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.

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

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 wk of low-volume high-intensity interval training (HIIT) versus 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) or HIIT (n = 9, 10 × 1 min at ∼90% maximal heart rate) or to a nonexercising control group (n = 9). Exercising groups trained three times per week and measurements were taken every 3 wk. The rate of muscle deoxygenation (i.e., deoxygenated hemoglobin and myoglobin concentration, Δ[HHb + Mb]) profiles of the vastus lateralis muscle were normalized 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 %Δ[HHb + Mb] versus %PO slope of the first linear segment (slope1) was reduced (P < 0.05) beyond 3 wk 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.

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

PURPOSE: The time constant of phase II pulmonary oxygen uptake kinetics ([Formula: see text]) 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 [Formula: see text] in healthy active individuals, likely because [Formula: see text] is limited by metabolic inertia (rather than oxygen delivery) in these individuals. Since [Formula: see text] is more influenced by oxygen delivery in type 2 diabetes (T2D), this study tested the hypothesis that PE would reduce [Formula: see text] in T2D during work-to-work cycle exercise. METHODS: 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. RESULTS: Subsequent to PE, [Formula: see text] 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 [Formula: see text] slow component ([Formula: see text]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 [Formula: see text] slow component to end-exercise in both groups (P < 0.001), while [HHb + Mb] kinetics remained unchanged. CONCLUSIONS: PE accelerates [Formula: see text] in T2D, likely by negating the O2 delivery limitation extant in the unprimed condition, and reduces the [Formula: see text]As possibly due to changes in muscle fibre activation.

Venous occlusion plethysmography vs. Doppler ultrasound in the assessment of leg blood flow kinetics during different intensities of calf exercise.

PURPOSE: It has recently been shown that venous occlusion plethysmography (VOP) can successfully assess the rate of increase in leg blood flow (LBF) (LBF kinetics) responses during calf exercise, but there is lack of data supporting its validity. METHODS: Using Doppler ultrasound (DU) as a criterion standard technique, we tested the hypothesis that VOP would provide similar estimates of LBF kinetics responses as DU during calf plantar-flexion exercise at a range of different intensities. Ten healthy men performed repeated intermittent calf plantar-flexion contractions (3 s duty cycles, 1 s contraction/2 s relaxation) at 30, 50 and 70% maximum voluntary contraction (MVC) on different days. RESULTS: Resting LBF values were significantly (P < 0.05) larger for DU than VOP but the overall mean LBF responses during exercise were not different (P > 0.05) between DU and VOP (30% MVC: 330 ± 78 vs. 313 ± 92 ml/min; 50% MVC: 515 ± 145 vs. 483 ± 164 ml/min; 70% MVC: 733 ± 218 vs. 616 ± 229 ml/min). LBF kinetics analyses revealed that the end-amplitude at the highest intensity (70% MVC) was significantly higher when measured by DU compared with VOP, but all other kinetics parameters were not different between VOP and DU. CONCLUSIONS: 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 exercise accelerates oxygen uptake kinetics during high-intensity cycle exercise in middle-aged individuals with type 2 diabetes.

Background: The primary phase time constant of pulmonary oxygen uptake kinetics ( V · O 2 τ p) during submaximal efforts is longer in middle-aged people with type 2 diabetes (T2D), partly due to limitations in oxygen supply to active muscles. This study examined if a high-intensity "priming" exercise (PE) would speed V · O 2 τ p during a subsequent high-intensity cycling exercise in T2D due to enhanced oxygen delivery. Methods: Eleven (4 women) middle-aged individuals with type 2 diabetes and 11 (4 women) non-diabetic controls completed four separate cycling bouts each starting at an 'unloaded' baseline of 10 W and transitioning to a high-intensity constant-load. Two of the four cycling bouts were preceded by priming exercise. The dynamics of pulmonary V · O 2 and muscle deoxygenation (i.e. deoxygenated haemoglobin and myoglobin concentration [HHb + Mb]), were calculated from breath-by-breath and near-infrared spectroscopy data at the vastus lateralis, respectively. Results: At baseline V · O 2 τ p, was slower (p < 0.001) in the type 2 diabetes group (48 ± 6 s) compared to the control group (34 ± 2 s) but priming exercise significantly reduced V · O 2 τ p (p < 0.001) in type 2 diabetes (32 ± 6 s) so that post priming exercise it was not different compared with controls (34 ± 3 s). Priming exercise reduced the amplitude of the V · O 2 slow component (As) in both groups (type 2 diabetes: 0.26 ± 0.11 to 0.16 ± 0.07 L/min; control: 0.33 ± 0.13 to 0.25 ± 0.14 L/min, p < 0.001), while [HHb + Mb] kinetics remained unchanged. Conclusion: These results suggest that in middle-aged men and women with T2D, PE speeds V · O 2 τ p likely by a better matching of O2 delivery to utilisation and reduces the V · O 2 As during a subsequent high-intensity exercise.

Differential effects of sex on adaptive responses of skeletal muscle vasodilation to exercise training in type 2 diabetes.

AIMS: We tested the hypotheses that exercise training improves the peak and dynamic responses of leg vascular conductance (LVC) in males and females with type 2 diabetes (T2DM). METHODS: Forty-one males and females with T2DM were assigned to two training groups and two control groups. Twelve weeks of aerobic/resistance training was performed three times per week, 60-90 min per session. Responses of calf muscle blood flow and systemic arterial pressure during incremental and constant-load (30% maximal voluntary contraction) intermittent plantar-flexion protocols in the supine position were recorded. RESULTS: Training significantly increased peak LVC in males (4.86 ± 1.88 to 6.06 ± 2.06 ml·min-1·mm Hg-1) and females (3.91 ± 1.13 to 5.40 ± 1.38 ml·min-1·mm Hg-1) with no changes in control groups. For dynamic responses, training significantly increased the amplitude of the fast growth phase of LVC (1.81 ± 1.12 to 2.68 ± 1.01 ml·min-1·mm Hg-1) and decreased the time constant of the slow growth phase (43.6 ± 46.4 s to 16.1 14.0 s) in females, but no improvements were observed in control females or in any of the two male groups. CONCLUSIONS: These data suggest that training increases the peak vasodilatory response in males and females, whereas the speed of the dynamic response of vasodilation is improved in females but not males.

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.

Post-exercise Cold Water Immersion Does Not Improve Subsequent 4-km Cycling Time-Trial Compared With Passive and Active Recovery in Normothermia.

Background: We investigated whether a brief cold water immersion between two cycling time trials (TT) improves the performance of the latter compared with passive and active recovery in normothermic conditions (~20°C). Methods: In Experiment 1 10 active participants (4 women) completed two 4-km TT (Ex1 and Ex2, each preceded by a 12 min moderate-intensity warm-up) separated by a 15 min recovery period consisting of: (a) passive rest (PAS) or (b) 5 min cold water immersion at 8°C (CWI-5). In Experiment 2, 13 different active males completed the same Ex1 and Ex2 bouts separated by a 15 min recovery consisting of: (a) PAS, (b) 10 min cold water immersion at 8°C (CWI-10) or (c) 15 min of moderate-intensity active recovery (ACT). Results: In both experiments, the time to complete the 4-km TT-s was not different (P > 0.05, ES = 0.1) among the trials neither in Ex1 (Experiment 1: PAS: 414 ± 39 s; CWI-5: 410 ± 39 s; Experiment 2: PAS: 402 ± 41 s; CWI-10: 404 ± 43 s; ACT: 407 ± 41 s) nor Ex2 (Experiment 1: PAS: 432 ± 43 s; CWI-5: 428 ± 47 s; Experiment 2: PAS: 418 ± 52 s; CWI-10: 416 ± 57 s; ACT: 421 ± 50 s). In addition, in all conditions, the time to complete the time trials was longer (P < 0.05, ES = 0.4) in Ex2 than Ex1. Core temperature was lower (P < 0.05) during the majority of Ex2 after CW-5 compared with passive rest (Experiment 1) and after CWI-10 compared with PAS and ACT (Experiment 2). Perceived exertion was also lower (P < 0.05) at mid-point of Ex2 after CWI-5 compared with PAS (Experiment 1) as well as overall lower during the CWI-10 compared with PAS and ACT conditions (Experiment 2). Conclusion: A post-exercise 5-10 min cold water immersion does not influence subsequent 4-km TT performance in normothermia, despite evoking reductions in thermal strain.

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

We assessed the time-course of changes in oxygen uptake (V̇o2) and muscle deoxygenation (i.e., deoxygenated hemoglobin and myoglobin, [HHb + Mb]) kinetics during transitions to moderate-intensity cycling following 12 wk 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, 10 × 1 min at ∼90% maximal heart rate), or nonexercising control (n = 9) groups. Exercising groups trained three times per week, and measurements were taken every 3 wk. [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]/ΔV̇o2 ratio. 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, whereas 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 wk, 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.NEW & NOTEWORTHY High-intensity interval training and moderate-intensity continuous training elicited faster pulmonary oxygen uptake (V̇o2) kinetics during moderate-intensity cycling within 3 wk of training with no further changes thereafter in individuals with type 2 diabetes. These adaptations were accompanied by unaltered near-infrared spectroscopy-derived muscle deoxygenation (i.e. deoxygenated hemoglobin and myoglobin concentration, [HHb+Mb]) kinetics and transiently reduced Δ[HHb+Mb]-to-ΔV̇o2 ratio, suggesting an enhanced blood flow distribution within the active muscles subsequent to both training interventions.

Effects of exercise training and sex on dynamic responses of O2 uptake in type 2 diabetes.

Effects of training and sex on oxygen uptake 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 oxygen uptake (τp oxygen uptake) and with greater effect in males than females. Forty-one subjects with T2DM were assigned to 2 training groups (Tmale, Tfemale) and 2 control groups (Cmale, Cfemale), and were assessed before and after a 12-week intervention period. Twelve weeks of aerobic/resistance training was performed 3 times per week, 60-90 min per session. Assessments included ventilatory threshold (VT), peak oxygen uptake, τp oxygen uptake (80%VT), and dynamic responses of cardiac output, mean arterial pressure and systemic vascular conductance (80%VT). Training significantly decreased τp oxygen uptake 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 τp oxygen uptake 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 peak oxygen uptake in both sexes (12%-13%) but did not alter systemic cardiovascular dynamics in either sex. Training improved oxygen uptake dynamics to a similar extent in males and females in the absence of changes in systemic cardiovascular dynamics. Novelty Similar training improvements in oxygen uptake dynamics were observed in males and females with T2DM. In both sexes these improvements occurred without changes in systemic cardiovascular dynamics.

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

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.

Influence of type 2 diabetes on muscle deoxygenation during ramp incremental cycle exercise.

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 (1.59 (1.14) vs 1.23 (0.51)). Both groups displayed a near-plateau in Δ[HHb+Mb] at an exercise intensity (%PO) not different amongst 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.