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One hundred twenty-eight healthy volunteers (81 women, 47 men) older than 55 yr of age were studied with an incremental progressive cycle ergometer test to a symptom-limited, maximal tolerable work load. Mean (+/- SD) age was 66 +/- 6 yr in women and 66 +/- 5 years in men. Subjects with a history of ischemic heart disease, diabetes, pulmonary disease, or neuromuscular disease were excluded. Smokers were included, but all subjects had normal FEV1 and FVC. The objective of the study was to compare measured values of VO2max and Wmax in this older population with previously published predicted values based on subjects of all ages. We found that Wmax observed exceeded Wmax predicted by 9.5 +/- 22% (mean +/- SD) and that VO2max observed exceeded VO2max predicted by 17.5 +/- 22%. Because of this systematic underestimate of VO2max and Wmax by the previous prediction equations, we constructed new prediction equations for use in subjects older than 55 yr of age using height, weight, age, and sex as variables. We conclude that these new prediction equations more accurately predict Wmax and VO2max in subjects older than 55 yr of age because they are based solely on subjects in this age group.

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A previously healthy 38-year-old triathlete prepared for a swim in a cold (15°C) lake by drinking 1/2 L of a protein supplement and putting on a wetsuit. After swimming approximately 500 m, she developed dyspnea. She stopped momentarily and then continued on, but developed further dyspnea associated with chest constriction and wheezing. Her exercise tolerance deteriorated dramatically, such that she had to be towed to shore by another swimmer. Throughout the swim and rescue procedure her head was not submerged and she did not aspirate lake water.Upon reaching the shore, the patient's symptoms continued, and she also developed hemoptysis. Nevertheless, she was able to drive herself to the the emergency department at the nearest hospital, 15 minutes away.In the emergency department, the patient was found to be in moderate respiratory distress, tachypneic, able to speak only in brief phrases, and profoundly hypoxemic (blood pressure = 119/72 mm Hg; heart rate = 72 beats/ min; respiratory rate = 32 breaths/min; SaO 2 = 72% on room air). There was no jugular venous distension, no cardiac murmurs or gallops, and no dependent edema, but there was diffuse wheezing on auscultation of the chest.Laboratory investigations showed borderline elevation of the D-dimer, but results of troponin I tests and the ECG were normal. The initial sitting anterior-posterior chest xray is shown in Figure 1.This patient's most likely diagnosis is: a) food-associated exercise-induced anaphylaxis; b) cold urticaria; c) swimming-induced pulmonary edema; or d) cardiogenic pulmonary edema. For the Answer to this Challenge, see page 297.This article has been peer reviewed. Can J Emerg Med 2006;8(4):281

T he correct answer to this Diagnostic Challenge is swimming-induced pulmonary edema (SIPE). Cardiogenic pulmonary edema is an unlikely diagnosis in this case. Even without knowing the results of serial troponin determinations, the diagnosis of acute myocardial infarction leading to severe congestive heart failure would be almost impossible with a normal ECG; and as indicated below. Of note, a delayed echocardiogram revealed a normal ejection fraction, suggesting a non-cardiogenic etiology.Food-associated, exercise-induced anaphylaxis has been described, 1 especially in teenaged women, and it can produce pulmonary edema; 2 however, this patient lacked wheals and gastrointestinal symptoms, as well as vascular collapse, which are key features of the syndrome.Cold urticaria may often involve the respiratory tract (hoarseness, dyspnea and wheezing), gastrointestinal and the cardiovascular systems (hypotension, tachycardia and arrhythmia), 3 and shock-like symptoms have been reported after aquatic exposures. 4,5 However, most typically patients with this condition develop diffuse pruritus and wheals with angioedema, 3 and our patient had none of these manifestations. CommentaryIn racing thoroughbreds, marked increases in pulmonary vascular pressures contribute to stress failure of pulmonary capillaries 6,7 causing lung bleeding. After brief, vigorous exercise in elite human athletes with a previous history suggestive of lung bleeding, increased concentrations of red blood cells and protein have been demonstrated in broncho-alveolar lavage fluid. These findings imply that intense exercise can impair the integrity of the pulmonary capillaries of the blood-gas barrier (BGB). 8 Chest CT scans of highly trained athletes after a triathlon competition demonstrated enhanced lung density and greater numbers of opacities suggesting an increase in pulmonary extravascular fluid. 9 Although rare in people exercising on land, pulmonary edema is more routinely reported in individuals participating in swimming or other immersion-related sports. 10 Adir and coworkers describe a series of 70 teen athletes who, over a 3-year period, developed SIPE. 10 All cases occurred in trainees who were swimming semi-reclined in warm https://www.cambridge.org/core/terms. https://doi