Abstract

A significant number of highly trained endurance runners have been observed to display an inadequate hyperventilatory response to intense exercise. Two potential mechanisms include low ventilatory responsiveness to hypoxia and ventilatory limitation as a result of maximum expiratory flow rates being achieved. To test the hypothesis that expiratory flow limitation can complicate determination of ventilatory responsiveness during exercise the following study was performed. Sixteen elite male runners were categorized based on expiratory flow limitation observed in flow volume loops collected during the final minute of progressive exercise to exhaustion. Eight flow limited (FL) (VO2max, 75.9+/-2.4 mL x kg(-1) x min(-1); expiratory flow limitation, 47.3+/-20.4%) and eight non-flow limited subjects (NFL) (VO2max, 75.6+/-4.8 mL x kg(-1) x min(-1); expiratory flow limitation, 0.3+/-0.8%) were tested for hypoxic ventilatory responsiveness (HVR). Independent groups ANOVA revealed no significant differences between FL and NFL for VO2max, VE max (136.2+/-16.0 vs 137.5+/-21.6 L x min(-1)), VE/VO2, (28.4+/-3.2 vs 27.6+/-2.9 L x lO2(-1)), VE/VCO2 (24.8+/-3.1 vs 24.4+/-2.0 L x lCO2(-1)), HVR (0.2+/-0.2 vs 0.3+/-0.1 L x %SaO2(-1)), or SaO2 at max (89.1+/-2.4 vs 86.6+/-4.1%). A significant relationship was observed between HVR and SaO2 (r = 0.92, P < or = 0.001) in NFL that was not present in FL. Conversely, a significant relationship between VE/VO2 and SaO2 (r = 0.79, P < or = 0.019) was observed in FL but not NFL. Regression analysis indicated that the HVR-SaO2 and SaO2-VE/VO2 relationships differed between groups. When flow limitation is controlled for, HVR plays a more significant role in determining SaO2 in highly trained athletes than has been previously suggested.

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