Abstract

In healthy subjects expiratory flow limitation (EFL) during exercise can lower O2 delivery to the working muscles. We hypothesized that if this affects exercise performance it should influence O2 kinetics at the end of exercise when the O2 debt is repaid. We performed an incremental exercise test on six healthy males with a Starling resistor in the expiratory line limiting expiratory flow to ∼ 1 l s−1 to determine maximal EFL exercise workload (Wmax). In two more square-wave exercise runs subjects exercised with and without EFL at Wmax for 6 min, while measuring arterial O2 saturation (% SaO2), end-tidal pressure of CO2 (PETCO2) and breath-by-breath O2 consumption {({dot{V}}hbox{O}_{2})} taking into account changes in O2 stored in the lungs. Over the last minute of EFL exercise, mean PETCO2 (54.7 ± 9.9 mmHg) was significantly higher (P < 0.05) compared to control (41.4 ± 3.9 mmHg). At the end of EFL exercise %SaO2 fell significantly by 4 ± 3%. When exercise stopped, EFL was removed, and we continued to measure {{dot{V}}hbox{O}_{2}.} During recovery, there was an immediate step increase in {{dot{V}}hbox{O}_{2},} so that repayment of EFL O2 debt started at a higher {{dot{V}}hbox{O}_{2}} than control. Recovery {{dot{V}}hbox{O}_{2}} kinetics after EFL exercise was best characterized by a double-exponential function with fundamental and slow time constants of 27 ± 11 and 1,020 ± 305 s, compared to control values of 41 ± 10 and 1,358 ± 320 s, respectively. EFL O2 debt was 52 ± 22% greater than control (2.19 ± 0.58 vs. 1.49 ± 0.38 l). We conclude that EFL exercise increases the O2 debt and leads to hypoxemia in part due to hypercapnia.

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