VO2 kinetics in intermittent exercise over a range of duty-cycle durations tended to associate with blood [lactate] profiles, similarly to previous demonstrations for sustained constant-load exercise.
Background-Pulmonary diffusion is impaired at rest in patients with chronic heart failure (CHF) and has been implicated in the generation of symptoms and exercise intolerance. The aim of this study was to determine whether pulmonary diffusion is impaired during exercise in CHF, to examine its relationship to pulmonary blood flow, and to consider its functional significance in relation to metabolic gas exchange. Methods and Results-Carbon monoxide transfer factor (TLCO) and pulmonary blood flow (Q C ) were measured by a rebreathe technique at rest and during steady-state cycling at 30 W in 24 CHF patients and 10 control subjects. Both patients and control subjects were able to raise TLCO and Q C during exercise. However, the patient group had a lower diffusion for a given blood flow (TLCO/Q C ) both at rest (3.6Ϯ0.16 and 4.8Ϯ0.23 mL ⅐ L Ϫ1 ⅐ mm Hg Ϫ1 ; PϽ0.001) and during exercise (2.8Ϯ0.16 and 3.4Ϯ0.13 mL ⅐ L Ϫ1 ⅐ mm Hg Ϫ1 for CHF patients and control subjects, respectively; PϽ0.05). TLCO/Q C was related to the ventilatory equivalent for carbon dioxide (VEVCO 2 ) production at 30 W (TLCO/Q c versus VEVCO 2 , rϭϪ0.58, PϽ0.01) and to peak exercise oxygen consumption measured during a progressive test (TLCO/Qc versus VO 2peak , rϭ0.57, PϽ0.01) in these patients. Conclusions-Patients with CHF are able to recruit reserves of TLCO and Q C during exercise. However, the TLCO/Q C ratio is consistently impaired in these patients and relates to both exercise hyperpnea and peak exercise oxygen consumption. Whether this impairment in alveolar gas exchange is reversible in CHF and therefore is a potential target for therapy has yet to be determined.
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