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

We compared the time constant () of the fundamental phase of pulmonary oxygen uptake (V̇o) kinetics between young adult men with type 1 diabetes and healthy control subjects. We also assessed the impact of priming exercise on , 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 . A subset of seven participants with type 1 diabetes performed an additional eight visits, in which critical power, , and muscle deoxyhemoglobin + myoglobin ([HHb+Mb], via near-infrared spectroscopy) kinetics (described by a time constant, τ) were determined with (PRI) and without (CON) a prior 6-min bout of heavy exercise. was greater in participants with type 1 diabetes compared with control subjects (type 1 diabetes 50 ± 13 vs. control 32 ± 12 s; < 0.001). Critical power was greater in PRI compared with CON (PRI 161 ± 25 vs. CON 149 ± 22 W; < 0.001), whereas (PRI 36 ± 15 vs. CON 50 ± 21 s; = 0.006) and τ (PRI 10 ± 5 vs. CON 17 ± 11 s; = 0.037) were reduced in PRI compared with CON. Type 1 diabetes patients showed slower pulmonary V̇o kinetics compared with control subjects; priming exercise speeded V̇o 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 is an independent determinant of critical power in this population. Patients with type 1 diabetes demonstrated slower oxygen uptake (V̇o) kinetics compared with healthy control subjects. Furthermore, a prior bout of high-intensity exercise speeded V̇o kinetics and increased critical power in people with type 1 diabetes. Prior exercise speeded muscle deoxygenation kinetics, indicating that V̇o 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.