Oxygen kinetics and debt during recovery from expiratory flow-limited exercise in healthy humans

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 (W _max). In two more square-wave exercise runs subjects exercised with and without EFL at W _max for 6 min, while measuring arterial O₂ saturation (% SaO₂), end-tidal pressure of CO₂ (P _ETCO₂) 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 P _ETCO₂ (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.