Priming exercise accelerates pulmonary oxygen uptake kinetics during "work-to-work" cycle exercise in middle-aged individuals with type 2 diabetes.

Abstract

The time constant of phase II pulmonary oxygen uptake kinetics ([Formula: see text]) is increased when high-intensity exercise is initiated from an elevated baseline (work-to-work). A high-intensity priming exercise (PE), which enhances muscle oxygen supply, does not reduce this prolonged [Formula: see text] in healthy active individuals, likely because [Formula: see text] is limited by metabolic inertia (rather than oxygen delivery) in these individuals. Since [Formula: see text] is more influenced by oxygen delivery in type 2 diabetes (T2D), this study tested the hypothesis that PE would reduce [Formula: see text] in T2D during work-to-work cycle exercise. Nine middle-aged individuals with T2D and nine controls (ND) performed four bouts of constant-load, high-intensity work-to-work transitions, each commencing from a baseline of moderate-intensity. Two bouts were completed without PE and two were preceded by PE. The rate of muscle deoxygenation ([HHb + Mb]) and surface integrated electromyography (iEMG) were measured at the right and left vastus lateralis, respectively. Subsequent to PE, [Formula: see text] was reduced (P = 0.001) in T2D (from 59 ± 17 to 37 ± 20s) but not (P = 0.24) in ND (44 ± 10 to 38 ± 7s). The amplitude of the [Formula: see text] slow component ([Formula: see text]2 As) was reduced (P = 0.001) in both groups (T2D: 0.16 ± 0.09 to 0.11 ± 0.04l/min; ND: 0.21 ± 0.13 to 0.13 ± 0.09l/min). This was accompanied by a reduction in ΔiEMG from the onset of [Formula: see text] slow component to end-exercise in both groups (P < 0.001), while [HHb + Mb] kinetics remained unchanged. PE accelerates [Formula: see text] in T2D, likely by negating the O2 delivery limitation extant in the unprimed condition, and reduces the [Formula: see text]As possibly due to changes in muscle fibre activation.