Pulmonary Oxygen Uptake Kinetics Research Articles

The Influence of Acute Hypoxia on Oxygen Uptake and Muscle Oxygenation Kinetics During Cycling Exercise in Prepubertal Boys.

To examine the effect of normobaric hypoxia on pulmonary oxygen uptake (V˙O2) and muscle oxygenation kinetics during incremental and moderate-intensity exercise in children. Eight prepubertal boys (9-11y)performed incremental cycle tests to exhaustion in both normoxia and hypoxia (fraction of inspired O2 of 15%) followed by repeat 6-minute transitions of moderate-intensity exercise in each condition over subsequent visits. Maximal oxygen uptake (V˙O2max) was reduced in hypoxia compared with normoxia (1.69 [0.20] vs 1.87 [0.26]L·min-1, P = .028), although the gas exchange threshold was not altered in absolute terms (P = .33) or relative to V˙O2max (P = .78). During moderate-intensity exercise, the phase II V˙O2 time constant (τ) was increased in hypoxia (18 [9] vs 24 [8]s, P = .025), with deoxyhemoglobin τ unchanged (17 [8] vs 16 [6], P ≥ .28). In prepubertal boys, hypoxia reduced V˙O2max and slowed V˙O2 phase II kinetics during moderate-intensity exercise, despite unchanged deoxyhemoglobin kinetics. These data suggest an oxygen delivery dependence of V˙O2max and moderate-intensity V˙O2 kinetics under conditions of reduced oxygen availability in prepubertal boys.

Measuring pulmonary oxygen uptake kinetics: Contemporary perspectives.

Measuring pulmonary oxygen uptake kinetics: Contemporary perspectives.

Oxygen Uptake and Bilaterally Measured Vastus Lateralis Muscle Oxygen Desaturation Kinetics in Well-Trained Endurance Cyclists.

The aim of the present study was to compare and analyse the relationships between pulmonary oxygen uptake and vastus lateralis (VL) muscle oxygen desaturation kinetics measured bilaterally with Moxy NIRS sensors in trained endurance athletes. To this end, 18 trained athletes (age: 42.4 ± 7.2 years, height: 1.837 ± 0.053 m, body mass: 82.4 ± 5.7 kg) visited the laboratory on two consecutive days. On the first day, an incremental test was performed to determine the power values for the gas exchange threshold, the ventilatory threshold (VT), and V̇O2max levels from pulmonary ventilation. On the second day, the athletes performed a constant work rate (CWR) test at the power corresponding to the VT. During the CWR test, the pulmonary ventilation characteristics, left and right VL muscle O2 desaturation (DeSmO2), and pedalling power were continuously recorded, and the average signal of both legs' DeSmO2 was computed. Statistical significance was set at p ≤ 0.05. The relative response amplitudes of the primary and slow components of VL desaturation and pulmonary oxygen uptake kinetics did not differ, and the primary amplitude of muscle desaturation kinetics was strongly associated with the initial response rate of oxygen uptake. Compared with pulmonary O2 kinetics, the primary response time of the muscle desaturation kinetics was shorter, and the slow component started earlier. There was good agreement between the time delays of the slow components describing global and local metabolic processes. Nevertheless, there was a low level of agreement between contralateral desaturation kinetic variables. The averaged DeSmO2 signal of the two sides of the body represented the oxygen kinetics more precisely than the right- or left-leg signals separately.

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 ( 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 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 10W and transitioning to a high-intensity constant-load. Two of the four cycling bouts were preceded by priming exercise. The dynamics of pulmonary 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 τ p, was slower (p < 0.001) in the type 2 diabetes group (48 ± 6s) compared to the control group (34 ± 2s) but priming exercise significantly reduced τ p (p < 0.001) in type 2 diabetes (32 ± 6s) so that post priming exercise it was not different compared with controls (34 ± 3s). Priming exercise reduced the amplitude of the slow component (As) in both groups (type 2 diabetes: 0.26 ± 0.11 to 0.16 ± 0.07L/min; control: 0.33 ± 0.13 to 0.25 ± 0.14L/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 τ p likely by a better matching of O2 delivery to utilisation and reduces the As during a subsequent high-intensity exercise.

Ischaemic preconditioning blunts exercise-induced mitochondrial dysfunction, speeds oxygen uptake kinetics but does not alter severe-intensity exercise capacity.

What is the central question of this study? Ischaemic preconditioning is a novel pre-exercise priming strategy. We asked whether ischaemic preconditioning would alter mitochondrial respiratory function and pulmonary oxygen uptake kinetics and improve severe-intensity exercise performance. What is the main finding and its importance? Ischaemic preconditioning expedited overall pulmonary oxygen uptake kinetics and appeared to prevent an increase in leak respiration, proportional to maximal electron transfer system and ADP-stimulated respiration, that was evoked by severe-intensity exercise in sham-control conditions. However, severe-intensity exercise performance was not improved. The results do not support ischaemic preconditioning as a pre-exercise strategy to improve exercise performance in recreationally active participants. We examined the effect of ischaemic preconditioning (IPC) on severe-intensity exercise performance, pulmonary oxygen uptake ( ) kinetics, skeletal muscle oxygenation (muscle tissue O2 saturation index) and mitochondrial respiration. Eight men underwent contralateral IPC (4×5min at 220mmHg) or sham-control (SHAM; 20mmHg) before performing a cycling time-to-exhaustion test (92% maximum aerobic power). Muscle (vastus lateralis) biopsies were obtained before IPC or SHAM and ∼1.5min postexercise. The time to exhaustion did not differ between SHAM and IPC (249±37vs. 240±32s; P=0.62). Pre- and postexercise ADP-stimulated (P) and maximal (E) mitochondrial respiration through protein complexes (C) I, II and IV did not differ (P>0.05). Complex I leak respiration was greater postexercise compared with baseline in SHAM, but not in IPC, when normalized to wet mass (P=0.01vs. P=0.19), mitochondrial content (citrate synthase activity, P=0.003vs. P=0.16; CI+IIP, P=0.03vs. P=0.23) and expressed relative to P (P=0.006vs. P=0.30) and E (P=0.004vs. P=0.26). The mean response time was faster (51.3±15.5vs. 63.7±14.5s; P=0.003), with a smaller slow component (270±105vs. 377±188mlmin-1 ; P=0.03), in IPC compared with SHAM. The muscle tissue O2 saturation index did not differ between trials (P>0.05). Ischaemic preconditioning expedited kinetics and appeared to prevent an increase in leak respiration through CI, when expressed proportional to E and P evoked by severe-intensity exercise, but did not improve exercise performance.

Oxygen uptake kinetics and ventilatory and metabolic parameters do not differ between moderate‐intensity front crawl and breaststroke swimming

Pulmonary oxygen uptake (V˙O2) kinetics have been well studied during land‐based exercise. However, less is known about V˙O2 kinetics during swimming exercise and comparisons between strokes is non‐existent. We aimed to characterize and compare the V˙O2 kinetics, ventilatory,e and metabolic response to constant velocity moderate‐intensity freely breathing front crawl (FC) and breaststroke (BR) swimming in a swimming flume. These two strokes reflect predominantly upper body versus lower body modes of swimming locomotion, respectively. Eight trained swimmers (4 females, 20 ± 1 years, 1.74 ± 0.06 m; 66.8 ± 6.3 kg) attended 5–6 laboratory‐based swimming sessions. The first two trials determined FC and BR V˙O2max and the ventilatory threshold (VT), respectively, during progressive intensity swimming to the limit of tolerance. Subsequent trials involved counterbalanced FC and BR transitions from prone floating to constant velocity moderate‐intensity swimming at 80% of the velocity at VT (vVT), separated by 30‐min recovery. Breath‐by‐breath changes in pulmonary gas exchange and ventilation were measured continuously using a snorkel and aquatic metabolic cart system. The ventilatory and metabolic responses were similar (p > 0.05) between strokes during maximal velocity swimming, however, vVT and maximal velocity were slower (p < 0.05) during BR . During moderate‐intensity swimming, V˙O2 kinetics, ventilatory and metabolic parameters were similar (p > 0.05) between strokes. In conclusion, when breathing ad libitum, V˙O2 kinetics during moderate‐intensity constant velocity swimming, and ventilatory and metabolic responses during moderate‐intensity and maximal velocity swimming, are similar between FC and BR strokes.

Training status affects between-protocols differences in the assessment of maximal aerobic velocity

PurposeContinuous incremental protocols (CP) may misestimate the maximum aerobic velocity (Vmax) due to increases in running speed faster than cardiorespiratory/metabolic adjustments. A higher aerobic capacity may mitigate this issue due to faster pulmonary oxygen uptake (dot{V}O2) kinetics. Therefore, this study aimed to compare three different protocols to assess Vmax in athletes with higher or lower training status.MethodsSixteen well-trained runners were classified according to higher (HI) or lower (LO) dot{V}O2maxdot{V}O2-kinetics was calculated across four 5-min running bouts at 10 km·h−1. Two CPs [1 km·h−1 per min (CP1) and 1 km·h−1 every 2-min (CP2)] were performed to determine Vmaxdot{V}O2max, lactate-threshold and submaximal dot{V}O2/velocity relationship. Results were compared to the discontinuous incremental protocol (DP).ResultsVmax, dot{V}O2max, dot{V}CO2 and VE were higher [(P < 0.05,(ES:0.22/2.59)] in HI than in LO. dot{V}O2-kinetics was faster [P < 0.05,(ES:-2.74/ − 1.76)] in HI than in LO. dot{V}O2/velocity slope was lower in HI than in LO [(P < 0.05,(ES:-1.63/ − 0.18)]. Vmax and dot{V}O2/velocity slope were CP1 > CP2 = DP for HI and CP1 > CP2 > DP for LO. A lower [P < 0.05,(ES:0.53/0.75)] Vmax-difference for both CP1 and CP2 vs DP was found in HI than in LO. Vmax-differences in CP1 vs DP showed a large inverse correlation with Vmax, dot{V}O2max and lactate-threshold and a very large correlation with dot{V}O2-kinetics.ConclusionsHigher aerobic training status witnessed by faster dot{V}O2 kinetics led to lower between-protocol Vmax differences, particularly between CP2 vs DP. Faster kinetics may minimize the mismatch issues between metabolic and mechanical power that may occur in CP. This should be considered for exercise prescription at different percentages of Vmax.

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.

Oxygen Uptake Kinetics in Endurance Trained Youth and Adult Cyclists

Previous studies reported faster pulmonary oxygen uptake kinetics at the onset of exercise in untrained youth compared with adults. Whether or not these differences are identical for trained groups have not been examined. The purpose of this study was to compare ˙VO2 kinetics of youth and adult cyclists at moderate and heavy-intensity exercise. Thirteen adult (age: 23.2 ± 4.8 years; ˙VO2peak 68.4 ± 6.8 mL·min-1.kg-1) and thirteen youth cyclists (age: 14.3 ± 1.5 years; ˙VO2peak 61.7 ± 4.3 mL·min-1.kg-1) completed a series of 6-min square wave exercises at moderate and heavy-intensity exercise at 90 rev·min-1. A two-way repeated-measure ANOVA was conducted to identify differences between groups and intensities. The time constant, time delay and the mean response time were not significantly different between youth and adult cyclists (p > 0.05). We found significant differences between intensities, with a faster time constant during moderate than heavy-intensity exercise in youth (24.1 ± 7.0 s vs. 31.8 ± 5.6 s; p = 0.004) and adults (22.7 ± 5.6 s vs. 28.6 ± 5.7 s; p < 0.001). The present data suggest that the effect of training history in adult cyclists compensate for the superior primary response of the oxygen uptake kinetics typically seen in youth compared to adults. Furthermore, the ˙VO2 response is dependent of work rate intensity in trained youth and adult cyclists.

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

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. 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. Subsequent to PE, [Formula: see text] was reduced (P = 0.001) in T2D (from 59 ± 17 to 37 ± 20s) but not (P = 0.24) in ND (44 ± 10 to 38 ± 7s). 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 ± 0.04l/min; ND: 0.21 ± 0.13 to 0.13 ± 0.09l/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. 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.

Effect of priming exercise and body position on pulmonary oxygen uptake and muscle deoxygenation kinetics during cycle exercise.

We hypothesized that the performance of prior heavy exercise would speed pulmonary oxygen uptake (V̇o2) kinetics (i.e., as described by the time constant, [Formula: see text]) and reduce the amplitude of muscle deoxygenation (deoxy[heme]) kinetics in the supine (S) but not upright (U) body position. Seventeen healthy men completed heavy-intensity constant-work rate exercise tests in S and U consisting of two bouts of 6-min cycling separated by 6-min cycling at 20 W. Pulmonary V̇o2 was measured breath by breath; total and deoxy[heme] were determined via time-resolved near-infrared spectroscopy (NIRS) at three muscle sites. Priming exercise reduced [Formula: see text] in S (bout 1: 36 ± 10 vs. bout 2: 28 ± 10 s, P < 0.05) but not U (bout 1: 27 ± 8 s vs. bout 2: 25 ± 7 s, P > 0.05). Deoxy[heme] amplitude was increased after priming in S (bout 1: 25-28 μM vs. bout 2: 30-35 μM, P < 0.05) and U (bout 1: 13-18 μM vs. bout 2: 17-25 μM, P > 0.05), whereas baseline total[heme] was enhanced in S (bout 1: 110-179 μM vs. bout 2: 121-193 μM, P < 0.05) and U (bout 1: 123-186 μM vs. bout 2: 137-197 μM, P < 0.05). Priming exercise increased total[heme] in both S and U, likely indicating enhanced diffusive O2 delivery. However, the observation that after priming the amplitude of the deoxy[heme] response was increased in S suggests that the reduction in [Formula: see text] subsequent to priming was related to a combination of both enhanced intracellular O2 utilization and increased O2 delivery.NEW & NOTEWORTHY Here we show that oxygen uptake (V̇o2) kinetics are slower in the supine compared with upright body position, an effect that is associated with an increased amplitude of skeletal muscle deoxygenation in the supine position. After priming in the supine position, the amplitude of muscle deoxygenation remained markedly elevated above that observed during upright exercise. Hence, the priming effect cannot be solely attributed to enhanced O2 delivery, and enhancements to intracellular O2 utilization must also be contributory.

Test–retest reliability of pulmonary oxygen uptake and muscle deoxygenation during moderate- and heavy-intensity cycling in youth elite-cyclists

ABSTRACT To establish the test–retest reliability of pulmonary oxygen uptake (V̇O2), muscle deoxygenation (deoxy[haem]) and tissue oxygen saturation (StO2) kinetics in youth elite-cyclists. From baseline pedalling, 15 youth cyclists completed 6-min step transitions to a moderate- and heavy-intensity work rate separated by 8 min of baseline cycling. The protocol was repeated after 1 h of passive rest. V̇O2 was measured breath-by-breath alongside deoxy[haem] and StO2 of the vastus lateralis by near-infrared spectroscopy. Reliability was assessed using 95% limits of agreement (LoA), the typical error (TE) and the intraclass correlation coefficient (ICC). During moderate- and heavy-intensity step cycling, TEs for the amplitude, time delay and time constant ranged between 3.5–21.9% and 3.9–12.1% for V̇O2 and between 6.6–13.7% and 3.5–10.4% for deoxy[haem], respectively. The 95% confidence interval for estimating the kinetic parameters significantly improved for ensemble-averaged transitions of V̇O2 (p < 0.01) but not for deoxy[haem]. For StO2, the TEs for the baseline, end-exercise and the rate of deoxygenation were 1.0–42.5% and 1.1–5.5% during moderate- and heavy-intensity exercise, respectively. The ICC ranged from 0.81 to 0.99 for all measures. Test–retest reliability data provide limits within which changes in V̇O2, deoxy[haem] and StO2 kinetics may be interpreted with confidence in youth athletes.

Influence Of Body Position On Pulmonary Oxygen Uptake And Muscle Deoxygenation Kinetics During Cycle Exercise

Whether pulmonary oxygen uptake (VO2) kinetics are limited by O2 delivery remains contentious. Previous studies have demonstrated that the time constant of pulmonary VO2 kinetics (τVO2) is greater during supine compared to upright cycle exercise, presumably reflecting the superimposition of an O2 availability limitation. However, interpretation of these studies is compromised by their use of superficial single-site measurements using continuous-wave near-infrared spectroscopy (NIRS), which is unable to determine absolute [heme]. PURPOSE: To determine the impact of body position (i.e. upright [U] vs. supine [S]) on the kinetics of pulmonary VO2, as well as muscle deoxygenation (deoxy[heme]) kinetics and total[heme] using time-resolved (TR-)NIRS. METHODS: 7 healthy men completed an incremental ramp test to determine VO2 max and the gas exchange threshold in the supine position. 4 visits followed whereby pulmonary VO2 and deoxy[heme] kinetics and total[heme] were determined via TR-NIRS at three muscle sites (deep [VLd] and superifical [VLs] vastus lateralis and superficial rectus femoris [RFs]) in two conditions: 1) during S heavy intensity constant work rate exercise at 40%Δ (between ventilatory threshold and VO2 max); and 2) during U exercise at the same absolute work rate. RESULTS: τVO2 was increased during S compared to U (S: 42 ± 12 vs. U: 32 ± 9 s, P = 0.03). The fundamental phase τdeoxy[heme] was greater (i.e. slower) in S compared to U for each muscle site (VLd S: 19 ± 10 vs. U: 8 ± 5 s; VLs S: 16 ± 7 vs. U: 10 ± 3 s; RFs S: 20 ± 7 vs. U: 11 ± 3 s, P = 0.002) and its amplitude was greater in S compared to U for RFs only (S: 27.4 ± 12.1 vs. U: 9.1 ± 2.5 μM, P = 0.008). Total[heme] did not differ between U and S for any muscle site (all P > 0.05). CONCLUSION: The slowing of pulmonary VO2 kinetics for S versus U occurs concomitant with a depressed rate of muscle(s) deoxygenation. This finding suggests that supine exercise results in a relatively greater fall in muscle VO2 when compared to O2 delivery kinetics at least for VLd and VLs. The increased amplitude of deoxy[heme] in S for RFs suggests an increase in O2 extraction to compensate for impaired muscle perfusion in S compared to U.

Oral Contraceptive Use Influences On-Kinetic Adaptations to Sprint Interval Training in Recreationally-Active Women.

IntroductionOral contraceptive (OC) use influences peak exercise responses to training, however, the influence of OC on central and peripheral adaptations to exercise training are unknown. This study investigated the influence of OC use on changes in time-to-fatigue, pulmonary oxygen uptake, cardiac output, and heart rate on-kinetics, as well as tissue saturation index to 4 weeks of sprint interval training in recreationally active women.MethodsWomen taking an oral contraceptive (OC; n = 25) or experiencing natural menstrual cycles (MC; n = 22) completed an incremental exercise test to volitional exhaustion followed by a square-wave step-transition protocol to moderate (90% of power output at ventilatory threshold) and high intensity (Δ50% of power output at ventilatory threshold) exercise on two separate occasions. Time-to-fatigue, pulmonary oxygen uptake on-kinetics, cardiac output, and heart rate on-kinetics, and tissue saturation index responses were assessed prior to, and following 12 sessions of sprint interval training (10 min × 1 min efforts at 100–120% PPO in a 1:2 work:rest ratio) completed over 4 weeks.ResultsTime-to-fatigue increased in both groups following training (p < 0.001), with no difference between groups. All cardiovascular on-kinetic parameters improved to the same extent following training in both groups. Greater improvements in pulmonary oxygen up-take kinetics were seen at both intensities in the MC group (p < 0.05 from pre-training) but were blunted in the OC group (p > 0.05 from pre-training). In contrast, changes in tissue saturation index were greater in the OC group at both intensities (p < 0.05); with the MC group showing no changes at either intensity.DiscussionOral contraceptive use may reduce central adaptations to sprint interval training in women without influencing improvements in exercise performance - potentially due to greater peripheral adaptation. This may be due to the influence of exogenous oestradiol and progestogen on cardiovascular function and skeletal muscle blood flow. Further investigation into female-specific influences on training adaptation and exercise performance is warranted.

Influence of muscle oxygenation and nitrate-rich beetroot juice supplementation on O2 uptake kinetics and exercise tolerance

We tested the hypothesis that acute supplementation with nitrate (NO3−)-rich beetroot juice (BR) would improve quadriceps muscle oxygenation, pulmonary oxygen uptake (V˙O2) kinetics and exercise tolerance (Tlim) in normoxia and that these improvements would be augmented in hypoxia and attenuated in hyperoxia. In a randomised, double-blind, cross-over study, ten healthy males completed two-step cycle tests to Tlim following acute consumption of 210 mL BR (18.6 mmol NO3−) or NO3−-depleted beetroot juice placebo (PL; 0.12 mmol NO3−). These tests were completed in normobaric normoxia [fraction of inspired oxygen (FIO2): 21%], hypoxia (FIO2: 15%) and hyperoxia (FIO2: 40%). Pulmonary V˙O2 and quadriceps tissue oxygenation index (TOI), derived from multi-channel near-infrared spectroscopy, were measured during all trials. Plasma [nitrite] was higher in all BR compared to all PL trials (P < 0.05). Quadriceps TOI was higher in normoxia compared to hypoxia (P < 0.05) and higher in hyperoxia compared to hypoxia and normoxia (P < 0.05). Tlim was improved after BR compared to PL ingestion in the hypoxic trials (250 ± 44 vs. 231 ± 41 s; P = 0.006; d = 1.13), with the magnitude of improvement being negatively correlated with quadriceps TOI at Tlim (r = −0.78; P < 0.05). Tlim was not improved following BR ingestion in normoxia (BR: 364 ± 98 vs. PL: 344 ± 78 s; P = 0.087, d = 0.61) or hyperoxia (BR: 492 ± 212 vs. PL: 472 ± 196 s; P = 0.273, d = 0.37). BR ingestion increased peak V˙O2 in hypoxia (P < 0.05), but not normoxia or hyperoxia (P > 0.05). These findings indicate that BR supplementation is more likely to improve Tlim and peak V˙O2 in situations when skeletal muscle is more hypoxic.

Limitations to exercise tolerance in type 1 diabetes: the role of pulmonary oxygen uptake kinetics and priming exercise.

We compared the time constant () of the fundamental phase of pulmonary oxygen uptake (V̇o2) kinetics between young adult men with type 1 diabetes and healthy control subjects. We also assessed the impact of priming exercise on , critical power, and muscle deoxygenation in a subset of participants with type 1 diabetes. Seventeen men with type 1 diabetes and 17 healthy male control subjects performed moderate-intensity exercise to determine . A subset of seven participants with type 1 diabetes performed an additional eight visits, in which critical power, , and muscle deoxyhemoglobin + myoglobin ([HHb+Mb], via near-infrared spectroscopy) kinetics (described by a time constant, τ[HHb+Mb]) were determined with (PRI) and without (CON) a prior 6-min bout of heavy exercise. was greater in participants with type 1 diabetes compared with control subjects (type 1 diabetes 50 ± 13 vs. control 32 ± 12 s; P < 0.001). Critical power was greater in PRI compared with CON (PRI 161 ± 25 vs. CON 149 ± 22 W; P < 0.001), whereas (PRI 36 ± 15 vs. CON 50 ± 21 s; P = 0.006) and τ[HHb+Mb] (PRI 10 ± 5 vs. CON 17 ± 11 s; P = 0.037) were reduced in PRI compared with CON. Type 1 diabetes patients showed slower pulmonary V̇o2 kinetics compared with control subjects; priming exercise speeded V̇o2 and [HHb + Mb] kinetics and increased critical power in a subgroup with type 1 diabetes. These data therefore represent the first characterization of the power-duration relationship in type 1 diabetes and the first experimental evidence that is an independent determinant of critical power in this population.NEW & NOTEWORTHY Patients with type 1 diabetes demonstrated slower oxygen uptake (V̇o2) kinetics compared with healthy control subjects. Furthermore, a prior bout of high-intensity exercise speeded V̇o2 kinetics and increased critical power in people with type 1 diabetes. Prior exercise speeded muscle deoxygenation kinetics, indicating that V̇o2 kinetics in type 1 diabetes are limited primarily by oxygen extraction and/or intracellular factors. These findings highlight the potential for interventions that decrease metabolic inertia for enhancing exercise tolerance in this condition.

Effect of Hyperoxia on Critical Power and V˙O2 Kinetics during Upright Cycling.

Critical power (CP) is a fundamental parameter defining high-intensity exercise tolerance; however, its physiological determinants are incompletely understood. The present study determined the impact of hyperoxia on CP, the time constant of phase II pulmonary oxygen uptake kinetics (τV˙O2), and muscle oxygenation (assessed by near-infrared spectroscopy) in nine healthy men performing upright cycle ergometry. Critical power was determined in normoxia and hyperoxia (fraction of inspired O2 = 0.5) via four severe-intensity constant load exercise tests to exhaustion on a cycle ergometer, repeated once in each condition. During each test, τV˙O2 and the time constant of muscle deoxyhemoglobin kinetics (τ[HHb]), alongside absolute concentrations of muscle oxyhemoglobin ([HbO2]), were determined. Critical power was greater (hyperoxia, 216 ± 30 W vs normoxia, 197 ± 29 W; P < 0.001), whereas W' was reduced (hyperoxia, 15.4 ± 5.2 kJ; normoxia, 17.5 ± 4.3 W; P = 0.037) in hyperoxia compared with normoxia. τV˙O2 (hyperoxia, 35 ± 12 s vs normoxia, 33 ± 10 s; P = 0.33) and τ[HHb] (hyperoxia, 11 ± 5 s vs normoxia, 14 ± 5 s; P = 0.65) were unchanged between conditions, whereas [HbO2] during exercise was greater in hyperoxia compared with normoxia (hyperoxia, 73 ± 20 vs normoxia, 66 ± 15 μM; P < 0.001). This study provides novel insights into the physiological determinants of CP and by extension, exercise tolerance. Microvascular oxygenation and CP were improved during exercise in hyperoxia compared with normoxia. Importantly, the improved microvascular oxygenation afforded by hyperoxia did not alter τV˙O2, suggesting that microvascular O2 availability is an independent determinant of the upper limit for steady-state exercise, that is, CP.

Speeding of oxygen uptake kinetics is not different following low-intensity blood-flow-restricted and high-intensity interval training.

What is the central question of this study? Can interval blood-flow-restricted (BFR) cycling training, undertaken at a low intensity, promote a similar adaptation to oxygen uptake ( ) kinetics to high-intensity interval training? What is the main finding and its importance? Speeding of pulmonary on-kinetics in healthy young subjects was not different between low-intensity interval BFR training and traditional high-intensity interval training. Given that very low workloads are well tolerated during BFR cycle training and speed on-kinetics, this training method could be used when high mechanical loads are contraindicated. Low-intensity blood-flow-restricted (BFR) endurance training is effective to increase aerobic capacity. Whether it speeds pulmonary oxygen uptake ( ), CO2 output ( ) and ventilatory ( ) kinetics has not been examined. We hypothesized that low-intensity BFR training would reduce the phase2 time constant (τp ) of , and by a similar magnitude to traditional high-intensity interval training (HIT). Low-intensity interval training with BFR served as a control. Twenty-four participants (25±6years old; maximal 46±6mlkg-1 min-1 ) were assigned to one of the following: low-intensity BFR interval training (BFR; n=8); low-intensity interval training without BFR (LOW; n=7); or high-intensity interval training without BFR (HIT; n=9). Training was 12 sessions of two sets of five to eight×2min cycling and 1min resting intervals. LOW and BFR were conducted at 30% of peak incremental power (Ppeak ), and HIT was at ∼103% Ppeak . For BFR, cuffs were inflated on both thighs (140-200mmHg) during exercise and deflated during rest intervals. Six moderate-intensity step transitions (30% Ppeak ) were averaged for analysis of pulmonary on-kinetics. Both BFR (pre- versus post-training τp =18.3±3.2 versus 14.5±3.4s; effect size=1.14) and HIT (τp =20.3±4.0 versus 13.1±2.9s; effect size=1.75) reduced the τp (P<0.05). As expected, there was no change in LOW ( τp =17.9±6.2 versus 17.7±4.3s; P=0.9). The kinetics of and were speeded only after HIT (38.5±10.6%, P<0.001 and 31.2±24.7%, P=0.004, respectively). Both HIT and low-intensity BFR training were effective in speeding moderate-intensity kinetics. These data support the findings of others that low-intensity cycling training with BFR increases muscle oxidative capacity.

Relationship between (non)linear phase II pulmonary oxygen uptake kinetics with skeletal muscle oxygenation and age in 11–15 year olds

What is the central question of this study? Do the phase II parameters of pulmonary oxygen uptake ( ) kinetics display linear, first-order behaviour in association with alterations in skeletal muscle oxygenation during step cycling of different intensities or when exercise is initiated from an elevated work rate in youths. What is the main finding and its importance? Both linear and non-linear features of phase II kinetics may be determined by alterations in the dynamic balance between microvascular O2 delivery and utilization in 11-15year olds. The recruitment of higher-order (i.e. type II) muscle fibres during 'work-to-work' cycling might be responsible for modulating kinetics with chronological age. This study investigated in 19 male youths (mean age: 13.6±1.1years, range: 11.7-15.7years) the relationship between pulmonary oxygen uptake ( ) and muscle deoxygenation kinetics during moderate- and very heavy-intensity 'step' cycling initiated from unloaded pedalling (i.e. U→M and U→VH) and moderate to very heavy-intensity step cycling (i.e. M→VH). Pulmonary was measured breath-by-breath along with the tissue oxygenation index (TOI) of the vastus lateralis using near-infrared spectroscopy. There were no significant differences in the phase II time constant ( ) between U→M and U→VH (23±6 vs. 25±7s; P=0.36); however, the was slower during M→VH (42±16s) compared to other conditions (P<0.001). Quadriceps TOI decreased with a faster (P<0.01) mean response time (MRT; i.e. time delay + τ) during U→VH (14±2s) compared to U→M (22±4s) and M→VH (20±6s). The difference (Δ) between the and MRT-TOI was greater during U→VH compared to U→M (12±7vs. 2±7s, P<0.001) and during M→VH (23±15s) compared to other conditions (P<0.02), suggesting an increased proportional speeding of fractional O2 extraction. The slowing of the during M→VH relative to U→M and U→VH correlated positively with chronological age (r=0.68 and 0.57, respectively, P<0.01). In youths, 'work-to-work' transitions slowed microvascular O2 delivery-to-O2 utilization with alterations in phase II dynamics accentuated between the ages of 11 and 15years.

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.