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Maximal accumulated oxygen deficit in patients with chronic heart failure.
Medicine and Science in Sports and Exercise 2006 March
PURPOSE: To evaluate feasibility and repeatability of maximal accumulated oxygen deficit (MAOD) measurement in patients with chronic heart failure (CHF) and asymptomatic left ventricular dysfunction (ALVD), and to identify MAOD predictors employable in the clinical setting.
METHODS: We studied 10 CHF and 5 ALVD patients. Five normals (N) were used as controls. All subjects underwent a ramp incremental cardiopulmonary exercise test (CPX), three moderate-intensity constant-power exercise tests (CPET) at 30, 60, and 90% of ventilatory anaerobic threshold (VAT) power, and three severe-intensity CPET (1-2, 2-3, and >3 min in duration). MAOD was calculated as the difference between accumulated O2 demand and uptake during severe-intensity CPET. Postexercise lactate (PEL) was measured at 2, 4, 6, and 8 min of recovery after CPX and severe-intensity CPET.
RESULTS: MAOD did not vary with increasing severe-intensity CPET duration in any study subgroup. MeanMAOD (mean of the three severe-intensity CPET) was lower in the CHF than ALVD or N subgroups (12.2 +/- 4.9 vs 23.7 +/- 11.8 and 24.8 +/- 8.2 mL x kg(-1), P < 0.05), with comparable lean body mass values. In the total study population, meanMAOD was significantly but not highly correlated with peak VO2 and PEL from CPX, PEL from severe-intensity CPET, and O2 deficit and steady-state VO2 from moderate-intensity CPET. Intraclass correlation coefficient of MAOD measurement in CHF and ALVD was 0.98.
CONCLUSIONS: MAOD is repeatedly measurable in patients with CHF by a single severe-intensity CPET. MAOD of CHF patients is lower than that of age-matched ALVD patients and N, and this finding is muscle mass-independent. Finally, ergospirometric parameters and PEL from CPX, PEL from severe-intensity CPET, and VO2 on-kinetic descriptors from moderate-intensity CPET seem useless to reliably predict MAOD in CHF patients.
METHODS: We studied 10 CHF and 5 ALVD patients. Five normals (N) were used as controls. All subjects underwent a ramp incremental cardiopulmonary exercise test (CPX), three moderate-intensity constant-power exercise tests (CPET) at 30, 60, and 90% of ventilatory anaerobic threshold (VAT) power, and three severe-intensity CPET (1-2, 2-3, and >3 min in duration). MAOD was calculated as the difference between accumulated O2 demand and uptake during severe-intensity CPET. Postexercise lactate (PEL) was measured at 2, 4, 6, and 8 min of recovery after CPX and severe-intensity CPET.
RESULTS: MAOD did not vary with increasing severe-intensity CPET duration in any study subgroup. MeanMAOD (mean of the three severe-intensity CPET) was lower in the CHF than ALVD or N subgroups (12.2 +/- 4.9 vs 23.7 +/- 11.8 and 24.8 +/- 8.2 mL x kg(-1), P < 0.05), with comparable lean body mass values. In the total study population, meanMAOD was significantly but not highly correlated with peak VO2 and PEL from CPX, PEL from severe-intensity CPET, and O2 deficit and steady-state VO2 from moderate-intensity CPET. Intraclass correlation coefficient of MAOD measurement in CHF and ALVD was 0.98.
CONCLUSIONS: MAOD is repeatedly measurable in patients with CHF by a single severe-intensity CPET. MAOD of CHF patients is lower than that of age-matched ALVD patients and N, and this finding is muscle mass-independent. Finally, ergospirometric parameters and PEL from CPX, PEL from severe-intensity CPET, and VO2 on-kinetic descriptors from moderate-intensity CPET seem useless to reliably predict MAOD in CHF patients.
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