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Quantitating exercise ventilatory and gas exchange dynamics affords insights into physiological control processes and cardiopulmonary dysfunction. We designed a novel waveform, the chirp waveform, to efficiently extract moderate-intensity exercise response dynamics. In the chirp waveform, work rate fluctuates sinusoidally with constant amplitude as sinusoidal period decreases progressively from ∼8.5 to 1.4 min over 30 min of cycle ergometry. We hypothesized that response dynamics of pulmonary ventilation (V̇e) and gas exchange [oxygen uptake (V̇o 2 ) and carbon dioxide output (V̇co 2 )] extracted from chirp waveform are similar to those obtained from stepwise transitions. Thirty-one participants [14 young healthy, 7 older healthy, and 10 patients with chronic obstructive pulmonary disease (COPD)] exercised on three occasions. Participants first performed ramp-incremental exercise for gas exchange threshold (GET) determination. In randomized order, the next two visits involved either chirp or stepwise waveforms. Work rate amplitude (20 W to ∼95% GET work rate) and exercise duration (30 min) were the same for both waveforms. A first-order linear transfer function with a single system gain ( G ) and time constant (τ) characterized response dynamics. Agreement between model parameters extracted from chirp and stepwise waveforms was established using Bland-Altman analysis and Rothery's concordance coefficient (RCC). V̇e, V̇o 2 , and V̇co 2 G s showed no systematic bias ( P > 0.178) and moderate-to-good agreement (RCC > 0.772, P < 0.01) between waveforms. Similarly, no systematic bias ( P = 0.815) and good agreement (RCC = 0.837, P < 0.001) was found for τV̇o 2 . Despite moderate agreement for τV̇co 2 (RCC = 0.794, P < 0.001) and τV̇e (RCC = 0.722, P = 0.083), chirp τ was less [-6.9(11.7) s and -12.2(22.5) s, respectively]. We conclude that the chirp waveform is a promising method for measuring exercise response dynamics and investigating physiological control mechanisms. NEW & NOTEWORTHY We investigated the ability of a novel waveform to extract exercise ventilatory and gas exchange dynamics. In the chirp waveform, work rate fluctuates sinusoidally with constant amplitude as sinusoidal period decreases progressively over 30 min of exercise. In a study of 31 healthy individuals and patients with COPD, comparison of exercise dynamics derived from chirp to those from stepwise waveforms suggests that the chirp waveform is a promising method for derivation of exercise response dynamics.

This study compared cardiovascular and metabolic responses during concentric and eccentric stepping. Eight participants (5 m, 3f; 22 ± 2 years) performed maximal concentric and eccentric ramp incremental tests on a modified stepping ergometer. Subsequently, three randomized 15-min constant-power tests were performed (1) concentric stepping at 90% of the concentric lactate threshold (LT), (2) eccentric stepping at the same power, and (3) eccentric stepping at the same oxygen uptake (V̇O 2 ). At equivalent power (36 ± 6 W, p = 0.62), eccentric stepping resulted in 46 ± 8% lower V̇O 2 , 16 ± 6% lower heart rate (HR), and 11 ± 5% lower mean arterial blood pressure compared to concentric (p < 0.01). Matching V̇O 2 required 65 ± 19% more power during eccentric stepping (p < 0.01). During this test, eccentric V̇O 2 and HR continued to increase, resulting in a 22 ± 29% higher V̇O 2 and 19 ± 16% higher HR in the final minute (p < 0.001). Reduced cardiorespiratory demand during eccentric stepping at the same power as concentric demonstrates a higher eccentric power is required to produce the same V̇O 2 . However, despite being below the concentric LT, eccentric V̇O 2 and HR continued to increase past the predicted steady state, indicating a higher exercise intensity., (© 2024 The Author(s). Physiological Reports published by Wiley Periodicals LLC on behalf of The Physiological Society and the American Physiological Society.)

We hypothesize that the V˙O2 time constant (τV˙O2) determines exercise tolerance by defining the power output associated with a "critical threshold" of intramuscular metabolite accumulation (e.g., inorganic phosphate), above which muscle fatigue and work inefficiency are apparent. Thereafter, the V˙O2 "slow component" and its consequences (increased pulmonary, circulatory, and neuromuscular demands) determine performance limits., (Copyright © 2021 by the American College of Sports Medicine.)

Introduction: The mechanism(s) of exercise intolerance at V˙O2max remain poorly understood. In health, standard ramp-incremental (RI) exercise is limited by fatigue-induced reductions in maximum voluntary cycling power. Whether neuromuscular fatigue also limits exercise when the RI rate is slow and RI peak power at intolerance is lower than standard RI exercise, is unknown., Methods: In twelve healthy participants, maximal voluntary cycling power was measured during a short (~6 s) isokinetic effort at 80 rpm (Piso) at baseline and, using an instantaneous switch from cadence-independent to isokinetic cycling, immediately at the limit of RI exercise with RI rates of 50, 25, and 10 W·min-1 (RI-50, RI-25, and RI-10). Breath-by-breath pulmonary gas exchange was measured throughout., Results: Baseline Piso was not different among RI rates (analysis of variance; P > 0.05). Tolerable duration increased with decreasing RI rate (RI-50, 411 ± 58 s vs RI-25, 732 ± 93 s vs RI-10, 1531 ± 288 s; P < 0.05). At intolerance, V˙O2peak was not different among RI rates (analysis of variance; P > 0.05), but RI peak power decreased with RI rate (RI-50, 361 ± 48 W vs RI-25, 323 ± 39 W vs RI-10, 275 ± 38 W; P < 0.05). Piso at intolerance was 346 ± 43 W, 353 ± 45 W, and 392 ± 69 W for RI-50, RI-25, and RI-10, respectively (P < 0.05 for RI-10 vs RI-50 and RI-25). At intolerance, in RI-50 and RI-25, Piso was not different from RI peak power (P > 0.05), thus there was no "power reserve." In RI-10, Piso was greater than RI peak power at intolerance (P < 0.001), that is, there was a "power reserve.", Conclusions: In RI-50 and RI-25, the absence of a power reserve suggests the neuromuscular fatigue-induced reduction in Piso coincided with V˙O2max and limited the exercise. In RI-10, the power reserve suggests neuromuscular fatigue was insufficient to limit the exercise, and additional mechanisms contributed to intolerance at V˙O2max., (Copyright © 2021 by the American College of Sports Medicine.)

Key Points: Continuous high-intensity constant-power exercise is unsustainable, with maximal oxygen uptake (V̇O2 max ) and the limit of tolerance attained after only a few minutes. Performing the same power intermittently reduces the O 2 cost of exercise and increases tolerance. The extent to which this dissociation is reflected in the intramuscular bioenergetics is unknown. We used pulmonary gas exchange and 31 P magnetic resonance spectroscopy to measure whole-body V̇O2, quadriceps phosphate metabolism and pH during continuous and intermittent exercise of different work:recovery durations. Shortening the work:recovery durations (16:32 s vs. 32:64 s vs. 64:128 s vs. continuous) at a work rate estimated to require 110% peak aerobic power reduced V̇O2, muscle phosphocreatine breakdown and muscle acidification, eliminated the glycolytic-associated contribution to ATP synthesis, and increased exercise tolerance. Exercise intensity (i.e. magnitude of intramuscular metabolic perturbations) can be dissociated from the external power using intermittent exercise with short work:recovery durations., Abstract: Compared with work-matched high-intensity continuous exercise, intermittent exercise dissociates pulmonary oxygen uptake (V̇O2) from the accumulated work. The extent to which this reflects differences in O 2 storage fluctuations and/or contributions from oxidative and substrate-level bioenergetics is unknown. Using pulmonary gas-exchange and intramuscular 31 P magnetic resonance spectroscopy, we tested the hypotheses that, at the same power: ATP synthesis rates are similar, whereas peak V̇O2 amplitude is lower in intermittent vs. continuous exercise. Thus, we expected that: intermittent exercise relies less upon anaerobic glycolysis for ATP provision than continuous exercise; shorter intervals would require relatively greater fluctuations in intramuscular bioenergetics than in V̇O2 compared to longer intervals. Six men performed bilateral knee-extensor exercise (estimated to require 110% peak aerobic power) continuously and with three different intermittent work:recovery durations (16:32, 32:64 and 64:128 s). Target work duration (576 s) was achieved in all intermittent protocols; greater than continuous (252 ± 174 s; P < 0.05). Mean ATP turnover rate was not different between protocols (∼43 mm min -1 on average). However, the intramuscular phosphocreatine (PCr) component of ATP generation was greatest (∼30 mm min -1 ), and oxidative (∼10 mm min -1 ) and anaerobic glycolytic (∼1 mm min -1 ) components were lowest for 16:32 and 32:64 s intermittent protocols, compared to 64:128 s (18 ± 6, 21 ± 10 and 10 ± 4 mm min -1 , respectively) and continuous protocols (8 ± 6, 20 ± 9 and 16 ± 14 mm min -1 , respectively). As intermittent work duration increased towards continuous exercise, ATP production relied proportionally more upon anaerobic glycolysis and oxidative phosphorylation, and less upon PCr breakdown. However, performing the same high-intensity power intermittently vs. continuously reduced the amplitude of fluctuations in V̇O2 and intramuscular metabolism, dissociating exercise intensity from the power output and work done., (© 2017 The Authors. The Journal of Physiology published by John Wiley & Sons Ltd on behalf of The Physiological Society.)

Phase 2 pulmonary oxygen uptake kinetics (ϕ2 τV̇o 2P ) reflect muscle oxygen consumption dynamics and are sensitive to changes in state of training or health. This study identified an unbiased method for data collection, handling, and fitting to optimize V̇o 2P kinetics estimation. A validated computational model of V̇o 2P kinetics and a Monte Carlo approach simulated 2 × 10 5 moderate-intensity transitions using a distribution of metabolic and circulatory parameters spanning normal health. Effects of averaging (interpolation, binning, stacking, or separate fitting of up to 10 transitions) and fitting procedures (biexponential fitting, or ϕ2 isolation by time removal, statistical, or derivative methods followed by monoexponential fitting) on accuracy and precision of V̇o 2P kinetics estimation were assessed. The optimal strategy to maximize accuracy and precision of τV̇o 2P estimation was 1-s interpolation of 4 bouts, ensemble averaged, with the first 20 s of exercise data removed. Contradictory to previous advice, we found optimal fitting procedures removed no more than 20 s of ϕ1 data. Averaging method was less critical: interpolation, binning, and stacking gave similar results, each with greater accuracy compared with analyzing repeated bouts separately. The optimal procedure resulted in ϕ2 τV̇o 2P estimates for transitions from an unloaded or loaded baseline that averaged 1.97 ± 2.08 and 1.04 ± 2.30 s from true, but were within 2 s of true in only 47-62% of simulations. Optimized 95% confidence intervals for τV̇o 2P ranged from 4.08 to 4.51 s, suggesting a minimally important difference of ~5 s to determine significant changes in τV̇o 2P during interventional and comparative studies. NEW & NOTEWORTHY We identified an unbiased method to maximize accuracy and precision of oxygen uptake kinetics (τV̇o 2P ) estimation. The optimum number of bouts to average was four; interpolation, bin, and stacking averaging methods gave similar results. Contradictory to previous advice, we found that optimal fitting procedures removed no more than 20 s of phase 1 data. Our data suggest a minimally important difference of ~5 s to determine significant changes in τV̇o 2P during interventional and comparative studies., (Copyright © 2017 the American Physiological Society.)

IntroductionSeveral studies report that pulmonary oxygen uptake (V̇O 2 ) at the respiratory compensation point (RCP) is equivalent to the V̇O 2 at critical power (CP), suggesting that the variables can be used interchangeably to demarcate the threshold between heavy and severe intensity domains. However, if RCP is a valid surrogate for CP, their values should correspond even when assessed in patients with chronic obstructive pulmonary disease (COPD) in whom the "normal" mechanisms linking CP and RCP are impeded. The aim of this study was to compare V̇O 2 at CP with V̇O 2 at RCP in patients with COPD.MethodsTwenty-two COPD patients (14 male/8 female; forced expiratory volume in 1 s, 46% ± 17% pred) performed ramp-incremental cycle ergometry to intolerance (5-10 W·min -1 ) for the determination of gas exchange threshold (GET) and RCP. CP was calculated from the asymptote of the hyperbolic power-duration relationship from 3-5 constant-power exercise tests to intolerance. CP was validated with a 20-min constant-power ride.ResultsGET was identified in 20 of 22 patients at a V̇O 2 of 0.93 ± 0.18 L·min -1 (75% ± 13% V̇O 2peak ), whereas RCP was identified in just 3 of 22 patients at a V̇O 2 of 1.40 ± 0.39 L·min -1 (85% ± 2% V̇O 2peak ). All patients completed constant-power trials with no difference in peak physiological responses relative to ramp-incremental exercise ( P > 0.05). CP was 46 ± 22 W, which elicited a V̇O 2 of 1.04 ± 0.29 L·min -1 (90% ± 9% V̇O 2peak ) during the validation ride. The difference in V̇O 2 at 15 and 20 min of the validation ride was 0.00 ± 0.04 L, which was not different from a hypothesized mean of 0 ( P = 0.856), thereby indicating a V̇O 2 steady state.ConclusionsIn COPD patients, who present with cardiopulmonary and/or respiratory-mechanical dysfunction, CP can be determined in the absence of RCP. Accordingly, CP and RCP are not equivalent in this group.

The article discusses a study on patients with chronic obstructive pulmonary disease (COPD) and the differentiation between critical power (CP) and the respiratory compensation point (RCP) during exercise tests, emphasizing that despite some physiological similarities.

Background: Athletic training leads to remodelling of both left and right ventricles with increased myocardial mass and cavity dilatation. Whether changes in cardiac strain parameters occur in response to training is less well established. In this study we investigated the relationship in trained athletes between cardiovascular magnetic resonance (CMR) derived strain parameters of cardiac function and fitness. Methods: Thirty five endurance athletes and 35 age and sex matched controls underwent CMR at 3.0 T including cine imaging in multiple planes and tissue tagging by spatial modulation of magnetization (SPAMM). CMR data were analysed quantitatively reporting circumferential strain and torsion from tagged images and left and right ventricular longitudinal strain from feature tracking of cine images. Athletes performed a maximal ramp-incremental exercise test to determine the lactate threshold (LT) and maximal oxygen uptake ... Results: LV circumferential strain at all levels, LV twist and torsion, LV late diastolic longitudinal strain rate, RV peak longitudinal strain and RV early and late diastolic longitudinal strain rate were all lower in athletes than controls. On multivariable linear regression only LV torsion (beta = -0.37, P = 0.03) had a significant association with LT. Only RV longitudinal late diastolic strain rate (beta = -0.35, P = 0.03) had a significant association with ... Conclusions: This cohort of endurance athletes had lower LV circumferential strain, LV torsion and biventricular diastolic strain rates than controls. Increased LT, which is a major determinant of performance in endurance athletes, was associated with decreased LV torsion. Further work is needed to understand the mechanisms by which this occurs. [ABSTRACT FROM AUTHOR]

Purpose: We aimed to measure 1) the dynamics of locomotor fatigue during constant supra-critical power cycling and 2) the magnitude of any reserve in locomotor power at intolerance to constant and ramp-incremental cycling in recreationally active volunteers. Methods: Fifteen participants (7 women and 8 men, 22 ± 3 yr, 3.34 ± 0.67 L·min−1 V˙O2peak) completed ramp-incremental and very-heavy constant power (205 ± 46 W) exercise to the limit of tolerance. Immediately after intolerance, the ergometer was switched into the isokinetic mode, and participants completed a short (~5 s) maximal isokinetic effort at 70 rpm. The time course of locomotor fatigue during constant supra-critical power exercise was characterized with these short maximal isokinetic sprints at 30, 60, 120, and 180 s and at the limit of tolerance. Each bout was terminated after the isokinetic sprint. Results: Constant power exercise duration was 312 ± 37 s. Isokinetic power production values at 30, 60, 120, and 180 s and at the limit of tolerance (at 312 ± 37 s) was 609 ± 165, 503 ± 195, 443 ± 157, 449 ± 133, and 337 ± 94 W, respectively. Of the total decline in isokinetic power, ~36% occurred within the first minute of exercise, and significant (P < 0.05) reductions in isokinetic power occurred at all time points versus the baseline maximal isokinetic power (666 ± 158 W). In addition, a significant power reserve of 132 ± 74 W (64% of the task requirement) and 119 ± 80 W (47%) was present at the limit of constant power and ramp-incremental exercise, respectively. Conclusions: Locomotor fatigue occurred rapidly during supracritical power exercise with pseudo-exponential kinetics. Instantaneous isokinetic power production at the limit of tolerance exceeded that of the task requirement, regardless of the constant or ramp work rate profile. Thus, the perceptual and physiologic limits were dissociated at the limit of tolerance in recreationally active volunteers. [ABSTRACT FROM AUTHOR]