Why the study?
Does combined exposure to NO2 and O3 reduce exercise-induced cardiac output in healthy older adults?
Does combined exposure to NO2 and O3 reduce exercise-induced cardiac output in healthy older adults?
Combined exposure to NO2 and O3 blunts the exercise-induced increase in cardiac output in healthy older adults, potentially due to the systemic vasodilator effects of inhaled reaction products.
Combined NO2/O3 exposure may blunt exercise cardiac output in older adults; leaves open clinical relevance and need for prospective studies.
Eight healthy adults (56-85 yrs) were exposed in an environmental chamber to filtered air (FA), 0.60 ppm NO2, 0.45 ppm O3, and 0.60 ppm NO2 + 0.45 ppm O3 to investigate the effects of NO2 and O3 exposure on cardiac output. The subjects were exposed to each condition for two hours, while they exercised and rested in alternating 20-min periods. Minute ventilation averaged 26-29 l/min among the four exposures. Cardiac output was measured by the noninvasive impedance cardiography method, and was recorded prior to each exposure with the subject at rest, and during the last five minutes of each exercise period. There were no differences in cardiac output at preexposure among the four exposures. The exercise-induced increase in cardiac output with NO2/O3 exposure was significantly smaller (P < 0.05) than with the FA or O3 alone exposures. Reaction products of inhaled NO2 are known to cross the lung membranes, probably as a nitrate or nitrite. NO2 and O3 are also known to react together to form nitrate and nitrite. We hypothesize that a nitrate or nitrite reaction product of inhaled O3 and NO2 crosses the lung membrane into the general circulation, where it functions as a vasodilator, thereby reducing cardiac output.
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Deborah M. Drechsler-Parks (1995) studied this question.
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