Abstract

ObjectivesThis study sought to test whether insulin improves exercise ventilatory efficiency (VE/VCO2slope) and oxygen uptake at peak exercise (peak VO2) in patients with type 2 diabetes–heart failure (HF) comorbidity. BackgroundIn type 2 diabetes–HF comorbidity, depression of alveolar–capillary diffusion (DLCO) correlates with deterioration of exercise VE/VCO2slope and peak VO2. Insulin potentiates DLCOin these patients. MethodsExercise ventilatory efficiency and peak VO2(cycle ergometry ramp protocol), as well as DLCOat rest and its subdivisions (membrane conductance [DM] and pulmonary capillary blood volume [VC]) were assessed in 18 patients with type 2 diabetes–HF comorbidity at baseline and after 50 ml of saline + regular insulin (10 IU), or saline, was infused on consecutive days, according to a random crossover design. Glycemia was kept at pre-insulin level for the experiment duration. ResultsBaseline DLCO, DM, peak VO2, and VE/VCO2slope were compromised in these patients. At measurements performed in the 60 min after infusions, compared with at baseline, saline was ineffective, whereas insulin augmented peak VO2(+13.5%) and lowered VE/VCO2slope (−18%), and also increased time to anaerobic threshold (+29.4%), maximal O2pulse (+12.3%), aerobic efficiency (+21.2%), DLCO(+12.5%), and DM(+21.6%), despite a reduction in VC(−16.3%); insulin did not vary cardiac index and ejection fraction at rest. Changes in peak VO2and VE/VCO2slope (r = 0.67, p = 0.002; r = −0.73, p < 0.001, respectively) correlated with those in DLCO. These responses were unrelated to glycohemoglobin and baseline fasting blood sugar. They were persistent at 6 h after insulin infusion, and were undetectable at 24 h. ConclusionsIn diabetes–HF comorbidity, insulin causes a prolonged improvement in physical performance through activation of multiple factors, among which facilitation of gas conductance seems to be predominant.

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