Pulmonary Oxygen Uptake Kinetics Assessment in Basketball-Trained Boys During Early Adolescence

New FindingsWhat 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 (V˙O2) kinetics, skeletal muscle oxygenation (muscle tissue O2 saturation index) and mitochondrial respiration. Eight men underwent contralateral IPC (4 × 5 min at 220 mmHg) or sham‐control (SHAM; 20 mmHg) before performing a cycling time‐to‐exhaustion test (92% maximum aerobic power). Muscle (vastus lateralis) biopsies were obtained before IPC or SHAM and ∼1.5 min postexercise. The time to exhaustion did not differ between SHAM and IPC (249 ± 37 vs. 240 ± 32 s; 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 = 0.01 vs. P = 0.19), mitochondrial content (citrate synthase activity, P = 0.003 vs. P = 0.16; CI+IIP, P = 0.03 vs. P = 0.23) and expressed relative to P (P = 0.006 vs. P = 0.30) and E (P = 0.004 vs. P = 0.26). The V˙O2 mean response time was faster (51.3 ± 15.5 vs. 63.7 ± 14.5 s; P = 0.003), with a smaller slow component (270 ± 105 vs. 377 ± 188 ml min−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 V˙O2 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.

The aim of the present study was to investigate whether a single-compartment (SCM) and a multi-compartment (MCM) venous return model will produce significantly different time-delaying and distortive effects on pulmonary oxygen uptake (V̇o2pulm) responses with equal cardiac outputs (Q̇) and muscle oxygen uptake (V̇o2musc) inputs. For each model, 64 data sets were simulated with alternating Q̇ and V̇o2musc kinetics-time constants (τ) ranging from 10 to 80 s-as responses to pseudorandom binary sequence work rate (WR) changes. Kinetic analyses were performed by using cross-correlation functions (CCFs) between WR with V̇o2pulm and V̇o2musc. Higher maxima of the CCF courses indicate faster system responses-equal to smaller τ values of the variables of interest (e.g., τV̇o2musc). The models demonstrated a highly significant relationship for the resulting V̇o2pulm responses ( r = 0.976, P < 0.001, n = 64). Both models showed significant differences between V̇o2pulm and V̇o2musc kinetics for τV̇o2musc ranging from 10 to 30 s ( P < 0.05 each). In addition, a significant difference in V̇o2pulm kinetics ( P < 0.05) between the models was observed for very fast V̇o2musc kinetics (τ = 10 s). The combinations of fast Q̇ dynamics and slow V̇o2musc kinetics yield distinct deviations in the resultant V̇o2pulm responses compared with V̇o2musc kinetics. Therefore, the venous return models should be used with care and caution if the aim is to infer V̇o2musc by means of V̇o2pulm kinetics. Finally, the resultant V̇o2pulm responses seem to be complex and most likely unpredictable if no cardiodynamic measurements are available in vivo. NEW & NOTEWORTHY A single-compartment and a multi-compartment venous return model were tested to see whether they result in different pulmonary oxygen uptake (V̇o2pulm) kinetics from equal cardiac output and muscle oxygen uptake (V̇o2musc) kinetics. To infer V̇o2musc kinetics by means of V̇o2pulm kinetics, both models should only be used for V̇o2musc time constants ranging from 40 to 80 s. The resultant V̇o2pulm responses seem to be complex and most likely unpredictable if no cardiodynamic measurements are available.

The effect of organ transplantation on arterial compliance, pulmonary oxygen uptake (VO2p) and heart rate kinetics during the 6-minute walk test (6-MWT) remains unknown. Twenty-two thoracic (heart and/or lung) organ transplant recipients (TOTR, 51+/-12 years) and 30 abdominal (kidney, kidney-pancreas, or liver) organ transplant recipients (AOTR, 46+/-11 years) from the 2006 Canadian Transplant Games, and 37 healthy controls (HC) completed a 6-MWT. VO2p, heart rate kinetics, and arterial compliance were determined. The 6-MWT distance and highest VO2p were significantly lower in TOTR and AOTR versus HC. The highest 6-MWT heart rate was lower in TOTR (11%) and AOTR (13%) versus HC. VO2p kinetics were slower in TOTR (52+/-11 sec, P<or=0.001) and AOTR (45+/-24 sec, P<or=0.001) versus HC (28+/-9 sec). Heart rate kinetics were slower in TOTR (100+/-49 sec) versus AOTR (41+/-21 sec, P<or=0.001) and HC (34+/-21 sec, P<or=0.001), but not between AOTR and HC. Small and large artery compliance were 26% (P=0.007) and 19% (P=0.004) lower, respectively, in TOTR versus HC. Large artery compliance was 14% lower in TOTR versus AOTR (P=0.017). 6-MWT distance was significantly related to VO2p kinetics (r=-0.35) and the highest 6-MWT VO2p (r=0.72). TOTR and AOTR have abnormal VO2p kinetics, which is secondary to prolonged heart rate kinetics and impaired vascular function in TOTR, but not AOTR.

It is unclear whether pulmonary oxygen uptake (Vo2) kinetics demonstrate linear, first-order behavior during supra gas exchange threshold exercise. Resolution of this issue is pertinent to the elucidation of the factors regulating oxygen uptake (Vo2) kinetics, with oxygen availability and utilization proposed as putative mediators. To reexamine this issue with the advantage of a relatively large sample size, 50 young (24 ± 4 yr) and 15 late middle-aged (54 ± 3 yr) participants completed repeated bouts of moderate and heavy exercise. Pulmonary gas exchange, heart rate (HR), and cardiac output (Q) variables were measured throughout. The phase II τ was slower during heavy exercise in both young (moderate: 22 ± 9; heavy: 29 ± 9 s; P ≤ 0.001) and middle-aged (moderate: 22 ± 9; heavy: 30 ± 8 s; P ≤ 0.001) individuals. The HR τ was slower during heavy exercise in young (moderate: 33 ± 10; heavy: 44 ± 15 s; P ≤ 0.05) and middle-aged (moderate: 30 ± 12; heavy: 50 ± 20 s; P ≤ 0.05) participants, and the Q τ showed a similar trend (young moderate: 21 ± 13; heavy: 28 ± 16 s; middle-aged moderate: 32 ± 13; heavy: 40 ± 15 s; P ≥ 0.05). There were no differences in primary component Vo2 kinetics between age groups, but the middle-aged group had a significantly reduced Vo2 slow component amplitude in both absolute (young: 0.25 ± 0.09; middle-aged: 0.11 ± 0.06 l/min; P ≤ 0.05) and relative terms (young: 15 ± 10; middle-aged: 9 ± 4%; P ≤ 0.05). Thus Vo2 kinetics do not demonstrate dynamic linearity during heavy intensity exercise. Speculatively, the slower phase II τ during heavy exercise might be attributable to reduced oxygen availability. Finally, the primary and slow components of Vo2 kinetics appear to be differentially influenced by middle age.

Modeling a physiological system's response to a stressor, such as muscular exercise, demands more than a mathematically adequate characterization of its transient response profile: adequacy and appropriateness are not synonymous. The model constituents should be reflective of the system's

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.

The existence of time-delayed phases ([1][1]) is not supported by oxygen uptake kinetics data. Despite many attempts for a number of years, no convincing physiological mechanism for such behavior has been proven to exist. The reason is that these time-delayed phases are a figment of the incorrect

Pulmonary oxygen uptake (V˙O2) kinetics and heart rate kinetics are influenced by age and fitness. Muscular V˙O2 kinetics can be estimated from heart rate and pulmonary V˙O2. In this study the applicability of a test using pseudo-random binary sequences in combination with a model to estimate muscular V˙O2 kinetics was tested. Muscular V˙O2 kinetics were expected to be faster than pulmonary V˙O2 kinetics, slowed in aged subjects and correlated with maximum V˙O2 and heart rate kinetics. 27 elderly subjects (73±3 years; 81.1±8.2 kg; 175±4.7 cm) participated. Cardiorespiratory kinetics were assessed using the maximum of cross-correlation functions, higher maxima implying faster kinetics. Muscular V˙O2 kinetics were faster than pulmonary V˙O2 kinetics (0.31±0.1 vs. 0.29±0.1 s; p=0.004). Heart rate kinetics were not correlated with muscular or pulmonary V˙O2 kinetics or maximum V˙O2. Muscular V˙O2 kinetics correlated with maximum V˙O2 (r=0.35; p=0.033). This suggests, that muscular V˙O2 kinetics are faster than estimates from pulmonary V˙O2 and related to maximum V˙O2 in aged subjects. In the future this experimental approach may help to characterize alterations in muscular V˙O2 under various conditions independent of motivation and maximal effort.

The aim of the present study was to determine whether glutamine ingestion, which has been shown to enhance the exercise-induced increase in the tricarboxylic acid intermediate (TCAi) pool size, resulted in augmentation of the rate of increase in oxidative metabolism at the onset of exercise. In addition, the potential interaction with oxygen availability was investigated by completing exercise in both normoxic and hyperoxic conditions. Eight male cyclists cycled for 6 min at 70% VO2max following consumption of a drink (5 ml kg body mass(-1)) containing a placebo or 0.125 g kg body mass(-1) of glutamine in normoxic (CON and GLN respectively) and hyperoxic (HYP and HPG respectively) conditions. Breath-by-breath pulmonary oxygen uptake and continuous, non-invasive muscle deoxygenation (via near infrared spectroscopy: NIRS) data were collected throughout exercise. The time constant of the phase II component of pulmonary oxygen uptake kinetics was unchanged between trials (CON: 21.5 +/- 3.0 vs. GLN: 18.2 +/- 1.3 vs. HYP: 18.9 +/- 2.0 vs. HPG: 18.6 +/- 1.2 s). There was also no alteration of the kinetics of relative muscle deoxygenation as measured via NIRS (CON: 5.9 +/- 0.7 vs. GLN: 7.3 +/- 0.8 vs. HYP: 6.5 +/- 0.9 vs. HPG: 5.2 +/- 0.4 s). Conversely, the mean response time of pulmonary oxygen uptake kinetics was faster (CON: 33.4 +/- 1.2 vs. GLN: 29.8 +/- 2.3 vs. HYP: 33.2 +/- 2.6 vs. HPG: 31.6 +/- 2.6 s) and the time at which muscle deoxygenation increased above pre-exercise values was earlier (CON: 9.6 +/- 0.9 vs. GLN: 8.7 +/- 1.1 vs. HYP: 8.5 +/- 0.8 vs. HPG: 8.4 +/- 0.7 s) following glutamine ingestion. In normoxic conditions, plasma lactate concentration was lower following glutamine ingestion compared to placebo. Whilst the results of the present study provide some support for the present hypothesis, the lack of any alteration in the time constant of pulmonary oxygen uptake and muscle deoxygenation kinetics suggest that the normal exercise induced expansion of the TCAi pool size is not limiting to oxidative metabolism at the onset of cycle exercise at 70% VO2max.

The aim of this pilot study was to investigate whether there are differences in heart rate and oxygen uptake kinetics in type 2 diabetes patients, considering their cardiovascular medication. It was hypothesized that cardiovascular medication would affect heart rate and oxygen uptake kinetics and that this could be detected using a standardized exercise test. 18 subjects were tested for maximal oxygen uptake. Kinetics were measured in a single test session with standardized, randomized moderate-intensity work rate changes. Time series analysis was used to estimate kinetics. Greater maxima in cross-correlation functions indicate faster kinetics. 6 patients did not take any cardiovascular medication, 6 subjects took peripherally acting medication and 6 patients were treated with centrally acting medication. Maximum oxygen uptake was not significantly different between groups. Significant main effects were identified regarding differences in muscular oxygen uptake kinetics and heart rate kinetics. Muscular oxygen uptake kinetics were significantly faster than heart rate kinetics in the group with no cardiovascular medication (maximum in cross-correlation function of muscular oxygen uptake vs. heart rate; 0.32±0.08 vs. 0.25±0.06; p=0.001) and in the group taking peripherally acting medication (0.34±0.05 vs. 0.28±0.05; p=0.009) but not in the patients taking centrally acting medication (0.28±0.05 vs. 0.30±0.07; n.s.). It can be concluded that regulatory processes for the achievement of a similar maximal oxygen uptake are different between the groups. The used standardized test provided plausible results for heart rate and oxygen uptake kinetics in a single measurement session in this patient group.

The aim of the study was to test whether or not the arteriovenous oxygen concentration difference (avDO2) kinetics at the pulmonary (avDO2pulm) and muscle (avDO2musc) levels is significantly different during dynamic exercise. A re-analysis involving six publications dealing with kinetic analysis was utilized with an overall sample size of 69 participants. All studies comprised an identical pseudorandom binary sequence work rate (WR) protocol-WR changes between 30 and 80W-to analyze the kinetic responses of pulmonary ([Formula: see text]) and muscle ([Formula: see text]) oxygen uptake kinetics as well as those of avDO2pulm and avDO2musc. A significant difference between [Formula: see text] (0.395 ± 0.079) and [Formula: see text] kinetics (0.330 ± 0.078) was observed (p < 0.001), where the variables showed a significant relationship (rSP=0.744, p < 0.001). There were no significant differences between avDO2musc (0.446 ± 0.077) and avDO2pulm kinetics (0.451 ± 0.075), which are highly correlated (r = 0.929, p < 0.001). It is suggested that neither avDO2pulm nor avDO2musc kinetic responses seem to be responsible for the differences between estimated [Formula: see text] and measured [Formula: see text] kinetics. Obviously, the conflation of avDO2 and perfusion ([Formula: see text] ) at different points in time and at different physiological levels drive potential differences in [Formula: see text] and [Formula: see text] kinetics. Therefore, [Formula: see text] should, in general, be considered whenever oxygen uptake kinetics are analyzed or discussed.

Pulmonary oxygen uptake, heart rate (HR), and deoxyhemoglobin (HHb) kinetics were studied in a group of older adults exercising in hypoxic conditions. Fourteen healthy older adults (aged 66 ± 6 years) performed 4 exercise sessions that consisted of (i) an incremental test to exhaustion on a cycloergometer while breathing normoxic room air (fractional inspired oxygen (FiO(2)) = 20.9% O(2)); (ii) an incremental test to exhaustion on a cycloergometer while breathing hypoxic room air (FiO(2) = 15% O(2)); (iii) 3 repeated square wave cycling exercises at moderate intensity while breathing normoxic room air; and (iv) 3 repeated square wave cycling exercises at moderate intensity while breathing hypoxic room air. During all exercise sessions, pulmonary gas exchange was measured breath-by-breath; HHb was determined on the vastus lateralis muscle by near-infrared spectroscopy; and HR was collected beat-by-beat. The pulomary oxygen uptake kinetics became slower in hypoxia (31 ± 9 s) than in normoxia (27 ± 7 s) because of an increased mismatching between O(2) delivery to O(2) utilization at the level of the muscle. The HR and HHb kinetics did not change between hypoxia and normoxia.

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.

Exercise intolerance is a hallmark feature in heart failure with preserved ejection fraction (HFpEF). Prior heavy exercise ("priming exercise") speeds pulmonary oxygen uptake (V̇o2p) kinetics in older adults through increased muscle oxygen delivery and/or alterations in mitochondrial metabolic activity. We tested the hypothesis that priming exercise would speed V̇o2p on-kinetics in patients with HFpEF because of acute improvements in muscle oxygen delivery. Seven patients with HFpEF performed three bouts of two exercise transitions: MOD1, rest to 4-min moderate-intensity cycling and MOD2, MOD1 preceded by heavy-intensity cycling. V̇o2p, heart rate (HR), total peripheral resistance (TPR), and vastus lateralis tissue oxygenation index (TOI; near-infrared spectroscopy) were measured, interpolated, time-aligned, and averaged. V̇o2p and HR were monoexponentially curve-fitted. TPR and TOI levels were analyzed as repeated measures between pretransition baseline, minimum value, and steady state. Significance was P < 0.05. Time constant (τ; tau) V̇o2p (MOD1 49 ± 16 s) was significantly faster after priming (41 ± 14 s; P = 0.002), and the effective HR τ was slower following priming (41 ± 27 vs. 51 ± 32 s; P = 0.025). TPR in both conditions decreased from baseline to minimum TPR ( P < 0.001), increased from minimum to steady state ( P = 0.041) but remained below baseline throughout ( P = 0.001). Priming increased baseline ( P = 0.003) and minimum TOI ( P = 0.002) and decreased the TOI muscle deoxygenation overshoot ( P = 0.041). Priming may speed the slow V̇o2p on-kinetics in HFpEF and increase muscle oxygen delivery (TOI) at the onset of and throughout exercise. Microvascular muscle oxygen delivery may limit exercise tolerance in HFpEF.

The aim of the present study was to examine whether improvements in pulmonary oxygen uptake (V̇o2) kinetics following a short period of high-intensity training (HIT) would be associated with improved skeletal muscle mitochondrial function. Ten untrained male volunteers (age 26 ± 2 yr; mean ± SD) performed six HIT sessions (8-12 × 60 s at incremental test peak power; 271 ± 52 W) over a 2-wk period. Before and after the HIT period, V̇o2 kinetics was modeled during moderate-intensity cycling (110 ± 19 W). Mitochondrial function was assessed with high-resolution respirometry (HRR), and maximal activities of oxidative enzymes citrate synthase (CS) and cytochrome c oxidase (COX) were accordingly determined. In response to HIT, V̇o2 kinetics became faster (τ: 20.4 ± 4.4 vs. 28.9 ± 6.1 s; P < 0.01) and fatty acid oxidation (ETFP) and leak respiration (LN) both became elevated (P < 0.05). Activity of CS and COX did not increase in response to training. Both before and after the HIT period, fast V̇o2 kinetics (low τ values) was associated with large values for ETFP, electron transport system capacity (ETS), and electron flow specific to complex II (CIIP) (P < 0.05). Collectively, these findings support that selected measures of mitochondrial function obtained with HRR are important for fast V̇o2 kinetics and better markers than maximal oxidative enzyme activity in describing the speed of the V̇o2 response during moderate-intensity exercise.