Although the lungs are a critical component of exercise performance, their response to exercise and other environmental stresses is often overlooked when evaluating pulmonary performance during high workloads. Exercise can produce capillary leakage, particularly when left atrial pressure increases related to left ventricular (LV) systolic or diastolic failure. Diastolic LV dysfunction that results in elevated left atrial pressure during exercise is particularly likely to result in pulmonary edema and capillary hemorrhage. Data from race horses, endurance athletes, and triathletes support the concept that the lungs can react to exercise and immersion stress with pulmonary edema and pulmonary hemorrhage. Immersion in water by swimmers and divers can also increase stress on pulmonary capillaries and result in pulmonary edema. Swimming-induced pulmonary edema and immersion pulmonary edema in scuba divers are well-documented events caused by the fluid shifts that occur with immersion, elevated pulmonary venous pressure during extreme exercise, and negative alveolar pressure due to inhalation resistance. Prevention strategies include avoiding extreme exercise, avoiding over hydration, and assuring that inspiratory resistance is minimized. Figure 1. Pulmonary capillary wedge pressure (PCWP) measured during increasing exercise intensity, determined by oxygen consumption (VO 2 ), in well-trained (circles) and average-trained (squares) men with a mean age of 29.6. Note that the well-trained subjects preserved normal levels of PCWP until they reached high levels of exercise, while the average-trained men demonstrated increases in PCWP at lower levels of exercise intensity. Adapted from Stickland et al.
4MDCVJ | XII (2) 2016 94 houstonmethodist.org/debakey-journal of interstitial hemorrhage and fluid accumulation following a high workload in one horse that developed EIPH. West et al. 9 suggested that two factors contributed to this problem in horses: (1) They were likely to have a congenital weakness of pulmonary capillaries that resulted in capillary rupture at high pulmonary venous and capillary pressure, and (2) they developed high pulmonary venous pressure due to failure of the left ventricle with subsequent elevation of LV end diastolic pressure during high workloads.Human studies of lung responses to high workloads 10 corroborate the studies of West et al. to some extent. Zavorsksy et al. 11 studied individuals under several different workloads and performed lung imaging to document the presence or absence of lung edema. Radiographic image readers were blinded to the exposures and reported visual evidence of lung fluid. In individuals undergoing a diagnostic graded exercise test, no evidence of lung edema was noted. However, 15% of individuals who ran on a treadmill at 70% of maximum capacity for 2 hours demonstrated evidence of pulmonary edema, as did 65% of those who ran at maximum capacity for 7 minutes. Similar findings were noted in female athletes.12 Pingitore et al. examined 48 athletes before and aft...