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

Abstract

We compared the time constant (<mml:math xmlns:mml="http://www.w3.org/1998/Math/MathML"><mml:mrow><mml:msub><mml:mi>τ</mml:mi><mml:mrow><mml:mover><mml:mtext>V</mml:mtext><mml:mo>̇</mml:mo></mml:mover><mml:msub><mml:mi>O</mml:mi><mml:mn>2</mml:mn></mml:msub></mml:mrow></mml:msub></mml:mrow></mml:math>) 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 <mml:math xmlns:mml="http://www.w3.org/1998/Math/MathML"><mml:mrow><mml:msub><mml:mi>τ</mml:mi><mml:mrow><mml:mover><mml:mtext>V</mml:mtext><mml:mo>̇</mml:mo></mml:mover><mml:msub><mml:mi>O</mml:mi><mml:mn>2</mml:mn></mml:msub></mml:mrow></mml:msub></mml:mrow></mml:math>, 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 <mml:math xmlns:mml="http://www.w3.org/1998/Math/MathML"><mml:mrow><mml:msub><mml:mi>τ</mml:mi><mml:mrow><mml:mover><mml:mtext>V</mml:mtext><mml:mo>̇</mml:mo></mml:mover><mml:msub><mml:mi>O</mml:mi><mml:mn>2</mml:mn></mml:msub></mml:mrow></mml:msub></mml:mrow></mml:math>. A subset of seven participants with type 1 diabetes performed an additional eight visits, in which critical power, <mml:math xmlns:mml="http://www.w3.org/1998/Math/MathML"><mml:mrow><mml:msub><mml:mi>τ</mml:mi><mml:mrow><mml:mover><mml:mtext>V</mml:mtext><mml:mo>̇</mml:mo></mml:mover><mml:msub><mml:mi>O</mml:mi><mml:mn>2</mml:mn></mml:msub></mml:mrow></mml:msub></mml:mrow></mml:math>, 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. <mml:math xmlns:mml="http://www.w3.org/1998/Math/MathML"><mml:mrow><mml:msub><mml:mi>τ</mml:mi><mml:mrow><mml:mover><mml:mtext>V</mml:mtext><mml:mo>̇</mml:mo></mml:mover><mml:msub><mml:mi>O</mml:mi><mml:mn>2</mml:mn></mml:msub></mml:mrow></mml:msub></mml:mrow></mml:math> was greater in participants with type 1 diabetes compared with control subjects (type 1 diabetes 50 ± 13 vs. control 32 ± 12 s; <i>P</i> < 0.001). Critical power was greater in PRI compared with CON (PRI 161 ± 25 vs. CON 149 ± 22 W; <i>P</i> < 0.001), whereas <mml:math xmlns:mml="http://www.w3.org/1998/Math/MathML"><mml:mrow><mml:msub><mml:mi>τ</mml:mi><mml:mrow><mml:mover><mml:mtext>V</mml:mtext><mml:mo>̇</mml:mo></mml:mover><mml:msub><mml:mi>O</mml:mi><mml:mn>2</mml:mn></mml:msub></mml:mrow></mml:msub></mml:mrow></mml:math> (PRI 36 ± 15 vs. CON 50 ± 21 s; <i>P</i> = 0.006) and τ_[HHb+Mb] (PRI 10 ± 5 vs. CON 17 ± 11 s; <i>P</i> = 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 <mml:math xmlns:mml="http://www.w3.org/1998/Math/MathML"><mml:mrow><mml:msub><mml:mi>τ</mml:mi><mml:mrow><mml:mover><mml:mtext>V</mml:mtext><mml:mo>̇</mml:mo></mml:mover><mml:msub><mml:mi>O</mml:mi><mml:mn>2</mml:mn></mml:msub></mml:mrow></mml:msub></mml:mrow></mml:math> is an independent determinant of critical power in this population.<b>NEW & NOTEWORTHY</b> 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.