body height (kg/m2). BMI cannot solely or accurately depict health status; indeed, some individual’s weight is not affected at any stage of an ED despite the presence of severe illness, reflecting the need to evaluate the medical and psychological parameters of an individual’s health for a more accurate understanding [60]. However, BMI is still often used to help assess medical status in individuals with an ED, and a BMI < 75% of median values for age, sex, and height is suggested to indicate hospitalization [146]. Engaging in intense endurance or strength training exercise with a BMI < 13.5 kg/m2 may be contraindicated due to health and performance consequences from energy deficiency (e.g., increased risk of pericardial effusion and other effects of LEA; [59, 60]. Engaging in high impact activity < 16 kg/m2 [147], is suggested to be avoided due to the detrimental and widespread effects of LEA.

Appropriate exercise engagement may also be determined via progression of weight recovery considering an individual’s premorbid weight history [22, 148, 149]. For example, a weight loss of 5–10% in one month may contraindicate return to sport [57]. Another suitable marker of body composition is a prolonged low body fat percentage [measured by dual-energy X-ray absorptiometry (DEXA) or less accurately, anthropometry]. McCallum et al. also propose that prior to engagement in regular endurance or other rigorous training, an individual should restore to at least 90% of their target body weight [78].

Low bone mineral density

Bone mineral density (BMD) is the amount of mineral density, particularly calcium and phosphorous, present in a volume of bone. Low BMD occurs when chronic LEA triggers a physiological adaptation within the bone to conserve energy for the vital organ systems [150]. Bone adaptations in the presence of chronic LEA include reduced oestrogen concentration, which is also involved in the disruption or elimination of reproductive function to conserve energy, as well as the suppression of some metabolic hormones [150]. Hormonal changes resulting from LEA can cause the uncoupling of bone turnover, whereby low levels of oestrogen permit increased bone resorption and, combined with the changes in metabolic hormones, cause decreased bone formation [150]. BMD and bone mineral geometry may be compromised most when accompanied by a low BMI, late menarche, or when amenorrhea persists for several years [151]. Although regular exercise engagement typically encourages bone growth [151], during a state of hypoestrogenism, exercise negates the usual positive effects of weight-bearing exercise [144].

Low BMD occurs in men and women, although sex differences may exist [152]. For example, one study suggests men with AN may display greater bone loss at the lumbar spine, as well as a faster rate of bone health decline, compared to women, with up to 65% of men experiencing low bone density as a symptom of their ED [152]. Once bone breakdown occurs, it may take months to years to recover following the resumption of adequate energy availability and recovered menses; however, in some cases, it may never fully recover [150, 153]. Consequences of poor bone health can include pain and disability, stress fractures and breaks, permanent rounding of the upper back due to micro fractures (kyphosis), and may require the use of a walker aid or pain medications, which can cause dependency and constipation, amongst other negative sequelae [60]. LEA prior to puberty may be particularly damaging to bone, as it may directly stunt both vital bone growth, as well as important sexual development that contributes to bone growth [154]. Recovery from bone growth delays can be challenging, and interruptions to bone accrual during adolescence and early adulthood can lead to osteoporosis and stress fractures [151].

Howgate and colleagues recommend high impact activity may be contraindicated until a BMI of 16 kg/m2 is reached to prevent compromise to bone health [147]. Furthermore, unmodified exercise in the presence of LEA, amenorrhea, and low BMD increases one’s risk of bone stress injury and stress fractures [57, 155]. Miller and colleagues (2006) found that in those with an ED that the greatest increases in lumbar spine and hip bone densityoccurred in patients who increased their body weight to 85% IBW and resumed menses (having had at least one menses in the past three month). Importantly, they found that increase in FFM was a better determinate improve BMD than adipose tissue gain highlighting the importance of resistance training for this group [156]. Thus, if low BMD presents in the absence of low BMI, malnutrition, LEA, or sex hormone disturbances. strength training can improve low BMD in men and women [157].

Superior mesenteric artery syndrome

Superior mesenteric artery (SMA) syndrome is caused by the compression of the duodenum due to a diminished fat pad from weight loss that would usually separate the aorta and superior mesenteric artery [127]. Symptoms of SMA syndrome can include upper quadrant abdominal pain soon after eating, early satiety, nausea, and vomiting [127]. SMA is most commonly found in children or individuals with a low BMI and can resolve with weight gain [158, 159]. However, as SMA syndrome occurs in severly underweight individuals, it may be prudent to modify exercise during this time.

Peripheral edema

Peripheral edema is the retention of fluid, most commonly in one’s extremities, and is particularly prominent in individuals with AN [160]. Higher intensity exercise can increase edema, which may already be aggravated during refeeding, or due to renal filtration of insulin or due to high levels of carbohydrate consumption [21]. Thus, exercise may be contraindicated in the presence of peripheral edema [21].

Exercise contraindication, modification, or with caution in the context of EDs

Recommendations for exercise modifications and exercise contraindications prior to exercise engagement are summarized in Table 2. Interestingly, some of the medical complications and associated exercise recommendations were documented through non-ED research publications, and research guiding modification of specific times, types, and intensity of exercise in the presence of each complication or contraindication is lacking. Table 2 highlights important gaps in the research literature on ED and exercise duration, type, intensity, and frequency to be able to provide science-based exercise recommendations.

Table 2 Summary of exercise recommendation evidence

Implications for practice

Given the serious concerns for safety with exercise among medically and physiologically compromised individuals with EDs, ED treatment teams and practioners understandably tend to recommend abstinence from exercise during ED treatment. However, research over the last two decades has demonstrated that complete restriction from exercise is not necessary or appropriate in many cases, and may actually do more harm than good [161]. The purpose of the current review was to provide a comprehensive summary of the medical and physiological complications of EDs that may be exacerbated among individuals who engage in dysfunctional exercise, and to offer an initial set of recommendations for incorporating exercise during ED treatment based on our findings. We have summarized the complications and recommendations in Table 1 and Table 2, respectively, to serve as a resource for members of ED treatment teams to help evaluate more readily and confidently whether exercise is safe for individual patients and when modifications and caution may be warranted. The information provided from this review may also be used in conjunction with the Safe Exercise at Every Stage guideline to help ED clinicians better address and manage dysfunctional exercise during treatment [165]. Ultimately, it is our hope that this knowledge will further empower clinicians in this challenging area of ED treatment.

Implications for future research

Our review highlights some critical gaps in the literature on exercise in ED contexts. There was limited evidence for guiding specific recommendations for exercise duration, type, intensity, and frequency in the presence of each complication. This includes a lack of differentiation between the mechanical versus metabolic loading of exercise and how these may uniquely impact the safety of a given exercise. For example, recommendations based upon exercise “intensity” alone may be misleading as they do not account for the differential demands of high mechanical and low metabolic loading versus low mechanical and high metabolic loading. This information is needed to inform the development of guidelines to best assess and manage exercise in ED populations [17]. Future research must prioritise increasing our knowledge of exercise as well as further adaptations relevant for special ED populations, such as athletes, youth, or individuals with comorbid conditions such as diabetes mellitus.

Most clinicians treating ED have not received adequate training in exercise interventions [162], with many highlighting their lack of knowledge and fears surrounding exercise as reasons for which they avoid addressing exercise with their clients [163]. Therefore, the inclusion of an exercise professional (e.g., accredited exercise physiologist, athletic therapist) with specialized training in ED as part of the treatment team may offer a depth of knowledge surrounding exercise physiology not otherwise available [162]. Even with this addition, determining readiness to return to exercise for those with ED has long been debated, with little evidence-based research currently guiding treatment [164]. As mentioned above, guidelines such as the Safe Exercise at Every Stage (SEES) Guideline [165]for adults with an ED [165], or SEES-Athlete version or RED-S CAT for athletes with an ED [166, 167] may provide guidance for practitioners aiming to determine physical and psychological readiness for exercise engagement.


This narrative review outlined the medical and physiological complications of EDs which can be negatively exacerbated for individuals who engage in dysfunctional exercise. These complications should be monitored in individuals with EDs to determine whether exercise is contraindicated, or whether it can be used in a modified or cautionary way. Importantly, if exercise in ED recovery is nutritionally supported and safely modified, it can facilitate ED treatment and recovery, and bring health benefits to individuals living with an ED [17, 168, 169]. Clinicians working with individuals with ED require clear guidelines to aid decision-making as it relates to exercise engagement during treatment.

Availability of data and materials

All data generated or analysed during this study are included in this published article [and its supplementary information files].



Anorexia nervosa purging subtype


Anorexia nervosa


Binge eating disorder


Bulimia nervosa


Bone mineral density


Body mass index


Beats per minute


Blood Urea Nitrogen


Dysfunctional exercise


Dual-energy X-ray absorptiometry


Eating disorder not otherwise specified


Eating disorders


Fat free mass


Functional hypothalamic amenorrhea






Low energy availability


Optimal energy availability


Resting metabolic rate


Superior mesenteric artery


Maximal oxygen uptake


Urine Specific Gravity


  1. Fichter MM, Quadflieg N. Mortality in eating disorders - results of a large prospective clinical longitudinal study. Int J Eat Disord. 2016;49:391–401.

    Article  Google Scholar 

  2. Grilo CM, Mitchell JE. T treatment of eating disorders NYTGP. Treat Eat Disorders Clin Handb. 2011.

    Article  Google Scholar 

  3. van Hoeken D, Hoek HW. Review of the burden of eating disorders: mortality, disability, costs, quality of life, and family burden. Curr Opin Psychiatry. 2020;33:521–7.

    Article  Google Scholar 

  4. Mandelli L, Arminio A, Atti A-R, et al. Suicide attempts in eating disorder subtypes: a meta-analysis of the literature employing DSM-IV, DSM-5, or ICD-10 diagnostic criteria. Psychol Med. 2019;49:1237–49.

    Article  Google Scholar 

  5. Smith KE, Mason TB, Crosby RD, et al. A comparative network analysis of eating disorder psychopathology and co-occurring depression and anxiety symptoms before and after treatment. Psychol Med. 2019;49:314–24.

    Article  Google Scholar 

  6. Smith AR, Zuromski KL, Dodd DR. Eating disorders and suicidality: what we know, what we don’t know, and suggestions for future research. Curr Opin Psychol. 2018;22:63–7.

    Article  Google Scholar 

  7. Elran-Barak R, Goldschmidt AB. Differences in severity of eating disorder symptoms between adults with depression and adults with anxiety. Eat Weight Disord Stud Anorexia, Bulimia Obes. 2021;26:1409–16.

    Article  Google Scholar 

  8. Shroff H, Reba L, Thornton LM, et al. Features associated with excessive exercise in women with eating disorders. Int J Eat Disord. 2006;39:454–61.

    Article  Google Scholar 

  9. Dalle Grave R, Calugi S, Marchesini G. Compulsive exercise to control shape or weight in eating disorders: prevalence, associated features, and treatment outcome. Compr Psychiatry. 2008;49:346–52.

    Article  Google Scholar 

  10. Hausenblas HA, Cook BJ, Chittester NI. Can exercise treat eating disorders? Exerc Sport Sci Rev. 2008;36:43–7.

    Article  Google Scholar 

  11. Calogero RM, Pedrotty-Stump KN. Incorporating exercise into eating disorder treatment and recovery: cultivating a mindful approach. Treat Eat Disord. 2010.

    Article  Google Scholar 

  12. Dittmer N, Jacobi C, Voderholzer U. Compulsive exercise in eating disorders: proposal for a definition and a clinical assessment. J Eat Disord. 2018;6:42.

    Article  Google Scholar 

  13. Bratland-Sanda S, Mathisen TF, Sundgot-Borgen J, et al. Defining compulsive exercise in eating disorders: acknowledging the exercise paradox and exercise obsessions. J Eat Disord. 2019;7:8.

    Article  Google Scholar 

  14. Carter JC, Blackmore E, Sutandar-Pinnock K, Woodside D. B Relapse in anorexia nervosa: a survival analysis. Psychol Med. 2004;34:671–9.

    Article  Google Scholar 

  15. Meyer C, Taranis L, Goodwin H, et al. Compulsive exercise and eating disorders. Eur Eat Disord Rev. 2011;19:174–89.

    Article  Google Scholar 

  16. Strober M, Freeman R, Morrell W. The long-term course of severe anorexia nervosa in adolescents: survival analysis of recovery, relapse, and outcome predictors over 10–15 years in a prospective study. Int J Eat Disord. 1997;22:339–60.;2-N.

    Article  Google Scholar 

  17. Hallward L, di Marino A, Duncan LR. A systematic review of treatment approaches for compulsive exercise among individuals with eating disorders. Eat Disord 2021;

  18. Mathisen TF, Bratland-Sanda S, Rosenvinge JH, et al. Treatment effects on compulsive exercise and physical activity in eating disorders. J Eat Disord. 2018.

    Article  Google Scholar 

  19. Davis C, Kennedy SH. The role of physical activity in the development and maintenance of eating disorders SEE PROFILE. Citeseer. 1994;24:957–67.

    Article  Google Scholar 

  20. Hechler T, Beumont P, Marks P, et al. How do clinical specialists understand the role of physical activity in eating disorders? Eur Eat Disord Rev. 2005;13:125–32.

    Article  Google Scholar 

  21. Beumont PJV, Arthur B, Russell JD, et al. Excessive physical activity in dieting disorder patients: proposals for a supervised exercise program. Int J Eat Disord. 1994;15:21–36.;2-K.

    Article  Google Scholar 

  22. Calogero RM, Pedrotty KN. Eating disorders the practice and process of healthy exercise: an investigation of the treatment of exercise abuse in women with eating disorders. Taylor & Francis. 2004;12:273–91.

    Article  Google Scholar 

  23. Ng LWC, Ng DP, Wong WP. Is supervised exercise training safe in patients with anorexia nervosa? A meta-analysis. Physiotherapy. 2013;99:1–11.

    Article  Google Scholar 

  24. Quesnel DA, Libben MD, Oelke N, et al. Is abstinence really the best option? Exploring the role of exercise in the treatment and management of eating disorders. Eat Disord. 2018;26:290–310.

    Article  Google Scholar 

  25. Calogero R, Pedrotty K. Targeting exercise abuse in women with eating disorders: A test of an innovative treatment program. 2003;:12–4.

  26. Schlegel S, Hartmann A, Fuchs R, et al. The Freiburg sport therapy program for eating disordered outpatients: a pilot study. Eat Weight Disord Stud Anorexia, Bulimia Obes. 2015;20:319–27.

    Article  Google Scholar 

  27. Vancampfort D, Vanderlinden J, De Hert M, et al. A systematic review of physical therapy interventions for patients with anorexia and bulemia nervosa. Disabil Rehabil. 2014;36:628–34.

    Article  Google Scholar 

  28. Moola FJ, Gairdner SE, Amara CE. Exercise in the care of patients with anorexia nervosa: a systematic review of the literature. Ment Health Phys Act. 2013;6:59–68.

    Article  Google Scholar 

  29. Carei TR, Fyfe-Johnson AL, Breuner CC, et al. Randomized controlled clinical trial of yoga in the treatment of eating disorders. J Adolesc Health. 2010;46:346–51.

    Article  Google Scholar 

  30. Karlsen KE, Vrabel K, Bratland-Sanda S, et al. Effect of Yoga in the treatment of eating disorders: a single-blinded randomized controlled trial with 6-months follow-up. Int J Yoga. 2018;11:166–9.

    Article  Google Scholar 

  31. Chantler I, Szabo C, Green K. Muscular strength changes in hospitalized anorexic patients after an eight week resistance training program. Int J Sports Med. 2006;27:660–5.

    Article  Google Scholar 

  32. Szabo CP, Green K. Hospitalized anorexics and resistance training: Impact on body composition and psychological well-being A preliminary study. Eat Weight Disord Stud Anorexia, Bulimia Obes. 2002;7:293–7.

    Article  Google Scholar 

  33. Agne A, Quesnel DA, Larumbe-Zabala E, et al. Progressive resistance exercise as complementary therapy improves quality of life and body composition in anorexia nervosa: a randomized controlled trial. Complement Ther Clin Pract. 2022;48: 101576.

    Article  Google Scholar 

  34. del Valle MF, Pérez M, Santana-Sosa E, et al. Does resistance training improve the functional capacity and well being of very young anorexic patients? A randomized controlled trial. J Adolesc Health. 2010;46:352–8.

    Article  Google Scholar 

  35. Fernandez-del-Valle M, Larumbe-Zabala E, Villaseñor-Montarroso A, et al. Resistance training enhances muscular performance in patients with anorexia nervosa: a randomized controlled trial. Int J Eat Disord. 2014;47:601–9.

    Article  Google Scholar 

  36. Tokumura M, Yoshiba S, Tanaka T, et al. Prescribed exercise training improves exercise capacity of convalescent children and adolescents with anorexia nervosa. Eur J Pediatr. 2003;162:430–1.

    Article  Google Scholar 

  37. Duesund L, Skårderud F. Use the body and forget the body: treating anorexia nervosa with adapted physical activity. Clin Child Psychol Psychiatry. 2003;8:53–72.

    Article  Google Scholar 

  38. Duesund L, Jespersen E. Skill acquisition in ski instruction and the skill model’s application to treating anorexia nervosa. Bull Sci Technol Soc. 2004;24:225–33.

    Article  Google Scholar 

  39. Mathisen TF, Rosenvinge JH, Friborg O, et al. Is physical exercise and dietary therapy a feasible alternative to cognitive behavior therapy in treatment of eating disorders? A randomized controlled trial of two group therapies. Int J Eat Disord. 2020;53:574–85.

    Article  Google Scholar 

  40. Catalan-Matamoros D, Helvik-Skjaerven L, Labajos-Manzanares MT, et al. A pilot study on the effect of basic body awareness therapy in patients with eating disorders: a randomized controlled trial. Clin Rehabil. 2011;25:617–26.

    Article  Google Scholar 

  41. Mitchell JE, King WC, Pories W, et al. Binge eating disorder and medical comorbidities in bariatric surgery candidates. Int J Eat Disord. 2015;48:471–6.

    Article  Google Scholar 

  42. Zhang J, Abbasi O, Malevanchik L, et al. Pilot study of the prevalence of binge eating disorder in non-alcoholic fatty liver disease patients. Ann Gastroenterol. 2017;30:664–9.

    Article  Google Scholar 

  43. Kessler RC, Berglund PA, Chiu WT, et al. The prevalence and correlates of binge eating disorder in the world health organization world mental health surveys. Biol Psychiatry. 2013;73:904–14.

    Article  Google Scholar 

  44. Oh H, Stickley A, Singh F, et al. Self-reported asthma diagnosis and mental health: findings from the collaborative psychiatric epidemiology surveys. Psychiatry Res. 2019;271:721–5.

    Article  Google Scholar 

  45. Alonso J, de Jonge P, Lim CCW, et al. Association between mental disorders and subsequent adult onset asthma. J Psychiatr Res. 2014;59:179–88.

    Article  Google Scholar 

  46. Lee I, Cooney LG, Saini S, et al. Increased risk of disordered eating in polycystic ovary syndrome. Fertil Steril. 2017;107:796–802.

    Article  Google Scholar 

  47. Hudson JI, Lalonde JK, Coit CE, et al. Longitudinal study of the diagnosis of components of the metabolic syndrome in individuals with binge-eating disorder. Am J Clin Nutr. 2010;91:1568–73.

    Article  Google Scholar 

  48. Turner G, Quigg S, Davoren P, et al. Resources to guide exercise specialists managing adults with diabetes. Sports Med Open. 2019;5:20.

    Article  Google Scholar 

  49. Avallone KM, McLeish AC. Asthma and aerobic exercise: a review of the empirical literature. J Asthma. 2013;50:109–16.

    Article  Google Scholar 

  50. Kanaley JA, Colberg SR, Corcoran MH, et al. Exercise/physical activity in individuals with type 2 diabetes: a consensus statement from the american college of sports medicine. Med Sci Sports Exerc. 2022;54:353–68.

    Article  Google Scholar 

  51. Andersen LL, Saervoll CA, Mortensen OS, et al. Effectiveness of small daily amounts of progressive resistance training for frequent neck/shoulder pain: randomised controlled trial. Pain. 2011;152:440–6.

    Article  Google Scholar 

  52. Loucks AB, Heath EM. Induction of low-T3 syndrome in exercising women occurs at a threshold of energy availability. Am J Physiol. 1994;266:R817–23.

    Article  Google Scholar 

  53. Loucks AB. Energy availability, not body fatness, regulates reproductive function in women. Exerc Sport Sci Rev. 2003;31:144–8.

    Article  Google Scholar 

  54. Loucks AB, Kiens B, Wright HH. Energy availability in athletes. J Sports Sci. 2011;29:S7-15.

    Article  Google Scholar 

  55. Gaudiani JL, Sabel AL, Mascolo M, et al. Severe anorexia nervosa: outcomes from a medical stabilization unit. Int J Eat Disord. 2012;45:85–92.

    Article  Google Scholar 

  56. Tarnopolsky MA, Zawada C, Richmond LB, et al. Gender differences in carbohydrate loading are related to energy intake. J Appl Physiol. 2001;91:225–30.

    Article  Google Scholar 

  57. Mountjoy M, Sundgot-Borgen J, Burke L, et al. The IOC consensus statement: beyond the female athlete triad-relative energy deficiency in sport (RED-S). Br J Sports Med. 2014;48:491–7.

    Article  Google Scholar 

  58. Woods AL, Garvican-Lewis LA, Lundy B, et al. New approaches to determine fatigue in elite athletes during intensified training: resting metabolic rate and pacing profile. PLoS One. 2017.

    Article  Google Scholar 

  59. Mountjoy M, Sundgot-Borgen JK, Burke LM, et al. IOC consensus statement on relative energy deficiency in sport (RED-S): 2018 update. Br J Sports Med. 2018.

    Article  Google Scholar 

  60. Gaudiani JL. Sick enough: a guide to the medical complications of eating disorders. New York: Routledge; 2018.

    Book  Google Scholar 

  61. El Ghoch M, Soave F, Calugi S, et al. Eating disorders, physical fitness and sport performance: a systematic review. Nutrients. 2013;5:5140–60.

    Article  Google Scholar 

  62. Quesnel DA, Cook B, Caperchione C. Guiding principles to inform future exercise protocols for eating disorder treatment. Health Fit J Can. 2020;13:3–15.

    Article  Google Scholar 

  63. Gianini LM, Klein DA, Call C, et al. The reinforcing effect of exercise in anorexia nervosa: clinical correlates and relationship to outcome. Eat Disord. 2016;24:412–23.

    Article  Google Scholar 

  64. American Psychiatric Association. Diagnostic and statistical manual of mental disorders. 5th ed. Washington, DC: 2013.

  65. Mehler P, Anderson A. Eating disorders: a guide to medical care and complications - google books. 2017.,+P.+%26+Andersen,+A.+(2017).+&ots=ydskspyGQe&sig=BrhJ4jKSRv5saWSzRWX5b_BUIZI&redir_esc=y#v=onepage&q=Mehler%2C%20P.%20%26%20Andersen%2C%20A.%20(2017).&f=false Accessed 19 Jan 2022

  66. Mehler PS, Walsh K. Electrolyte and acid-base abnormalities associated with purging behaviors. Int J Eat Disord. 2016;49:311–8.

    Article  Google Scholar 

  67. Lindsay B. Sweating rate and sweat sodium concentration in athletes: a review of methodology and intra/interindividual variability. Sports Med. 2017;47:111–28.

    Article  Google Scholar 

  68. Mcardle WD, Katch FI, Katch VL. Exercise physiology: nutrition, energy, and human performance. Philadelphia: Lippincott Williams & Wilkins; 2015.

    Google Scholar 

  69. Nilsson L, Karlsen C. Kvinnors upplevelser av att leva med anorexia nervosa: Ett patientperspektiv. 2020. Accessed 12 Sep 2022.

  70. Mascolo M, Chu ES, Mehler PS. Abuse and clinical value of diuretics in eating disorders therapeutic applications. Int J Eat Disord. 2011;44:200–2.

    Article  Google Scholar 

  71. Raj KS, Keane-Miller C, Golden NH. Hypomagnesemia in adolescents with eating disorders hospitalized for medical instability. Nutr Clin Pract. 2012;27:689–94.

    Article  Google Scholar 

  72. Imbierowicz K, Curkovic I, Braks K, et al. Effect of weight-regulating practices on potassium level in patients with anorexia or bulimia nervosa. Eur Eat Disord Rev. 2004;12:300–6.

    Article  Google Scholar 

  73. Green M, Herrick A, Kroska E, et al. Cardiac biomarkers of disordered eating: a case for decreased mean R wave amplitude. Psychiatry Res. 2019;272:555–61.

    Article  Google Scholar 

  74. Green M, Rogers J, Nguyen C, et al. Cardiac risk and disordered eating: decreased R wave amplitude in women with bulimia nervosa and women with subclinical binge/purge symptoms. Eur Eat Disord Rev. 2016;24:455–9.

    Article  Google Scholar 

  75. Green MA, Miles L, Sage E, et al. Cardiac biomarkers of disordered eating as a function of diagnostic subtypes. Eat Behav. 2020;39: 101425.

    Article  Google Scholar 

  76. American Heart Association. Low blood pressure - when blood pressure is too low. 2022.

  77. Baker LB. Sweating rate and sweat sodium concentration in athletes: a review of methodology and intra/interindividual variability. Sports Med. 2017;47:111–28.

    Article  Google Scholar 

  78. McCallum K, Bermudez O, Ohlemeyer C, et al. How should the clinician evaluate and manage the cardiovascular complications of anorexia nervosa? Eat Disord. 2006;14:73–80.

    Article  Google Scholar 

  79. Oświecimska J ZKAPRWP-KASMDA. Effects of neuroendocrine changes on results of ambulatory blood pressure monitoring (ABPM) in adolescent girls with anorexia nervosa. Neuro Endocrinol Lett 2007;28.

  80. Hypertension Society of Canada. Health behaviour management. 2022.

  81. American Heart Association. Health Threats from High Blood Pressure|American Heart Association. 2022. Accessed 27 May 2022

  82. Olguin P, Fuentes M, Gabler G, et al. Medical comorbidity of binge eating disorder. Eat Weight Disord Stud Anorexia, Bulimia Obes. 2016;22:13–26.

    Article  Google Scholar 

  83. Raggi A, Curone M, Bianchi Marzoli S, et al. Impact of obesity and binge eating disorder on patients with idiopathic intracranial hypertension. Cephalalgia. 2017;37:278–83.

    Article  Google Scholar 

  84. Ruggeri-McKinley AN, McKinley BC. The commonly missed diagnosis of intracranial hypotension. Interdiscip Neurosurg. 2016;4:11–2.

    Article  Google Scholar 

  85. Sharman JE, la Gerche A, Coombes JS. Exercise and cardiovascular risk in patients with hypertension. Am J Hypertens. 2015;28:147–58.

    Article  Google Scholar 

  86. American Heart Association. About arrhythmia. 2016.

  87. Spaulding-Barclay MA, Stern J, Mehler PS. Cardiac changes in anorexia nervosa. Cardiol Young. 2016;26:623–8.

    Article  Google Scholar 

  88. Sachs KV, Harnke B, Mehler PS, et al. Cardiovascular complications of anorexia nervosa: a systematic review. Int J Eat Disord. 2016;49:238–48.

    Article  Google Scholar 

  89. American Heart Association. Bradycardia: Slow heart rate. 2021.

  90. Kollai M, Bonyhay I, Jokkel G, et al. Cardiac vagal hyperactivity in adolescent anorexia nervosa. Eur Heart J. 1994;15:1113–8.

    Article  Google Scholar 

  91. Nagata JM, Carlson JL, Golden NH, et al. Associations between exercise, bone mineral density, and body composition in adolescents with anorexia nervosa. Eat Weight Disord Stud Anorexia, Bulimia Obesity. 2019;24:939–45.

    Article  Google Scholar 

  92. Nudel DB, Gootman N, Nussbaum MP, et al. Altered exercise performance and abnormal sympathetic responses to exercise in patients with anorexia nervosa. J Pediatr. 1984;105:34–7.

    Article  Google Scholar 

  93. Gibbons RJ, Balady GJ, Timothy Bricker J, et al. ACC/AHA 2002 guideline update for exercise testing: summary article. J Am Coll Cardiol. 2002;40:1531–40.

    Article  Google Scholar 

  94. Fletcher GF, Ades PA, Kligfield P, et al. Exercise standards for testing and training. Circulation. 2013;128:873–934.

    Article  Google Scholar 

  95. American College of Sport Medicine. ACSM’s guidelines for exercise testing and prescription. 10th ed. Wolters Kluwer Health, Philadelphia, PA, 2018

  96. American Heart Association. Tachycardia: Fast heart rate. 2021.

  97. Tokumura M, Watanabe H, Esaki T. Convalescent resting tachycardia predicts unfavorable outcome of anorexia nervosa. Pediatr Int. 2012;54:844–8.

    Article  Google Scholar 

  98. Raj SR. Postural tachycardia syndrome (POTS). Circulation. 2013;127:2336–42.

    Article  Google Scholar 

  99. Grubb BP, Kanjwal Y, Kosinski DJ. The postural tachycardia syndrome: a concise guide to diagnosis and management. J Cardiovasc Electrophysiol. 2005.

    Article  Google Scholar 

  100. Grubb BP. Postural tachycardia syndrome. Circulation. 2008;117:2814–7.

    Article  Google Scholar 

  101. Grubb BP, Kanjwal Y, Karabin B, et al. Orthostatic hypotension and autonomic failure: a concise guide to diagnosis and management. Clin Med Cardiol. 2008.

    Article  Google Scholar 

  102. Jacob G, Costa F, Shannon JR, Robertson RM, Robertson D, Wathen M, Black B. The neuropathic postural tachycardia syndrome. N Engl J Med. 2000;343:1008–14.

    Article  Google Scholar 

  103. Fu Q, VanGundy TB, Galbreath MM, Shibata S, Jain M, Hastings JL, Levine B. D cardiac origins of the postural orthostatic tachycardia syndrome. J Am Coll Cardiol. 2010;55:2858–68.

    Article  Google Scholar 

  104. Sheldon RS, Grubb BP, Olshansky B, et al. 2015 heart rhythm society expert consensus statement on the diagnosis and treatment of postural tachycardia syndrome, inappropriate sinus tachycardia, and vasovagal syncope. Heart Rhythm. 2015;12:e41-63.

    Article  Google Scholar 

  105. Freeman R, Wieling W, Axelrod FB, et al. Consensus statement on the definition of orthostatic hypotension, neurally mediated syncope and the postural tachycardia syndrome. Autonomic Neurosci Basic Clin. 2011;161:46–8.

    Article  Google Scholar 

  106. Lanier JB, Mote MB, Clay EC. Evaluation and management of orthostatic hypotension. 2011.

  107. Garson A. How to measure the QT interval-what is normal? Am J Cardiol. 1993;72:B14–6.

    Article  Google Scholar 

  108. Drew BJ, Ackerman MJ, Funk M, et al. Prevention of Torsade de Pointes in Hospital Settings A scientific statement from the american heart association and the american college of cardiology foundation endorsed by the american association of critical-care nurses and the international society. J Am Coll Cardiol. 2010;55:934–47.

    Article  Google Scholar 

  109. Krantz MJ, Sabel AL, Sagar U, et al. Factors influencing QT prolongation in patients hospitalized with severe anorexia nervosa. Gen Hosp Psychiatry. 2012;34:173–7.

    Article  Google Scholar 

  110. Laitinen T, Lyyra-Laitinen T, Huopio H, et al. Electrocardiographic alterations during hyperinsulinemic hypoglycemia in healthy subjects. Ann Noninvasive Electrocardiol. 2008;13:97–105.

    Article  Google Scholar 

  111. Electrocardiogram (ECG or EKG)|American Heart Association. Accessed 25 Nov 2020

  112. Mehler PS. Diagnosis and care of patients with anorexia nervosa in primary care settings. Ann Intern Med. 2001;134:1048–59.

    Article  Google Scholar 

  113. Voderholzer U, Haas V, Correll CU, et al. Medical management of eating disorders: an update. Curr Opin Psychiatry. 2020;33:542–53.

    Article  Google Scholar 

  114. Stone MS, Martyn L, Weaver CM. Potassium intake, bioavailability, hypertension, and glucose control. Nutrients. 2016.

    Article  Google Scholar 

  115. Funayama M, Mimura Y, Takata T, et al. Hypokalemia in Patients with eating disorders is associated with binge-purge behavior, lower body mass index, and hypoalbuminemia ~predicting hypokalemia during refeeding. Publ Online First. 2021.

    Article  Google Scholar 

  116. American Heart Association. Part 10.1: life-threatening electrolyte abnormalities. Circulation 2005;112:IV121–5. doi:

  117. Agency for Clinical Innovation. Phosphate - Hypophosphatemia. 2017.

  118. Nielsen FH, Lukaski HC. Update on the relationship between magnesium and exercise. Magnes Res. 2006;19(6):180–9.

  119. Hoorn EJ, Bovée DM, Geerse DA, Visser WJ. Diet-exercise-induced hypokalemic metabolic alkalosis. Am J Med. 2020;133(11):e667–9.

  120. Henry DA. Hyponatremia. Ann Intern Med. 2015.

    Article  Google Scholar 

  121. Rosner MH, Kirven J. Exercise-associated hyponatremia. Clin J Am Soc Nephrol 2007;2(1):151–61.

  122. Nishita JK, Ellinwood EH, Rockwell WJK. Hypothermia in anorexia nervosa: an increase in nonshivering thermogenesis? Int J Eat Disord. 1985;4:307–19.;2-H.

    Article  Google Scholar 

  123. Luck P, Wakeling A. Set-point displacement for behavioural thermoregulation in anorexia nervosa. Clin Sci. 1982;62:677–82.

    Article  Google Scholar 

  124. Schumann GB, Schweitzer SC. Examination of urine. In: Clinical chemistry, theory, analysis and correlation. St. Louis: Mosby: Year Book Inc. 1996. 1118–9.

  125. Hanachi M, Melchior JC, Crenn P. Hypertransaminasemia in severely malnourished adult anorexia nervosa patients: risk factors and evolution under enteral nutrition. Clin Nutr. 2013;32:391–5.

    Article  Google Scholar 

  126. American Academy of Family Physicians. RC, Hustead TR. American family physician. American Academy of Family Physicians 1970. (accessed 20 Jan 2022).

  127. Mehler PS, Brown C. Anorexia nervosa - medical complications. J Eat Disord. 2015;3:1–8.

    Article  Google Scholar 

  128. de Caprio C, Alfano A, Senatore I, et al. Severe acute liver damage in anorexia nervosa: two case reports. Nutrition. 2006;22:572–5.

    Article  Google Scholar 

  129. Henriksson J. Effect of exercise on amino acid concentrations in skeletal muscle and plasma. J Exp Biol 1991;160.

  130. Rich LM, Caine MR, Findling JW, et al. Hypoglycemic coma in Anorexia Nervosa. Arch Intern Med. 1990;150:894.

    Article  Google Scholar 

  131. Brun JF, Dumortier M, Fedou C, et al. Exercise hypoglycemia in nondiabetic subjects. Diabet Metab. 2001;27:92–106.

    Google Scholar 

  132. Riedlinger C, Schmidt G, Weiland A, et al. Which symptoms, complaints and complications of the gastrointestinal tract occur in patients with eating disorders? A systematic review and quantitative analysis. Front Psychiatry. 2020;11:195.

    Article  Google Scholar 

  133. Canadian Diabetic Association. About Diabetes. 2022.

  134. Lumb A. Diabetes and exercise. Clin Med (Lond). 2014;14:673–6.

    Article  Google Scholar 

  135. Baksh G. Refeeding Guideline May 2018. 2017. (accessed 20 Jan 2022).

  136. Melin A, Tornberg ÅB, Skouby S, et al. Energy availability and the female athlete triad in elite endurance athletes. Scand J Med Sci Sports. 2015;25:610–22.

    Article  Google Scholar 

  137. Gordon CM, Ackerman KE, Berga SL, et al. Functional hypothalamic amenorrhea: an endocrine society clinical practice guideline. J Clin Endocrinol Metab. 2017;102:1413–39.

    Article  Google Scholar 

  138. Nattiv A. The female athlete triad: ACSM position stand. Med Sci Sports Exerc. 2007;39:1867–82.

    Article  Google Scholar 

  139. Berga SL, Loucks TL. Use of cognitive behavior therapy for functional hypothalamic amenorrhea. In: Annals of the New York Academy of Sciences. Blackwell Publishing Inc. 2006. 114–29. doi:

  140. Ålgars M, Huang L, von Holle AF, et al. Binge eating and menstrual dysfunction. J Psychosom Res. 2014;76:19–22.

    Article  Google Scholar 

  141. Warren MP, Perlroth NE. The effects of intense exercise on the female reproductive system. J Endocrinol. 2001;170:3–11.

    Article  Google Scholar 

  142. Scheid JL, Toombs RJ, Ducher G, et al. Estrogen and peptide YY are associated with bone mineral density in premenopausal exercising women. Bone. 2011;49:194–201.

    Article  Google Scholar 

  143. Zanker CL, Swaine IL. Bone turnover in amenorrhoeic and eumenorrhoeic women distance runners. Scand J Med Sci Sports. 2007;8:20–6.

    Article  Google Scholar 

  144. Kandemir N, Slattery M, Ackerman KE, et al. Bone parameters in anorexia nervosa and athletic amenorrhea: comparison of two hypothalamic amenorrhea states. J Clin Endocrinol Metab. 2018;103:2392–402.

    Article  Google Scholar 

  145. Silveira LG. Article in seminars in reproductive medicine. Semin Reprod Med. 2002;12:41–63.

    Article  Google Scholar 

  146. Geller, J., Goodrich, S., Chan, K., Cockell, S., & Srikameswaran S. Clinical practice guidelines for the BC eating disorder continuum of services. BC Ministry of Health Services,. 2012;:3–170.

  147. Howgate DJ, Graham SM, Leonidou A, et al. Bone metabolism in anorexia nervosa: molecular pathways and current treatment modalities. Osteoporos Int. 2013;24:407–21.

    Article  Google Scholar 

  148. Cook B, Wonderlich S, JM-M and science, et al. Exercise in eating disorders treatment: systematic review and proposal of guidelines. 2016;48:1408.

  149. Noetel M, Dawson L, Hay P, et al. The assessment and treatment of unhealthy exercise in adolescents with anorexia nervosa: a Delphi study to synthesize clinical knowledge. Int J Eat Disord. 2017;50:378–88.

    Article  Google Scholar 

  150. De Souza MJ. The female athlete triad and implications for sports nutrition strategies for recovery. 2019. (accessed 27 Nov 2020).

  151. Mallinson RJ, Williams NI, Gibbs JC, et al. Current and past menstrual status is an important determinant of femoral neck geometry in exercising women. Bone. 2016;88:101–12.

    Article  Google Scholar 

  152. Mehler PS, Sabel AL, Watson T, et al. High risk of osteoporosis in male patients with eating disorders. Int J Eat Disord. 2008;41:666–72.

    Article  Google Scholar 

  153. Warren MP, Brooks-Gunn J, Fox RP, et al. Osteopenia in exercise-associated amenorrhea using ballet dancers as a model: a longitudinal study. J Clin Endocrinol Metab. 2002;87:3162–8.

    Article  Google Scholar 

  154. Schneider JE, Wade GN. Inhibition of reproduction in se rvice of energy balance.In: Wallen K, Schneider JE (eds) Reproduction in context: social and environmental influences on reproductive physiology and behavior, Cambridge: The MIT Press; 35.

  155. Barrack MT, Gibbs JC, DeSouza MJ, et al. Higher incidence of bone stress injuries with increasing female athlete triad-related risk factors a prospective multisite study of exercising girls and women. 2014;42:949–58.

  156. Miller KK, Lee EE, Lawson EA, et al. Determinants of skeletal loss and recovery in anorexia nervosa. J Clin Endocrinol Metab. 2006;91:2931–7.

    Article  Google Scholar 

  157. Watson S, Weeks B, Weis L, et al. High-intensity resistance and impact training improves bone mineral density and physical function in postmenopausal women with osteopenia and osteoporosis: the LIFTMOR randomized controlled trial. J Bone Miner Res. 2019;34:572.

    Article  Google Scholar 

  158. Arthurs OJ, Mehta U, Set PAK. Nutcracker and SMA syndromes: What is the normal SMA angle in children? Eur J Radiol. 2012;81:e854–61.

    Article  Google Scholar 

  159. Shetty AK, Schmidt-Sommerfeld E, Haymon M-L, et al. Radiological case of the month. Arch Pediatr Adolesc Med. 1999;153:303.

    Article  Google Scholar 

  160. Derman O, Kılıç EZ. Edema can be a handicap in treatment of anorexia nervosa. 2009. (accessed 20 Jan 2022).

  161. Mathisen TF, Sundgot-Borgen J, Bulik CM, et al. The neurostructural and neurocognitive effects of physical activity: a potential benefit to promote eating disorder recovery. Int J Eat Disord. 2021;54:1766–70.

    Article  Google Scholar 

  162. Bergmeier HJ, Morris H, Mundell N, et al. What role can accredited exercise physiologists play in the treatment of eating disorders? A descriptive study. Eat Disord 2019;

  163. Quesnel DA, Libben M, Caperchione CM. Preliminary assessment criteria for prescribing exercise when treating eating disorders: What do the experts have to say? Ment Health Phys Act. 2018;15:27–33.

    Article  Google Scholar 

  164. Davies RR. The treatment of compulsive physical activity in anorexia nervosa lacks a conceptual base. Adv Eat Disord. 2015;3:103–12.

    Article  Google Scholar 

  165. Dobinson A, Cooper M, Quesnel D. The safe exercise for every stage guideline – A clinical tool for treating and managing dysfunctional exercise in eating disorders. 2019. Accessed 23 May 2020

  166. Quesnel DA, Cooper M, Dobinson A. Safe exercise at every stage - athelte. 2020.

  167. Mountjoy M, Sundgot-Borgen J, Burke L, et al. The IOC relative energy deficiency in sport clinical assessment tool (RED-S CAT). Br J Sports Med Published Online First. 2015.

    Article  Google Scholar 

  168. Vancampfort D, Vanderlinden J, de Hert M, et al. A systematic review on physical therapy interventions for patients with binge eating disorder. Published Online First. 2013.

    Article  Google Scholar 

  169. Hausenblas HA, Downs DS. Exercise dependence: a systematic review. Psychol Sport Exerc. 2002;3:89–123.

    Article  Google Scholar 

Download references


We have no acknowledgments to make.


There is no funding, grants or awards to be disclosed in relation to this project.

Author information

Authors and Affiliations



DQ and MC undertook the conceptualization, article review process and manuscript writing. AD helped with the initial review process and writing. MFD reviewed and contributed to the manuscript. RC provided editing, clarifying scope and aim and final review of the manuscript. All authors read and approved the final manuscript.

Corresponding author

Correspondence to Danika A. Quesnel.

Ethics declarations

Ethical approval information

Given that this is a narrative review, this was no applicable.

Consent for publications

Not applicable.

Competing interests

DQ, MC, and AD receive training fees from the safe exercise at every stage guidelines. The remaining authors declare no competing interests.

Additional information

Publisher's Note

Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.

Rights and permissions

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit The Creative Commons Public Domain Dedication waiver ( applies to the data made available in this article, unless otherwise stated in a credit line to the data.

Reprints and permissions

About this article

Check for updates. Verify currency and authenticity via CrossMark

Cite this article

Quesnel, D.A., Cooper, M., Fernandez-del-Valle, M. et al. Medical and physiological complications of exercise for individuals with an eating disorder: A narrative review. J Eat Disord 11, 3 (2023).

Download citation

  • Received:

  • Accepted:

  • Published:

  • DOI: