title: Oxygen kinetics and debt during recovery from expiratory flow-limited exercise in healthy humans.
abstract: In healthy subjects expiratory flow limitation (EFL) during exercise can lower O(2) delivery to the working muscles. We hypothesized that if this affects exercise performance it should influence O(2) kinetics at the end of exercise when the O(2) 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 approximately 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 O(2) saturation (% SaO(2)), end-tidal pressure of CO(2) (P (ET)CO(2)) and breath-by-breath O(2) consumption VO2 taking into account changes in O(2) stored in the lungs. Over the last minute of EFL exercise, mean P (ET)CO(2) (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 %SaO(2) fell significantly by 4 +/- 3%. When exercise stopped, EFL was removed, and we continued to measure VO2. During recovery, there was an immediate step increase in [Formula: see text] so that repayment of EFL O(2) debt started at a higher VO2 than control. Recovery VO2 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 O(2) debt was 52 +/- 22% greater than control (2.19 +/- 0.58 vs. 1.49 +/- 0.38 l). We conclude that EFL exercise increases the O(2) debt and leads to hypoxemia in part due to hypercapnia.
authors.affiliation: Department of Critical Care Medicine and Pulmonary Services, G. P. Livanos and M. Simou Laboratories, Evangelismos Hospital, National and Kapodistrian University of Athens, Athens, Greece. gianvog@phed.uoa.gr
authors.forename: I
authors.initials: I
authors.lastname: Vogiatzis
authors.forename: S
authors.initials: S
authors.lastname: Zakynthinos
authors.forename: O
authors.initials: O
authors.lastname: Georgiadou
authors.forename: S
authors.initials: S
authors.lastname: Golemati
authors.forename: A
authors.initials: A
authors.lastname: Pedotti
authors.forename: P T
authors.initials: PT
authors.lastname: Macklem
authors.forename: C
authors.initials: C
authors.lastname: Roussos
authors.forename: A
authors.initials: A
authors.lastname: Aliverti
mesh_terms: D002245:Carbon Dioxide / Q000378:metabolism; D002302:Cardiac Output; D017079:Exercise Tolerance; D045853:Exhalation; D005541:Forced Expiratory Volume; D006801:Humans; D006935:Hypercapnia / Q000378:metabolism / Q000503:physiopathology; D000860:Hypoxia / Q000378:metabolism / Q000503:physiopathology; D007700:Kinetics; D008297:Male; D008954:Models, Biological; D018482:Muscle, Skeletal / Q000378:metabolism*; D010100:Oxygen / Q000097:blood / Q000378:metabolism*; D010101:Oxygen Consumption; D029424:Pulmonary Disease, Chronic Obstructive / Q000503:physiopathology; D012123:Pulmonary Ventilation; D012016:Reference Values
chemical_list: D002245:Carbon Dioxide; D010100:Oxygen