Abstract
We compared the time constant () 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 , 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[HHb+Mb]) 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; P < 0.001). Critical power was greater in PRI compared with CON (PRI 161 ± 25 vs. CON 149 ± 22 W; P < 0.001), whereas (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 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.
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