We assessed the time course of changes in oxygen uptake (V̇O2) and muscle deoxygenation (i.e., deoxygenated haemoglobin and myoglobin, [HHb+Mb]) kinetics during transitions to moderate-intensity cycling following 12-weeks of low-volume high-intensity interval training (HIIT) vs. moderate-intensity continuous training (MICT) in adults with type 2 diabetes (T2D). Participants were randomly assigned to MICT (n=10, 50 min of moderate-intensity cycling), HIIT (n=9, 10x1 min at ~90% maximal heart rate) or non-exercising control (n=9) groups. Exercising groups trained 3 times per week and measurements were taken every 3 weeks. [HHb+Mb] kinetics were 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]/ΔV̇O2ratio. The pretraining time constant of the primary phase of V̇O2 (τV̇O2p ) decreased (P<0.05) at wk 3 of training in both MICT (from 44±12 to 32±5 s) and HIIT (from 42±8 to 32 ± 4 s) with no further changes thereafter; while no changes were reported in controls. The pretraining overall dynamic response of muscle deoxygenation (τ'[HHb+Mb]) was faster than τV̇O2p in all groups, resulting in Δ[HHb+Mb]/V̇O2p showing a transient "overshoot" relative to the subsequent steady-state level. After 3 wks, the Δ[HHb+Mb]/V̇O2p overshoot was eliminated only in the training groups, so that τ'[HHb+Mb] was not different to τV̇O2p in MICT and HIIT. The enhanced V̇O2 kinetics response consequent to both MICT and HIIT in T2D was likely attributed to a training-induced improvement in matching of O2 delivery to utilization.

We tested the hypothesis that type 2 diabetes (T2D) alters the profile of muscle fractional oxygen (O2) extraction (near-infrared spectroscopy) during incremental cycle exercise. Seventeen middle-aged individuals with uncomplicated T2D and 17 controls performed an upright ramp test to exhaustion. The rate of muscle deoxygenation (i.e. deoxygenated haemoglobin and myoglobin concentration, Δ[HHb+Mb]) profiles of the vastus lateralis muscle were normalised to 100% of the response, plotted against % power output (PO) and fitted with a double linear regression model. Peak oxygen uptake was significantly (P<0.05) reduced in individuals with T2D. The %Δ[HHb+Mb]/%PO slope of the first linear segment of the double linear regression function was significantly (P<0.05) steeper in T2D than controls (1.810.61 vs 1.350.43). Both groups displayed a near-plateau in Δ[HHb+Mb] at an exercise intensity (%PO) not different among them. Such findings suggest that a reduced O2 delivery to active muscles is an important underlying cause of exercise intolerance during a maximum graded test in middle-aged individuals with T2D.

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.

Given that these slight differences in amplitude observed during exercise can be explained by differences in vascular regions which the two techniques assess, our results suggest that VOP can accurately assess LBF kinetics responses during calf plantar-flexion exercise at intensities between 30 and 70% MVC.

Priming e ercise accelerates pulmonar o gen uptake kinetics during work-to-work c cle e ercise in middle-2 aged individuals with type 2 diabetes.

Effects of training and sex on V̇O2 dynamics during exercise in type 2 diabetes mellitus (T2DM) are not well established. We tested the hypotheses that exercise training improves the time constant of the primary phase of V̇O2 (taupV̇O2) and with greater effect in males than females. Forty-one subjects with T2DM were assigned to two training groups (Tmale, Tfemale) and two control groups (Cmale, Cfemale), assessed before and after a 12-week intervention period. Twelve weeks of aerobic/resistance training was performed three times per week, 60-90 minutes per session. Assessments included ventilatory threshold (VT), V̇O2peak, taupV̇O2 (80 %VT) and dynamic responses of cardiac output, mean arterial pressure and systemic vascular conductance (80 %VT). Training significantly decreased taupV̇O2 in males by a mean of 20 % (Tmale = 42.7±6.2 to 34.3±7.2 s) and females by a mean of 16 % (Tfemale = 42.2±9.3 to 35.4±8.6 s); whereas taupV̇O2 was not affected in controls (Cmale = 41.6±9.8 to 42.9±7.6 s; Cfemale = 40.4±12.2 to 40.6±13.4 s). Training increased V̇O2peak in both sexes (12-13 %) but did not alter systemic cardiovascular dynamics in either sex. Training improved V̇O2 dynamics to a similar extent in males and females in the absence of changes in systemic cardiovascular dynamics. Novelty Bullets Similar training improvements in V̇O2 dynamics were observed in males and females with type 2 diabetes. In both sexes these improvements occurred without changes in systemic cardiovascular dynamics.

In the present study we assessed the time course of adaptations in peak oxygen uptake (V̇O2peak) and muscle fractional oxygen (O2) extraction (using near-infrared spectroscopy) following 12 weeks of low-volume high-intensity interval training (HIIT) vs. moderate-intensity continuous endurance training (MICT) in adults with uncomplicated type 2 diabetes (T2D). Participants with T2D were randomly assigned to MICT (n = 12, 50 min of moderate-intensity cycling), HIIT (n = 9, 10 x 1 min at ~90% maximal heart rate) or to a non-exercising control group (n = 9). Exercising groups trained 3 times per week and measurements were taken every 3 weeks. The rate of muscle deoxygenation (i.e. deoxygenated haemoglobin and myoglobin concentration, Δ[HHb+Mb]) profiles of the vastus lateralis muscle were normalised to 100% of the response, plotted against % power output (PO) and fitted with a double linear regression model. V̇O2peak increased (P<0.05) by week 3 of MICT (+17%) and HIIT (+8%), with no further significant changes thereafter. Total increases in V̇O2peak posttraining (P<0.05) were 27% and 14% respectively. The %∆[HHb+Mb] vs %PO slope of the first linear segment (slope1) was reduced (P<0.05) beyond 3 weeks of HIIT and MICT with no further significant changes thereafter. No changes in V̇O2peak or slope1 were observed in the control group. Low-volume HIIT and MICT induced improvements in V̇O2peak following a similar time course and these improvements were likely, at least in part, due to an improved microvascular O2 delivery.

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