Objectives: This study sought to test whether insulin improves exercise ventilatory efficiency (VE/VCO2 slope) and oxygen uptake at peak exercise (peak VO2) in patients with type 2 diabetes-heart failure (HF) comorbidity.
Background: In type 2 diabetes-HF comorbidity, depression of alveolar-capillary diffusion (DL(CO)) correlates with deterioration of exercise VE/VCO2 slope and peak VO2. Insulin potentiates DL(CO) in these patients.
Methods: Exercise ventilatory efficiency and peak VO2 (cycle ergometry ramp protocol), as well as DL(CO) at rest and its subdivisions (membrane conductance [D(M)] and pulmonary capillary blood volume [V(C)]) 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.
Results: Baseline DL(CO), D(M), peak VO2, and VE/VCO2 slope 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/VCO(2) slope (-18%), and also increased time to anaerobic threshold (+29.4%), maximal O2 pulse (+12.3%), aerobic efficiency (+21.2%), DL(CO) (+12.5%), and D(M) (+21.6%), despite a reduction in V(C) (-16.3%); insulin did not vary cardiac index and ejection fraction at rest. Changes in peak VO2 and VE/VCO2 slope (r = 0.67, p = 0.002; r = -0.73, p < 0.001, respectively) correlated with those in DL(CO). 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.
Conclusions: In 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.