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Blood lactate accumulation and muscle deoxygenation during incremental exercise.
Authors:B Grassi  V Quaresima  C Marconi  M Ferrari  P Cerretelli
Institution:Istituto di Tecnologie Biomediche Avanzate, Consiglio Nazionale delle Ricerche, I-20090 Segrate (MI), Italy. grassi@itba.mi.cnr.it
Abstract:Near-infrared spectroscopy (NIRS) could allow insights into controversial issues related to blood lactate concentration (La](b)) increases at submaximal workloads (). We combined, on five well-trained subjects mountain climbers; peak O(2) consumption (VO(2peak)), 51.0 +/- 4.2 (SD) ml. kg(-1). min(-1)] performing incremental exercise on a cycle ergometer (30 W added every 4 min up to voluntary exhaustion), measurements of pulmonary gas exchange and earlobe La](b) with determinations of concentration changes of oxygenated Hb (DeltaO(2)Hb]) and deoxygenated Hb (DeltaHHb]) in the vastus lateralis muscle, by continuous-wave NIRS. A "point of inflection" of La](b) vs. was arbitrarily identified at the lowest La](b) value which was >0.5 mM lower than that obtained at the following. Total Hb volume (DeltaO(2)Hb + HHb]) in the muscle region of interest increased as a function of up to 60-65% of VO(2 peak), after which it remained unchanged. The oxygenation index (DeltaO(2)Hb - HHb]) showed an accelerated decrease from 60- 65% of VO(2 peak). In the presence of a constant total Hb volume, the observed DeltaO(2)Hb - HHb] decrease indicates muscle deoxygenation (i.e., mainly capillary-venular Hb desaturation). The onset of muscle deoxygenation was significantly correlated (r(2) = 0.95; P < 0.01) with the point of inflection of La](b) vs., i.e., with the onset of blood lactate accumulation. Previous studies showed relatively constant femoral venous PO(2) levels at higher than approximately 60% of maximal O(2) consumption. Thus muscle deoxygenation observed in the present study from 60-65% of VO(2 peak) could be attributed to capillary-venular Hb desaturation in the presence of relatively constant capillary-venular PO(2) levels, as a consequence of a rightward shift of the O(2)Hb dissociation curve determined by the onset of lactic acidosis.
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