Limitations to exercise tolerance in type 1 diabetes: the role of pulmonary oxygen uptake kinetics and priming exercise

Abstract

We compared the time constant (${\tau }_{\dot{\text{V}}{O}_2}$) of the fundamental phase of pulmonary oxygen uptake (V̇o₂) kinetics between young adult men with type 1 diabetes and healthy control subjects. We also assessed the impact of priming exercise on ${\tau }_{\dot{\text{V}}{O}_2}$, critical power, and muscle deoxygenation in a subset of participants with type 1 diabetes. Seventeen men with type 1 diabetes and 17 healthy male control subjects performed moderate-intensity exercise to determine ${\tau }_{\dot{\text{V}}{O}_2}$. A subset of seven participants with type 1 diabetes performed an additional eight visits, in which critical power, ${\tau }_{\dot{\text{V}}{O}_2}$, and muscle deoxyhemoglobin + myoglobin ([HHb+Mb], via near-infrared spectroscopy) kinetics (described by a time constant, τ_[HHb+Mb]) were determined with (PRI) and without (CON) a prior 6-min bout of heavy exercise. ${\tau }_{\dot{\text{V}}{O}_2}$ was greater in participants with type 1 diabetes compared with control subjects (type 1 diabetes 50 ± 13 vs. control 32 ± 12 s; P < 0.001). Critical power was greater in PRI compared with CON (PRI 161 ± 25 vs. CON 149 ± 22 W; P < 0.001), whereas ${\tau }_{\dot{\text{V}}{O}_2}$ (PRI 36 ± 15 vs. CON 50 ± 21 s; P = 0.006) and τ_[HHb+Mb] (PRI 10 ± 5 vs. CON 17 ± 11 s; P = 0.037) were reduced in PRI compared with CON. Type 1 diabetes patients showed slower pulmonary V̇o₂ kinetics compared with control subjects; priming exercise speeded V̇o₂ and [HHb + Mb] kinetics and increased critical power in a subgroup with type 1 diabetes. These data therefore represent the first characterization of the power-duration relationship in type 1 diabetes and the first experimental evidence that ${\tau }_{\dot{\text{V}}{O}_2}$ is an independent determinant of critical power in this population.NEW & NOTEWORTHY Patients with type 1 diabetes demonstrated slower oxygen uptake (V̇o₂) kinetics compared with healthy control subjects. Furthermore, a prior bout of high-intensity exercise speeded V̇o₂ kinetics and increased critical power in people with type 1 diabetes. Prior exercise speeded muscle deoxygenation kinetics, indicating that V̇o₂ kinetics in type 1 diabetes are limited primarily by oxygen extraction and/or intracellular factors. These findings highlight the potential for interventions that decrease metabolic inertia for enhancing exercise tolerance in this condition.

Keywords: critical power; exercise tolerance; muscle deoxygenation kinetics; oxygen uptake kinetics; priming exercise; type 1 diabetes.