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

The time constant of phase II pulmonary oxygen uptake kinetics ( $${\dot{\text{V}}\text{O}}_{2} \, \tau_{{\text{p}}}$$ ) 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 $${\dot{\text{V}}\text{O}}_{2} \, \tau_{{\text{p}}}$$ in healthy active individuals, likely because $${\dot{\text{V}}\text{O}}_{2} \, \tau_{{\text{p}}}$$ is limited by metabolic inertia (rather than oxygen delivery) in these individuals. Since $${\dot{\text{V}}\text{O}}_{2} \, \tau_{{\text{p}}}$$ is more influenced by oxygen delivery in type 2 diabetes (T2D), this study tested the hypothesis that PE would reduce $${\dot{\text{V}}\text{O}}_{2} \, \tau_{{\text{p}}}$$ 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, $${\dot{\text{V}}\text{O}}_{2} \, \tau_{{\text{p}}}$$ was reduced (P = 0.001) in T2D (from 59 ± 17 to 37 ± 20 s) but not (P = 0.24) in ND (44 ± 10 to 38 ± 7 s). The amplitude of the $${\dot{\text{V}}\text{O}}_{{2}}$$ slow component ( $${\dot{\text{V}}\text{O}}_{2} \, \tau_{{\text{p}}}$$ 2 As) was reduced (P = 0.001) in both groups (T2D: 0.16 ± 0.09 to 0.11 ± 0.04 l/min; ND: 0.21 ± 0.13 to 0.13  ± 0.09 l/min). This was accompanied by a reduction in ΔiEMG from the onset of $${\dot{\text{V}}\text{O}}_{{2}}$$ slow component to end-exercise in both groups (P < 0.001), while [HHb + Mb] kinetics remained unchanged. PE accelerates $${\dot{\text{V}}\text{O}}_{2} \, \tau_{{\text{p}}}$$ in T2D, likely by negating the O2 delivery limitation extant in the unprimed condition, and reduces the $${\dot{\text{V}}\text{O}}_{{2}}$$ As possibly due to changes in muscle fibre activation.