To determine if the gas exchange anaerobic threshold (GeAT) is altered by increases in cardiac function, 7 chronic heart failure (CHF) patients (age 56.4± 7.6 years) were studied by withdrawal and subsequent réintroduction of inotropic medication, digoxin, to evaluate the sensitivity and feasibility of utilizing GeAT during exercise testing as an additional marker of improved cardiac function. Treadmill tests using a modified Naughton treadmill protocol were done 1 week apart. Blood sampling was done prior to each exercise session to determine digoxin levels. Expired gases were collected using an automated metabolic measurement cart. GeAT was determined by examination of the plots of O(2) consumption (VO(2)) versus minute ventilation (V(E)), as well as end-tidal O(2) and CO(2). Dead space/tidal volume ratios (V(D)/V(T)) were calculated from expired gas variables at submaximal and peak exercise levels. Peak exercise rate pressure product increased from 18.7 to 22.7 bpm X mm Hg X 10^-3 on digoxin. VO(2) peak and relative GeAT (GeAT(rei)) were unchanged with digoxin (1.50 ± 0.58 to 1.60 ± 0.48 l ∙ min^-1, and from 70.3 ± 14.6 to 76.7 ± 11.3% of VO(2) peak, respectively). Absolute GeAT(GeAT(abs)) increased from 1.07 ± 0.39 to 1.23 ± 0.39 l ∙ min^-1 (p < 0.01)when on digoxin. No changes in V(D)/V(T) were observed at submaximal versus maximal exercise, nor with digoxin, suggesting that altered ventilation/perfusion imbalances were not related to the increased V(E) and GeAT during exercise under the off- or on-digoxin conditions. These data suggest that although VO(2) peak remains relatively unchanged with digoxin, the increase in GeAT(abs)(reflecting postponed skeletal muscle anaerobic metabolism) might constitute a more sensitive noninvasive marker of changes in blood flow and exercise capacity in CHF patients than VO(2) peak. Since peak systolic blood pressure increased on digoxin, GeAT might reflect increased myocardial function.

Keywords:
Chronic heart failure, Ventilation threshold, Exercise testing, Exercise capacity, Digoxin
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1992
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