The maximal metabolic responses of 11 paraplegic wheelchair road racers were evaluated with 2 wheelchair exercise protocols: increasing speed and increasing resistance. The maximal heart rates, minute ventilations and oxygen uptakes were similar for the 2 tests, indicating that either protocol is suitable for maximal wheelchair dynamometer exercise tests for groups. The resulting data were then compared to published data on maximal arm exercise by athletic and non athletic paraplegics and ambulatory males of the same age group. The combined mean values for both exercise tests of maximal oxygen consumption rate (V02rnax = 37.4 ml/kg/min) , minute ventilation (VE = 109.4 l/min) , respira tory exchange quotient (RQrnax = 1.18) and heart rate (187 beats/min) are in the mid range of reported data on wheelchair athletes. The mean RQ and heart rate values were similar to those achieved by ambulatory individuals performing maximal exercise tests. The mean V02rnax of 37.4 ml/kg/min in our subjects is comparable to that achieved by sedentary ambulatory males of this age group. The data and the comparison to published data suggest several conclusions: in some parameters elite male paraplegic road racers have maximal values similar to those of ambulatory males, and in others they have maximal values substantially lower than might be expected; there is considerable variability among paraplegics in the metabolic responses to maximal exercise, most likely related to differences in cardiovascular fitness; and paraplegics can improve their cardiovascular fitness by training.
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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