Abstract
Background
Swimming-induced pulmonary oedema (SIPO) has predominantly been reported in swimmers. However, to date, no review has specifically explored the scientific literature concerning the occurrence and characteristics of SIPO in triathletes. Therefore, this review aims to summarize and discuss the current evidence on SIPO in the context of triathlon.
Methods
We conducted a narrative review to summarize the current scientific literature on SIPO in triathletes. A structured search of two major databases—PubMed and Scopus—was conducted using free-text terms related to SIPO and triathlon. The search included articles published up to January 2025, with no language restrictions. After removing duplicates and excluding animal or in vitro studies, as well as unrelated articles based on title and abstract screening, a total of 48 relevant publications were included for analysis.
Results
The reports on SIPO in triathletes are mainly case reports or case studies on a single athlete or a small number (case series) of triathletes. Most reported cases involved middle-aged women (30–60 years) participating in IRONMAN® 70.3 and IRONMAN® triathlons. The prevalence of SIPO in triathletes is reported to be less than 1.5%. Risk factors for SIPO in triathletes are female sex, age over 50 years, hypertension, fish oil consumption, highly trained individuals, competitive exercise, wet suit compression, longer race distances (i.e. IRONMAN® 70.3 or IRONMAN®) and a cold (water) environment. The symptoms and outcome are similar to those observed in swimmers and other aquatic athletes.
Conclusions
In summary, the results regarding the prevalence, symptoms and risk factors of SIPO in triathletes are comparable to those in other aquatic athletes. SIPO occurs only in IRONMAN® 70.3 and IRONMAN® races, but has not been reported in the Olympic distance triathlon or triathlons longer than the IRONMAN® race distance.
Keywords: Pulmonary involvement, Coughing, Shortness of breath, Strenuous physical activity, Cold water
Abbreviations
- CRP
C-reactive protein
- CT
Computed tomography
- EAH
Exercise-associated hyponatremia
- ECG
Electrocardiogram
- EIPE
Exercise-induced pulmonary oedema
- IPO
Immersion pulmonary oedema
- LV
Left ventricle
- LVA
Left ventricular area
- LVH
Left ventricular hypertrophy
- RVS
Right ventricular surface area
- SCUBA
Self-Contained Underwater Breathing Apparatus
- SIPO
Swimming-induced pulmonary oedema
- TCM
Takotsubo cardiomyopathy
1. Introduction
Triathlon is a multidisciplinary endurance sport—or ultra-endurance sport when its total duration exceeds 6 hour (h)—comprising sequential swimming, cycling and running over varying distances. Although it is becoming increasingly popular among both sexes and all ages, participation in this sport is not without risks and may result in health conditions such as hyperthermia and exertional heatstroke,1 gastrointestinal symptoms,2 muscular exhaustion, and musculoskeletal injuries,3 as well as dizziness.4
In addition to these medical concerns, increased scientific interest has recently focused on swimming-induced pulmonary oedema (SIPO) in triathletes in case reports or case studies.5, 6, 7, 8, 9 SIPO is a form of exertional pulmonary oedema characterized by fluid accumulation in the lungs during swimming or other forms of water-based exercise.10,11 SIPO was first described in scuba divers in 1981.12 Since then, SIPO has been reported in various aquatic athletes, including triathletes.13 Clinically, SIPO is characterized by the acute onset of dyspnea, coughing, and in some instances, hemoptysis, typically triggered during or shortly after water immersion.14 The underlying mechanisms and clinical consequences of SIPO remain incompletely understood, and the specific factors predisposing individuals to its occurrence have yet to be established.15 The pathophysiology of SIPO involves a combination of increased pulmonary capillary pressure, cold-induced peripheral vasoconstriction, and central blood volume redistribution leading to central blood pooling.5 SIPO occurs in aquatic activities such as swimming,16,17 snorkeling,18,19 scuba diving,16,17,20, 21, 22 combat swimming,23 special tactics military training,11 United States Navy Sea, Air, and Land candidates,24 underwater military recruits,25 breath-hold diving,26, 27, 28 ice diving at high altitude,29 open-water swimming,30,31 and triathlon,32 and even in young and healthy individuals.17
To date, research on SIPO has mainly been reported for swimmers.33 Little is known about SIPO in triathletes,33 as the prevalence of SIPO in triathlon has been reported to be low at ∼1.5%.34,35 Nevertheless, the increasing popularity of triathlon,36 has resulted in SIPO being more frequently acknowledged.
Although SIPO is often self-limiting, in severe cases it can result in life-threatening respiratory distress, making it an important concern for athletes, coaches and medical professionals. Despite the increasing awareness of SIPO, research focusing on triathletes remains limited, with most of the available literature comprising case reports and small case series.32,37,38 Further research into the prevalence, risk factors and outcomes of SIPO in triathletes is needed to improve prevention and management strategies.
Therefore, this review aims to summarize the current scientific literature on SIPO in triathletes, highlighting its epidemiology, risk factors, clinical presentation and management approaches. Given the increasing participation in triathlon worldwide, a comprehensive understanding of SIPO in this population is essential for clinicians, researchers and sports science professionals.39,40 This synthesis of current knowledge seeks to support future research and provide information for preventive and therapeutic interventions in endurance athletes. Although the prevalence of SIPO is low in triathlon, it will help triathletes and coaches to prevent SIPO in triathlon races. Especially since triathletes may die during the swimming split due to SIPE.41
2. Methods
The study was designed as a narrative review and the relevant literature was searched using a predefined search algorithm.42 Studies eligible for inclusion were those investigating swimming-induced pulmonary oedema in triathletes of all race distances.
2.1. Literature search strategy
The selected articles were related to swimming-induced pulmonary oedema in triathletes and were published until the end of January 2025, with no language restrictions. The search for sources of high-quality scientific information was conducted using two of the most widely used information databases in health and sports sciences – PubMed and Scopus.43 Free-text words were employed in the search.44 The following search terms were used: ((swimming induced pulmonary oedema triathlon) OR (swimming induced pulmonary oedema triathlete) OR (swimming induced pulmonary oedema triathlon) OR (swimming induced pulmonary oedema triathlete) OR (immersion pulmonary oedema (IPO)) OR (swimming-induced pulmonary oedema (SIPO) OR (exercise-induced pulmonary oedema (EIPE))). We found a total of 19 articles in the PubMed database (title) and 27 papers in the SCOPUS (title). In the end, a total of 46 articles were considered. Duplicates, animal studies, in vitro studies and articles not related to the topic were excluded after the initial screening of the search results (title and abstract screening). Further relevant studies were detected among the reference lists of the identified full-text articles and through a search in similar articles and citations (PubMed database). After selecting all relevant articles, a total of 33 publications were considered.
3. Results
The reports on SIPO in triathletes are mainly case reports or case studies on a single athlete or a small number (case series) of triathletes (Table 1).6,7,9,10,32,37,38,45, 46, 47, 48, 49, 50, 51 Most reported cases involved women,6,7,9,10,37,45,47,49,51 of an average age from 30 to 60 years.6,7,10,32,37,45,47,49,51 However, two male triathletes competing in the ‘Norseman Xtreme Triathlon’ have also been reported.32
Table 1.
Case reports of SIPO in triathletes.
| Case description | Reference |
|---|---|
| Subject: 58-year-old female triathlete in an IRONMAN® 70.3 competition. Observation: Acute dyspnea during the swimming split. Outcome: Complete resolution within 24 h of presentation | 10 |
| Subject: 37-year-old male triathlete. Observation: Two episodes of acute onset of severe dyspnea, cough and expectoration of pink frothy sputum during the swimming stage of two different races. On both occasions, the athlete was able to continue the cycling split of the race but at a slower pace and symptoms improved spontaneously once he reached the shore and rested. Outcome: All investigations conducted were normal, leading to the diagnosis of SIPO. | 47 |
| Subject: 57-year-old female triathlete. Observation: She was experiencing critical lung oedema during low intensity open-water swimming. Outcome: X-ray of the chest three months after the lung oedema showed a complete resolution of the oedema | 45 |
| Subject: 50-year-old male triathlete attempting his third IRONMAN®. Observation: He developed worsening dyspnea during the cycling and running splits, progressing to a cough productive of pink sputum and then hemoptysis. Outcome: He completed the IRONMAN® and clinical assessment was consistent with acute pulmonary oedema. | 48 |
| Subject: 55-year-old female triathlete. Observation: She developed recurrent episodes of SIPO. Outcome: She had two hospital admissions with pulmonary oedema after developing breathlessness while swimming, including a near-drowning experience in an open-water swim. | 37 |
| Subject: 38-year-old male triathlete who participated in a triathlon race. Observation: He experienced difficulty in breathing after swimming and was moved to a first-aid center. His initial oxygen saturation was 82% and a thoracic computed tomography scan showed bilateral ground glass opacity in the peripheral lungs. Outcome: His diagnosis was noncardiogenic pulmonary oedema associated with exercise or swimming. | 46 |
| Subjects: Five patients. Observation: They presented to an on-site medical team with concurrent hemoptysis and shortness of breath at a recent triathlon event. Outcome: After initial management in the field, three of the five patients were transported to hospital via ambulance for further management. | 50 |
| Subject: 45-year-old female IRONMAN® triathlete. Observation: She presented with somnolence and convulsions after finishing her first IRONMAN® triathlon. Besides the neurological symptoms she had a swollen face and swollen ankles. Rales could be heard on pulmonary auscultation. Radiological examination revealed pulmonary as well as cerebral oedema. She developed respiratory and hemodynamic failure, had to be intubated, mechanically ventilated and needed catecholamines. Outcome: One year later, she was again participant of the IRONMAN® triathlon. | 49 |
| Subjects: Three cases of recreational triathletes (two women and one men) aged 50–60 years competing in mass participation triathlons. Observation: They presented with SIPO following water immersion. They all presented with acute dyspnea on exiting the water. Two also presented with chest pain and hemoptysis. Outcome: They were subsequently diagnosed with Takotsubo cardiomyopathy (TCM). | 6 |
| Subject: 48-year-old female triathlete. Observation: She had a sudden attack of severe dyspnea during an amateur sports competition. The incident happened in a lake at a water temperature of 17 °C). After the triathlete swam a distance of 200–300 m she developed severe shortness of breath, which made it impossible to continue competing. The electrocardiogram was normal. Chest radiography (X-ray) revealed areas of marked parenchymal thickening in the lower and middle lung fields bilaterally. Echocardiographic evaluation of the right and left ventricular relations at different time points during the period of patient care; a marked change in the ratio between the right and the left ventricle areas (RVS/LVA) over several days of follow-up. Outcome: On the third hospital day, the patient did not report any complaints. Radiographic examination revealed regression of parenchymal lesions. The patient was reassessed 30 days after the incident. Laboratory tests showed complete normalization. Based on the overall clinical presentation and the results of additional examinations, the patient was diagnosed with immersion pulmonary oedema (IPO), also referred to as swimming-induced pulmonary oedema (SIPO), with features of acute right ventricular heart failure. | 7 |
| Subject: 31-year-old active-duty U.S. Army female triathlete with a past medical history of anorexia in remission. Observation: She presented with acute onset shortness of breath and chest pressure occurring within 250 m of the swimming portion of IRONMAN® 70.3 triathlon in water with a temperature of 70 °F (21.1 °C). She subsequently partially removed her wet suit and swam for a rescue kayak. Outcome: The patient was treated with 2 liters supplemental oxygen and 20 mg of intravenous furosemide. After treatment, she reported subjective improvement and was able to ambulate in the hallways with oxygen saturation ranging between 97% and 98% on room air. She was offered hospital admission for observation but refused and was released from the Emergency Department 5 h later. | 9 |
|
Subject: 30-year-old male professional triathlete competing in Norseman Xtreme Triathlon. Observation: During the swim, he wore a well-fitted wetsuit and neoprene swim cap. He later reported that he felt increasingly breathless and was struggling to keep the usual pace in the water just minutes after the start. He had not aspirated during the swim. He presented with shortness of breath, chest tightness and coughing up pink sputum during the last part of the bike phase. He reported an improvement in breathing during the first major uphill of the bike phase and increasing symptoms during the downhill. Observation: He managed to complete the 180 km long bike phase, but due to coughing and increased shortness of breath, he was forced to withdraw from the race just a few meters into the run phase and was transferred to the hospital. He had end-expiratory crackles bilaterally and a productive cough with pink sputum. He had facial oedema but no cyanosis. An echocardiogram was performed at arrival at the emergency department that showed a well-contracting, normal-sized left ventricle and mildly dilated right ventricle. A thoracic computed tomography (CT) scan showed bilateral ground glass opacity in the peripheral lungs but no pulmonary embolism. Due to the complete regression of symptoms, no treatment other than rehydration and oxygen was given during hospitalization. He was discharged from hospital the following day. Subject: 40-year-old female age group triathlete competing in Norseman Xtreme Triathlon. Observation: During the swim, she wore a well-fitted wetsuit and neoprene swim cap. She later reported that he felt increasingly breathless and was struggling to keep the usual pace in the water just minutes after the start. She had not aspirated during the swim. She presented with shortness of breath, chest tightness and coughing up pink sputum during the last part of the bike phase. She reported an improvement in breathing during the first major uphill of the bike phase and increasing symptoms during the downhill. Outcome: She was taken out of the competition by one of the race doctors. She was transferred to the nearest local medical center for further treatment but recovered quickly after being treated with oxygen and hospitalization was not indicated. Subject: 34-year-old male age group triathlete competing in Norseman Xtreme Triathlon. Observation: During the swim, he wore a well-fitted wetsuit and neoprene swim cap. He later reported that he felt increasingly breathless and was struggling to keep the usual pace in the water just minutes after the start. He had not aspirated during the swim. He presented with shortness of breath, chest tightness and coughing up pink sputum during the last part of the bike phase. He reported an improvement in breathing during the first major uphill of the bike phase and increasing symptoms during the downhill. Observation: He managed to complete the 180 km long bike phase, but due to coughing and increased shortness of breath, he was forced to withdraw from the race just a few meters into the run phase and was transferred to the hospital. Clinical examination reported end-expiratory crackles bilaterally but otherwise normal findings. No echocardiogram was performed. He was given diuretics and was discharged from the hospital with complete regression of symptoms the following day. |
32 |
|
Subject: 60-year-old male IRONMAN® triathlete. Observation: He became severely breathless while taking part in the swimming phase of an IRONMAN® triathlon. Thirty minutes into the open water swim, wearing a wetsuit, with a lake temperature of 13 °C, he developed sudden onset dyspnea. A doctor at the scene found widespread respiratory crackles, a systemic arterial oxygen saturation of 86% on air, a blood pressure of 131/82, respiratory rate 20 breaths per minute and heart rate of 77 bpm. On arrival at the hospital, he had an oxygen saturation of 95% on air with mid-zone crackles bilaterally. Electrocardiogram (ECG) showed non-pathological Q waves and saddle T waves with no ischaemic changes. A chest X-ray and routine bloods tests were normal with a C-reactive protein (CRP) of < 1 mg/L. An echocardiogram showed a left ventricular (LV) anteroseptal wall thickness of 14 mm, inferolateral wall of 12 mm, LV ejection fraction of > 55% and a mildly dilated left atrium of 29 cm2. A coronary computed tomography was normal. A diagnosis of probable SIPO was made. Outcome: He was discharged the following day with no on-going treatment and advice about the risk of recurrence. Subject: 55-year-old female triathlete, who regularly competed at World Championship level. Observation: She presented following sudden onset of shortness of breath, chest tightness and coughing up pink frothy sputum while undertaking a training swim in open water. In the Emergency Department, she had end-expiratory crackles bilaterally, with a systemic arterial oxygen saturation of 95% on air and no peripheral oedema. A chest X-ray was normal. Her ECG, CRP, D-dimer and Troponin were normal. Outcome: Ten days later, she was reviewed in the cardiology clinic. An echocardiogram was normal with an LV ejection fraction of 57% by biplane Simpson's method and LV wall thickness of 9 mm. No further treatment was given, and the patient was advised of future recurrence risk. She began training again after this episode. She was given a presumptive diagnosis of swimming-induced pulmonary oedema. |
38 |
Note: CRP, C-reactive protein; CT, computed tomography; ECG, electrocardiogram; IPO, immersion pulmonary oedema; LV, left ventricle; LVA, left ventricular area; RVS, right ventricular surface area. SIPO, swimming-induced pulmonary oedema; TCM, Takotsubo cardiomyopathy.
3.1. Prevalence of SIPO
The prevalence of SIPO in triathletes ranges from as low as 0.01%31 to 0.9%52 and 1.4%.13 No cases of SIPO were detected in the triathlon races at the 2020 Olympic Games in Tokyo.53
3.2. Risk factors for SIPO
Based on current knowledge, the female sex seems to be more prone to SIPO than the male sex,5,13,35 age over 50 years,5 hypertension,13,35,38 fish oil intake,13,35 highly trained individuals,38 competitive exercise,38 wet suit compression,5 long course distance (i.e. IRONMAN® 70.3 or IRONMAN®)13,35 and a cold (water) environment5,38 are considered risk factors for SIPO in triathletes.
3.3. Symptoms
The main symptoms include acute and partially severe dyspnea,6,7,10,47,48,52 shortness of breath,10,32,50,52 chest tightness,32 chest pain,6 cough10,32,47,52 and occasionally blood-tinged sputum10 or hemoptysis7,47,48,50,52 during the swimming portion of the race. According to Grünig et al.14 analysis of 38 cases, the primary symptoms at presentation were dyspnea (79%), cough (71%) and hemoptysis (68%). However, in some instances, symptoms may also occur later in the race during the cycling split.32 One problem is also that symptoms of SIPO can recur in the next races.6,47
3.4. Outcome
Symptoms usually subside within an instant to ∼48 h.7,47,48 In severe cases, athletes are transported to a hospital50 but often discharged the following day.6,32 SIPO also appears to be associated with exercise-associated hyponatremia (EAH).49
Death due to SIPO should not occur in triathletes during the swimming part of the race54, 55, 56 or after the swimming split of the race.54,57 Current evidence does not suggest that SIPO is a common cause of swimming-related deaths.54
Rather, there is strong evidence that sudden deaths in triathletes are often associated with cardiac abnormalities.33 SIPO in triathletes may be associated with Takotsubo cardiomyopathy.6 However, left ventricular hypertrophy (LVH) as a marker of swimming-induced pulmonary oedema (SIPO) was present in a greater than expected proportion of triathletes who died during the swimming portion.58
3.5. Prevention
The use of sildenafil as prophylaxis against SIPO was described in a case report of a 46-year-old female ultra-triathlete with a history of at least five SIPO episodes. She has had no recurrences during 20 subsequent triathlons while taking 50 mg of sildenafil before each swim.51 Sildenafil may reduce pulmonary vascular pressure and resistance in SIPO-susceptible swimmers in cold water.59 Since LVH has been found in triathletes who died while training for or during a triathlon event, the importance of testing for LVH in triathletes as a predictor of adverse outcomes should be considered.58
4. Discussion
This review aimed to consolidate current knowledge SIPO in triathletes—a condition that remains underrecognized despite its potentially serious clinical implications. While the available literature primarily consists of case reports and small case series, synthesizing this evidence reveals meaningful patterns regarding the prevalence, risk factors, clinical presentation, and outcomes of SIPO in the triathlon context.
4.1. Prevalence and comparative context
The reported prevalence of SIPO in triathletes ranges from 0.01% to 1.4%, with most estimates clustering below 1.5%. Interestingly, these values appear to be higher than those reported among open-water swimmers. For example, a large-scale Swedish cohort study covering over 47 000 open-water swimming distances found SIPO incidence rates of 0.75% in women and 0.09% in men, with incidence rising with age.31 The incidence increased with increasing age from 0.08% in the youngest age group (18–30 years) to 1.1% in the oldest age group (≥ 61 years).31 However, a literature review reported an incidence of SIPO of 1.1%–1.8% for swimming and diving.60 This discrepancy may be due to the unique demands and constraints of triathlon events, such as time-pressured swim starts, cumulative physical stress, psychological tension, or cold-water exposure under competition conditions. These findings suggest that SIPO may be more than just a rare complication—it may represent an underappreciated physiological stress response in a susceptible subgroup of triathletes.
4.2. Symptoms and clinical course
The clinical presentation of SIPO in triathletes typically includes acute dyspnea, cough, chest tightness, and occasionally hemoptysis, occurring during or shortly after swimming. The symptoms reported for SIPO in triathletes are the same as reported for other aquatic athletes such as swimmers, snorkelers and scuba divers, with coughing, shortness of breath and sometimes blood-tinged sputum.61 While most cases are self-limiting, resolving within 24–48 h, others may require emergency medical attention and hospitalization. Rarely, symptoms persist into the cycling segment of the race or occur in a delayed fashion.
Some case reports also suggest a link between SIPO and Takotsubo cardiomyopathy6 or LVH,58 which could indicate underlying myocardial stress. However, it remains unclear whether SIPO is a causal factor in such cardiomyopathies or whether both conditions reflect a common stress-related etiology. Although SIPO has been proposed as a possible cause of sudden deaths in triathletes, current evidence suggests that cardiac arrhythmias or structural heart disease are more commonly implicated. In a case report of a female triathlete, the authors argued that SIPO was due to a combination of stress-induced diastolic dysfunction, a tendency to vasoconstriction upon stress, and possibly paroxysmal atrial fibrillation induced by increased atrial pressure during the event.45
4.3. Risk factors for SIPO
In swimmers, there is, based on a systematic review, only limited evidence to suggest that there are pre-existing risk factors leading to SIPO with exposure to strenuous physical activity while swimming.33 When considering the literature on SIPO in sports disciplines other than triathlon, risk factors for SIPO include age > 50 years, female sex, fish oil consumption, overhydration before exercise, tight wetsuits, long course distances, hypertension, cold water exposure and physically trained individuals such as endurance athletes.35,60 Cold water appears to be the most important risk factor for SIPO in swimmers. A systematic review suggested a moderate association between water temperature and the prevalence of SIPO.33 Ultra-endurance exercise can lead to severe hyponatremia, pulmonary and cerebral oedema.49 This is caused mainly by fluid overload due to excessive drinking62 and a release of antidiuretic hormone induced by hypovolemia and stress which impairs the excretion of free water.63 Moderate fluid intake during performance is important.64
Female sex seems to be a risk factor to develop SIPO in triathletes. The case reports available in the literature suggest that SIPO in triathletes predominantly affects women. Similarly, a literature review focusing on swimmers identified female sex as a potential risk factor for developing SIPO.60 This is also reported in case reports.65 Here, biological factors may be determinants for SIPO. However, it is important to conduct future studies on this topic to establish inferences. The literature consistently reports a higher prevalence of SIPO among female triathletes, particularly those aged 30–60 years. Several factors may explain this sex disparity. Women generally have smaller lung volumes, different pulmonary vascular compliance, and may exhibit heightened vascular responses to cold exposure.66 Hormonal influences, such as the vasodilatory effects of estrogen and progesterone, may also affect capillary hydrostatic pressure regulation.67 However, the predominance of female cases could also reflect reporting or participation bias, as women in triathlon are often highly trained and health-conscious, potentially leading to greater awareness and diagnosis of symptoms.68 This pattern warrants further investigation through sex-stratified physiological studies.
The age of the athletes also needs to be considered as a potential risk to develop SIPO. The age of the athletes developing SIPO was reported to be at ⁓30–60 years. This is most likely because athletes of this age compete in both IRONMAN® 70.369 and IRONMAN®.70 A literature review on SIPO in swimmers also reported that age over 50 years is a risk factor for SIPO,60 which was also highlighted in the results of the present review.
The length of a triathlon race might also be considered a risk factor. IRONMAN® 70.3 and IRONMAN® races were mainly mentioned in the case reports. Also, ‘Norseman Xtreme Triathlon’ is a long-distance triathlon covering the full IRONMAN® distance but does not belong to the IRONMAN® race series.32 Reports of athletes competing in longer triathlon races are missing. This is most likely due to the lower popularity of these races71 compared to IRONMAN® 70.372 and IRONMAN®.73 An important aspect regarding IRONMAN® races is water temperature. For professional IRONMAN® triathletes, the optimal water temperature was ⁓22 °C and warmer74 whereas it was ⁓23–25 °C for age group IRONMAN® triathletes.36 Higher water temperature might prevent triathletes from developing SIPO. In ‘Norseman Xtreme Triathlon’, water temperature lies at 14–17 °C and air temperature at 6–10 °C.32
Environmental and equipment-related risks do also exist. Cold water and wetsuit compression emerge as important extrinsic factors contributing to SIPO pathophysiology. The use of wetsuit influences the higher SIPO incidence among triathletes, as tight wetsuits, especially those with full-length leg coverage, are considered a risk factor for SIPO.5 Cold exposure triggers peripheral vasoconstriction, increasing central blood volume and pulmonary capillary pressures.75 Meanwhile, tight wetsuits may mechanically restrict chest wall expansion, further elevating intrathoracic pressure.76 These conditions may exacerbate the natural hemodynamic shifts during immersion, particularly in long-course events (IRONMAN® 70.3 and IRONMAN® distances), where the physical demand is greatest.
A noteworthy consideration is the interaction of multiple risk factors. For example, an older female athlete with hypertension, wearing a tight wetsuit, and swimming in cold water may face compounded risk due to synergistic physiological stressors. Elderly triathletes can, however, also have pre-existing diseases such as coronary artery disease38 or cardiomyopathy.6 Despite the low prevalence, the potential for rapid onset and life-threatening symptoms underscores the need for pre-race screening and awareness among medical personnel.
A more analytical approach summarizing the main findings is presented in Table 2. To complement the descriptive synthesis, we have included a summary table that categorizes the strength of evidence for each reported risk factor associated with SIPO in triathletes. This classification is based on the type of supporting evidence (e.g., case reports, case series, reviews) and the consistency of findings across studies. Cold water immersion stands out with the strongest support, backed by both physiological rationale and systematic reviews. There is moderate evidence for factors such as female sex, age over 50, tight wetsuit compression, race distance, high-intensity exertion, and being a highly trained individual. Other factors, such as hypertension and overhydration leading to EAH, are supported by limited or emerging evidence, respectively. Fish oil intake and Takotsubo cardiomyopathy currently rely on anecdotal reports. This table offers a clearer understanding of the relative importance of different risk factors and can help guide future research priorities and targeted preventive strategies.
Table 2.
Strength of evidence for risk factors of SIPO in triathletes.
| Risk Factor | Strength of Evidence | Type of Evidence | Representative References |
|---|---|---|---|
| Cold water immersion | Strong | Systematic reviews, case series | 5, 33, 35, 38, 60 |
| Female sex | Moderate | Case reports, reviews, observational | 5, 13, 35, 49, 60, 65 |
| Age over 50 | Moderate | Case reports, reviews | 5, 60 |
| Hypertension | Limited | Case reports | 13, 35, 38 |
| Fish oil consumption | Limited | Case reports | 13, 35 |
| Tight wetsuit compression | Moderate | Case reports, physiological rationale | 5, 60 |
| High-intensity exertion | Moderate | Case reports, physiological rationale | 38, 49 |
| Overhydration/EAH | Emerging | Case reports, reviews | 49, 60 |
| Left ventricular hypertrophy | Emerging | Pathophysiological reports | 6, 58 |
| Takotsubo cardiomyopathy | Limited | Retrospective case series | 6 |
| Race distance (IRONMAN®) | Moderate | Case reports | 13, 32, 35 |
| Highly trained individuals | Moderate | Case reports, reviews | 38, 60 |
Note: Strong - multiple consistent case series or supported by systematic reviews/meta-analyses. Moderate - supported by several case reports or repeated thematic evidence + biological plausibility. Limited - isolated case reports or inconsistently reported findings. Emerging - growing hypothesis with some support from physio pathological studies but still preliminary.
4.4. Sports practice and SIPO
SIPO represents a significant risk, especially during intense physical exertion and immersion in challenging environments. The current review highlighted that factors such as systemic hypertension, aging and dehydration can exacerbate the risk of SIPO.25,37,77 However, adaptation through regular, structured training can notably enhance the body's ability to cope with these stressors, potentially reducing the likelihood of subsequent SIPO episodes.35 Case reports indicated that after full recovery from SIPO, the athletes can safely re-engage in water activities when monitored properly, with adaptations supporting improved pulmonary and cardiovascular function.37,61 Structured training protocols may focus on gradual progression and recovery to ensure that the athletes maintain their physiological resilience, which is crucial for minimizing future SIPO vulnerability32,77 Although SIPO can be a serious concern, the adaptive capacity of sports and exercise regimes offers a plausible pathway toward safer engagement in aquatic sports.9,78
4.5. Prevention and management strategies
The fact that the symptoms of SIPO can recur37 needs to make athletes and coaches aware of preventive strategies. Therefore, it is important to make an accurate diagnosis as these individuals may be at an increased risk of future life-threatening episodes.37
Preventive strategies are currently limited but promising. One case report documented the successful use of sildenafil prophylaxis in a triathlete with recurrent SIPO episodes, likely due to its effect on reducing pulmonary vascular resistance.51 However, this approach requires further validation in controlled trials. Additionally, testing for left ventricular hypertrophy—either via ECG or echocardiography—could be considered in triathletes with known cardiovascular risk factors or prior SIPO symptoms.79
Race organizers and medical personnel might consider implementing pre-race risk screening protocols, particularly in cold water events, to identify at-risk individuals.80 Educational efforts directed at coaches and athletes could also enhance early recognition and reporting of symptoms.81 For example, equipment for measuring oxygen saturation should be available for the medical staff on site.32
4.6. The aspect of late-onset oedema
In some instances, a certain degree of exercise-induced pulmonary oedema (often subclinical) can also be observed in the context of intense and/or prolonged endurance exercise, even without immersion in cold water. The oedema can be diagnosed by radiological techniques such as lung ultrasound and altered diffuse by functional measurements. Indeed, in ‘Norseman Xtreme Triathlon’, three cases of suspected late-presenting SIPO have been reported with shortness of breath, chest tightness and coughing up pink sputum during the last part of the cycling split.32
4.7. Association between EAH and SIPO?
SIPO appears to be associated with EAH in developing pulmonary and cerebral oedema.48 It has been reported that EAH was considerably higher in ultra-triathletes82 compared to IRONMAN® triathletes.83 While 26% of Triple Iron ultra-triathletes (8 out of 31 finishers at Triple Iron Triathlon Germany) developed EAH,82 only 18% of IRONMAN® triathletes (58 out of 330 finishers at IRONMAN® New Zealand) suffered from EAH.83 One case study reported that SIPO appears to be associated with EAH in developing pulmonary and cerebral oedema.49 It has been shown that EAH was considerably higher in females compared to male long-distance swimmers. The prevalence of EAH was investigated in 25 male and 11 female open-water ultra-endurance swimmers participating in the ‘Marathon-Swim’ in Lake Zurich, Switzerland, covering a distance of 26.4 km. While only two men (8%) developed EHA, four women (36%) were diagnosed with EAH at the finish line, with one woman being symptomatic with a plasma sodium [Na (+)] of 127 mmol/L.84 A potential connection between EAH and SIPO could be fluid overload in athletes developing EAH. Fluid overload might also lead to pulmonary oedema. The systematic determination of [Na (+)] in triathletes developing SIPO might reveal EAH and confirm this assumption.
4.8. Implications for future research
The fact that the results are based on case reports might considerably affect the strength of the conclusions. Based on the fact that SIPO also appears to be associated with EAH in developing pulmonary and cerebral oedema,48 future studies might investigate the prevalence of pre-race EAH when triathletes overhydrate before the race to prevent dehydration during the race.85 EAH appears to be considerably higher in female swimmers compared to male swimmers84 and athletes in other sports disciplines.86 Another case involved a female swimmer who developed exercise-associated hyponatremic encephalopathy after completing a 20-km open-water swim, which was accompanied by altered consciousness and seizures.87 A statement by Hew-Butler et al.88 reported that EAH is significantly more prevalent in female endurance athletes compared to their male counterparts. This is thought to be due to differences in body composition, hormonal influences and fluid regulation behaviors. These findings suggest that female swimmers and triathletes may be at higher risk for EAH, highlighting the importance of monitoring fluid intake and sodium levels during endurance swimming events.
4.9. Future research directions
Current knowledge on SIPO in triathletes remains limited and largely anecdotal. Future research should aim to:
-
•
Establish standardized diagnostic criteria for SIPO in both clinical and race settings.
-
•
Develop prospective surveillance systems to better capture incidence data.
-
•
Explore sex-specific and age-related physiological mechanisms through comparative studies.
-
•
Test intervention strategies, such as pre-swim pharmacological prophylaxis or equipment modifications (e.g., wetsuit design).
-
•
Investigate potential biomarkers or imaging techniques to detect early or subclinical pulmonary fluid shifts
4.10. Limitations
This narrative review about SIPO in triathletes is limited due to the fact that the results are mainly based on case reports or case series. This approach may have the potential for a selection bias and a lack of reproducibility. A narrative review using case studies, particularly regarding the small sample size and the non-systematic selection of cases, has limitations. The case studies predominantly featured 30-60-year-old females, introducing a selection bias. Conclusions labeling female sex and age as independent risk factors are overgeneralized and lack robust epidemiological support.
5. Conclusions
In summary, SIPO in triathletes does not appear to differ from SIPO in other aquatic activities in terms of prevalence, symptoms and risk factors. SIPO only occurs in IRONMAN® 70.3 and IRONMAN® races, but has not been reported in Olympic distance or longer triathlon distances than the IRONMAN® race distance. The lack of reports on these distances could be due to a lack of research or an actual absence of cases. Future studies need to investigate whether this is due to a true absence or a lack of available data. SIPO in triathletes, while rare, presents a clinically relevant challenge that intersects physiology, environment, and equipment. A more nuanced understanding of its triggers and manifestations will aid in developing preventive and therapeutic interventions. Given the global rise in triathlon participation, this condition merits heightened attention within sports medicine, cardiopulmonary research, and athlete safety protocols. We recommend standardized data collection at triathlons and routine cardiovascular screening for at-risk athletes.
CRediT authorship contribution statement
Beat Knechtle: Writing – original draft, Conceptualization. Pantelis T. Nikolaidis: Writing – review & editing. Daniela Chlíbková: Writing – review & editing. Luciano Bernardes Leite: Writing – review & editing. Pedro Forte: Writing – review & editing. Marilia Santos Andrade: Writing – review & editing. Katja Weiss: Writing – review & editing. Thomas Rosemann: Writing – review & editing. Sasa Duric: Writing – review & editing.
Declaration of competing interest
Beat Knechtle is an Editorial Board Member for Sports Medicine and Health Science and was not involved in the editorial review or the decision to publish this article. Otherwise, the authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.
Acknowledgements
Luciano Bernardes Leite thanks the Fundação de Amparo à Pesquisa do Estado de Minas Gerais (FAPEMIG) for the scholarship.
Footnotes
Peer review under the responsibility of Editorial Board of Sports Medicine and Health Science
References
- 1.Armstrong L.E., Johnson E.C., Adams W.M., Jardine J.F. Hyperthermia and exertional heatstroke during running, cycling, open water swimming, and triathlon events. Open Access J Sports Med. 2024;15:111–127. doi: 10.2147/OAJSM.S482959. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 2.Nilssen P.K., Connolly C.P., Johnson K.B., et al. Medical encounters and treatment outcomes in Ironman-distance triathlon. Med Sci Sports Exerc. 2023;55(11):1968–1976. doi: 10.1249/MSS.0000000000003235. [DOI] [PubMed] [Google Scholar]
- 3.Feletti F., Saini G., Naldi S., et al. Injuries in medium to long-distance triathlon: a retrospective analysis of medical conditions treated in three editions of the Ironman competition. J Sports Sci Med. 2022;21(1):58–67. doi: 10.52082/jssm.2022.58. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 4.Manninen I.K., Jutila T., Hirvonen T., et al. Dizzy triathlete: Evidence supporting vestibular etiology. Scand J Med Sci Sports. 2021;31(12):2267–2271. doi: 10.1111/sms.14041. [DOI] [PubMed] [Google Scholar]
- 5.Barouch L.A. Swimming-induced pulmonary edema: an underrecognized cause of triathlon-associated medical emergencies. JACC Case Rep. 2022;4(17):1094–1097. doi: 10.1016/j.jaccas.2022.05.019. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 6.Rigler C., Menon G., Lipworth S., et al. Case series of triathletes with Takotsubo cardiomyopathy presenting with swimming-induced pulmonary edema. Transl Sports Med. 2022;2022 doi: 10.1155/2022/3602505. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 7.Sobieszek A., Konopka M., Cacko M., Kuch M., Braksator W. Immersion pulmonary oedema in a triathlete: a diagnostic challenge in sports cardiology. J Ultrason. 2021;21(86):e252–e257. doi: 10.15557/JoU.2021.0041. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 8.Grant A.J., Kanwal A., Shah A.B. Swimming: what the sports cardiologist should know. Curr Treat Options Cardiovasc Med. 2020;22(70):1–9. doi: 10.1007/s11936-020-00876-0. [DOI] [Google Scholar]
- 9.Haran J.B., Donaldson C., Kicker P.W. Swimming-induced pulmonary edema in an active-duty female triathlete. Mil Med. 2020;185(9-10):e1897–e1899. doi: 10.1093/milmed/usaa118. [DOI] [PubMed] [Google Scholar]
- 10.Paz P., Makram J., Mallah H., Mantilla B., Ball S., Nugent K. Swimming-induced pulmonary edema. SAVE Proc. 2020;33(3):409–412. doi: 10.1080/08998280.2020.1735236. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 11.O'Keefe C.L., Clemente Fuentes R.W., Salinas E. Swimming-induced pulmonary edema in a member participating in a special tactics selection course. Aerosp Med Hum Perform. 2024;95(12):937–939. doi: 10.3357/AMHP.6516.2024. [DOI] [PubMed] [Google Scholar]
- 12.Wilmshurst P., Nuri M., Crowther A., Betts J., Webb-Peploe M. Forearm vascular response in subjects who develop recurrent pulmonary oedema when scuba diving: a new syndrome. Br Heart J. 1981;45 [Google Scholar]
- 13.Miller C.C., 3rd, Calder-Becker K., Modave F. Swimming-induced pulmonary edema in triathletes. Am J Emerg Med. 2010;28(6):941–946. doi: 10.1016/j.ajem.2009.08.004. [DOI] [PubMed] [Google Scholar]
- 14.Grünig H., Nikolaidis P.T., Moon R.E., Knechtle B. Diagnosis of swimming-induced pulmonary edema: a review. Front Physiol. 2017;8:652. doi: 10.3389/fphys.2017.00652. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 15.Adir Y., Shupak A., Gil A., et al. Swimming-induced pulmonary edema: clinical presentation and serial lung function. Chest. 2004;126(2):394–399. doi: 10.1378/chest.126.2.394. [DOI] [PubMed] [Google Scholar]
- 16.Bove A.A. Cardiovascular concerns in water sports. Clin Sports Med. 2015;34(3):449–460. doi: 10.1016/j.csm.2015.02.003. [DOI] [PubMed] [Google Scholar]
- 17.Peacher D.F., Martina S.D., Otteni C.E., et al. Immersion pulmonary edema and comorbidities: case series and updated review. Med Sci Sports Exerc. 2015;47(6):1128–1134. doi: 10.1249/MSS.0000000000000524. [DOI] [PubMed] [Google Scholar]
- 18.Cochard G., Henckes A., Deslandes S., et al. Swimming-induced immersion pulmonary edema while snorkeling can be rapidly life-threatening: case reports. Undersea Hyperb Med. 2013;40(5):411–416. [PubMed] [Google Scholar]
- 19.Foti P.R., Wilcox C.M., Goto R.S. Factors contributing to snorkel drowning in Hawai‘i. Hawaii J Health Soc Welf. 2022;81(3):71. [PMC free article] [PubMed] [Google Scholar]
- 20.Morimatsu Y., Nasu M., Murata Y., et al. Severe immersion pulmonary edema in a novice elderly scuba diver after heavy alcohol intake. Acute Med Surg. 2021;8(1) doi: 10.1002/ams2.703. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 21.Bove A.A. Pulmonary aspects of exercise and sports. Methodist Debakey Cardiovasc J. 2016;12(2):93–97. doi: 10.14797/mdcj-12-2-93. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 22.Wilmshurst P.T., Nuri M., Crowther A., Webb-Peploe M.M. Cold-induced pulmonary oedema in scuba divers and swimmers and subsequent development of hypertension. Lancet. 1989;1(8629):62–65. doi: 10.1016/s0140-6736(89)91426-8. [DOI] [PubMed] [Google Scholar]
- 23.Kwek W., Seah M., Chow W. Swimming-induced pulmonary edema in a tropical climate: a case report. Undersea Hyperb Med. 2017;44(3):293–296. [PubMed] [Google Scholar]
- 24.Volk C., Spiro J., Boswell G., et al. Incidence and impact of swimming-induced pulmonary edema on Navy SEAL candidates. Chest. 2021;159(5):1934–1941. doi: 10.1016/j.chest.2020.11.019. [DOI] [PubMed] [Google Scholar]
- 25.Borza M.L., Blonien N.E. Swimming-induced pulmonary edema found in a U.S. Navy Basic Underwater Demolition/SEAL recruit. Cureus. 2022;14(9) doi: 10.7759/cureus.29417. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 26.Lindholm P., Ekborn A., Oberg D., Gennser M. Pulmonary edema and hemoptysis after breath-hold diving at residual volume. J Appl Physiol. 2008;104(4):912–917. doi: 10.1152/japplphysiol.01127.2007. [DOI] [PubMed] [Google Scholar]
- 27.Linér M.H., Andersson J.P. Pulmonary edema after competitive breath-hold diving. J Appl Physiol. 2008;104(4):986–990. doi: 10.1152/japplphysiol.00641.2007. [DOI] [PubMed] [Google Scholar]
- 28.Yu E., Dong G.Z., Patron T., et al. Occurrence and resolution of freediving-induced pulmonary syndrome in breath-hold divers: an online survey of lung squeeze incidents. Diving Hyperb Med. 2024;54(4):281–286. doi: 10.28920/dhm54.4.281-286. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 29.Sanou A.Z., Murray R.L., Hernandez E., Sherrier D. An unusual presentation of pulmonary edema during an ice dive at altitude. Mil Med. 2023;188(1-2):392–397. doi: 10.1093/milmed/usac081. [DOI] [PubMed] [Google Scholar]
- 30.Shupak A., Weiler-Ravell D., Adir Y., et al. Pulmonary oedema induced by strenuous swimming: a field study. Respir Physiol. 2000;121(1):25–31. doi: 10.1016/s0034-5687(00)00109-2. [DOI] [PubMed] [Google Scholar]
- 31.Hårdstedt M., Kristiansson L., Seiler C., Braman Eriksson A., Sundh J. Incidence of swimming-induced pulmonary edema: a cohort study based on 47,600 open-water swimming distances. Chest. 2021;160(5):1789–1798. doi: 10.1016/j.chest.2021.06.034. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 32.Melau J., Bonnevie-Svendsen M., Mathiassen M., et al. Late-presenting swimming-induced pulmonary edema: a case report series from the Norseman Xtreme Triathlon. Sports (Basel) 2019;7(6):137. doi: 10.3390/sports7060137. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 33.Hohmann E., Glatt V., Tetsworth K. Swimming-induced pulmonary oedema in athletes: a systematic review and best evidence synthesis. BMC Sports Sci Med Rehabil. 2018;10:18. doi: 10.1186/s13102-018-0107-3. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 34.Miller I.L. Meyer & Meyer Sport; 2011. Fearless Swimming for Triathletes: Improve your Open Water Skills. Maidenhead. [Google Scholar]
- 35.Spencer S., Dickinson J., Forbes L. Occurrence, risk factors, prognosis and prevention of swimming-induced pulmonary oedema: a systematic review. Sports Med Open. 2018;4(1):43. doi: 10.1186/s40798-018-0158-8. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 36.Knechtle B., Villiger E., Weiss K., et al. The fastest nonprofessional age group Ironman triathletes in the world originate from Europe. Sci Rep. 2025;15(1):1028. doi: 10.1038/s41598-024-84008-9. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 37.Smith R., Brooke D., Kipps C., Skaria B., Subramaniam V. A case of recurrent swimming-induced pulmonary edema in a triathlete: the need for awareness. Scand J Med Sci Sports. 2017;27(10):1130–1135. doi: 10.1111/sms.12736. [DOI] [PubMed] [Google Scholar]
- 38.Casey H., Dastidar A.G., MacIver D. Swimming-induced pulmonary oedema in two triathletes: a novel pathophysiological explanation. J R Soc Med. 2014;107(11):450–452. doi: 10.1177/0141076814543214. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 39.Knechtle B., Knechtle P., Lepers R. Participation and performance trends in ultra-triathlons from 1985 to 2009. Scand J Med Sci Sports. 2011;21(6):e82–e90. doi: 10.1111/j.1600-0838.2010.01160.x. [DOI] [PubMed] [Google Scholar]
- 40.Meili D., Knechtle B., Rüst C.A., Rosemann T., Lepers R. Participation and performance trends in 'Ultraman Hawaii' from 1983 to 2012. Extreme Physiol Med. 2013;2(1):25. doi: 10.1186/2046-7648-2-25. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 41.Diehm C. SIPE-syndrom: Tod im kalten Wasser. CardioVasc. 2017;17:57. doi: 10.1007/s15027-017-1119-8. [DOI] [Google Scholar]
- 42.Baethge C., Goldbeck-Wood S., Mertens S. SANRA-a scale for the quality assessment of narrative review articles. Res Integr Peer Rev. 2019;4:5. doi: 10.1186/s41073-019-0064-8. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 43.Falagas M.E., Pitsouni E.I., Malietzis G.A., Pappas G. Comparison of PubMed, scopus, web of science, and google scholar: strengths and weaknesses. FASEB J. 2008;22(2):338–342. doi: 10.1096/fj.07-9492LSF. [DOI] [PubMed] [Google Scholar]
- 44.DeMars M.M., Perruso C. MeSH and text-word search strategies: precision, recall, and their implications for library instruction. J Med Libr Assoc. 2022;110(1):23–33. doi: 10.5195/jmla.2022.1283. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 45.Lønborg A.V., Mathæussen A. Swimming-induced pulmonary oedema. Ugeskr Laeger. 2021;183(26) [PubMed] [Google Scholar]
- 46.Yamanashi H., Koyamatsu J., Nobuyoshi M., Murase K., Maeda T. Exercise-induced pulmonary edema in a triathlon. Case Rep Med. 2015;2015 doi: 10.1155/2015/968152. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 47.Spiteri D.B., Debono R., Micallef-Stafrace K., Xuereb R.G. Recurrent swimming-induced pulmonary oedema (SIPE) in a triathlete. Int Sportmed J (ISMJ) 2011;12(3):141–144. [Google Scholar]
- 48.Beale A., Gong F.F., La Gerche A. Exercise-induced pulmonary oedema in endurance triathletes. Int J Cardiol. 2016;203:980–981. doi: 10.1016/j.ijcard.2015.11.116. [DOI] [PubMed] [Google Scholar]
- 49.Richter S., Betz C., Geiger H. Schwere Hyponatriämie mit Lungen- und Hirnödem bei einer Ironman-Triathletin. Dtsch Med Wochenschr. 2007;132(36):1829–1832. doi: 10.1055/s-2007-984973. [DOI] [PubMed] [Google Scholar]
- 50.Ma J.L., Dutch M.J. Extreme sports: extreme physiology. Exercise-induced pulmonary oedema. Emerg Med Australas. 2013;25(4):368–371. doi: 10.1111/1742-6723.12101. [DOI] [PubMed] [Google Scholar]
- 51.Martina S.D., Freiberger J.J., Peacher D.F., et al. Sildenafil: possible prophylaxis against swimming-induced pulmonary oedema. Med Sci Sports Exerc. 2017;49(9):1755–1757. doi: 10.1249/MSS.0000000000001293. [DOI] [PubMed] [Google Scholar]
- 52.Moon R.E., Beck T.P. Cold water, hard swim, shortness of breath: how to assess? Chest. 2020;158(4):1329–1330. doi: 10.1016/j.chest.2020.05.541. [DOI] [PubMed] [Google Scholar]
- 53.Yagi M., Kasanami R., Tarumi Y., Dohi K. Medical care management based on disaster medicine for the triathlon events at the XXXII Olympiad and Tokyo 2020 Paralympic Games. Int J Environ Res Publ Health. 2023;20(19):6891. doi: 10.3390/ijerph20196891. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 54.Asplund C.A., Creswell L.L. Hypothesised mechanisms of swimming-related death: a systematic review. Br J Sports Med. 2016;50(22):1360–1366. doi: 10.1136/bjsports-2015-094722. [DOI] [PubMed] [Google Scholar]
- 55.Dressendorfer R. Triathlon swim deaths. Curr Sports Med Rep. 2015;14(3):151–152. doi: 10.1249/JSR.0000000000000142. [DOI] [PubMed] [Google Scholar]
- 56.Grant A.J., Kanwal A., Shah A.B. Swimming: what the sports cardiologist should know. Curr Treat Options Cardiovasc Med. 2020;22(12):70. doi: 10.1007/s11936-020-00876-0. [DOI] [Google Scholar]
- 57.Eichner E.R. The mystery of swimming deaths in athletes. Curr Sports Med Rep. 2011;10(1):3–4. doi: 10.1249/JSR.0b013e318205e0f6. [DOI] [PubMed] [Google Scholar]
- 58.Moon R.E., Martina S.D., Peacher D.F., Kraus W.E. Deaths in triathletes: immersion pulmonary oedema as a possible cause. BMJ Open Sport Exerc Med. 2016;2(1) doi: 10.1136/bmjsem-2016-000146. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 59.Moon R.E., Martina S.D., Peacher D.F., et al. Swimming-induced pulmonary oedema: pathophysiology and risk reduction with sildenafil. Circulation. 2016;133(10):988–996. doi: 10.1161/CIRCULATIONAHA.115.019464. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 60.Kumar M., Thompson P.D. A literature review of immersion pulmonary edema. Phys Sportsmed. 2019;47(2):148–151. doi: 10.1080/00913847.2018.1546104. [DOI] [PubMed] [Google Scholar]
- 61.Steele S., Brahmbhatt S., Patel D. Swimming-induced pulmonary edema: evaluation, diagnosis, and treatment. Curr Sports Med Rep. 2024;23(4):124–129. doi: 10.1249/JSR.0000000000001157. [DOI] [PubMed] [Google Scholar]
- 62.Rogers I.R., Hew-Butler T. Exercise-associated hyponatremia: overzealous fluid consumption. Wilderness Environ Med. 2009;20(2):139–143. doi: 10.1580/08-WEME-CON-231R2.1. [DOI] [PubMed] [Google Scholar]
- 63.Schrier R.W., Goldberg J.P. The physiology of vasopressin release and the pathogenesis of impaired water excretion in adrenal, thyroid, and edematous disorders. Yale J Biol Med. 1980;53(6):525–541. [PMC free article] [PubMed] [Google Scholar]
- 64.Belval L.N., Hosokawa Y., Casa D.J., et al. Practical hydration solutions for sports. Nutrients. 2019;11(7):1550. doi: 10.3390/nu11071550. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 65.Stellrecht M., Wedekind H. Akut einsetzende dyspnoe, husten und hämoptysen bei einer 46-jährigen bisher gesunden schwimmerin [Sudden-onset dyspnea, cough and hemoptysis in a previously healthy 46-year-old female swimmer] Internist. 2022;63(1):110–114. doi: 10.1007/s00108-021-01160-4. [DOI] [PubMed] [Google Scholar]
- 66.Sheel A.W., Richards J.C., Foster G.E., Guenette J.A. Sex differences in respiratory exercise physiology. Sports Med. 2004;34(9):567–579. doi: 10.2165/00007256-200434090-00002. [DOI] [PubMed] [Google Scholar]
- 67.Stone J.C., MacDonald M.J. The impacts of endogenous progesterone and exogenous progestin on vascular endothelial cell and smooth muscle cell function: a narrative review. Vasc Pharmacol. 2023;152 doi: 10.1016/j.vph.2023.107209. [DOI] [PubMed] [Google Scholar]
- 68.Poczta J., Almeida N., Malchrowicz-Mośko E. Socio-psychological functions of men and women triathlon participation. Int J Environ Res Publ Health. 2021;18(22) doi: 10.3390/ijerph182211766. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 69.Knechtle B., Valero D., Villiger E., et al. Comparing the performance gap between males and females in the older age groups in IRONMAN® 70.3: an internet-based cross-sectional study of more than 800,000 race records. Sports Med Open. 2023;9(1):88. doi: 10.1186/s40798-023-00636-x. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 70.Stiefel M., Knechtle B., Rüst C.A., Rosemann T., Lepers R. The age of peak performance in Ironman triathlon: a cross-sectional and longitudinal data analysis. Extreme Physiol Med. 2013;2(1):27. doi: 10.1186/2046-7648-2-27. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 71.Sousa C.V., Nikolaidis P.T., Knechtle B. Ultra-triathlon: pacing, performance trends, the role of nationality, and sex differences in finishers and non-finishers. Scand J Med Sci Sports. 2020;30(3):556–563. doi: 10.1111/sms.13598. [DOI] [PubMed] [Google Scholar]
- 72.Thuany M., Valero D., Villiger E., et al. A machine learning approach to finding the fastest race course for professional athletes competing in Ironman® 70.3 races between 2004 and 2020. Int J Environ Res Publ Health. 2023;20(4):3619. doi: 10.3390/ijerph20043619. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 73.Knechtle B., Valero D., Villiger E., et al. The influence of origin and race location on performance in Ironman® age group triathletes. PLoS One. 2024;19(12) doi: 10.1371/journal.pone.0315064. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 74.Knechtle B., Thuany M., Valero D., et al. The association of origin and environmental conditions with performance in professional Ironman triathletes. Sci Rep. 2025;15(1):2700. doi: 10.1038/s41598-025-86033-8. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 75.Rintamäki H. Human responses to cold. Alaska Med. 2007;49(2 Suppl):29–31. [PubMed] [Google Scholar]
- 76.Tetzlaff K., Thomas P.S. Short- and long-term effects of diving on pulmonary function. Eur Respir Rev. 2017;26(143) doi: 10.1183/16000617.0097-2016. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 77.Smith R., Ormerod J.O.M., Sabharwal N., Kipps C. Swimming-induced pulmonary edema: current perspectives. Open Access J Sports Med. 2018;9:131–137. doi: 10.2147/OAJSM.S140028. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 78.Hårdstedt M., Seiler C., Kristiansson L., et al. Swimming-induced pulmonary edema: diagnostic criteria validated by lung ultrasound. Chest. 2020;158(4):1586–1595. doi: 10.1016/j.chest.2020.04.028. [DOI] [PubMed] [Google Scholar]
- 79.Liu C.W., Wu F.H., Hu Y.L., et al. Left ventricular hypertrophy detection using electrocardiographic signal. Sci Rep. 2023;13(1):2556. doi: 10.1038/s41598-023-28325-5. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 80.Sewry N., Schwellnus M., Borjesson M., Swanevelder S., Jordaan E. Pre-race screening and stratification predicts adverse events: a 4-year study in 29,585 ultra-marathon entrants, SAFER X. Scand J Med Sci Sports. 2020;30(7):1205–1211. doi: 10.1111/sms.13659. [DOI] [PubMed] [Google Scholar]
- 81.Bengtsson D., Stenling A., Nygren J., Ntoumanis N., Ivarsson A. The effects of interpersonal development programmes with sport coaches and parents on youth athlete outcomes: a systematic review and meta-analysis. Psychol Sport Exerc. 2024;70 doi: 10.1016/j.psychsport.2023.102558. [DOI] [PubMed] [Google Scholar]
- 82.Rüst C.A., Knechtle B., Knechtle P., Rosemann T. Higher prevalence of exercise-associated hyponatremia in triple iron ultra-triathletes than reported for ironman triathletes. Chin J Physiol. 2012;55(3):147–155. doi: 10.4077/CJP.2012.BAA010. [DOI] [PubMed] [Google Scholar]
- 83.Speedy D.B., Noakes T.D., Rogers I.R., et al. Hyponatremia in ultradistance triathletes. Med Sci Sports Exerc. 1999;31(6):809–815. doi: 10.1097/00005768-199906000-00008. [DOI] [PubMed] [Google Scholar]
- 84.Wagner S., Knechtle B., Knechtle P., Rüst C.A., Rosemann T. Higher prevalence of exercise-associated hyponatremia in female than in male open-water ultra-endurance swimmers: the ‘Marathon-Swim’ in Lake Zurich. Eur J Appl Physiol. 2012;112(3):1095–1106. doi: 10.1007/s00421-011-2070-5. [DOI] [PubMed] [Google Scholar]
- 85.Samuels B. The importance of pre-hydration: are you drinking enough before race day? Sci Sports. 2025 https://www.scienceinsport.com/sports-nutrition/importance-pre-hydration-drinking-enough-race-day Available at: [Google Scholar]
- 86.Knechtle B., Gnädinger M., Knechtle P., et al. Prevalence of exercise-associated hyponatremia in male ultraendurance athletes. Clin J Sport Med. 2011;21(3):226–232. doi: 10.1097/JSM.0b013e31820cb021. [DOI] [PubMed] [Google Scholar]
- 87.Rogers I.R., Grainger S., Nagree Y. Exercise-associated hyponatremic encephalopathy in an endurance open water swimmer. Wilderness Environ Med. 2015;26(1):59–61. doi: 10.1016/j.wem.2014.07.010. [DOI] [PubMed] [Google Scholar]
- 88.Hew-Butler T., Rosner M.H., Fowkes-Godek S., et al. Statement of the third international exercise-associated hyponatremia consensus development conference, Carlsbad, California, 2015. Clin J Sport Med. 2015;25(4):303–320. doi: 10.1097/JSM.0000000000000221. [DOI] [PubMed] [Google Scholar]
