Influence of priming exercise on oxygen uptake and muscle deoxygenation kinetics during moderate-intensity cycling in type 2 diabetes.

The pulmonary oxygen uptake (V̇o) kinetics during the transition to moderate-intensity exercise is slowed in individuals with type 2 diabetes (T2D), at least in part because of limitations in O delivery. The present study tested the hypothesis that a prior heavy-intensity warm-up or "priming" exercise (PE) bout would accelerate V̇o kinetics in T2D, because of a better matching of O delivery to utilization. Twelve middle-aged individuals with T2D and 12 healthy controls (ND) completed moderate-intensity constant-load cycling bouts either without (Mod A) or with (Mod B) prior PE. The rates of muscle deoxygenation (i.e., deoxygenated hemoglobin and myoglobin concentration, [HHb+Mb]) and oxygenation (i.e., tissue oxygenation index) were continuously measured by near-infrared spectroscopy at the vastus lateralis muscle. The local matching of O delivery to O utilization was assessed by the Δ[HHb+Mb]-to-ΔV̇o ratio. Both groups demonstrated an accelerated V̇O kinetics response during Mod B compared with Mod A (T2D, 32 ± 9 vs. 42 ± 12 s; ND, 28 ± 9 vs. 34 ± 8 s; means ± SD) and an elevated muscle oxygenation throughout Mod B, whereas the [HHb+Mb] amplitude was greater during Mod B only in individuals with T2D. The [HHb+Mb] kinetics remained unchanged in both groups. In T2D, Mod B was associated with a decrease in the "overshoot" relative to steady state in the Δ[HHb+Mb]-to-ΔV̇o ratio (1.17 ± 0.17 vs. 1.05 ± 0.15), whereas no overshoot was observed in the control group before (1.04 ± 0.12) or after (1.01 ± 0.12) PE. Our findings support a favorable priming-induced acceleration of the V̇o kinetics response in middle-aged individuals with uncomplicated T2D attributed to an enhanced matching of microvascular O delivery to utilization. Heavy-intensity "priming" exercise (PE) elicited faster pulmonary oxygen uptake (V̇o) kinetics during moderate-intensity cycling exercise in middle-aged individuals with type 2 diabetes (T2D). This was accompanied by greater near-infrared spectroscopy-derived muscle deoxygenation (i.e., deoxygenated hemoglobin and myoglobin concentration, [HHb+Mb]) responses and a reduced Δ[HHb+Mb]-to-ΔV̇o ratio. This suggests that the PE-induced acceleration in oxidative metabolism in T2D is a result of greater O extraction and better matching between O delivery and utilization.