Contribution of pulmonary stores to oxygen uptake

Influence of expiratory flow-limitation during exercise on systemic oxygen delivery in humans

“…We corrected for the sampling rates of the O 2 and CO 2 meters. We took into account the changes in the gas stored in the lung (Auchincloss et al 1970;Capelli et al 2001) and we avoided problems due to time dilation and compression (Farmery and Hahn 2001). The breath-by-breath technique has been validated and shown to measure V 0 O 2 accurately (Aliverti et al 2004a).…”

“…The difference in area between the two curves gives V O 2 ;m : However, the volume of O 2 exchanged at the mouth differs from V O 2 taken up by pulmonary capillaries ðV O 2 ;A Þ if the amount of O 2 stored within the lung changes. This occurs if the volume inspired is different from the volume expired in a given respiratory cycle, and/or if alveolar concentrations of O 2 change (Auchincloss et al 1970;Capelli et al 2001). The changes in O 2 stored within the lung must be subtracted from V O 2 ;m in order to obtain V O 2 ;A : This can be done if one knows the absolute gas volume and the alveolar O 2 concentrations at the beginning and end of a breath.…”

Exercise on‐transition uncoupling of ventilatory, gas exchange and cardiac hemodynamic kinetics accompany pulmonary oxygen stores depletion to impact exercise intolerance in human heart failure

“…Observations taken from separate studies of healthy adults across the ageing spectrum as well as those with cardiac disease (not specific to HF) indeed suggest the exercise on‐transition balance between the availability, depletion and repletion of O 2stores plays an appreciable role in dynamic adjustments that occur between ventilation, gas exchange and cardiac haemodynamics . The effect of temporal dyssynchrony across ventilation, gas exchange and cardiac haemodynamics followed by dynamic O 2store availability and utilization is particularly important within the exercise on‐transition phase heading towards windows of highly O 2 ‐dependent metabolic demand .…”

“…Lengthened O 2 kinetics demonstrated by HF also relate with integrative pathophysiology linked to features such as slowed response rates for adjustments in blood flow and oxidative phosphorylation relative to adenosine tri‐phosphate requirement . Separately, others report for adults without HF, those with delayed exercise on‐transition O 2 could also be expected to demonstrate asynchronous responsiveness across E , CO 2 and cardiac haemodynamics . Thus, while it is still unknown for human HF, an overall lack of confluence at the exercise on‐transition for aforementioned key physiological responses may be a precipitating factor for high and early recruitment of O 2 ‐independent metabolic contributions to total metabolic demand, narrowing of the predominant oxidative metabolic window of exercise and closely following exercise intolerance …”

“…With slowed E responsiveness relative to that for O 2 , CO 2 and cardiac haemodynamics at the exercise on‐transition, it has been proposed in those without HF that this may provoke rapid depletion of O 2stores and a lessened ability of this mechanism to contribute to subsequent increases in oxidative metabolic demand . The gross physiological uncoupling of O 2 transport features within the exercise on‐transition window may serve as a potent mechanism leading to ventilatory demand that is persistently exaggerated for a given workload domain …”