The time course of pulmonary diffusion capacity changes following maximal exercise
Creators: name: Sheel, Andrew William
Publisher: name: University of British Columbia
Year: 2009

description: Pulmonary gas transport has not been typically recognized as a limiting factor to physical exercise. Dempsey et al. (1984; 1986) have suggested that the pulmonary system remains unchanged despite chronic aerobic training. Adaptations to other physiological systems may impose metabolic demands which the respiratory system can not meet. In essence, the lung's capacity for gas exchange becomes surpassed by other training adaptations. Supporting evidence is seen as decreases in arterial oxygenation at near maximal work rates in highly trained male endurance athletes (Dempsey et al., 1984; Powers et al., 1988; 1989; Hopkins and McKenzie 1989). Decreased arterial oxygenation has been termed exercise-induced arterial hypoxemia (EIH), and has direct consequences on VO₂max (Lawler et al., 1988; Powers et al., 1989; Martin and O'Kroy, 1993) and maximal performance capacity (Koskolou and McKenzie, 1994). It is estimated that approximately fifty percent of highly trained male endurance athletes exhibit EIH (Powers et al., 1988; 1993; Martin et al., 1992b). One mechanism that has been advanced to explain this phenomenon is a diffusion limitation. Diffusion capacity of the lung (DL) may be depressed during exercise and not allow for complete gas equilibrium to occur. If a structural alteration were present during exercise, it would continue to depress DL during recovery. To investigate the time course of change in pulmonary diffusion capacity for carbon monoxide (DL[sub co]) ten (N=10) highly trained male cyclists (HT) and ten (N=10) moderately (MT) male subjects were selected for this study. Subjects cycled to exhaustion to determine maximal oxygen consumption (VO₂max) on an electronically braked cycle ergometer (Mijnhardt KEM-3) (mean ± SD; HT VO₂max = 68.0 ± 4.9; MT VO₂max = 51.6 ± 4.7 mL-kg⁻¹Emin⁻¹). Percent arterial oxygen saturation (%SaO₂) was monitored by a pulse oximeter (Ohmeda Biox 3740) to determine if subjects demonstrated exercise-induced arterial hypoxemia (defined as %SaO₂ ≤ 91%) (%SaO₂min HT = 91.4 ± 1.6; MT = 94.6 ± 1.1). At a second data collection period, pulmonary function testing was performed. All subjects demonstrated normal pulmonary function. Initial diffusion measurements were made to obtain resting DL[sub CO]. diffusion capacity of the alveolar membrane (DM), and pulmonary capillary blood volume (Vc). Both spirometry and diffusion measurements were made using the same apparatus (Collins PLUS DS II). DM and Vc were calculated by measuring DL[sub CO] at two inspired O₂ concentrations using the technique of Roughton &amp; Forster (1957). Subjects then cycled to fatigue at a workrate that corresponded to the highest workrate attained during the VO₂max test. Expired gases and %SaO₂ data were collected during the time to fatigue cycle test. Five additional measurements of pulmonary diffusion were made at 1, 2, 4, 6 and 24 hours following the cycle test. One hour post-exercise, DL[sub CO] was significantly decreased in both groups compared to baseline. The decrease reached a minimum value at 6 hrs and approached normal values 24 hrs after the exercise. Only HT subjects exhibited EIH yet both groups experienced similar changes in DL[sub CO] The correlation between %SaO₂min and change in DL[sub CO] was low (r=-0.3), implying that EIH can not be explained by post exercise decrease in DL[sub CO]. The change in DL[sub CO] can be explained primarily by a parallel decrease in Vc. Vc decreased below baseline values in both groups, perhaps indicating a compensatory shunting mechanism. A smaller degree of change was observed in DM, and played less of a role in the decreased DL[sub CO]- The results of this study are the first to compare diffusion capacity in two separate groups, based on training status, following maximal exercise. Both moderately trained and highly trained subjects exhibited similar decreases in pulmonary diffusing capacity. This supports the theory that the lung may not adapt to aerobic training and behaves in a similar manner regardless of training status.