Muscle deoxygenation during ramp incremental cycle exercise in older adults with type 2 diabetes.

PURPOSE: To explore profiles of fractional O2 extraction (using near-infrared spectroscopy) during ramp incremental cycling in older individuals with type 2 diabetes (T2D). METHODS: Twelve individuals with T2D (mean ± SD, age: 63 ± 3 years) and 12 healthy controls (mean age: 65 ± 3 years) completed a ramp cycling exercise. Rates of muscle deoxygenation (i.e., deoxygenated haemoglobin and myoglobin, Δ[HHb + Mb]) profiles of the vastus lateralis muscle were normalised to 100% of the response, plotted against absolute (W) and relative (%peak) power output (PO) and fitted with a double linear regression model. RESULTS: Peak oxygen uptake (V̇O2peak) was significantly (P < 0.01) reduced in T2D (23.0 ± 4.2 ml.kg-1.min-1) compared with controls (28.3 ± 5.3 ml.kg-1.min-1). The slope of the first linear segment of the model was greater (median (interquartile range)) in T2D (1.06 (1.50)) than controls (0.79 (1.06)) when Δ%[HHb + Mb] was plotted as a function of PO. In addition, the onset of the second linear segment of the Δ%[HHb + Mb]/PO model occurred at a lower exercise intensity in T2D (101 ± 35 W) than controls (140 ± 34 W) and it displayed a near-plateau response in both groups. When the relationship of the Δ%[HHb + Mb] profile was expressed as a function of %PO no differences were observed in any parameters of the double linear model. CONCLUSIONS: These findings suggest that older individuals with uncomplicated T2D demonstrate greater fractional oxygen extraction for a given absolute PO compared with older controls. Thus, the reductions in V̇O2peak in older people with T2D are likely influenced by impairments in microvascular O2 delivery.

Low-volume HIIT and MICT speed V̇o2 kinetics during high-intensity "work-to-work" cycling with a similar time-course in type 2 diabetes.

We assessed the rates of adjustment in oxygen uptake (V̇o2) and muscle deoxygenation [i.e., deoxygenated hemoglobin and myoglobin, (HHb + Mb)] during the on-transition to high-intensity cycling initiated from an elevated baseline (work-to-work, w-to-w) before training and at weeks 3, 6, 9, and 12 of low-volume high-intensity interval training (HIIT) and moderate-intensity continuous training (MICT) in type 2 diabetes (T2D). Participants were randomly assigned to MICT (n = 11, 50 min of moderate-intensity cycling), HIIT (n = 8, 10 × 1 min of high-intensity cycling separated by 1 min of light cycling) or nonexercising control (n = 9) groups. Exercising groups trained three times per week. Participants completed two w-to-w transitions at each time point consisting of sequential step increments to moderate- and high-intensity work-rates. [HHb + Mb] kinetics were measured by near-infrared spectroscopy at the vastus lateralis muscle. The pretraining time constant of the primary phase of V̇o2 (V̇o2 τp) and the amplitude of the V̇o2 slow component (V̇o2As) of the high-intensity w-to-w bout decreased (P < 0.05) by a similar magnitude at week 3 of training in both MICT (from 56 ± 9 to 43 ± 6 s, and from 0.17 ± 0.07 to 0.09 ± 0.05 L/min, respectively) and HIIT (from 56 ± 8 to 42 ± 6 s, and from 0.18 ± 0.05 to 0.09 ± 0.08 L/min, respectively) with no further changes thereafter. No changes were reported in controls. The parameter estimates of Δ[HHb + Mb] remained unchanged in all groups. MICT and HIIT elicited comparable improvements in V̇o2 kinetics without changes in muscle deoxygenation kinetics during high-intensity exercise initiated from an elevated baseline in T2D despite training volume and time commitment being ∼50% lower in the HIIT group.NEW & NOTEWORTHY Three weeks of high-intensity interval training and moderate-intensity continuous training decreased the time constant of the primary phase of oxygen uptake (V̇o2) and amplitude of the V̇o2 slow component during a high-intensity exercise initiated from an elevated baseline, a protocol that mimics the abrupt metabolic transitions akin to those in daily life, in type 2 diabetes. These V̇o2 kinetics improvements were maintained until the end of the 12-wk intervention without changes in muscle deoxygenation kinetics.