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

Abstract

The pulmonary oxygen uptake (V̇o2) 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 O2 delivery. The present study tested the hypothesis that a prior heavy-intensity warm-up or “priming” exercise (PE) bout would accelerate V̇o2 kinetics in T2D, because of a better matching of O2 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 O2 delivery to O2 utilization was assessed by the Δ[HHb+Mb]-to-ΔV̇o2 ratio. Both groups demonstrated an accelerated V̇O2 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-ΔV̇o2 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 V̇o2 kinetics response in middle-aged individuals with uncomplicated T2D attributed to an enhanced matching of microvascular O2 delivery to utilization. NEW & NOTEWORTHY Heavy-intensity “priming” exercise (PE) elicited faster pulmonary oxygen uptake (V̇o2) 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-ΔV̇o2 ratio. This suggests that the PE-induced acceleration in oxidative metabolism in T2D is a result of greater O2 extraction and better matching between O2 delivery and utilization.

Time-course of V̇o2 kinetics responses during moderate-intensity exercise subsequent to HIIT versus moderate-intensity continuous training in type 2 diabetes

“…It is possible that the high rates or 'steps' of muscle fiber recruitment and repetitive shear stress during the HIIT exercise sessions influenced the current outcome (39). However, it remains unclear why a levelling off in the V ̇O2 kinetics When applying this measure simultaneously with V ̇O2 kinetics measurements, our laboratory recently showed that the rate of adjustment in the NIRS-derived [HHb+Mb] was faster than the adjustment in τV ̇O2p in uncomplicated T2D, suggesting an over reliance in fractional oxygen extraction and thus, a reduced blood flow response (66). Findings in keeping with T2D-induced impairments in the dynamic response of vasodilation and matching of capillary blood flow to metabolism in contracting myocytes (30,38,57,58,60).…”

“…Although the mechanisms governing the impaired τV ̇O2P herein are not well understood, they are likely influenced, at least partly, by cardiovascular defects, for example impaired left ventricular filling (83,84), and/or limitations in peripheral O 2 delivery/supply to contracting muscles in the lower limbs (8,30,31,34,38,59), although restrictions in the oxygen extraction ability have also been reported (29,65). Our laboratory recently showed a larger mismatch in local (microvascular) O 2 delivery to utilization in the quadriceps muscle in T2D compared with healthy controls, which was accompanied with slowed τV ̇O2p (66). This was reflected by a greater ratio of change in near-infrared spectroscopy (NIRS)-derived deoxygenated hemoglobin and myoglobin concentration ([HHb+Mb] to change in V ̇O2 (Δ[HHb+Mb]/ΔV ̇O2 ) (66).…”

“…Our laboratory recently showed a larger mismatch in local (microvascular) O 2 delivery to utilization in the quadriceps muscle in T2D compared with healthy controls, which was accompanied with slowed τV ̇O2p (66). This was reflected by a greater ratio of change in near-infrared spectroscopy (NIRS)-derived deoxygenated hemoglobin and myoglobin concentration ([HHb+Mb] to change in V ̇O2 (Δ[HHb+Mb]/ΔV ̇O2 ) (66). This is consistent with findings showing a transient lowering of capillary PO 2 at the onset of exercise in rodent models with T2D, thereby limiting O 2 transport from the capillary to the myocyte (10) as well as reduced microvascular blood flow responses during transitions to moderate-intensity cycling in adults with uncomplicated T2D (7).…”

Time course of changes in V̇o2peak and O2 extraction during ramp cycle exercise following HIIT versus moderate-intensity continuous training in type 2 diabetes

“…The impairments in V ̇O2peak in T2D might be influenced by cardiovascular limitations at a systemic level, such as impaired left ventricular filling (68, 69), and limitations in peripheral vasodilation and/or microvascular function in the lower limbs (5,18,19,25,27,32,49,52,65). Regarding peripheral O2 delivery constraints, Kiely et al (26) initially reported reduced peak leg haemodynamic and vasodilatory responses during an incremental calf plantar-flexion exercise in uncomplicated T2D.…”

Electrochemical Monitoring of Subcutaneous Tissue pO2 Fluctuations during Exercise Using a Semi‐implantable Needle Electrode

“…In clinical situations radical oxygenation failure is seen classically in cardiovascular shock, rapid blood loss, injury, critical illness or sepsis [2]. There may also be failures of local circulation compromising specific peripheral tissues as in peripheral vascular disease and late diabetes [3]. Measurement of tissue oxygen partial pressure (pO 2 ) has the potential to provide a metabolic 'short-hand' of the balance between the adequacy of a blood supply and cellular oxygenation demand [2].…”