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.

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.

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.

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.

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.

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.

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.

A 2.5 min cold water immersion improves prolonged intermittent sprint performance.

OBJECTIVES: We investigated if cold water immersion (CWI) affects exercise performance during a prolonged intermittent sprint test (IST), designed to mimic activity patterns of team-sports. DESIGN: Randomized-crossover design. METHODS: Ten male team-sport players completed 3 IST protocols (two 40-min "halves" of repeated 2-min blocks consisting of a 8-s "all-out" sprint, 100-s active recovery and 12-s rest) on a cycle ergometer at normothermic conditions. Each "half" was separated by a 15 min recovery period of either: (i) passive rest, (ii) 5-min CWI at 8 °C (CWI-5) or (iii) 2.5-min CWI at 8 °C (CWI-2.5), in a random counterbalanced order. RESULTS: Physical performance, core temperature (Tcore) and heart rate were not different among conditions in the first half. In the passive rest trial, total work (TW) and peak power (PP) were lower during the second half (TW: 5.04 ±â€¯1.11 kJ; PP: 929 ±â€¯286 W) than the first half (TW: 5.66 ±â€¯1.02 kJ; PP: 1009 ±â€¯266 W); while TW and PP were not different between halves following CWI-5 (first half, TW: 5.34 ±â€¯1.02 kJ, PP: 1016 ±â€¯283 W; second half, TW: 5.19 ±â€¯1.38 kJ; PP: 996 ±â€¯318 W) and CWI-2.5 (first half, TW: 5.47 ±â€¯1.19 kJ, PP: 966 ±â€¯261 W; second half, TW: 5.25 ±â€¯1.17 kJ; PP: 952 ±â€¯231 W). Tcore was lower until the 20th minute of the second half after CWI-5 and CWI-2.5 compared with passive rest. CONCLUSIONS: A post-exercise 2.5-5-min CWI attenuates the reductions in prolonged sprint performance that occur in the second half of team sports, due, at least partly, to reductions in core temperature and associated increase in heat storage.

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.

Effect of obesity on oxygen uptake and cardiovascular dynamics during whole-body and leg exercise in adult males and females.

Obesity has been associated with a slowing of V˙O2 dynamics in children and adolescents, but this problem has not been studied in adults. Cardiovascular mechanisms underlying this effect are not clear. In this study, 48 adults (18 males, 30 females) grouped according to body mass index (BMI) (lean < 25 kg·m-2 , overweight = 25-29.9 kg·m-2 , obese ≥30 kg·m-2 ) provided a fasting blood sample, completed a maximal graded exercise test and six bouts of submaximal exercise on a cycle ergometer, and performed two protocols of calf exercise. Dynamic response characteristics of V˙O2 and leg vascular conductance (LVC) were assessed during cycling (80% ventilatory threshold) and calf exercise (30% MVC), respectively. Dynamic responses of cardiac output, mean arterial pressure and total systemic vascular conductance were also assessed during cycling based on measurements at 30 and 240 sec. The time constant of the second phase of the V˙O2 response was significantly greater in obese than lean subjects (39.4 (9.2) vs. 29.1 (7.6) sec); whereas dynamic responses of cardiac output and systemic vascular conductance were not affected by BMI. For calf exercise, the time constant of the second growth phase of LVC was slowed significantly in obese subjects (22.1 (12.7) sec) compared with lean and overweight subjects (11.6 (4.5) sec and 13.4 (6.7) sec). These data show that obesity slows dynamic responses of V˙O2 during cycling and the slower phase of vasodilation in contracting muscles of male and female adults.

Lack of age-specific influence on leg blood flow during incremental calf plantar-flexion exercise in men and women.

PURPOSE: Age-related exercising leg blood flow (LBF) responses during dynamic knee-extension exercise and forearm blood flow responses during handgrip exercise are preserved in normally active men but attenuated in activity-matched women. We explored whether these age- and sex-specific effects are also apparent during isometric calf plantar-flexion incremental exercise. METHODS: Normally active young men (YM, n = 15, 24 ± 2 years), young women (YW, n = 8, 22 ± 1 years), older men (OM, n = 13, 70 ± 7 years) and older women (OW, n = 10, 64 ± 7 years) were tested. LBF was measured between contractions using venous occlusion plethysmography. RESULTS: Peak force obtained was higher (P < 0.05) in men compared with women and in young compared with older individuals. However, peak LBF (YM; 971 ± 328 ml min-1, OM; 985 ± 504 ml min-1, YW; 844 ± 366 ml min-1, OW; 960 ± 244 ml min-1) and peak leg vascular conductance [LVC = LBF/(MAP + hydrostatic pressure)] responses (YM; 6.0 ± 1.8 ml min-1 mmHg-1, OM; 5.5 ± 2.8 ml min-1 mmHg-1, YW; 5.3 ± 2.1 ml min-1 mmHg-1, OW; 5.5 ± 1.6 ml min-1 mmHg-1) were similar among the four groups. Furthermore, the hyperaemic (YM; 8.8 ± 3.7 ml min-1 %Fpeak-1 OM; 8.3 ± 5.4 ml min-1 %Fpeak-1, YW; 8.2 ± 3.5 ml min-1 %Fpeak-1, OW; 9.6 ± 2.2 ml min-1 %Fpeak-1) and vasodilatory responses (YM; 0.053 ± 0.020 ml min-1 mmHg-1 %Fpeak-1, OM; 0.048 ± 0.028 ml min-1 mmHg-1 %Fpeak-1, YW; 0.051 ± 0.019 ml min-1 mmHg-1 %Fpeak-1, OW; 0.055 ± 0.014 ml min-1 mmHg-1 %Fpeak-1) were not different among the four groups. These results were accompanied by similar resting LBF responses among groups and were not affected when data were normalised to estimated leg muscle mass. CONCLUSIONS: Our results demonstrate that exercising LBF responses during isometric incremental calf muscle exercise are preserved in older men and women, suggesting that the previously observed age-related attenuations in leg and forearm hyperaemia among women may be muscle-group specific.

The Use of Microtechnology to Monitor Collision Performance in Professional Rugby Union.

PURPOSE: To determine if microtechnology-derived collision loads discriminate between collision performance and compare the physical and analytical components of collision performance between positional groups. METHODS: Thirty-seven professional male rugby union players participated in this study. Collision events from 11 competitive matches were coded using specific tackle and carry classifications based on the ball-carrier's collision outcome. Collisions were automatically detected using 10 Hz microtechnology units. Collision events were identified, coded (as tackle or carry), and timestamped at the collision contact point using game analysis software. Attacking and defensive performances of 1609 collision events were analyzed. RESULTS: Collision loads were significantly greater during dominant compared with neutral and passive collisions (P < .001; effect size [ES] = 0.53 and 0.80, respectively), tackles (P < .0001; ES = 0.60 and 0.56, respectively), and carries (P < .001; ES = 0.48 and 0.79, respectively). Overall, forwards reported a greater number and frequency of collisions but lower loads per collision and velocities at collision point than did backs. Microtechnology devices can also accurately, sensitively, and specifically identify collision events (93.3%, 93.8%, and 92.8%, respectively). CONCLUSION: Microtechnology is a valid means of discriminating between tackle and carry performance. Thus, microtechnology-derived collision load data can be utilized to track and monitor collision events in training and games.

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.

The effects of a 16-week aerobic exercise programme on cognitive function in people living with HIV.

High levels of cardiovascular fitness and physical activity are associated with higher levels of cognitive function in people with HIV, thus, they may reduce the risk of developing HIV-associated neurocognitive disorder (HAND). This study aimed to investigate the effects of a 16-week aerobic exercise intervention on cognitive function in people with HIV. Eleven participants living with HIV were recruited into the study. Participants were randomised into either an exercise group (n = 5), that completed a 16-week aerobic exercise programme training, 3 times per week (2 supervised sessions and one unsupervised session) or a control group (n = 6) that received no intervention. Outcomes measured included cognitive function (Montreal cognitive assessment (MOCA) and the Trail making tests A and B), aerobic fitness (modified Bruce protocol), sleep quality (Pittsburgh sleep quality index; PSQI) and physical activity levels (seven-day accelerometry). At baseline, higher levels of moderate physical activity were positively correlated with higher MOCA scores and levels of aerobic fitness were negatively associated with Trail A scores (P = 0.04 and P = 0.001 respectively). However, exercise training did not induce any significant improvements in cognitive function or aerobic fitness. The overall mean adherence rate to the exercise programme was 60%. In conclusion, in the present study a 16-week aerobic exercise intervention did not affect the cognitive function of participants with HIV. It is likely that longer intervention periods and/or higher adherence rates to exercise might be needed for an aerobic exercise programme to be effective in improving cognitive function in a cohort with no baseline cognitive impairments.

Postexercise cold-water immersion improves intermittent high-intensity exercise performance in normothermia.

A brief cold water immersion between 2 continuous high-intensity exercise bouts improves the performance of the latter compared with passive recovery in the heat. We investigated if this effect is apparent in normothermic conditions (∼19 °C), employing an intermittent high-intensity exercise designed to reflect the work performed at the high-intensity domain in team sports. Fifteen young active men completed 2 exhaustive cycling protocols (Ex1 and Ex2: 12 min at 85% ventilatory threshold (VT) and then an intermittent exercise alternating 30-s at 40% peak power (Ppeak) and 30 s at 90% Ppeak to exhaustion) separated by 15 min of (i) passive rest, (ii) 5-min cold-water immersion at 8 °C, and (iii) 10-min cold-water immersion at 8 °C. Core temperature, heart rate, rates of perceived exertion, and oxygen uptake kinetics were not different during Ex1 among conditions. Time to failure during the intermittent exercise was significantly (P < 0.05) longer during Ex2 following the 5- and 10-min cold-water immersions (7.2 ± 3.5 min and 7.3 ± 3.3 min, respectively) compared with passive rest (5.8 ± 3.1 min). Core temperature, heart rate, and rates of perceived exertion were significantly (P < 0.05) lower during most periods of Ex2 after both cold-water immersions compared with passive rest. The time constant of phase II oxygen uptake response during the 85% VT bout of Ex2 was not different among the 3 conditions. A postexercise, 5- to 10-min cold-water immersion increases subsequent intermittent high-intensity exercise compared with passive rest in normothermia due, at least in part, to reductions in core temperature, circulatory strain, and effort perception.

Influence of menopause and Type 2 diabetes on pulmonary oxygen uptake kinetics and peak exercise performance during cycling.

We investigated if the magnitude of the Type 2 diabetes (T2D)-induced impairments in peak oxygen uptake (V̇O2) and V̇O2 kinetics was affected by menopausal status. Twenty-two women with T2D (8 premenopausal, 14 postmenopausal), and 22 nondiabetic (ND) women (11 premenopausal, 11 postmenopausal) matched by age (range = 30-59 yr) were recruited. Participants completed four bouts of constant-load cycling at 80% of their ventilatory threshold for the determination of V̇O2 kinetics. Cardiac output (CO) (inert gas rebreathing) was recorded at rest and at 30 s and 240 s during two additional bouts. Peak V̇O2 was significantly (P < 0.05) reduced in both groups with T2D compared with ND counterparts (premenopausal, 1.79 ± 0.16 vs. 1.55 ± 0.32 l/min; postmenopausal, 1.60 ± 0.30 vs. 1.45 ± 0.24 l/min). The time constant of phase II of the V̇O2 response was slowed (P < 0.05) in both groups with T2D compared with healthy counterparts (premenopausal, 29.1 ± 11.2 vs. 43.0 ± 12.2 s; postmenopausal, 33.0 ± 9.1 vs. 41.8 ± 17.7 s). At rest and during submaximal exercise absolute CO responses were lower, but the "gains" in CO larger (both P < 0.05) in both groups with T2D. Our results suggest that the magnitude of T2D-induced impairments in peak V̇O2 and V̇O2 kinetics is not affected by menopausal status in participants younger than 60 yr of age.