Coupling of [Formula: see text] and [Formula: see text] kinetics: insights from multiple exercise transitions below the estimated lactate threshold.

During a step-change in exercise power output (PO), ventilation ([Formula: see text]) increases with a similar time course to the rate of carbon dioxide delivery to the lungs ([Formula: see text]). To test the strength of this coupling, we compared [Formula: see text] and [Formula: see text] kinetics from ten independent exercise transitions performed within the moderate-intensity domain. Thirteen males completed 3-5 repetitions of ∆40 W step transitions initiated from 20, 40, 60, 80, 100, and 120 W on a cycle ergometer. Preceding the ∆40 W step transitions from 60, 80, 100, and 120 W was a 6 min bout of 20 W cycling from which the transitions of variable ∆PO were examined. Gas exchange ([Formula: see text] and oxygen uptake, [Formula: see text]) and [Formula: see text] were measured by mass spectrometry and volume turbine. The kinetics of the responses were characterized by the time constant (τ) and amplitude (Δ[Formula: see text]/Δ[Formula: see text]). Overall, [Formula: see text] kinetics were consistently slower than [Formula: see text] kinetics (by ~ 45%) and τ[Formula: see text] rose progressively with increasing baseline PO and with heightened ∆PO from a common baseline. Compared to τ[Formula: see text], τ[Formula: see text] was on average slightly greater (by ~ 4 s). Repeated-measures analysis of variance revealed that there was no interaction between τ[Formula: see text] and τ[Formula: see text] in either the variable baseline (p = 0.49) and constant baseline (p = 0.56) conditions indicating that each changed in unison. Additionally, for Δ[Formula: see text]/Δ[Formula: see text], there was no effect of either variable baseline PO (p = 0.05) or increasing ΔPO (p = 0.16). These data provide further evidence that, within the moderate-intensity domain, both the temporal- and amplitude-based characteristics of V̇E kinetics are inextricably linked to those of [Formula: see text].

Data analysis technique influences blood flow kinetics parameter estimates for moderate- and heavy-intensity exercise transitions.

NEW FINDINGS: What is the central question of this study? During exercise, there are fluctuations in conduit artery blood flow (BF) caused by both cardiac and muscle contraction-relaxation cycles. What is the optimal method to process Doppler ultrasound-measured BF for the purpose of characterizing the dynamic response of BF during step-transitions in exercise? What is the main finding and its importance? Continuous BF data were processed in relation to either cardiac or muscle contraction-relaxation cycles and computed based on 'binned' or 'rolling' averages over one, two or five consecutive cycles. Kinetics characterization revealed no data processing technique-specific differences in steady-state BF, but variability in the rapidity at which BF attained steady-state (i.e., mean response time) was observed. ABSTRACT: The overall rate of blood flow (BF) adjustment (i.e., kinetics) from the onset of an exercise transition can be quantified by the mean response time (MRT). However, the BF response profile can be distorted during rhythmic, dynamic exercise consequent to variations caused by the cardiac cycle (HR) and the muscle contraction-relaxation (CR) cycle. We examined the extent to which distortions imposed by HR and CR cycles affected BF kinetics. Eight healthy, young men (27 (4) years; mean (SD)) performed transitions of alternate-leg knee-extension exercise from 3 W to either a moderate- (MOD) or heavy-intensity (HVY) power output. Femoral artery BF was continuously measured by Doppler ultrasound and averaged over one, two or five 'binned' (e.g., HR2b, etc.) or 'rolling' (e.g., CR5r, etc.) HR and CR cycles. Among analysis techniques, there were no differences for steady-state BF values at the 3 W baseline. In MOD, MRT using contraction-relaxation cycle (CR1) was smaller than most other analysis techniques. For both MOD and HVY, the 95% confidence interval for MRT was generally larger when using HR- compared to CR-related methods, and monoexponential fits based on 'rolling' averages (HR2r, HR5r, CR2r, CR5r) had a poorer ability to estimate the true end-exercise BF in HVY than in MOD. When modelling BF kinetics, we conclude that the CR1 method is a good option because of its ability to accurately estimate the 'data-determined' end-exercise BF value from the 'model-derived' response, maintain a relatively high density of data points during the transition and yield a relatively small 95% CI.

The influence of metabolic and circulatory heterogeneity on the expression of pulmonary oxygen uptake kinetics in humans.

We examined the relationship amongst baseline work rate (WR), phase II pulmonary oxygen uptake (V̇(O2p)) time constant (τV̇(O2p)) and functional gain (G(P)=ΔV̇(O2p)/ΔWR) during moderate-intensity exercise. Transitions were initiated from a constant or variable baseline WR. A validated circulatory model was used to examine the role of heterogeneity in muscle metabolism (V̇(O2m)) and blood flow (Q̇(m)) in determining V̇(O2p) kinetics. We hypothesized that τV̇(O2p) and G(P) would be invariant in the constant baseline condition but would increase linearly with increased baseline WR. Fourteen men completed three to five repetitions of ∆40 W step transitions initiated from 20, 40, 60, 80, 100 and 120 W on a cycle ergometer. The ∆40 W step transitions from 60, 80, 100 and 120 W were preceded by 6 min of 20 W cycling, from which the progressive ΔWR transitions (constant baseline condition) were examined. The V̇(O2p) was measured breath by breath using mass spectrometry and a volume turbine. For a given ΔWR, both τV̇(O2p) (22-35 s) and G(P) (8.7-10.5 ml min(-1) W(-1)) increased (P < 0.05) linearly as a function of baseline WR (20-120 W). The τV̇(O2p) was invariant (P < 0.05) in transitions initiated from 20 W, but G(P) increased with ΔWR (P < 0.05). Modelling the summed influence of multiple muscle compartments revealed that τV̇(O2p) could appear fast (24 s), and similar to in vivo measurements (22 ± 6 s), despite being derived from τV̇(O2p) values with a range of 15-40 s and τQ̇(m) with a range of 20-45 s, suggesting that within the moderate-intensity domain phase II V̇(O2p) kinetics are slowed dependent on the pretransition WR and are strongly influenced by muscle metabolic and circulatory heterogeneity.

Slowed muscle oxygen uptake kinetics with raised metabolism are not dependent on blood flow or recruitment dynamics.

Oxygen uptake kinetics (τVO2) are slowed when exercise is initiated from a raised metabolic rate. Whether this reflects the recruitment of muscle fibres differing in oxidative capacity, or slowed blood flow (Q) kinetics is unclear. This study determined τVO2 in canine muscle in situ, with experimental control over muscle activation and Q during contractions initiated from rest and a raised metabolic rate. The gastrocnemius complex of nine anaesthetised, ventilated dogs was isolated and attached to a force transducer. Isometric tetanic contractions (50 Hz; 200 ms duration) via supramaximal sciatic nerve stimulation were used to manipulate metabolic rate: 3 min stimulation at 0.33 Hz (S1), followed by 3 min at 0.67 Hz (S2). Circulation was initially intact (SPON), and subsequently isolated for pump-perfusion (PUMP) above the greatest value in SPON. Muscle VO2 was determined contraction-by-contraction using an ultrasonic flowmeter and venous oximeter, and normalised to tension-time integral (TTI). τVO2/TTI and τQ were less in S1SPON (mean ± s.d.: 13 ± 3 s and 12 ± 4 s, respectively) than in S2SPON (29 ± 19 s and 31 ± 13 s, respectively; P < 0.05). τVO2/TTI was unchanged by pump-perfusion (S1PUMP, 12 ± 4 s; S2PUMP, 24 ± 6 s; P < 0.001) despite increased O2 delivery; at S2 onset, venous O2 saturation was 21 ± 4% and 65 ± 5% in SPON and PUMP, respectively. VO2 kinetics remained slowed when contractions were initiated from a raised metabolic rate despite uniform muscle stimulation and increased O2 delivery. The intracellular mechanism may relate to a falling energy state, approaching saturating ADP concentration, and/or slowed mitochondrial activation; but further study is required. These data add to the evidence that muscle VO2 control is more complex than previously suggested.

Breath-by-breath pulmonary O2 uptake kinetics: effect of data processing on confidence in estimating model parameters.

To improve the signal-to-noise ratio of breath-by-breath pulmonary O2 uptake (V̇O2p) data, it is common practice to perform multiple step transitions, which are subsequently processed to yield an ensemble-averaged profile. The effect of different data-processing techniques on phase II V̇O2p kinetic parameter estimates (V̇O2p amplitude, time delay and phase II time constant (τV̇O2p)] and model confidence [95% confidence interval (CI95)] was examined. Young (n = 9) and older men (n = 9) performed four step transitions from a 20 W baseline to a work rate corresponding to 90% of their estimated lactate threshold on a cycle ergometer. Breath-by-breath V̇O2p was measured using mass spectrometry and volume turbine. Mono-exponential kinetic modelling of phase II V̇O2p data was performed on data processed using the following techniques: (A) raw data (trials time aligned, breaths of all trials combined and sorted in time); (B) raw data plus interpolation (trials time aligned, combined, sorted and linearly interpolated to second by second); (C) raw data plus interpolation plus 5 s bin averaged; (D) individual trial interpolation plus ensemble averaged [trials time aligned, linearly interpolated to second by second (technique 1; points joined by straight-line segments), ensemble averaged]; (E) 'D' plus 5 s bin averaged; (F) individual trial interpolation plus ensemble averaged [trials time aligned, linearly interpolated to second by second (technique 2; points copied until subsequent point appears), ensemble averaged]; and (G) 'F' plus 5 s bin averaged. All of the model parameters were unaffected by data-processing technique; however, the CI95 for τV̇O2p in condition 'D' (4 s) was lower (P < 0.05) than the CI95 reported for all other conditions (5-10 s). Data-processing technique had no effect on parameter estimates of the phase II V̇O2p response. However, the narrowest interval for CI95 occurred when individual trials were linearly interpolated and ensemble averaged.

Pulmonary O2 uptake kinetics during moderate-intensity exercise transitions initiated from low versus elevated metabolic rates: insights from manipulations in cadence.

INTRODUCTION: The rate of adjustment (τ) of phase II pulmonary O2 uptake (VO2p) is slower when exercise transitions are initiated from an elevated baseline work rate (WR) and metabolic rate (MR). In this study, combinations of cycling cadence (40 vs. 90 rpm) and external WR were used to examine the effect of prior MR on τVO2p. METHODS: Eleven young men completed transitions from 20 W (BSL) to 90% lactate threshold, with transitions performed as two steps of equal ∆WR (LS, lower step; US, upper step), while maintaining a cadence of (1) 40 rpm, (2) 90 rpm, and (3) 40 rpm but with the WRs elevated to match the higher VO2p associated with 90 rpm cycling (40MATCH); transitions lasted 6 min. VO2p was measured breath-by-breath using mass spectrometry and turbinometry; vastus lateralis muscle deoxygenation [HHb] was measured using near-infrared spectroscopy. VO2p and HHb responses were modeled using nonlinear least squares regression analysis. RESULTS: VO2p at BSL, LS and US was similar for 90 rpm and 40MATCH, but greater than in 40 rpm. Compared to 90 rpm, τVO2p at 40 rpm was shorter (p < 0.05) in LS (18 ± 5 vs. 28 ± 8 s) but not in US (26 ± 8 vs. 33 ± 9 s), and at 40MATCH, τVO2p was lower (p < 0.05) (19 ± 6 s) in LS but not in US (34 ± 13 s) despite differing external WR and ∆WR. CONCLUSIONS: A similar overall adjustment of [HHb] and VO2p in LS and US across conditions suggested dynamic matching between microvascular blood flow and O2 utilization. Prior MR (rather than external WR per se) plays a role in the dynamic adjustment of pulmonary (and muscle) VO2p.

Effect of voluntary hyperventilation with supplemental CO2 on pulmonary O2 uptake and leg blood flow kinetics during moderate-intensity exercise.

Pulmonary O2 uptake (V(O2p)) and leg blood flow (LBF) kinetics were examined at the onset of moderate-intensity exercise, during hyperventilation with and without associated hypocapnic alkalosis. Seven male subjects (25 ± 6 years old; mean ± SD) performed alternate-leg knee-extension exercise from baseline to moderate-intensity exercise (80% of estimated lactate threshold) and completed four to six repetitions for each of the following three conditions: (i) control [CON; end-tidal partial pressure of CO2 (P(ET, CO2)) ~40 mmHg], i.e. normal breathing with normal inspired CO2 (0.03%); (ii) hypocapnia (HYPO; P(ET, CO2) ~20 mmHg), i.e. sustained hyperventilation with normal inspired CO2 (0.03%); and (iii) normocapnia (NORMO; P(ET, CO2) ~40 mmHg), i.e. sustained hyperventilation with elevated inspired CO2 (~5%). The V(O2p) was measured breath by breath using mass spectrometry and a volume turbine. Femoral artery mean blood velocity was measured by Doppler ultrasound, and LBF was calculated from femoral artery diameter and mean blood velocity. Phase 2 V(O2p) kinetics (τV(O2p)) was different (P < 0.05) amongst all three conditions (CON, 19 ± 7 s; HYPO, 43 ± 17 s; and NORMO, 30 ± 8 s), while LBF kinetics (τLBF) was slower (P < 0.05) in HYPO (31 ± 9 s) compared with both CON (19 ± 3 s) and NORMO (20 ± 6 s). Similar to previous findings, HYPO was associated with slower V(O2p) and LBF kinetics compared with CON. In the present study, preventing the fall in end-tidal P(CO2) (NORMO) restored LBF kinetics, but not V(O2p) kinetics, which remained 'slowed' relative to CON. These data suggest that the hyperventilation manoeuvre itself (i.e. independent of induced hypocapnic alkalosis) may contribute to the slower V(O2p) kinetics observed during HYPO.

Slowed oxygen uptake kinetics in hypoxia correlate with the transient peak and reduced spatial distribution of absolute skeletal muscle deoxygenation.

It remains unclear whether an overshoot in skeletal muscle deoxygenation (HHb; reflecting a microvascular kinetic mismatch of O2 delivery to consumption) contributes to the slowed adjustment of oxidative energy provision at the onset of exercise. We progressively reduced the fractional inspired O2 concentration (F(I,O2)) to investigate the relationship between slowed pulmonary O2 uptake (V(O2)) kinetics and the dynamics and spatial distribution of absolute[HHb]. Seven healthy men performed 8 min cycling transitions during normoxia (F(I,O2) = 0.21),moderate hypoxia (F(I,O2) = 0.16) and severe hypoxia (F(I,O2)= 0.12). V(O2) uptake was measured using a flowmeter and gas analyser system. Absolute [HHb] was quantified by multichannel,time-resolved near-infrared spectroscopy from the rectus femoris and vastus lateralis (proximal and distal regions), and corrected for adipose tissue thickness. The phase II V(O2) time constant was slowed (P <0.05) as F(I,O2) decreased (normoxia, 17 ± 3 s;moderate hypoxia, 22 ± 4 s; and severe hypoxia, 29 ± 9 s). The [HHb] overshoot was unaffected by hypoxia, but the transient peak [HHb] increased with the reduction in F(I,O2) (P <0.05). Slowed V(O2) kinetics in hypoxia were positively correlated with increased peak [HHb] in the transient (r(2) = 0.45; P <0.05), but poorly related to the [HHb] overshoot. A reduction of spatial heterogeneity in peak [HHb]was inversely correlated with slowed V(O2) kinetics (r(2) = 0.49; P <0.05). These data suggest that aerobic energy provision at the onset of exercise may be limited by the following factors: (i) the absolute ratio (i.e. peak [HHb]) rather than the kinetic ratio (i.e. [HHb] overshoot) of microvascular O2 delivery to consumption; and (ii) a reduced spatial distribution in the ratio of microvascular O2 delivery to consumption across the muscle.

Effect of moderate-intensity work rate increment on phase II τVO2, functional gain and Δ[HHb].

This study systematically examined the role of work rate (WR) increment on the kinetics of pulmonary oxygen uptake (VO(2p)) and near-infrared spectroscopy (NIRS)-derived muscle deoxygenation (Δ[HHb]) during moderate-intensity (Mod) cycling. Fourteen males (24 ± 5 years) each completed four to eight repetitions of Mod transitions from 20 to 50, 70, 90, 110 and 130 W. VO(2p) and Δ[HHb] responses were modelled as a mono-exponential; responses were then scaled to a relative % of the respective response (0-100 %). The Δ[HHb]/VO(2) ratio was calculated as the average Δ[HHb]/VO(2) during the 20-120 s period of the on-transient. When considered as a single group, neither the phase II VO(2p) time constant (τVO(2p); 27 ± 9, 26 ± 11, 25 ± 10, 27 ± 14, 29 ± 13 s for 50-130 W transitions, respectively) nor the Δ[HHb]/VO(2) ratio (1.04 ± 0.13, 1.10 ± 0.13, 1.08 ± 0.07, 1.09 ± 0.11, 1.09 ± 0.09, respectively) was affected by WR (p > 0.05); yet, the VO(2) functional gain (G; ΔVO(2)/ΔWR) increased with increasing WR transitions (8.6 ± 1.3, 9.1 ± 1.2, 9.5 ± 1.0, 9.5 ± 1.0, 9.9 ± 1.0 mL min(-1) W(-1); p < 0.05). When subjects were stratified into two groups [Fast (n = 6), τVO(2p130W) < 25 s < τVO(2p130W), Slower (n = 8)], a group by WR interaction was observed for τVO(2p). The increasing functional G persisted (p < 0.05) and did not differ between groups (p > 0.05). The Δ[HHb]/VO(2) ratio was smaller (p < 0.05) in the Fast than Slower group, but was unaffected by WR. In conclusion, the present study demonstrated (1) a non-uniform effect of Mod WR increment on τVO(2p); (2) that τVO(2p) in the Slower group is likely determined by an O(2) delivery limitation; and (3) that increasing Mod WR increments elicits an increased functional G, regardless of the τVO(2p) response.

Effect of acute hypoxia on muscle blood flow, VO2p, and [HHb] kinetics during leg extension exercise in older men.

The adjustment of pulmonary oxygen uptake (VO2p), heart rate (HR), limb blood flow (LBF), and muscle deoxygenation [HHb] was examined during the transition to moderate-intensity, knee-extension exercise in six older adults (70 ± 4 years) under two conditions: normoxia (FIO2 = 20.9 %) and hypoxia (FIO2 = 15 %). The subjects performed repeated step transitions from an active baseline (3 W) to an absolute work rate (21 W) in both conditions. Phase 2 VO2p, HR, LBF, and [HHb] data were fit with an exponential model. Under hypoxic conditions, no change was observed in HR kinetics, on the other hand, LBF kinetics was faster (normoxia 34 ± 3 s; hypoxia 28 ± 2), whereas the overall [HHb] adjustment (τ' = TD + τ) was slower (normoxia 28 ± 2; hypoxia 33 ± 4 s). Phase 2 VO2p kinetics were unchanged (p < 0.05). The faster LBF kinetics and slower [HHb] kinetics reflect an improved matching between O2 delivery and O2 utilization at the microvascular level, preventing the phase 2 VO2p kinetics from become slower in hypoxia. Moreover, the absolute blood flow values were higher in hypoxia (1.17 ± 0.2 L min(-1)) compared to normoxia (0.96 ± 0.2 L min(-1)) during the steady-state exercise at 21 W. These findings support the idea that, for older adults exercising at a low work rate, an increase of limb blood flow offsets the drop in arterial oxygen content (CaO2) caused by breathing an hypoxic mixture.

The effect of increasing work rate amplitudes from a common metabolic baseline on the kinetic response of V̇o2p, blood flow, and muscle deoxygenation.

A step-transition in external work rate (WR) increases pulmonary O2 uptake (V̇o2p) in a monoexponential fashion. Although the rate of this increase, quantified by the time constant (τ), has frequently been shown to be similar between multiple different WR amplitudes (ΔWR), the adjustment of O2 delivery to the muscle (via blood flow; BF), a potential regulator of V̇o2p kinetics, has not been extensively studied. To investigate the role of BF on V̇o2p kinetics, 10 participants performed step-transitions on a knee-extension ergometer from a common baseline WR (3 W) to: 24, 33, 45, 54, and 66 W. Each transition lasted 8 min and was repeated four to six times. Volume turbinometry and mass spectrometry, Doppler ultrasound, and near-infrared spectroscopy were used to measure V̇o2p, BF, and muscle deoxygenation (deoxy[Hb + Mb]), respectively. Similar transitions were ensemble-averaged, and phase II V̇o2p, BF, and deoxy[Hb + Mb] were fit with a monoexponential nonlinear least squares regression equation. With increasing ΔWR, τV̇o2p became larger at the higher ΔWRs (P < 0.05), while τBF did not change significantly, and the mean response time (MRT) of deoxy[Hb + Mb] became smaller. These findings that V̇o2p kinetics become slower with increasing ΔWR, while BF kinetics are not influenced by ΔWR, suggest that O2 delivery could not limit V̇o2p in this situation. However, the speeding of deoxy[Hb + Mb] kinetics with increasing ΔWR does imply that the O2 delivery-to-O2 utilization of the microvasculature decreases at higher ΔWRs. This suggests that the contribution of O2 delivery and O2 extraction to V̇O2 in the muscle changes with increasing ΔWR.NEW & NOTEWORTHY A step increase in work rate produces a monoexponential increase in V̇o2p and blood flow to a new steady-state. We found that step transitions from a common metabolic baseline to increasing work rate amplitudes produced a slowing of V̇o2p kinetics, no change in blood flow kinetics, and a speeding of muscle deoxygenation kinetics. As work rate amplitude increased, the ratio of blood flow to V̇o2p became smaller, while the amplitude of muscle deoxygenation became greater. The gain in vascular conductance became smaller, while kinetics tended to become slower at higher work rate amplitudes.

Identification of Non-Invasive Exercise Thresholds: Methods, Strategies, and an Online App.

During incremental exercise, two thresholds may be identified from standard gas exchange and ventilatory measurements. The first signifies the onset of blood lactate accumulation (the lactate threshold, LT) and the second the onset of metabolic acidosis (the respiratory compensation point, RCP). The ability to explain why these thresholds occur and how they are identified, non-invasively, from pulmonary gas exchange and ventilatory variables is fundamental to the field of exercise physiology and requisite to the understanding of core concepts including exercise intensity, assessment, prescription, and performance. This review is intended as a unique and comprehensive theoretical and practical resource for instructors, clinicians, researchers, lab technicians, and students at both undergraduate and graduate levels to facilitate the teaching, comprehension, and proper non-invasive identification of exercise thresholds. Specific objectives are to: (1) explain the underlying physiology that produces the LT and RCP; (2) introduce the classic non-invasive measurements by which these thresholds are identified by connecting variable profiles to underlying physiological behaviour; (3) discuss common issues that can obscure threshold detection and strategies to identify and mitigate these challenges; and (4) introduce an online resource to facilitate learning and standard practices. Specific examples of exercise gas exchange and ventilatory data are provided throughout to illustrate these concepts and a novel online application tool designed specifically to identify the estimated LT (θLT) and RCP is introduced. This application is a unique platform for learners to practice skills on real exercise data and for anyone to analyze incremental exercise data for the purpose of identifying θLT and RCP.

Influence of phase I duration on phase II VO2 kinetics parameter estimates in older and young adults.

Older adults (O) may have a longer phase I pulmonary O(2) uptake kinetics (Vo(2)(p)) than young adults (Y); this may affect parameter estimates of phase II Vo(2)(p). Therefore, we sought to: 1) experimentally estimate the duration of phase I Vo(2)(p) (EE phase I) in O and Y subjects during moderate-intensity exercise transitions; 2) examine the effects of selected phase I durations (i.e., different start times for modeling phase II) on parameter estimates of the phase II Vo(2)(p) response; and 3) thereby determine whether slower phase II kinetics in O subjects represent a physiological difference or a by-product of fitting strategy. Vo(2)(p) was measured breath-by-breath in 19 O (68 ± 6 yr; mean ± SD) and 19 Y (24 ± 5 yr) using a volume turbine and mass spectrometer. Phase I Vo(2)(p) was longer in O (31 ± 4 s) than Y (20 ± 7 s) (P < 0.05). In O, phase II τVo(2)(p) was larger (P < 0.05) when fitting started at 15 s (49 ± 12 s) compared with fits starting at the individual EE phase I (43 ± 12 s), 25 s (42 ± 10 s), 35 s (42 ± 12 s), and 45 s (45 ± 15 s). In Y, τVo(2)(p) was not affected by the time at which phase II Vo(2)(p) fitting started (τVo(2)(p) = 31 ± 7 s, 29 ± 9 s, 30 ± 10 s, 32 ± 11 s, and 30 ± 8 s for fittings starting at 15 s, 25 s, 35 s, 45 s, and EE phase I, respectively). Fitting from EE phase I, 25 s, or 35 s resulted in the smallest CI τVo(2)(p) in both O and Y. Thus, fitting phase II Vo(2)(p) from (but not constrained to) 25 s or 35 s provides consistent estimates of Vo(2)(p) kinetics parameters in Y and O, despite the longer phase I Vo(2)(p) in O.

A raised metabolic rate slows pulmonary O(2) uptake kinetics on transition to moderate-intensity exercise in humans independently of work rate.

During exercise below the lactate threshold (LT), the rate of adjustment (τ) of pulmonary VO(2) uptake (τ) is slowed when initiated from a raised work rate. Whether this is consequent to the intrinsic properties of newly recruited muscle fibres, slowed circulatory dynamics or the effects of a raised metabolism is not clear. We aimed to determine the influence of these factors on τV(O(2)) using combined in vivo and in silico approaches. Fifteen healthy men performed repeated 6 min bouts on a cycle ergometer with work rates residing between 20 W and 90% LT, consisting of the following: (1) two step increments in work rate (S1 and S2), one followed immediately by the other, equally bisecting 20 W to 90% LT; (2) two 20 W to 90% LT bouts separated by 30 s at 20 W to raise muscle oxygenation and pretransition metabolism (R1 and R2); and (3) two 20 W to 90% LT bouts separated by 12 min at 20 W allowing full recovery (F1 and F2). Pulmonary O(2) uptake was measured breath by breath by mass spectrometry and turbinometry, and quadriceps oxygenation using near-infrared spectroscopy. The influence of circulatory dynamics on the coupling of muscle and τV(O(2)) lung was assessed by computer simulations. The τV(O(2)) in R2 (32 ± 9 s) was not different (P > 0.05) from S2 (30 ± 10 s), but both were greater (P < 0.05) than S1 (20 ± 10 s) and the F control bouts (26 ± 10 s). The slowed V(O(2)) kinetics in R2 occurred despite muscle oxygenation being raised throughout, and could not be explained by slowed circulatory dynamics (τV(O(2)) predicted by simulations: S1 = R2 < S2). These data therefore suggest that the dynamics of muscle O(2) consumption are slowed when exercise is initiated from a less favourable energetic state.

Speeding of VO2 kinetics in response to endurance-training in older and young women.

The goal of this study was to examine the time-course of changes in oxygen uptake kinetics (τVO(2p)) during step-transitions from 20 W to moderate-intensity cycling in response to endurance-training in older (O) and young (Y) women. Six O (69 ± 7 years) and 8 Y (25 ± 5 years) were tested pre-training, and at 3, 6, 9, and 12 weeks of training. VO(2p) was measured breath-by-breath using a mass spectrometer. Changes in deoxygenated-hemoglobin concentration of the vastus lateralis (∆[HHb]) were measured by near-infrared spectroscopy in Y (but this was not possible in O). VO(2p) and ∆[HHb] were modeled with a mono-exponential. Training was performed on a cycle-ergometer three times per week for 45 min at ~70% of VO(2 peak). Pre-training τVO(2p) was greater (p < 0.05) in O (55 ± 16 s) than Y (31 ± 8 s). After 3 weeks training, τVO(2p) decreased (p < 0.05) in both O (35 ± 12 s) and Y (22 ± 4 s). A pre-training "overshoot" in the normalized ∆[HHb]/VO(2p) ratio relative to the subsequent steady-state level (interpreted as a mismatch of local O(2) delivery to muscle VO(2)) was observed in Y. Three weeks of training resulted in that "overshoot" being abolished. Thus there was a training-induced speeding of VO(2) kinetics in O and Y. In the Y this appeared to be the result of improved matching of local O(2) delivery to muscle VO(2). In O, inadequate systemic O(2) distribution (as indirectly expressed by the arterial-venous O(2) difference/VO(2p) ratio) seemed to play a role for the initial slower rate of adjustment in VO(2p).

Pulmonary O2 uptake and muscle deoxygenation kinetics are slowed in the upper compared with lower region of the moderate-intensity exercise domain in older men.

This study sought to determine the effect of the pre-transition work rate (WR) and WR transition magnitude on the adjustment of pulmonary oxygen uptake (VO(2p) kinetics) in older men. Seven men (69 ± 5 years; mean ± SD) each performed 4-6 cycling transitions from 20 W to either a WR corresponding to 90% estimated lactate threshold (full step, FS) or 2 equal-step transitions (lower step, LS; upper step, US) to the same end-exercise WR as in FS. Gas exchange was analysed breath-by-breath and muscle deoxygenation (∆[HHb]) was measured with NIRS. The time constant (τ) for VO(2p) was greater in US (53 ± 17 s) and FS (44 ± 11 s) compared to LS (37 ± 9 s); τVO(2p) for US also trended (p = 0.05) towards being greater than FS. The VO(2p) gain in US (9.97 ± 0.41 mL/min/W) was greater than LS (9.06 ± 1.17; p = 0.06) and FS (9.13 ± 0.54; p < 0.05). The O(2) deficit was greater in US (0.25 ± 0.08 L) than LS (0.19 ± 0.06 L); yet the 'accumulated O(2) deficit' (0.44 ± 0.13 L; O(2) deficit from LS + US) was similar to that of FS (0.42 ± 0.13 L; p = 0.38). The effective Δ[HHb] response time (τ'∆[HHb]) for US (36 ± 12 s) was greater than LS (27 ± 6 s; p = 0.07) and FS (26 ± 4 s; p < 0.05), suggesting that the slowed adjustment of muscle O(2) extraction was associated with the slowed VO(2) kinetics of the US. Despite already slowed VO(2p) kinetics, older men exhibit further slowing when small WR transitions are initiated from an elevated pre-transition WR, yet this results in no cumulative impact on O(2) deficit. This slowing in US compared to LS does not appear to be related to local O(2) availability.

Are the parameters of VO2, heart rate and muscle deoxygenation kinetics affected by serial moderate-intensity exercise transitions in a single day?

This study compared the parameter estimates of pulmonary oxygen uptake (VO(2p)), heart rate (HR) and muscle deoxygenation (Δ[HHb]) kinetics when several moderate-intensity exercise transitions (MODs) were performed during a single visit versus several MODs performed during separate visits. Nine subjects (24 ± 5 years, mean ± SD) each completed two successive cycling MODs on six occasions (1-6A and 1-6B) from 20 W to a work rate corresponding to 80% estimated lactate threshold with 6 min recovery at 20 W. During one visit, subjects completed two series of three MODs (6A-F), separated by 20 min rest. VO(2p) time constants (τVO(2p); 27 ± 10 s, 25 ± 12 s, 25 ± 11 s) were similar (p > 0.05) for MODs 1-6A, 1-6B and 6A-F, respectively. τVO(2p) had reproducibility 95% confidence intervals (CI(95)) of 8.3, 8.2, 4.7, 4.9 and 4.7 s when comparing single (1A vs. 2A), the average of two (1-2A vs. 3-4A), three (1-3A vs. 4-6A), four (1-2AB vs. 3-4AB) and six (1-3AB vs. 4-6AB) MODs, respectively. The effective Δ[HHb] response time (τ'Δ[HHb]) was unaffected across conditions (1-6A: 19 ± 2 s, 1-6B: 19 ± 3 s, 6A-F: 17 ± 4 s) with reproducibility CI(95) of 5.3, 4.5, 3.1, 2.9 and 3.3 s when a single, two, three, four and six MODs were compared, respectively. τHR was reduced in MODs 6A-F compared to 1-6A and 1-6B (23 ± 5 s, 25 ± 5 s, 27 ± 6 s, respectively). This study showed that parameter estimates of VO(2p), HR and Δ[HHb] kinetics are largely unaffected by data collection sequence, and the day-to-day reproducibility of τVO(2p) and τ'Δ[HHb] estimates, as determined by the CI(95), was appreciably improved by averaging of at least three MODs.

Muscle deoxygenation to VO2 relationship differs in young subjects with varying τVO2.

The relationship between the adjustment of muscle deoxygenation (∆[HHb]) and phase II VO(2p) was examined in subjects presenting with a range of slow to fast VO(2p) kinetics. Moderate intensity VO(2p) and ∆[HHb] kinetics were examined in 37 young males (24 ± 4 years). VO(2p) was measured breath-by-breath. Changes in ∆[HHb] of the vastus lateralis muscle were measured by near-infrared spectroscopy. VO(2p) and ∆[HHb] response profiles were fit using a mono-exponential model, and scaled to a relative % of the response (0-100%). The ∆[HHb]/∆VO(2p) ratio for each individual (reflecting the matching of O(2) distribution to O(2) utilization) was calculated as the average ∆[HHb]/∆VO(2p) response from 20 to 120 s during the exercise on-transient. Subjects were grouped based on individual phase II VO(2p) time-constant (τVO(2p)): <21 s [very fast (VF)]; 21-30 s [fast (F)]; 31-40 s [moderate (M)]; >41 s [slow (S)]. The corresponding ∆[HHb]/∆VO(2p) were 0.98 (VF), 1.05 (F), 1.09 (M), and 1.22 (S). The larger ∆[HHb]/∆VO(2p) in the groups with slower VO(2p) kinetics resulted in the ∆[HHb]/∆VO(2p) displaying a transient "overshoot" relative to the subsequent steady state level, which was progressively reduced as τVO(2) became smaller (r = 0.91). When τVO(2p) > ~20 s, the rate of adjustment of phase II VO(2p) appears to be mainly constrained by the matching of local O(2) distribution to muscle VO(2). These data suggest that in subjects with "slower" VO(2) kinetics, the rate of adjustment of VO(2) may be constrained by O(2) availability within the active tissues related to the matching of microvascular O(2) distribution to muscle O(2) utilization.

Effects of ammonium chloride ingestion on phosphocreatine metabolism during moderate- and heavy-intensity plantar-flexion exercise.

This study examined the effects of NH(4)Cl ingestion on phosphocreatine (PCr) metabolism during 9 min of moderate- (MOD) and heavy- (HVY) intensity constant-load isotonic plantar-flexion exercise. Healthy young adult male subjects (n = 8) completed both a control (CON) and NH(4)Cl ingestion (ACID) trial. Phosphorus-31 magnetic resonance spectroscopy was used to monitor changes in intracellular pH (pHi), [Pi], [PCr], and [ATP]. During the Middle (3-6 min) and Late (6-9 min) stages of HVY, ACID was associated with a higher (P < 0.05) intracellular hydrogen-ion concentration ([H(+)]i) [Middle: 246 (SD 36) vs. 202 (SD 36) mmol/l]; [Late: 236 (SD 35) vs. 200 (SD 39) mmol/l]. In addition, ACID was associated with a lower (P < 0.05) [PCr] relative to CON during the Early (0-3 min) [18.1 (SD 5.1) vs. 20.4 (SD 5.4) mmol/l] and Middle stages [14.1 (SD 5.4) vs. 16.7 (SD 6.0) mmol/l] of HVY. The amplitude of the primary component of PCr breakdown during the transition to HVY was greater in ACID than CON [14.5 (SD 5.8 vs. 11.3 (SD 4.8) mmol/l], however, the PCr slow component (continued slow decline in [PCr]) showed no difference (P > 0.05). The time constant for PCr breakdown (tauPCr) was greater in HVY than MOD for both conditions [58 (SD 22) vs. 28 (SD 15) s ACID; 51 (SD 20) vs. 29 (SD 14) s CON] (P < 0.05). In summary, ACID increased PCr breakdown during the transition from MOD to HVY, but did not increase the magnitude of the PCr slow component.