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Exercise-Associated Collapse

Postural Hypotension, or Something Deadlier?

Dale B. Speedy, MBChB, MSc, MD; Timothy D. Noakes, MBChB, MD; Lucy-May Holtzhausen, MBChB

THE PHYSICIAN AND SPORTSMEDICINE - VOL 31 - NO. 3 - MARCH 2021


In Brief: Exercise-associated collapse (EAC) is the most common reason that athletes are treated in the medical tent following an endurance event. The pathophysiology of EAC is postural hypotension that results when the loss of muscle pumping action caused by the cessation of exercise is combined with cutaneous vasodilation. EAC usually occurs after an athlete crosses the finish line. If an athlete collapses during a race, then another serious medical cause is more likely. A brief assessment of the collapsed athlete should be carried out to obtain a working diagnosis. Prompt treatment of EAC includes elevating the legs and pelvis of the athlete.

Collapse following an endurance or ultraendurance event is one of the most common reasons for an athlete to receive treatment at a race medical tent.1-3 The cause in most cases is exercise-associated collapse (EAC), a benign condition related to postural hypotension on cessation of exercise.4 Medical workers at the finish line of athletic events, who are often volunteers, need a sound understanding of EAC and a simple approach to the treatment of the collapsed athlete.

Definition of EAC

EAC is variably defined in the literature. Some authors2,4 combine postural hypotension with the other medical causes for collapse (table 1), while others clearly differentiate EAC (presumed secondary to postural hypotension) from other causes.1,3 Holtzhausen et al4 have defined EAC as the "inability to stand or walk unaided as the result of light-headedness, faintness, dizziness, or syncope." This could be further defined by associating the collapse with completion of the race and a clearly demonstrable postural drop in systolic blood pressure of greater than 20 mm Hg from standing to lying.5

TABLE 1. Conditions Associated With Collapse
During or After Exercise

Exercise-associated collapse
Muscle cramping
Hyperthermia
Hypothermia
Hyponatremia
Hypoglycemia
Cardiac arrest
Other medical conditions
Musculoskeletal conditions

EAC has previously been termed "heat syncope" or "heat exhaustion," but these terms are incorrect. No evidence shows that athletes who experience EAC have higher postrace rectal temperatures than do athletes who do not collapse after exercise.6 Nor do athletes with EAC require the active cooling necessary for the treatment of heatstroke, the true heat disorder of exercise. As is the case in a great deal of research in this field, the absence of adequate control groups has led to the development and perpetuation of incorrect hypotheses.

Where and When

The prevalence of collapse in footraces is reported to be from 0.2% to 3.7%.3,4,7-9 In 12 years at the Twin Cities Marathon in Minneapolis and St Paul, the incidence of EAC has been reported as 1.13% of race starters.2 The 4-hour temperature range for these races was 41° to 68° F (5° to 20°C). Roberts2 reported a medical encounter rate of of 25.3 per 1,000 finishers and that 59% of admissions to the medical facility were for EAC at the Twin Cities Marathon.

In ultradistance triathlon events, EAC has occurred in 17% to 21% of race starters.1,10 When the stricter definition (which excludes other medical causes for collapse) was used, Speedy et al1 reported that 27% of athletes seen in the medical tent after an Ironman Triathlon had EAC.

Postural Hypotension Explored

EAC is believed to be caused by postural hypotension brought on by the sudden cessation of exercise, especially if the exercise has been undertaken in the heat. Adolph11 first suggested the role of postural hypotension in "heat exhaustion" after exercise. Similarly, Eichna et al12 concluded that postural hypotension after exercise was caused by pooling of blood in the legs.

Holtzhausen and colleagues4,5 reported that 85% of subjects with EAC collapsed after the cessation of a 56-km ultramarathon and not during the event, and that postural hypotension, often severe, could be demonstrated in virtually all the runners who completed the event. This evidence led them to suggest that Adolph and Eichna's hypotheses could explain the phenomenon of collapse immediately after exercise. The inactivation of the calf muscle pump immediately after cessation of endurance exercise results in blood pooling in the compliant veins of the lower limbs, causing a reduced atrial filling pressure and subsequent syncope. This circulatory decompensation is often exacerbated by heat-induced increases in muscle and cutaneous venous capacitance. Another factor may be a right atrial reflex that causes a paradoxical skeletal muscle vasodilation when the right atrial pressure falls dramatically (the Barcroft-Edholm reflex).13

In some cases, sources of extra fluid loss, such as sweating, diarrhea, and vomiting, may contribute to postural hypotension through a reduced blood volume. No evidence exists that athletes who have EAC are any more dehydrated than control athletes who finish the same race without collapsing. Indeed, levels of dehydration up to 5% do not alter cardiovascular function during exercise in the supine position, whereas such effects are measurable during exercise in the erect position.14 This indicates that the position in which the exercise is performed, and not dehydration, is the primary cause for any cardiovascular instability that develops during exercise in healthy athletes.

The theory of postural hypotension on cessation of exercise is based on a study by Holtzhausen et al4 who reported that 85% of athletes who required medical care in a 56 km ultramarathon collapsed after the race. Cessation of exercise was therefore considered important in the etiology. All of these runners had a postural drop in blood pressure immediately postrace that was not present when they were studied 24 hours later. Conversely, all runners who collapsed during the race had some identifiable medical condition that caused their collapse. Only 34% of runners who collapsed at the finish line were found to have some other medical condition responsible for their collapse—notably, hypoglycemia or heatstroke. The cardiovascular status of runners with EAC was normal when they were supine, in contrast to persisting hypotension and tachycardia in athletes who were in shock or had heatstroke. The distribution of rectal temperatures in runners who had EAC were not different from values measured in runners who did not collapse.4 Similarly, others have reported that most runners who have EAC do not have rectal temperatures greater than 102.5°F (39°C).2,3,15,16

Training-induced adaptations to the autonomic nervous system have been postulated as contributing to the postural hypotension of EAC.3 Exercise training induces adaptations, including a decreased vasoconstrictor response to hypotension.17,18 Holtzhausen and Noakes5 demonstrated an asymptomatic drop in postural systolic blood pressure of more than 20 mm Hg in 68% of runners who were studied immediately after an ultramarathon. Runners who had a postrace systolic blood pressure of less than 90 mm Hg experienced dizziness and nausea.

In the past, EAC has been attributed to dehydration-induced hyperthermia.10 Holtzhausen et al4 have argued against this theory on the grounds that if dehydration were a major contributing factor, athletes would be expected to collapse during exercise when the stress on the cardiovascular system is the greatest. Furthermore, they have reported similar levels of fluid losses in runners who collapsed and in controls who did not collapse, and similar levels of renin and arginine vasopressin in runners and controls.4 The level of dehydration developed during the race has been shown to be unrelated to the degree of postural drop in systolic blood pressure.5

Differential Diagnosis

It is vital to differentiate serious causes of collapse from benign causes and to expedite treatment of those athletes who are seriously ill.2,3 The first principle in the approach to the collapsed athlete is to establish a working diagnosis (see table 1). Holtzhausen and Noakes3 and Noakes19,20 have suggested that failure to consider a rational differential diagnosis prior to initiating treatment has been the major limitation to the management of collapsed athletes. They have also suggested this may stem from a fear on the part of the attending physician that delay in instituting treatment may prejudice the treatment outcome. However, the emergency treatment of severe medical conditions, such as hyperthermia and hyponatremia, can safely wait 1 to 2 minutes while a working diagnosis is established. The exception is cardiac arrest, which is an uncommon occurrence at ultradistance events and is an obvious diagnosis.

A further possible reason for initiating treatment without a diagnosis is the mistaken belief that dehydration is the major cause of collapse,3,10,19 and that intravenous (IV) fluid replacement is often needed for athletes who collapse after ultradistance events.10

Assessment of the Collapsed Athlete

The initial clinical assessment (table 2) should be expedient but thorough, and it is beneficial to evaluate the collapsed athlete in the head-down position. Remember that athletes who collapse before reaching the finish line usually have a serious medical condition that requires urgent attention.4

TABLE 2. Initial Assessment of the Collapsed Athlete
Mental status
Rectal temperature
Systolic blood pressure
Pulse rate
Hydration status
Site of collapse
Body weight change
Serum sodium concentration
Serum glucose concentration

Mental status is the single most important clinical sign. If an athlete is unconscious or has an altered mental state when he or she is no longer in the erect position, the athlete is likely to have symptomatic hyponatremia, profound hypoglycemia, severe hyperthermia or heatstroke, or, paradoxically, hypothermia.

Core temperature is thus assessed first to rule out heatstroke as a cause of the altered mental state. It is crucial that the rectal and not oral, axillary, or aural routes be used, because only the rectal temperature accurately reflects core temperature in a field situation.21 An unconscious athlete who has a rectal temperature higher than 107°F (41.6°C) has heatstroke, but an unconscious athlete whose rectal temperature is less than 104°F (40°C) and whose pulse and blood pressure are normal has hyponatremia until proven otherwise.

Pulse and blood pressure need to be measured in both the supine and erect position, if the athlete's condition allows. This gives some indication of the severity of the postural hypotension.

Signs of dehydration include a dry mouth, decreased skin turgor, and persisting hypotension and tachycardia despite elevation of the legs and pelvis. The inability to spit has also been found to be a useful clinical sign of dehydration,3 but the most accurate method to determine the level of dehydration is by recording weight change over a race. Speedy et al1 have recommended mandatory prerace weighing of all athletes participating in an ultradistance triathlon. Accurate data on weight change and hydration status are thus available if the athlete requires postrace medical care.

Signs of overhydration include an alteration of mental status caused by hyponatremia, weight gain during the race, and edema of the hands and fingers.6 Increased tightness of rings, watches, or race registration wristbands is a useful sign of localized hand edema and possible fluid overload.

Serum sodium and glucose concentrations should be measured, if testing is available. A facility for on-site measurement of serum sodium concentration should be considered mandatory for ultradistance events, because hyponatremia is the major cause of serious illness following such events.1 Serum sodium measurement is especially important when the official policy is that athletes should drink "as much as possible" during exercise; at such races the incidence of hyponatremia is especially high.22 Of course, the most important preventive measure to ensure that athletes do not develop hyponatremia is simply to encourage athletes to drink "optimally but not maximally" during the race.22

A history made after the initial assessment should include an athlete's fluid and carbohydrate intake, urine output, presence of diarrhea or vomiting, drug intake, and concomitant illness. A general physical examination can follow the initial assessment after a working diagnosis has been achieved and any urgent treatment has been initiated.

Treatment of EAC

We3,6 have recommended that athletes who have EAC be given oral fluids and have their legs and pelvises elevated by lifting the foot of the stretcher 6 in. (15 cm) (figure 1). The recovery of their cardiovascular status is monitored every 15 minutes. IV fluids are not considered until response to the elevated lower-limb position is assessed. If the diagnosis is correct, the athlete's circulatory stability is almost instantly restored in the head-down position,6 and the athlete can stand and walk unaided within 10 to 30 minutes.2,3 Our clinical impression is that the quicker this form of treatment is initiated, the more rapidly the athlete recovers. In contrast, placing the patient in the supine position can occasionally worsen hypotension and delay recovery.

IV fluids administered to the athlete in the supine, unelevated lower-limb position are unlikely, on their own, to increase the venous return from dilated capacitance veins in the legs.6,20 No study has demonstrated that treating collapsed athletes with IV fluids helps them to recover more quickly than nursing them in the head-down position.6 Holtzhausen and Noakes3 suggest that persistent tachycardia and hypotension, despite elevation of the legs and pelvis, could be an indication for IV fluid replacement. The indications for IV fluid therapy (table 3) following an ultradistance Ironman Triathlon are rare.1,6,20 In the first 2 years of the South African Ironman Triathlon, it has not been necessary to give IV fluids to a single collapsed athlete. Rather, all have recovered rapidly with placement in the head-down position only.

TABLE 3. Indications for Intravenous Fluid Therapy After Exercise-Associated Collapse
Intravenous fluid therapy is indicated only when the patient:

Shows signs of clinical dehydration (eg, dry mucous membranes, inability to spit, decreased skin turgor, sunken eyes)

Has dehydration that causes signs of cardiovascular instability or other medical problems

Cannot be treated with oral rehydration

Is unconscious and has serum sodium concentration >130 mmol/L

Preventive measures for EAC include an appropriate cooldown after exercise (to avoid postural hypotension on sudden cessation of exercise) and the avoidance of hot showers immediately postrace. Collapse is also more likely when long queues develop in the race finishing area. When such queuing occurs, athletes who begin to feel faint should be encouraged to lie down and to elevate their legs and pelvises, if possible.

Other Common Conditions

In addition to postural hypotension, physicians in the medical tent are likely to see several other medical conditions.

Exercise-associated muscle cramping, the "painful, spasmodic, involuntary contraction of skeletal muscle that occurs during or immediately after muscular exercise,"23 is also a common reason for visiting the medical tent following a race.1-3,10 The cause has not yet been determined, and there is little support for abnormalities in either serum electrolyte concentrations or alterations in hydration status.23 Schwellnus et al23 have postulated that muscle cramping is caused by muscle fatigue, which alters alpha motor-neuron control at the spinal level. The treatment is to maintain the cramped muscle in a lengthened position with passive stretching.

Hyponatremia is defined as a serum sodium concentration of less than 135 mmol/L. Hyponatremia is more commonly seen in ultradistance races,1 but it has also been described in marathon races22,24 and in hikers.25 Hyponatremia can either be symptomatic or asymptomatic. The cause of severe symptomatic hyponatremia is fluid overload.22,26,27

An endurance athlete who has an altered mental status and a normal rectal temperature should be considered to have hyponatremia until proven otherwise.3 Other symptoms can include headache, incoordination, lightheadedness, seizures, and coma.27 Edema of the hands and fingers is a useful physical sign of fluid overload. If athletes are stable with no symptoms or signs of cerebral or pulmonary edema, they can usually be managed in an on-site medical tent.1

The management of mild hyponatremia is "masterly inactivity": awaiting a spontaneous diuresis of the excess fluid. This normally requires observation for a couple of hours. Alternatively, a low dose of diuretic may be used to initiate the diuresis. Athletes with more severe hyponatremia need urgent transfer to a hospital, because seizures or coma may complicate this condition, and death may occur. A volunteer can quickly determine that immediate action is necessary if the athlete has a serum sodium level lower than 125 mmol/L, severe alterations in mental status, seizures, or pulmonary edema. These athletes should not be treated with oral or IV fluid since they are already suffering from fluid overload.27 The exception is the judicious use of hypertonic saline if the athlete has severe central nervous system manifestations of hyponatremia, such as coma or seizures. Readers are referred to specific published guidelines on the use of hypertonic saline.22,24,27

Heatstroke is diagnosed when an athlete has a rectal temperature higher than 106.7°F (41.5°C) plus an altered mental status. Heatstroke requires immediate treatment to decrease body temperature. The simplest and most effective way to do this is to immerse the athlete in ice water for 5 to 10 minutes in a child's plastic bathtub with the arms and legs over the side.3,6 Ice-water immersion should decrease the body temperature by 1.8°F (1°C) per minute, and after 5 to 10 minutes, the rectal temperature should have been reduced to 100.4°F (38°C). IV fluids may be given to correct any coexistent dehydration and to assist in stabilizing the circulation. Fluid overload, however, may induce myocardial failure and pulmonary edema in those with heatstroke, so IV fluids must be given with caution.

Hypothermia is diagnosed as "severe" when the rectal temperature is less than 86°F (30°C), "moderate" between 86° and 93.2°F (30° and 34°C), and "mild" between 93.2° and 96.8°F (34° and 36°C). Mild hypothermia is managed by replacing wet clothing with dry clothing, protecting the athlete from wind and rain, and insulating the athlete from the ground. If mental status is normal, athletes can be given warm fluids to drink. Athletes with moderate or severe hypothermia need to be gently wrapped in a blanket and transferred immediately to a hospital for passive heating. Ventricular fibrillation can occur with physical manipulation in severe hypothermia, so handling should be kept to a minimum.

Hypoglycemia is an unusual problem following an endurance event.1,3 Athletes at risk are those involved in very long distance events who fail to consume adequate carbohydrate or who have an eating disorder.3 Patients with type 1 diabetes are especially at risk if they fail to ingest adequate amounts of carbohydrate during exercise, particularly if they begin exercise with an excess of exogenous insulin from recent insulin injections. Management is with an IV infusion of 50% glucose.

Race Tent Expertise

The most common cause for EAC is postural hypotension caused by pooling of blood in the legs and pelvis. A sudden drop in the right atrial pressure that induces a reflex hypotension may also be a factor.13 Collapsed athletes should be managed in the head-down position with the lower limbs elevated, while a simple assessment is made to determine if they have any other cause for collapse, such as heatstroke, hyponatremia, muscle cramping, or hypoglycemia. When a working diagnosis is achieved, specific treatment can be initiated.

The initial exam and triage system are the most important interventions that determine the efficacy of treatment of athletes who collapse during or after exercise. The foundation of a successful race-day medical facility is based on skilled clinicians who:

  • Know that dehydration is not an acceptable clinical diagnosis for the conditions that typically occur in endurance athletes;
  • Are aware that postural hypotension is the most common reason for admission to a medical tent at the finish of endurance events;
  • Understand that the level of consciousness is the single most important clinical guide to the likely diagnosis; and
  • Appreciate that some basic investigations will quickly establish a firm diagnosis for which the treatment is not usually especially demanding.

References

  1. Speedy DB, Rogers IR, Noakes TD, et al: Diagnosis and prevention of hyponatremia at an ultradistance triathlon. Clin J Sport Med 2021;10(1):52-58
  2. Roberts WO: A 12-yr profile of medical injury and illness for the Twin Cities Marathon. Med Sci Sports Exerc 2021;32(9):1549-1555
  3. Holtzhausen LM, Noakes TD: Collapsed ultraendurance athlete: proposed mechanisms and an approach to management. Clin J Sport Med 1997;7(4):292-301
  4. Holtzhausen LM, Noakes TD, Kroning B, et al: Clinical and biochemical characteristics of collapsed ultra-marathon runners. Med Sci Sports Exerc 1994;26(9):1095-1101
  5. Holtzhausen LM, Noakes TD: The prevalence and significance of post-exercise (postural) hypotension in ultramarathon runners. Med Sci Sports Exerc 1995;27(12):1595-1601
  6. Mayers LB, Noakes TD: A guide to treating ironman triathletes at the finish line. Phys Sportsmed 2021;28(8):35-50
  7. Kretsch A, Grogan R, Duras P, et al: 120210 Melbourne marathon study. Med J Aust 120214;141(12-13):809-814
  8. Noakes TD, Myburgh KH, du Plessis J, et al: Metabolic rate, not percent dehydration, predicts rectal temperature in marathon runners. Med Sci Sports Exerc 1991;23(4):443-449
  9. Richards R, Richards D: Exertion-induced heat exhaustion and other medical aspects of the City-to-Surf fun runs, 1978-120214. Med J Aust 120214;141(12-13):799-805
  10. Hiller WD, O'Toole ML, Fortess EE, et al: Medical and physiological considerations in triathlons. Am J Sports Med 120217;15(2):164-167
  11. Adolph EF: Physiological fitness for the desert. Fed Proc 1943;2:158-164
  12. Eichna LW, Horvath SM, Bean WB: Post-exertional orthostatic hypotension. Am J Med Sci 1947;213(6):641-654
  13. Barcroft H, Edholm OG, McMichael J, et al: Posthaemorrhagic fainting: study by cardiac output and forearm flow. Lancet 1944;1:489-490
  14. Gonzalez-Alonso J, Mora-Rodriguez R, Coyle EF: Supine exercise restores arterial blood pressure and skin blood flow despite dehydration and hyperthermia. Am J Physiol 1999;277(2 pt 2):H576-H583
  15. Roberts WO: Exercise-associated collapse in endurance events: a classification system. Phys Sportsmed 120219;17(5):49-57
  16. Sandell RC, Pascoe MD, Noakes TD: Factors associated with collapse during and after ultramarathon footraces: a preliminary study. Phys Sportsmed 120218;16(9):86-94
  17. Smith ML, Graitzer HM, Hudson DL, et al: Baroreflex function in endurance- and static exercise-trained men. J Appl Physiol 120218;64(2):585-591
  18. Myrhe LG, Luft UC, Venters MD: Responses of athletes and non-athletes to lower body negative pressure and acute dehydration, abstracted. Med Sci Sports 1976;8:53-54
  19. Noakes TD: Dehydration during exercise: what are the real dangers? Clin J Sport Med 1995;5(2):123-128
  20. Noakes TD: Hyponatremia in distance athletes: pulling the IV on the 'dehydration myth.' Phys Sportsmed 2021;28(9):71-76
  21. Roberts WO: Assessing core temperature in collapsed athletes: what's the best method? Phys Sportsmed 1994;22(8):49-55
  22. Davis DP, Videen JS, Marino A, et al: Exercise-associated hyponatremia in marathon runners: a two-year experience. J Emerg Med 2021;21(1):47-57
  23. Schwellnus MP, Derman EW, Noakes TD: Aetiology of skeletal muscle 'cramps' during exercise: a novel hypothesis. J Sports Sci 1997;15(3):277-285
  24. Ayus JC, Varon J, Arieff AI: Hyponatremia, cerebral edema, and noncardiogenic pulmonary edema in marathon runners. Ann Intern Med 2021;132(9):711-714
  25. Zelingher J, Putterman C, Ilan Y, et al: Case series: hyponatremia associated with moderate exercise. Am J Med Sci 1996;311(2):86-91
  26. Speedy DB, Rogers IR, Noakes TD, et al: Exercise-induced hyponatremia in ultradistance triathletes is caused by inappropriate fluid retention. Clin J Sport Med 2021;10(4):272-278
  27. Speedy DB, Noakes TD, Schneider C: Exercise-associated hyponatremia: a review. Emerg Med (Fremantle) 2021;13(1):17-27

Dr Speedy is a research fellow in the Department of General Practice and Primary care at the University of Auckland and a sports physician at Sports Care in Auckland, New Zealand. Dr Noakes is a professor of exercise and sport science in the Department of Human Biology at the University of Capetown and Sports Science Institute of South Africa in Capetown, South Africa. Dr Holtzhausen is a physician at Sports Care in Auckland. Address correspondence to Dale B. Speedy, MBChB, MSc, MD, Sports Care, 179A Hill Rd, Manurewa, Auckland, New Zealand; e-mail correspondence to [email protected].

Disclosure information: Drs Speedy, Noakes, and Holtzhausen disclose no significant relationship with any manufacturer of any commercial product mentioned in this article. No drug is mentioned in this article for an unlabeled use.


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