Overtraining Syndrome (OTS) in Three Endurance Athletes and Roads to Recovery

Summary

Overtraining syndrome (OTS) is a significant medical condition observed predominantly in endurance athletes and characterised by a decline in performance and disruptions in multiple physiological functions. Given the increasing popularity of endurance training and the complex nature of OTS diagnosis, there is a compelling need for comprehensive case studies. The case series summarises one professional runner, one competitive runner and one recreational runner who were diagnosed with OTS. Key parameters observed include symptoms, diagnostic journey, recovery initiatives and return-to-sport outcomes. All three athletes showed typical OTS manifestations, including impaired performance and multisystem dysfunction (ie, endocrine, nervous, immune and gastrointestinal systems). Following a mandated cessation from training, active recovery strategies were instituted. Two of the three athletes successfully returned to competition. Specific recovery patterns and potential relapse indicators were also identified. The comprehensive examination of the cases underscores the complex nature of OTS diagnosis, its multifaceted symptoms and the critical importance of structured recovery. The case series elucidates the importance of heightened awareness and early intervention to diagnose and manage OTS. In addition, we propose an anecdotal Return to Running Protocol individualised to the athlete’s response.

Background

Overtraining syndrome (OTS) is a severe medical condition predominantly observed in endurance and ultra-endurance athletes. This condition arises from a maladaptive physiological response with an aetiology and pathogenesis that remain multifaceted and largely elusive.^{1 2} It is widely accepted that excessive exercise or training, in isolation, is not the exclusive causative factor behind OTS.² Symptoms associated with OTS are variable but coincide with a decline in athletic performance due to over-reaching. Affected individuals often exhibit signs of inadequate rest and disturbances to critical physiological functions, encompassing endocrine imbalances, autonomic nervous system irregularities (like sympathetic–parasympathetic imbalances resulting in fatigue, depression and bradycardia), and disruptions in musculoskeletal, cardiovascular, immune and metabolic systems.^{2 3} There are many potential triggers for OTS (eg, sleep disturbance, altitude exposure, heat stress, work stress and social stress).^{1 2} Contemporary literature advises prevention and provides limited clinical recommendations for intervention beyond full rest.⁴ Definitive protocols for a safe return to sport or evidence-based methods to circumvent relapse are unknown to the authors.

The increasing appeal of running and endurance training across age groups and genders has highlighted the complexity and importance of OTS diagnosis. The low incidence of OTS can lead to misdiagnoses among athletes, coaches and even experienced medical professionals. Symptoms of OTS can affect elite and recreational athletes. Athletes accustomed to pushing their bodies beyond conventional thresholds are at an elevated risk.⁵

To our knowledge, this is the first manuscript with the aim to illuminate OTS through the examination of recent cases diagnosed in professional and non-professional endurance runners (two males and one female) diagnosed with the syndrome. Our narrative will show how each athlete, after a necessary hiatus from training, successfully transitioned through active recovery. Two of the three athletes returned to full competition. The third case is an athlete who is in recovery at 22 months from OTS diagnosis and is actively engaged in the Return to Running Protocol.

‘Diagnosis by exclusion’ refers to a medical approach to diagnose a condition by ruling out other diseases or conditions that present with similar symptoms. The process can be lengthy and involve an array of medical tests, all of which can be mentally, physically and emotionally taxing on athletes. For those eager to return to their sport, the ambiguity surrounding the timeline of diagnosis and recovery can be an added strain, emphasising the need for greater awareness and understanding of OTS among medical and sporting communities.

Case presentation: Case 1

An elite-level male competitive mountain runner with elite maximum oxygen consumption (VO₂ max) in his 30s had finished his best competitive ultramarathon season to date—competing in six of the most competitive ultramarathon races in the world with podium finishes in four races. This athlete took no time off from that season and continued training at a high level into the next race season. Additionally, he had a high-stress job.

While training 20–25 hours a week, he began experiencing heart palpitations, hyperventilation, muscle cramping, extreme fatigue, upper respiratory infections (URIs) and significant appetite swings. He ignored symptoms, continued training and entered his first race of the season.

Halfway through the first 50-mile race, he hyperventilated, experienced dizziness, was forced to walk and barely finished, noting decreased performance, profound fatigue and lack of vigour prior to and after the race.

Case 1: Investigations

He visited a sports medicine physician approximately 3 months after the onset of symptoms and impaired run performance. Blood test results were unremarkable. The doctor attributed his performance, fatigue and related symptoms to persistent URIs, strenuous training load, work-related stress and fatigue. He continued to train despite experiencing ongoing symptoms. 1 month later, he completed a highly competitive 100-mile race. Two-thirds of the way into the race, the same symptoms recurred but were more severe than before. He was forced to walk the last third of the race but did finish.

He had a very hard time recovering after the 100-mile race and experienced chronic fatigue, malaise, sleep disruptions and mild depression. The athlete only reduced the training load and then competed in another 100-mile race 3 months later. During this race, he again experienced the same symptoms of extreme fatigue, hyperventilation, racing heart rate (HR) and severe muscle cramps, but with new uncontrolled vomiting that caused him to withdraw at Mile 65.

Case 1: Treatment

After this race, he returned to the same sports medicine physician, now 6 months after the onset of symptoms. Laboratory results at that time were within normal ranges or otherwise unremarkable. However, a diagnosis of non-functional over-reaching and presumptive OTS was made based on decreased performance and clinical symptoms. The athlete was informed that the only significant intervention was rest; he was prescribed a 4-month rest period, which involved no running and keeping his HR below 120 beats per minute with any activity, based on 60% of his maximum HR by VO₂ max testing. The athlete primarily rested and complied with a limited HR during activity, which included light cross-country skiing and limited strength training.

Case 1: Outcome and Follow-up

After 4 months of rest, the athlete began planning his return to running. The physician advised him to remain intuitive to how he was feeling daily. This included acknowledging all the physical, emotional, work and relationship stressors in his life, as they all would impact his recovery. Six months after prescribed rest, he returned to running a few days a week with a goal HR below 140 beats per minute. If the athlete felt symptoms returning, he would add extra rest days. 7 months after diagnosis, he was able to gradually increase his training volume and intensity with higher HRs. 9 months after diagnosis and 15 months after the onset of symptoms and impaired run performance, he was able to race again without the prior noted OTS symptoms. This athlete has returned to sport fully; however, the athlete is not able to race at maximum effort in competitions.

Case presentation: Case 2

An ultra-distance runner in his 40s with an elite VO₂ max has a 5-year training history including 10–15 hours a week of training on average and non-professional competition. He took a planned leave of absence from his career to fully focus on training and racing. He relocated from sea level for altitude training for 3 months at 8000-10000 feet above sea level. Training history included 10–15 average hours a week and competition non-professionally for 5 years. Initial symptoms at altitude were subtle and included voice hoarseness, dehydration and non-exertional diarrhoea. While training at altitude, he also noticed a depressed HR that did not match the high effort of training activities. His sleep quantity was over 10 hours, but the quality was poor, leading to constant fatigue. It was presumed to be impaired performance due to high-altitude training.

Two months after completing a 100-mile ultramarathon and on returning to sea level, symptoms became more pronounced along with continued impaired performance. He suffered from excessive sweating (exertional and night sweats), episodic dizziness and palpitations. While participating in another ultramarathon (8800 feet peak altitude), he withdrew at the 40-mile point due to persistent dizziness.

His health and maladapted physiology continued to deteriorate over the next month, and symptoms included severe vertigo, new insomnia, intense migraines, pronounced cognitive fog, and temperature and light sensitivities. Prior medical history was negative for depression. More than a year after initial symptoms, he faced debilitating depression and mental despair due to symptom intensity and a lack of unifying diagnosis from multiple clinicians. Following the advice of a fellow athlete, he subsequently consulted with a specialist at a sports medicine centre approximately 12 months after the onset of symptoms and impaired performance, who diagnosed OTS.

Case 2: Investigations

After exhaustive medical evaluations, Lyme disease, cardiac disease, calcium imbalances, postural orthostatic tachycardia syndrome and relative energy deficiency in sport (RED-S) were ruled out. He had a complete endocrine evaluation including thyroid-stimulation hormone, T4, total testosterone, free testosterone, sex hormone-binding globulin, luteinising hormone, follicle-stimulating hormone (FSH), prolactin and cortisol. An MRI of the pituitary gland was conducted, which showed no structural abnormality. Adrenal insufficiency was ruled out. These labs were unremarkable except testosterone was 1.6 ng/dL (reference range: 1.8–6.8 ng/dL). Due to the absence of RED-S, he was diagnosed with OTS, which in turn led to hypogonadotropic hypogonadism.

Case 2: Treatment

Treatment included weekly testosterone injections for 2 months with no significant improvement in the patient’s symptoms. In addition, he was unable to continue training and was forced to allow physiological recovery.

Case 2: Outcome and Follow-up

Further medical complications included an obstructing calcium oxalate calculus with moderate hydronephrosis and a penile fracture with urethral laceration during sexual activity that required three surgeries and multiple visits to the emergency department.

Six months after the last testosterone injection, the athlete started naturopathy. This approach identified Helicobacter pylori (H. pylori) and Candida overgrowth in the gut. A naturopath prescribed daily testosterone cream applications and prescribed an antibiotic regimen targeting H. pylori, which brought about clinical improvement while also resting from training.

Over the next 2 years, the ultrarunner began to slowly recover, but the road to recovery was riddled with deceptive intervals of improvement and flares. As a result, the athlete had heightened vigilance for early warning signs of overtraining, such as a hoarse voice post-workout, sunken eyes, sleep disruptions and irregularities in HR or heart rate variability (HRV) data. Approximately 3 years from initial diagnosis and 4 years from the onset of impaired performance, the patient’s training hours surpassed his pre-OTS benchmarks, although at a 10–15% average lower HR intensity than his prior maximum rate. His success currently in competitive ultrarunning has exceeded his pre-OTS experience, including his body’s ability to recover naturally without relapse.

Case presentation: Case 3

A perimenopausal female recreational athlete intensified her athletic journey in her late 40s to improve her health. With the goal to eventually qualify for the Boston Marathon, she regularly performed endurance running, cross-trained with high-intensity interval training and performed vigorous hikes at elevation. Her training intensified during the COVID-19 pandemic, with no rest days for several months. While training and completing two regional marathons, she began having multiple musculoskeletal injuries, including stress reactions, hip tendinopathy and labral tear, and athletic pubalgia. Additional symptoms included significant weight and muscle loss, runner’s diarrhoea with incontinence, non-exertional diarrhoea, intermittent chest discomfort and symptoms consistent with potential perimenopause (ie, night sweats, dizziness and secondary amenorrhoea).

During peak training for her third marathon, in hopes of improving her constellation of symptoms, she increased her caloric intake, which was only 1300 calories daily, up to 2000 calories (31 cals/kg/day). This resulted in unusual, erratic and transient decreases in HR relative to her rate of perceived exertion (RPE), marking the onset of persistent impaired running performance. She was subsequently evaluated by a sports cardiologist due to her symptoms. At this time, she was in her 50s with an excellent VO₂ max, but decreased performance and ongoing symptoms led to a withdrawal just days before her scheduled race.

Case 3: Investigations

A cardiac evaluation for her chest pressure and dizziness returned normal results. A comprehensive gastrointestinal workup ruled out coeliac disease, H. pylori infection, Giardia, pancreatic exocrine insufficiency, bile acid bowel dysfunction and other rare conditions. Further tests for faecal incontinence, including anorectal manometry, rectal ultrasound and repeat colonoscopy were negative.

Through her clinical course, laboratory tests were conducted to rule out other causes for the decreased performance. A complete blood count, comprehensive metabolic panel, thyroid function tests, cortisol, adrenocorticotropic hormone, vitamin B12, folate, phosphorus, testosterone, estradiol and prealbumin were unremarkable, including no evidence for hypothalamic amenorrhoea.

Evaluation by a sports cardiologist included a review of her exercise history and additional cardiac testing. Her persistent resting bradycardia was deemed clinically consistent with her high fitness level. She was then diagnosed with OTS with RED-S. Additionally, a sleep study was performed and was negative for sleep apnoea as a cause of eventual metabolic alkalosis.

Case 3: Treatment

With the diagnosis of OTS and RED-S, she was prescribed rest, continued adequate nutrition and prioritisation of sleep. Pelvic floor physical therapy and loperamide (Imodium) were unsuccessful for faecal incontinence. Her musculoskeletal injuries were managed with physical therapy, acetaminophen, naproxen, other non-steroidal anti-inflammatories and ice. When her symptoms worsened, she received steroid and plasma-rich protein injections.

Case 3: Outcome and Follow-up

Initially, the OTS with RED-S diagnosis was treated with cessation of all training except core functional training three times per week for 30 min per session. Despite over 2 years of adequate caloric intake with return to pretraining body composition, impaired performance persists. Recovery was complicated by, but not limited to, the following: an acute URI with periorbital cellulitis, severe dizziness, persistent fatigue, headaches, finger stiffness, brain fog, tachypnoea and dyspnoea on exertion. Laboratory evaluations during this time showed increased FSH and decreased estradiol and testosterone levels consistent with a menopausal state. Strength training was started at 3 months postdiagnosis when her body composition returned to her pretraining state, but symptoms continued.

Six months after the diagnosis of OTS and RED-S, she was found to have metabolic alkalosis and respiratory acidosis. This state was made worse after a visit to a higher altitude, which triggered increasing night sweats and daytime sweating along with many of the aforementioned symptoms. Treatment included acetazolamide, walking while submerged to the neck in water, respiratory efficiency physical therapy and effervescent tablets for acute symptomatic relief. Her symptoms gradually improved over the next month with this treatment, with further improvements over 6–9 months. Subsequent investigations to delineate any underlying associated pathology did not reveal hypoxaemia, sleep disordered breathing or other contributing factors beyond her OTS. Finally, in the first year postdiagnosis, the athlete continued to have episodic symptoms of severe calf burning.

In the second year after OTS diagnosis and with the reintroduction of cardiorespiratory training, the athlete continued to have medical issues. At 15 months, she experienced night sweats (previously controlled), headaches, dizziness, balance problems and benign paroxysmal positional vertigo, along with intermittent nausea, loss of appetite, fatigue, brain fog, emotional sensitivity and chronotropic incompetence during exercise. These symptoms hindered her return to running primarily due to dyspnoea, disordered breathing and intense bilateral calf burning. At 18 months, she resumed hiking on a gradual schedule and completed her first successful hike with a steady 500-foot incline. However, within 48 hours, she presented to the emergency department with a partially obstructing calcium phosphate stone in the left proximal ureter requiring surgical treatment. As a result of the renal stone, the patient was switched from acetazolamide to an alternate regimen to decrease carbonic anhydrase activity (hydrochlorothiazide, cetirizine and aspirin). Remarkably, after precisely 12 months of treatment for symptomatic respiratory alkalosis, during a 30-minute training session, she began to run 5-minute intervals with 2-minute recovery walks. At 20 months, she returned to the emergency department with a lower gastrointestinal bleed of uncertain aetiology but possibly related to aspirin use. Aspirin was changed to low-dose aspirin, and the athlete continued cetirizine and hydrochlorothiazide. At this point, she started to run 15-minute intervals with 3-minute recovery walks during a 60-minute training session.

The athlete’s journey has been lengthy and involved multiple body systems—testing both her physical and emotional resilience. Previously content and optimistic, she faced periods of sadness as she drastically reduced or ceased most physical activities following her OTS diagnosis. Despite the challenges, she remains hopeful about returning to running, the sport that she loves.

At the time of this report, the athlete can run continuously for 45 min and has been able to tolerate altitude exposure to 5400 feet. She has postponed her next marathon, but plans to gradually build her marathon training once fully recovered from OTS.

Discussion

OTS is described in literature as a rare entity^{1 2}; however, it is the authors’ and athletes’ opinion that the condition is likely under-reported. In addition, OTS, postviral syndrome, postacute COVID-19 syndrome and myalgic encephalomyelitis/chronic fatigue syndrome have significant overlap of symptoms and may complicate diagnosis. RED-S must be recognised as a frequent contributing factor to OTS, but they can both exist individually.^{6 7} OTS is a state of maladapted physiology and not simply undernourished physiology. Our case series represents the common delay in diagnosis and significant disruption in the athlete’s life beyond impaired performance, not relieved with rest from training and adequate nutrition for training. The multiple symptoms and varied expression of OTS still respond to planned rest along with focusing on lifestyle medicine such as sleep, nutrition and stress resiliency. Unfortunately, not enough attention has been given to the existential stress experienced by an athlete in recommending forced rest while also experiencing many apparently unexplained symptoms.⁴ It is our hope that the anecdotal ‘Return to Running Protocol’ will help medical providers safely guide athletes back to running in a safe manner while recognising the stress and anxiousness experienced.

These athletes shared their case studies to show commonalities and presenting symptoms beyond an uncertain or vague decrease in performance. The diagnosis of OTS is often a process of elimination.1,3 Evaluations provide reassurance because the extensive testing was generally ‘normal’, but also frustrating because it signalled to the athlete that ‘everything is ok’ when they were keenly aware of the body’s inability to train or perform. The seriousness of OTS, because it is rare, is often misunderstood. The condition may continue to evolve through multiple body systems even after cessation of training.

A widely accepted return to running protocol does not exist following a diagnosis of OTS. In the absence of a formal guideline, the runners represented in this article were able to return to running based on a 3-phase approach from full stop to active recovery, progressively building training volume and load (See table 1). The proposed anecdotal ‘OTS Return to Running Protocol’ is based on general principles of sports medicine and consultation with coaching, nutrition and medical experts in OTS.^{8 9} All phases should be monitored by a multidisciplinary team with knowledge and experience with OTS consisting of the following: (1) sports medicine specialist, (2) sports registered dietitian with any concern for concurrent RED-S and (3) sport-specific coach.

Table 1. OTS Return to Running Protocol.

Phase	Action steps	Recovery prescription
Phase 1	Full stop in cardiovascular activity (except for very light intensity) and heavy strength training. Focus on proper fuelling and overcoming any prior relative energy deficiency.	Frequency: ≤3 days per week. Intensity: no increased HR or RR and RPE <3 (out of 10=very light activity). Time: <50% of weekly volume before a decrease in performance. Type: START walking, cycling, swimming—generally, non-impact, limited-weight bearing, along with tolerated core exercises.
Phase 2	Initiate approximately 12 weeks postdiagnosis; begin to reintroduce minimal cardiovascular activity for aerobic base.	Frequency: ≤4 days per week. Intensity: lower of HR <120 or 60% max HR (decrease with any symptoms) and RPE <4–6 (out of 10=moderate activity). NO intervals or tempo pace. Time: building up to 75%–80% of weekly running volume before a decrease in performance. For strength training, introduce short 30-minute sessions 1–2 times per week. Monitor how you feel during and after the session; increase/decrease accordingly. Type: START of running. CONTINUE walking, cycling and swimming. START hiking and resistance band cross-training.
Phase 3	Graduated re-entry informed by RPE and recovery parameters (ie, HRE).	Frequency: ≤5 days per week. Intensity: 90%–95% of time at the lower of HR <120 or 60% max HR (decrease with any symptoms) and RPE <4–6 (out of 10=moderate activity). 5%–10% of time with RPE 7–8 (out of 10=vigorous activity) with intervals or tempo pace. Time: building to 90%–100% of weekly volume before a decrease in performance, adding 1 then 2 episodes at RPE 7–8. Type: CONTINUE running, hiking, cycling, swimming, functional strength training.

HR, heart rate; HRE, heart rate variability; RPE, rate of perceived exertion; RR, respiratory rate.

These runners came to a full stop in running activity and all other cardiovascular activities in Phase 1. Like other protocols, when an athlete is injured or encounters a significant illness, training load is significantly reduced with consideration of the severity at initial diagnosis and medical attention for maladapted signals that may persist weeks to months after the athlete comes to a full stop.⁸ Duration of recovery is difficult to predict because it is individualised for each athlete, based on time to diagnosis, duration of impaired performance and degree of symptoms. If URI and/or urinary tract infection were present at diagnosis, infections were resolved before advancing exercise. Unlike injuries, multiple body systems are involved with a diagnosis of OTS; therefore, acute symptoms and coexisting medical conditions must return to baseline or resolve during Phase 1 in the Return to Running Protocol. In addition, focus was made to ensure adequate energy intake for recovery, which included weight gain for 2 of the 3 athletes. For some athletes, Phase 1 could extend 8 weeks or 2 years from presumed OTS diagnosis. The athlete should continue gentle active recovery to include walking, easy effort cycling or swimming, with an anecdotal recommendation to keep efforts well under 60% maximum HR. The athlete learns to watch and listen to cues from the body during this phase.

Beginning with Phase 1, the athletes monitored resting HR, HRV if previously used during training, and the athletes reported vigour and RPE of limited movement. If sleep was compromised in quality or duration, the athletes worked to restore it during Phase 1. Before advancing from Phase 1, these athletes achieved a basic level of general wellness, including mental clarity and resolution of any brain fog and/or mental health challenges. Phase 1 is a perfect time to focus on HRV trends if previously monitored, and can help guide the return to running with an educated sports medicine provider or coach. The state of physiology during recovery may be improved with HRV monitoring, but more research is needed.¹⁰

HRV is a measure of the natural millisecond variability variation in HR in response to one’s respiratory rate (RR). In short, it is accepted that a well-recovered athlete will have increased responsiveness to the RR due to higher relative parasympathetic tone—resulting in a higher HRV. On the contrary, a stressed body will have a higher relative sympathetic tone, leading to a lower HRV. It is generally accepted that the most reliable measurements for HRV are performed over 5–10 minutes in the same position (lying or sitting) and state (fasted with an empty bladder) among measurements. Each individual has a personal HRV range and average, and, as such, the use of HRV in training and return to running from OTS is highly individualised. Results are frequently normalised to the individual’s history and/or monitored with a 3- or 7-day rolling average. However, there are shortcomings in using only HRV to guide training and return to running. In more general populations not specific to OTS, a meta-analysis of HRV studies does find potential benefits of HRV-guided training, but the effect size may be small.¹⁰ However, in a disease state, such as OTS, the value added of training by HRV might be greater.

During reintroduction to sport, the coach and medical team must consider training stress. Stress-informed coaching considers weekly distance/volume in addition to intensity as measured by RPE, HR zones and possibly blood lactate level to avoid musculoskeletal injuries or over-reaching, along with psychological markers such as ‘vigour.’^{2 4 9}

When the athletes entered Phase 2 of the Return to Running Protocol, minimal cardiovascular activity and intensity were reintroduced. Running began with a very short period of time, and the athlete self-assessed the body’s response along with resting HR and HRV. These athletes began with HR at approximately 60% of maximum. If the first attempt at running was asymptomatic, then they repeated the same prescribed exercise a few days later. If still asymptomatic, then they considered increasing running volume over the first week with gradual incremental increases in subsequent weeks. It is recommended to add running volume over adding running intensity. If the athlete experiences symptoms while running volume increases, then pause cardiovascular activity and reduce volume until symptoms subside. During Phase 2, strength training can be initiated provided the HR stays low, and fatigue and symptoms are absent.

During Phase 3, athletes begin to increase short periods of running intensity with a slight drop in previously tolerated running volume. The athlete and coach should focus on HR during activity (speed drills, >60% max HR) and watch how the body responds to elevated HR and increased intensity through resting HR and HRV. Hiking can help build strength and power in the legs during this phase. These athletes avoided activities that created too much stress on the body (eg, heat training or altitude exposure).

After these runners executed phases 1–3 and were asymptomatic, then they were ready to re-enter traditional endurance training. Considering the limited number of OTS publications, the authors acknowledge that the anecdotal OTS Return to Running Protocol calls for more research and reporting—especially of cases with successful return to sport.

Patients’ perspectives.

CASE 1

Over Training Syndrome was a complete unknown to myself and my peers in the ultra-endurance world of running when I found myself confronting it. Over a decade ago, I was in peak fitness and the height of my racing career I, along with three other elite ultrarunners, found ourselves hollow shells of our former athletic selves, experiencing strange symptoms during training and racing. I suddenly went from confidently being able to race at the highest level to suddenly not being able to complete routine training runs, and unable to complete races. The physical symptoms ranged from chronic fatigue, muscle cramping, hyperventilating, dizziness, vomiting, upper respiratory illnesses and sleep disruption. Worse, however, were the mental and emotional symptoms; depression, malaise and questioning what was happening, with no concrete diagnosable medical issues that my primary care physician could pinpoint. I tried to continue training and racing, but everything got worse. I finally was able to consult with a Sports Medicine doctor that diagnosed me with over-reaching and over-training syndrome. An eventual hard-stop from running and training, for many months, helped me eventually return to my sport. However, I never felt I was able to regain my previous form or fitness. And I learnt during this time that many other athletes had, or were, experiencing similar things and no one could find medical support or resources that could help them, or understand what they were going through. I truly hope my case can help further educate and inform both the medical community and athletes, so others never get to the point of over-reaching or over training.

CASE 2

The symptoms of OTS started as confusing and annoying, and over time became life-changing and debilitating. At their worst, I couldn't get restful sleep, any exercise would result in migraines and bed rest for days. I couldn't think or talk clearly, and it felt like my body was falling apart. Going from someone who would run >100 miles/week in training to being unable to slowly jog 1 mile was frustrating. The lack of diagnosis or understanding by all of my initial medical support team, and their insistence that I was perfectly healthy, took a mental toll and resulted in a deep depression. Once I was finally diagnosed, the road to recovery and return to sport felt long and at times impossible. Through years of trial and error, I had to learn to listen more closely to my body’s signals. As a result, I am now able to spend more time running and climbing in the mountains than I could before, and I've had more competitive success in ultramarathons.

CASE 3

I had never heard of OTS. When I received the diagnosis, it took time for me to fully appreciate what it was, what body systems were linked to this diagnosis, how long I would need to rest and when I could run again. Then I wondered if I would have this forever. It was hard to stop running and hiking abruptly. It was unclear if I would ever run again. I had ‘red flags’ but they were easily dismissed. Training for an endurance event requires grit and intense training, even when you don’t feel good. Everyone thought I must be stressed, but I wasn’t. I watched the total body rash spread through my limbs and up to my eyelashes, but it was the pain that surprised me because all the teeth in my mouth hurt during this rash. Luckily the oral steroids corrected this quickly. I knew I was cycling between URI but thought it was just a ‘Runner’s Cough’ during winter months. I knew I was tired, but I ran early in the mornings. I knew my hip pain was flaring, but I was in peak training. I had an important deadline at work the week of my final marathon training run. I realise now it was a perfect storm. I thought once I went ‘full stop’ that everything would heal, but things continued to unravel after diagnosis. The worst part was still coming with a blood-base acid imbalance. I travelled to where I had run a marathon, but this time I couldn’t jog more than a few minutes without feeling ‘winded’. I had shortness of breath during exercise but also with speaking in meetings/presentations at work. I would cough when trying to speak, and my voice tone was quiet. My family asked me to repeat myself many times because I spoke quietly to them or mumbled my words as my breathing became shallower. I had debilitating bilateral calf burning/pain when I would attempt to run. My fingertips would turn red and burn, if I had exerted myself. We discovered I was breathing vertically, and I had to work with a Physical Therapist (PT) trained in respiratory efficiency to re-teach my body to breath diaphragmatically. I was a marathon runner—how was it possible that OTS attacked my breath, too? While I was working to improve my breathing, my right shoulder froze. What was I doing so wrong to cause yet another anatomy to fail me? I could barely comb my hair because the pain was limiting and severe. I restarted hiking on a wheel-chair path. Me—a good endurance runner and hiker now hiking with poles on a wheelchair path/trail. I remember being so excited to have finally accomplished a real hike and then 2 days later telling my husband ‘something is wrong’ and we went to the ER for the kidney stone. I was ashamed. I went from being able to run 4 hours to just barely 45 s. I felt like I was blindly waiting for the next landmine to explode inside me as OTS relentlessly attacked me. I was unable to participate in non-running activities, because I did not have the voice or stamina to sing with a choir that I had long been a member, nor did I have the strength to push clay together to make pottery without physically crashing. The grief of a life I used to know was strong. I learnt I had to exercise alone during recovery and go at my own speed when my HRV was balanced. Socially one of the most difficult parts was trying to explain what OTS is because it is ‘invisible’ to others and the name merely suggested I had just done one too many workouts. At 22 months postdiagnosis I’m beginning to jog again. It is hard and has taken a serious amount of persistence. My support team included close follow-up from a multidisciplinary team including a sports cardiologist, aerospace medicine physician and nurse, orthopaedic physician, respiratory physical therapist, mental performance coach, registered dietitian, strength trainer and run coach experienced with OTS. OTS completely changed my life. There are no support groups for OTS, and I am grateful to the athletes included in this article who have been my lifeline. I believe I may have died without the intervention of my sports cardiologist and Aerospace physician; they sought medical solutions and continue to believe in my full recovery. My deep wish is for my experience to help others. Running a marathon is not the hardest thing I have ever done. Waking up and living with OTS is the hardest thing I have ever done.

Learning points.

• Overtraining Syndrome (OTS) is a rare but devastating condition most often seen in endurance athletes.

• OTS can have many different presentations and roads to recovery. It is a multisystem disease that requires awareness of the condition and challenges in management to facilitate direction to appropriate specialists.

• Return to sport is possible after OTS, but requires a knowledge of potential triggers and roadblocks to recovery.

• A phased return to running is possible with interdisciplinary support and comanagement with the athlete, including close monitoring of training stress and the body’s response through subjective feelings, resting heart rate and heart rate variability.