Metabolic and hemodynamic responses of lower limb during exercise in patients with COPD |
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Authors: | Maltais Francois; Jobin Jean; Sullivan Martin J; Bernard Sarah; Whittom Francois; Killian Kieran J; Desmeules Marc; Belanger Marthe; LeBlanc Pierre |
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Abstract: | Premature lacticacidosis during exercise in patients with chronic obstructive pulmonarydisease (COPD) may play a role in exercise intolerance. In this study,we evaluated whether the early exercise-induced lactic acidosis inthese individuals can be explained by changes in peripheralO2 delivery( O2).Measurements of leg blood flow by thermodilution and of arterial andfemoral venous blood gases, pH, and lactate were obtained during astandard incremental exercise test to capacity in eight patients withsevere COPD and in eight age-matched controls. No significantdifference was found between the two groups in leg blood flow at restor during exercise at the same power outputs. Blood lactateconcentrations and lactate release from the lower limb were greater inCOPD patients at all submaximal exercise levels (allP < 0.05). Leg O2at a given power output was not significantly different between the twogroups, and no significant correlation was found between this parameterand blood lactate concentrations. COPD patients had lower arterial andvenous pH at submaximal exercise, and there was a significant positivecorrelation between venous pH at 40 W and the peakO2 uptake(r = 0.91, P < 0.0001). The correlation betweenvenous pH and peak O2 uptakesuggests that early muscle acidosis may be involved in early exercisetermination in COPD patients. The early lactate release from the lowerlimb during exercise could not be accounted for by changes inperipheral O2. The present results point to skeletal muscle dysfunction as being responsible for the early onset of lactic acidosis inCOPD. |
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