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.

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].

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.

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.

Power reserve following ramp-incremental cycling to exhaustion: implications for muscle fatigue and function.

In ramp-incremental cycling exercise, some individuals are capable of producing power output (PO) in excess of that produced at their limit of tolerance (LoT) whereas others cannot. This study sought to describe the 1) prevalence of a "power reserve" within a group of young men ( n = 21; mean ± SD: age 25 ± 4 yr; V̇o2max 45 ± 8 ml·kg-1·min-1); and 2) muscle fatigue characteristics of those with and without a power reserve. "Power reserve" (ΔPReserve) was determined as the difference between peak PO achieved during a ramp-incremental test to exhaustion and maximal, single-leg isokinetic dynamometer power determined within 45 s of completing the ramp-incremental test. Between-group differences in pre- vs. postexercise changes in voluntary and electrically stimulated single-leg muscle force production measures (maximal voluntary contraction torque, voluntary activation, maximal isotonic velocity and isokinetic power; 1-, 10-, 50-Hz torque; and 10/50-Hz ratio), V̇o2max, and constant-PO cycling time-to-exhaustion also were assessed. Frequency distribution analysis revealed a dichotomy in the prevalence of a power reserve within the sample resulting in two groups: 1) "No Reserve" (NRES: power reserve <5%; n = 10) and 2) "Reserve" (RES: power reserve >15%; n = 11). At the LoT, all participants had achieved V̇o2max. Muscle fatigue was evident in both groups, although the NRES group had greater reductions ( P < 0.05) in 10-Hz peak torque (PT), 10/50 Hz ratio, and maximal velocity. Time to the LoT during the constant PO test was 22 ± 16% greater ( P < 0.05) in RES (116 ± 19 s; PO = 317 ± 52 W) than in NRES (90 ± 23 s; PO = 337 ± 71 W), despite similar ramp-incremental exercise durations and V̇o2max between groups. Compared with the RES group, the NRES group accrued greater peripheral muscle fatigue at the LoT, suggesting that the mechanisms contributing to exhaustion in a ramp-incremental protocol are not uniform. NEW & NOTEWORTHY This study demonstrates that the mechanisms associated with the limit of tolerance during ramp-incremental cycling exercise differ between those who are capable of generating power output in excess of that at exercise termination vs. those who are not. Those without a "power reserve" exhibit greater peripheral muscle fatigue and reduced muscle endurance, supporting the hypothesis that exhaustion occurs at a specific level of neuromuscular fatigue. In contrast, those with a power reserve likely are limited by other mechanisms.

Using ramp-incremental V̇O2 responses for constant-intensity exercise selection.

Despite compelling evidence to the contrary, the view that oxygen uptake (V̇O2) increases linearly with exercise intensity (e.g., power output, speed) until reaching its maximum persists within the exercise physiology literature. This viewpoint implies that the V̇O2 response at any constant intensity is predictable from a ramp-incremental exercise test. However, the V̇O2 versus task-specific exercise intensity relationship constructed from ramp-incremental versus constant-intensity exercise are not equivalent preventing the use of V̇O2 responses from 1 domain to predict those of the other. Still, this "linear" translational framework continues to be adopted as the guiding principle for aerobic exercise prescription and there remains in the sport science literature a lack of understanding of how to interpret V̇O2 responses to ramp-incremental exercise and how to use those data to assign task-specific constant-intensity exercise. The objectives of this paper are to (i) review the factors that disassociate the V̇O2 versus exercise intensity relationship between ramp-incremental and constant-intensity exercise paradigms; (ii) identify when it is appropriate (or not) to use ramp V̇O2 responses to accurately assign constant-intensity exercise; and (iii) illustrate the technical and theoretical challenges with prescribing constant-intensity exercise solely on information acquired from ramp-incremental tests. Actual V̇O2 data collected during cycling exercise and V̇O2 kinetics modelling are presented to exemplify these concepts. Possible solutions to overcome these challenges are also presented to inform on appropriate intensity selection for individual-specific aerobic exercise prescription in both research and practical settings.

Slow V˙O2 kinetics in acute hypoxia are not related to a hyperventilation-induced hypocapnia.

We examined whether slower pulmonary O2 uptake (V˙O2p) kinetics in hypoxia is a consequence of: a) hypoxia alone (lowered arterial O2 pressure), b) hyperventilation-induced hypocapnia (lowered arterial CO2 pressure), or c) a combination of both. Eleven participants performed 3-5 repetitions of step-changes in cycle ergometer power output from 20W to 80% lactate threshold in the following conditions: i) normoxia (CON; room air); ii) hypoxia (HX, inspired O2 = 12%; lowered end-tidal O2 pressure [PETO2] and end-tidal CO2 pressure [PETCO2]); iii) hyperventilation (HV; increased PETO2 and lowered PETCO2); and iv) normocapnic hypoxia (NC-HX; lowered PETO2 and PETCO2 matched to CON). Ventilation was increased (relative to CON) and matched between HX, HV, and NC-HX conditions. During each condition VO2p˙ was measured and phase II V˙O2p kinetics were modeled with a mono-exponential function. The V˙O2p time constant was different (p < 0.05) amongst all conditions: CON, 26 ±â€¯11s; HV, 36 ±â€¯14s; HX, 46 ±â€¯14s; and NC-HX, 52 ±â€¯13s. Hypocapnia may prevent further slowing of V˙O2p kinetics in hypoxic exercise.

Effect of heavy-intensity 'priming' exercise on oxygen uptake and muscle deoxygenation kinetics during moderate-intensity step-transitions initiated from an elevated work rate.

We examined the effect of heavy-intensity 'priming' exercise on the rate of adjustment of pulmonary O2 uptake (τV˙O2p) initiated from elevated intensities. Fourteen men (separated into two groups: τV˙O2p≤25s [Fast] or τV˙O2p>25s [Slow]) completed step-transitions from 20W to 45% lactate threshold (LT; lower-step, LS) and 45% to 90%LT (upper-step, US) performed (i) without; and (ii) with US preceded by heavy-intensity exercise (HUS). Breath-by-breath V˙O2p and near-infrared spectroscopy-derived muscle deoxygenation ([HHb+Mb]) were measured. Compared to LS, τV˙O2p was greater (p<0.05) in US in both Fast (LS, 19±4s; US, 30±4s) and Slow (LS, 25±5s; US, 40±11s) with τV˙O2p in US being lower (p<0.05) in Fast. In HUS, τV˙O2p in Slow was reduced (28±8s, p<0.05) and was not different (p>0.05) from LS or Fast group US. In Slow, τ[HHb+Mb] increased (p<0.05) in US relative to HUS; this finding coupled with a reduced τV˙O2p indicates a priming-induced improvement in matching of muscle O2 delivery-to-O2 utilization during transitions from elevated intensities in those with Slow but not Fast V˙O2p kinetics.

The slow component of pulmonary O2 uptake accompanies peripheral muscle fatigue during high-intensity exercise.

During constant-power output (PO) exercise above lactate threshold (LT), pulmonary O2 uptake (V̇o2 p) features a developing slow component (V̇o2 pSC). This progressive increase in O2 cost of exercise is suggested to be related to the effects of muscle fatigue development. We hypothesized that peripheral muscle fatigue as assessed by contractile impairment would be associated with the V̇o2 pSC Eleven healthy men were recruited to perform four constant-PO tests at an intensity corresponding to ∼Δ60 (very heavy, VH) where Δ is 60% of the difference between LT and peak V̇o2 p The VH exercise was completed for each of 3, 8, 13, and 18 min (i.e., VH3, VH8, VH13, VH18) with each preceded by 3 min of cycling at 20 W. Peripheral muscle fatigue was assessed via pre- vs. postexercise measurements of quadriceps torque in response to brief trains of electrical stimulation delivered at low (10 Hz) and high (50 Hz) frequencies. During exercise, breath-by-breath V̇o2 p was measured by mass spectrometry and volume turbine. The magnitude of V̇o2 pSC increased (P < 0.05) from 224 ± 81 ml/min at VH3 to 520 ± 119, 625 ± 134, and 678 ± 156 ml/min at VH8, VH13, and VH18, respectively. The ratio of the low-to-high frequency (10/50 Hz) response was reduced (P < 0.05) at VH3 (-12 ± 9%) and further reduced (P < 0.05) at VH8 (-25 ± 11%), VH13 (-42 ± 19%), and VH18 (-46 ± 16%), mirroring the temporal pattern of V̇o2 pSC development. The reduction in 10/50 Hz ratio was correlated (P < 0.001, r(2) = 0.69) with V̇o2 pSC amplitude. The temporal and quantitative association of decrements in muscle torque production and V̇o2 pSC suggest a common physiological mechanism between skeletal muscle fatigue and loss of muscle efficiency.

Influence of muscle metabolic heterogeneity in determining the V̇o2p kinetic response to ramp-incremental exercise.

The pulmonary O2 uptake (V̇o2p) response to ramp-incremental (RI) exercise increases linearly with work rate (WR) after an early exponential phase, implying that a single time constant (τ) and gain (G) describe the response. However, variability in τ and G of V̇o2p kinetics to different step increments in WR is documented. We hypothesized that the "linear" V̇o2p-WR relationship during RI exercise results from the conflation between WR-dependent changes in τ and G. Nine men performed three or four repeats of RI exercise (30 W/min) and two step-incremental protocols consisting of four 60-W increments beginning from 20 W or 50 W. During testing, breath-by-breath V̇o2p was measured by mass spectrometry and volume turbine. For each individual, the V̇o2p RI response was characterized with exponential functions containing either constant or variable τ and G values. A relationship between τ and G vs. WR was determined from the step-incremental protocols to derive the variable model parameters. τ and G increased from 21 ± 5 to 98 ± 20 s and from 8.7 ± 0.6 to 12.0 ± 1.9 ml·min(-1)·W(-1) for WRs of 20-230 W, respectively, and were best described by a second-order (τ) and a first-order (G) polynomial function of WR (lowest Akaike information criterion score). The sum of squared residuals was not different (P > 0.05) when the V̇o2p RI response was characterized with either the constant or variable models, indicating that they described the response equally well. Results suggest that τ and G increase progressively with WR during RI exercise. Importantly, these relationships may conflate to produce a linear V̇o2p-WR response, emphasizing the influence of metabolic heterogeneity in determining the apparent V̇o2p-WR relationship during RI exercise.

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.

Changes in whole tissue heme concentration dissociates muscle deoxygenation from muscle oxygen extraction during passive head-up tilt.

Skeletal muscle deoxygenated hemoglobin and myoglobin concentration ([HHb]), assessed by near-infrared spectroscopy (NIRS), is commonly used as a surrogate of regional O2 extraction (reflecting the O2 delivery-to-consumption ratio, Q̇/V̇o2). However, [HHb] change (Δ[HHb]) is also influenced by capillary-venous heme concentration, and/or small blood vessel volume (reflected in total heme; [THb]). We tested the hypotheses that Δ[HHb] is associated with O2 extraction, and insensitive to [THb], over a wide range of Q̇/V̇o2 elicited by passive head-up tilt (HUT; 10-min, 15° increments, between -10° and 75°). Steady-state common femoral artery blood flow (FBF) was measured by echo-Doppler, and time-resolved NIRS measured [HHb] and [THb] of vastus lateralis (VL) and gastrocnemius (GS) in 13 men. EMG confirmed muscles were inactive. During HUT in VL [HHb] increased linearly (57 ± 10 to 101 ± 16 µM; P < 0.05 above 15°) and was associated (r(2) ∼ 0.80) with the reduction in FBF (618 ± 75 ml/min at 0° to 268 ± 52 ml/min at 75°; P < 0.05 above 30°) and the increase in [THb] (228 ± 30 vs. 252 ± 32 µM; P < 0.05 above 15°). GS response was qualitatively similar to VL. However, there was wide variation within and among individuals, such that the overall limits of agreement between Δ[HHb] and ΔFBF ranged from -35 to +19% across both muscles. Neither knowledge of tissue O2 saturation nor vascular compliance could appropriately account for the Δ[HHb]-ΔFBF dissociation. Thus, under passive tilt, [HHb] is influenced by Q̇/V̇o2, as well as microvascular hematocrit and/or tissue blood vessel volume, complicating its use as a noninvasive surrogate for muscle microvascular O2 extraction.

Exercise Intensity Thresholds: Identifying the Boundaries of Sustainable Performance.

UNLABELLED: Critical power (CP), respiratory compensation point (RCP), maximal lactate steady state (MLSS), and deoxyhemoglobin breakpoint ([HHb]BP) are alternative functional indices that are thought to demarcate the highest exercise intensity that can be tolerated for long durations. PURPOSE: We tested the hypothesis that CP, RCP, MLSS, and [HHb]BP occur at the same metabolic intensity by examining the pulmonary oxygen uptake (V˙)O2p and power output (PO) associated with each "threshold." METHODS: Twelve healthy men (mean ± SD age, 27 ± 3 yr) performed the following tests on a cycle ergometer: i) four to five exhaustive tests for determination of CP, ii) two to three 30-min constant-power trials for MLSS determination, and iii) a ramp incremental exercise test from which the V˙O2p and PO at RCP and [HHb]BP were determined. During each trial, breath-by-breath V˙O2p and ventilatory variables were measured with a metabolic cart and flowmeter turbine; near-infrared spectroscopy-derived [HHb] was monitored using a frequency domain multidistance system, and arterialized capillary blood lactate was sampled at regular intervals. RESULTS: There were no differences (P > 0.05) among the V˙O2p values associated with CP, RCP, MLSS, and [HHb]BP (CP, 3.29 ± 0.48; RCP, 3.34 ± 0.45; MLSS, 3.27 ± 0.44; [HHb]BP, 3.41 ± 0.46 L·min(-1)); however, the PO associated with RCP (262 ± 48 W) and [HHb]BP (273 ± 41 W) were greater (P < 0.05) than both CP (226 ± 45 W) and MLSS (223 ± 39 W), which, themselves, were not different (P > 0.05). CONCLUSIONS: Although the standard methods for determination of CP, RCP, MLSS, and [HHb]BP are different, these indices occur at the same V˙O2p, suggesting that i) they may manifest as a result of similar physiological phenomenon and ii) each provides a valid delineation between tolerable and intolerable constant-power exercise.

Effects of age and long-term endurance training on VO2 kinetics.

PURPOSE: This study examined the effects of age and training status on the pulmonary oxygen uptake (VO2p) kinetics of untrained and chronically trained young, middle-age, and older groups of men. METHODS: Breath-by-breath VO2p and near-infrared spectroscopy-derived muscle deoxygenation ([HHb]) were monitored continuously in young (20-39 yr) trained (YT, n = 8) and untrained (YuT, n = 8), middle-age (40-59 yr) trained (MT, n = 9) and untrained (MuT, n = 9), and older (60-85 yr) trained (OT, n = 9) and untrained (OuT, n = 8) men. On-transient VO2p and [HHb] responses to cycling exercise at 80% of the estimated lactate threshold (three repeats) were modeled as monoexponential. Data were scaled to a relative percentage of the response (0%-100%), the signals time aligned, and the individual [HHb]-to-VO2p ratio was calculated as the average [HHb]/VO2 during the 20- to 120-s period after exercise onset. RESULTS: The time constant for the adjustment of phase II pulmonary VO2 (τVO2p) was larger in OuT (42.0 ± 11.3 s) compared with that in YT (17.0 ± 7.5 s), MT (18.1 ± 5.3 s), OT (19.8 ± 5.4 s), YuT (25.7 ± 6.6 s), and MuT (24.4 ± 7.4 s) (P < 0.05). Similarly, the [HHb]/VO2 ratio was larger than 1.0 in OuT (1.30 ± 0.13, P < 0.05) and this value was larger than that observed in YT (1.01 ± 0.07), MT (1.04 ± 0.05), OT (1.04 ± 0.04), YuT (1.05 ± 0.03), and MuT (1.02 ± 0.09) (P < 0.05). CONCLUSIONS: This study showed that the slower VO2kinetics typically observed in older individuals can be prevented by long-term endurance training interventions. Although the role of O2 delivery relative to peripheral use cannot be elucidated from the current measures, the absence of age-related slowing of VO2 kinetics seems to be partly related to a preservation of the matching of O2 delivery to O2 utilization in chronically trained older individuals, as suggested by the reduction in the [HHb]/VO2 ratio.

Muscle O2 extraction reserve during intense cycling is site-specific.

The present study compared peak muscle deoxygenation ([HHb]peak) responses at three quadriceps sites during occlusion (OCC), ramp incremental (RI), severe- (SVR) and moderate-intensity (MOD) exercise. Seven healthy men (25 ± 4 yr) each completed a stationary cycling RI (20 W/min) test to determine [HHb]peak [at distal and proximal vastus lateralis (VLD and VLP) and rectus femoris (RF)], peak V̇O2 (V̇O(2peak)), gas exchange threshold (GET), and peak work rate (WR(peak)). Subjects also completed MOD (WR = 80% GET) and SVR exercise (WR corresponding to 120% V̇O(2peak)) with absolute [HHb] (quantified by multichannel, time-resolved near-infrared spectroscopy) and pulmonary VO2 (V̇O(2p)) monitored continuously. Additionally, [HHb] and total hemoglobin ([Hb]tot) were monitored at rest and during subsequent OCC (250 mmHg). Site-specific adipose tissue thickness was assessed (B-mode ultrasound), and its relationship with resting [Hb]tot was used to correct absolute [HHb]. For VLD and RF, [HHb]peak was higher (P < 0.05) during OCC (VLD = 111 ± 38, RF = 114 ± 26 µM) than RI (VLD 64 ± 14, RF = 85 ± 20) and SVR (VLD = 63 ± 13, RF = 81 ± 18). [HHb]peak was similar (P > 0.05) across these conditions at the VLP (OCC = 67 ± 17, RI = 69 ± 17, SVR = 63 ± 17 µM). [HHb] peaked and then decreased prior to exercise cessation during SVR at all three muscle sites. [HHb]peak during MOD was consistently lower than other conditions at all sites. A "[HHb] reserve" exists during intense cycling at the VLD and RF, likely implying either sufficient blood flow to meet oxidative demands or insufficient diffusion time for complete equilibration. In VLP this [HHb] reserve was absent, suggesting that a critical PO2 may be challenged during intense cycling.

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.

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.

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.