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~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 ð _ VO 2 Þ 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 _ VO 2 : During recovery, there was an immediate step increase in _ VO 2 ; so that repayment of EFL O 2 debt started at a higher _ VO 2 than control. Recovery _ VO 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 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.

Kinetics of muscle deoxygenation are accelerated at the onset of heavy-intensity exercise in patients with COPD: relationship to central cardiovascular dynamics

“…More specifically, the development of high mean intrathoracic pressures as V E increases in the transitional phase could dynamically impair the rate of right ventricle filling and left ventricle emptying in these patients. Recently, Vogiatzis et al (49) showed that normal subjects breathing with simulated expiratory flow limitation, similar to that found in advanced COPD, had significantly slower offtransient V O 2p kinetics compared with control values, suggesting that alterations in the mechanics of breathing can reduce muscle O 2 delivery enough to affect the kinetics of V O 2p .…”

“…Potential explanations for slower on-transient Q T (i.e., HR and SV) kinetics in COPD are as follows: 1) autonomic imbalance (26), 2) pulmonary vascular alterations (including pulmonary hypertension) (14), and/or 3) effects of mechanics of breathing on SV (1,2,49,50). The increase in HR through sympathetic activation is slower than that accomplished by parasympathetic withdrawal (51).…”

“…However, a different scenario may emerge during heavy (supra-"lactate threshold") exercise. In this situation, higher ventilation and disturbances in mechanics of breathing (1,2,49,50), hypoxemia (36,45), pulmonary hemodynamics (14), autonomic balance (26), and peripheral vasodilation (see DISCUSSION for details) could slow the response of systemic (central) and peripheral (microvascular) O 2 delivery to a point where the kinetics of V O 2 might become limited by O 2 availability (38).…”

Chest wall volume regulation during exercise in COPD patients with GOLD stages II to IV

“…Greater activation of abdominal muscles allowed GOLD stage II patients to dynamically hyperinflate much less than GOLD stages III and IV and probably led those patients to stop exercise from leg discomfort rather than dyspnoea (table 2). High expiratory pressures during exercise in patients with COPD [10,11,26] and healthy subjects [27,28] can cause adverse circulatory events that ultimately may impair exercise performance. Under this condition, high expiratory pressures during exercise in patients with GOLD stage II might have caused adverse circulatory effects that ultimately impaired exercise performance resulting in similar peak exercise tolerance in GOLD stages II and III (table 2).…”

Algorithms, modelling and $$ \dot{V}{\text{O}}_{ 2} $$ kinetics

“…Furthermore, using the directly measured B-by-B absolute values of V Ai-1 , they calculated B-by-B DVO 2s in steady-state (rest and exercise) and during rest-to-exercise transitions obtaining reliable measures of _ VO 2 and _ VCO 2 . Although a method based on the use of OEP, along with standard measures of respiratory gas fractions and flow at the mouth, appears highly promising for research and clinical applications (Vogiatzis et al 2007), it remains rather time-consuming and technically demanding. At its current stage of technical development, it cannot provide the user with immediate results.…”