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

摘要

We compared the time constant (tau( o2)) of the fundamental phase of pulmonary oxygen uptake ( o(2)) kinetics between young adult men with type 1 diabetes and healthy control subjects. We also assessed the impact of priming exercise on , tau( 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 moderateintensity exercise to determine tau( o2). A subset of seven participants with type 1 diabetes performed an additional eight visits, in which critical power, tau( o2), and muscle deoxyhemoglobin + myoglobin ([HHb+Mb]. via near-infrared spectroscopy) kinetics (described by a time constant, tau([HHb+Mb])) were determined with (PRI) and without (CON) a prior 6-min bout of heavy exercise. tau( o2) was greater in participants with type 1 diabetes compared with control subjects (type 1 diabetes 50 +/- 13 vs. control 32 +/- 12 s: P o2) (PRI 36 +/- 15 vs. CON 50 +/- 21 s; P = 0.006) and tau([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 o(2) kinetics compared with control subjects: priming exercise speeded o(2 )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( o2) is an independent determinant of critical power in this population.