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

© 2020 the American Physiological SocietyWe compared the time constant (τV·O2) of the fundamental phase of pulmonary oxygen uptake (V·O2) kinetics between young adult men with type 1 diabetes and healthy control subjects. We also assessed the impact of priming exercise on τV·O2, 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 τV·O2. A subset of seven participants with type 1 diabetes performed an additional eight visits, in which critical power, τV·O2, 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. τV·O2 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 τV·O2 (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 V· O2 kinetics compared with control subjects; priming exercise speeded V· O2 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 τV·O2 is an independent determinant of critical power in this population.