Breath-by-breath measurement of alveolar gas exchange must preserve mass balance and conform to a physiological definition of a breath.

Tidal breathing in awake humans is variable. This variability causes changes in lung gas stores that affect gas exchange measurements. To overcome this, several algorithms provide solutions for breath-by-breath alveolar gas exchange measurement; however, there is no consensus on a physiologically robust method suitable for widespread application.

Ventilation/carbon dioxide output relationships during exercise in health.

"Ventilatory efficiency" is widely used in cardiopulmonary exercise testing to make inferences regarding the normality (or otherwise) of the arterial CO tension ( ) and physiological dead-space fraction of the breath ( / ) responses to rapid-incremental (or ramp) exercise. It is quantified as: 1) the slope of the linear region of the relationship between ventilation (') and pulmonary CO output (' ); and/or 2) the ventilatory equivalent for CO at the lactate threshold ('/' [Formula: see text]) or its minimum value ('/' min), which occurs soon after [Formula: see text] but before respiratory compensation. Although these indices are normally numerically similar, they are not equally robust.

Reply to Garcia-Tabar et al.: Quality control of open-circuit respirometry: real-time, laboratory-based systems. Let us spread "good practice".

Purpose: This article is in response to the Letter of Garcia-Tabar et al. [Eur J Appl Physiol (in press), 2018] relating to the issue of post-test sensor calibration 'verification'. This issue is poorly addressed in contemporary patient-related position statements on cardiopulmonary exercise testing (CPET).

Open-circuit respirometry: real-time, laboratory-based systems.

This review explores the conceptual and technological factors integral to the development of laboratory-based, automated real-time open-circuit mixing-chamber and breath-by-breath (B × B) gas-exchange systems, together with considerations of assumptions and limitations. Advances in sensor technology, signal analysis, and digital computation led to the emergence of these technologies in the mid-20th century, at a time when investigators were beginning to recognise the interpretational advantages of nonsteady-state physiological-system interrogation in understanding the aetiology of exercise (in)tolerance in health, sport, and disease. Key milestones include the 'Auchincloss' description of an off-line system to estimate alveolar O uptake B × B during exercise.

Exercise Testing, Supplemental Oxygen, and Hypoxia.

Cardiopulmonary exercise testing (CPET) in hyperoxia and hypoxia has several applications, stemming from characterization of abnormal physiological response profiles associated with exercise intolerance. As altered oxygenation can impact the performance of gas-concentration and flow sensors and pulmonary gas exchange algorithms, integrated CPET system function requires validation under these conditions. Also, as oxygenation status can influence peak [Formula: see text]o, care should be taken in the selection of work-rate incrementation rates when CPET performance is to be compared with normobaria at sea level.

A 'ramp-sprint' protocol to characterise indices of aerobic function and exercise intensity domains in a single laboratory test.

Purpose: The lactate threshold (LT), critical power (CP) and maximum oxygen uptake (VO₂max) together partition exercise intensity domains by their common physiological, biochemical and perceptual response characteristics. CP is the greatest power output attainable immediately following intolerance at VO₂peak, and the asymptote of 3 min all-out exercise. Thus we reasoned that a maximal 'sprint' immediately following standard ramp-incremental exercise would allow characterisation of the three aerobic indices in a single test.

Muscle metabolism and activation heterogeneity by combined 31P chemical shift and T2 imaging, and pulmonary O2 uptake during incremental knee-extensor exercise.

The integration of skeletal muscle substrate depletion, metabolite accumulation, and fatigue during large muscle-mass exercise is not well understood. Measurement of intramuscular energy store degradation and metabolite accumulation is confounded by muscle heterogeneity. Therefore, to characterize regional metabolic distribution in the locomotor muscles, we combined 31P magnetic resonance spectroscopy, chemical shift imaging, and T2-weighted imaging with pulmonary oxygen uptake during bilateral knee-extension exercise to intolerance.

Respiratory and sleep disorders in mucopolysaccharidosis.

MPS encompasses a group of rare lysosomal storage disorders that are associated with the accumulation of glycosaminoglycans (GAG) in organs and tissues. This accumulation can lead to the progressive development of a variety of clinical manifestations. Ear, nose, throat (ENT) and respiratory problems are very common in patients with MPS and are often among the first symptoms to appear.

The contribution of "resting" body muscles to the slow component of pulmonary oxygen uptake during high-intensity cycling.

Oxygen uptake (VO2) kinetics during moderate constant-workrate (WR) exercise (>lactate-threshold (θL)) are well described as exponential. AboveθL, these kinetics are more complex, consequent to the development of a delayed slow component (VO2sc), whose aetiology remains controversial. To assess the extent of the contribution to the VO2sc from arm muscles involved in postural stability during cycling, six healthy subjects completed an incremental cycle-ergometer test to the tolerable limit for estimation of θL and determination of peak VO2.

Pulmonary O2 uptake kinetics as a determinant of high-intensity exercise tolerance in humans.

Tolerance to high-intensity constant-power (P) exercise is well described by a hyperbola with two parameters: a curvature constant (W') and power asymptote termed "critical power" (CP). Since the ability to sustain exercise is closely related to the ability to meet the ATP demand in a steady state, we reasoned that pulmonary O(2) uptake (Vo(2)) kinetics would relate to the P-tolerable duration (t(lim)) parameters. We hypothesized that 1) the fundamental time constant (τVo(2)) would relate inversely to CP; and 2) the slow-component magnitude (ΔVo(2sc)) would relate directly to W'.

Oxygen uptake kinetics during incremental- and decremental-ramp cycle ergometry.

The pulmonary oxygen uptake (VO2) response to incremental-ramp cycle ergometry typically demonstrates lagged-linear first-order kinetics with a slope of ~10-11 ml·min(-1)·W(-1), both above and below the lactate threshold (θL), i.e. there is no discernible VO2 slow component (or "excess" VO2) above θL.

Kinetics of the ventilatory and metabolic responses to moderate-intensity exercise in humans following prior exercise-induced metabolic acidaemia.

As the time constant of the phase 2 (ø2) ventilatory response (tauV'(E)) to moderate exercise (< lactate threshold, thetaL) is reduced by exogenous procedures that augment peripheral (carotid) chemosensitivity (hypoxia; chronic metabolic acidaemia), we examined whether an acute endogenous metabolic acidaemia had a similar effect. Six subjects completed two tests (A, B), each comprising two 6-min bouts separated by a 6-min "0" W recovery: A:- 90% thetaL, 90% thetaL; B:- supra-thetaL (50% between thetaL and peak V'O2), 90% thetaL. For Protocol A, the bout 2 sub-thetaL tauV'E was similar to bout 1.

Influence of cycling history on the ventilatory response to cycle-ergometry in humans: a role for respiratory memory?

The ventilatory (V' E) mechanisms subserving stability of alveolar and arterial PCO2 (PACO2, PaCO2) during moderate exercise (< lactate threshold, thetaL) remain controversial. As long-term modulation has been argued to be an important contributor to this control process, we proposed that subjects with no experience of cycling (NEx) might provide insight into this issue. With no exercise familiarization, 9 sedentary NEx subjects and 9 age-, sex-, and activity-matched controls (C) who had cycled regularly for recreational purposes since childhood completed a square-wave (6-min stage) cycle-ergometry test: 10 W-WR1-WR2-WR1-10 W; WR1 range 25-45 W, WR2 range 50-90 W.

Ventilatory control during intermittent high-intensity exercise in humans.

Intermittent supra-maximal cycling of varying work: recovery durations was used to explore the kinetics of respiratory compensation for the metabolic acidosis of high-intensity exercise (> lactate threshold, thetaL). For a 10:20s duty-cycle, blood [lactate] ([L-]) was not increased, and there was no evidence of respiratory compensation (RC); i.e, no increase in the ventilation (VE)-CO2 output (Vco2) slope, nor fall in end-tidal PCO2 (PETCO2).

Effects of formoterol on exercise tolerance in severely disabled patients with COPD.

Objective: We wished to evaluate the effects of inhaled formoterol, a long-acting beta(2)-adrenergic agonist, on exercise tolerance and dynamic hyperinflation (DH) in severely disabled chronic obstructive pulmonary disease (COPD) patients.

Design: In a two-period, crossover study, 21 patients with advanced COPD (FEV(1)=38.8+/-11.

Ventilatory control in humans: constraints and limitations.

Below the lactate threshold ((thetaL)), ventilation (V(E))responds in close proportion to CO(2) output to regulate arterial partial pressure of CO(2) (PaCO2). While ventilatory control models have traditionally included proportional feedback (central and carotid chemosensory) and feedforward (central and peripheral neurogenic) elements, the mechanisms involved remain unclear. Regardless, putative control schemes have to accommodate the close dynamic 'coupling' between and V(E) and V(CO2).

Indices of electromyographic activity and the "slow" component of oxygen uptake kinetics during high-intensity knee-extension exercise in humans.

The control of pulmonary oxygen uptake (VO2) kinetics above the lactate threshold (LT) is complex and controversial. Above LT, VO2 for square-wave exercise is greater than predicted from the sub-LT VO2-WR relationship, reflecting the contribution of an additional "slow" component (VO2(sc)). Investigators have argued for a contribution to this slow component from the recruitment of fast-twitch muscle fibres, which are less aerobically efficient than slow-twitch fibres.