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Effect of Altered Body CO 2 Stores on Pulmonary Gas Exchange Dynamics During Incremental Exercise in Humans
Author(s) -
Ozcelik O.,
Ward S. A.,
Whipp B. J.
Publication year - 1999
Publication title -
experimental physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.925
H-Index - 101
eISSN - 1469-445X
pISSN - 0958-0670
DOI - 10.1111/j.1469-445x.1999.01868.x
Subject(s) - hyperventilation , pco2 , bicarbonate , cycle ergometer , incremental exercise , lactic acidosis , acidosis , cardiology , medicine , carbon dioxide , lactic acid , respiration , metabolic acidosis , anesthesia , chemistry , anatomy , heart rate , biology , blood pressure , organic chemistry , bacteria , genetics
SUMMARY The lactate threshold is a widely used and, at times, controversial construct in exercise physiology and pathophysiology. Its non‐invasive estimation during incremental exercise depends upon CO 2 output increasing as a function of O 2 uptake, i.e. ‘V‐slope’, as a result of bicarbonate buffering during the lactic acidosis. However, we hypothesised that the V‐slope deflection could also occur as a consequence of metabolic CO 2 being diverted proportionally more into the CO 2 stores in the early phase of exercise. Eight healthy males performed two incremental exercise tests on a cycle ergometer, with and without controlled prior hyperventilation; the hyperventilation caused end‐tidal P CO2 to decline by [sim]10 mmHg, with the clearance of a CO 2 volume averaging 2547 ml. This corresponded to an ‘effective’ CO 2 capacitance of some 3·12 ml mmHg −1 kg −1 . Gas exchange was determined breath‐by‐breath, and blood was sampled from the dorsum of the heated hand. Our results demonstrate that the early dynamics of CO 2 wash‐in to the previously depleted body stores can result in a ‘pseudo‐threshold’, i.e. significantly before the onset of the actual lactic acidosis. Precautions should therefore be taken to avoid hyperventilation prior to non‐invasive estimation of the lactate threshold.