No abstract

To determine the precise nonsteady-state characteristics of ventilation (VE), O2 uptake (VO2), and CO2 output (VCO2) during moderate-intensity exercise, six subjects each underwent eight repetitions of 100-W constant-load cycling. The tests were preceded either by rest or unloaded cycling ("0" W). An early component of VE, VO2, and VCO2 responses, which was obscured on any single test by the breath-to-breath fluctuations, became apparent when the several repetitions were averaged. These early responses were abrupt when the work was instituted from rest but were much slower and smaller from the 0-W base line and corresponded to the phase of cardiodynamic gas exchange. Some 20 s after the onset of the work a further monoexponential increase to steady state occurred in all three variables, the time constants of which did not differ between the two types of test. Consequently, the exponential behavior of VE, VO2, and VCO2 in response to moderate exercise is best described by a model that incorporates only the second phase of the response.

The effects of prior exercise on O2 uptake (VO2) kinetics during supra-lactate threshold (LT) cycling were assessed in 11 subjects. Protocols consisted of two consecutive 6-min work bouts separated by 0 W (6 min) with 1) both bouts sub-LT, 2) both bouts supra-LT, 3) bout 1 sub-LT and bout 2 supra-LT, and 4) bout 1 supra-LT and bout 2 sub-LT. Sub-LT VO2 kinetics were similar whether the prior bout was supra- or sub-LT. The VO2 kinetics for supra-LT work preceded by a sub-LT "warm-up" were similar to those for supra-LT work that was not preceded by exercise (O-W warm-up): the "partial": O2 deficit averaged 2.64 vs. 2.57 liters, and the "effective" VO2 time constant averaged 56 vs. 65 s. Exercise responses (i.e., the change between O W and minute 6 of exercise) were unaffected for lactate concentration (4.58 vs. 4.50 meq/l), pH (-0.08 vs. -0.10), and CO2 output (VCO2; 2.65 vs. 2.49 l/min). However, when the supra-LT work was preceded by a supra-LT warm-up, VO2 kinetics were appreciably faster (O2 deficit = 1.82 liters, VO2 time constant = 37 s) relative to 0-W warm-up; the lactate (0.69 meq/l), pH (-0.01), and VCO2 (2.08 l/min) responses were smaller; and the effective VCO2 time constant was longer (58 vs. 43 s). The mechanism(s) that underlie this speeding of the VO2 kinetics cannot be firmly established, but we suggest that an improved muscle perfusion during the exercise may be involved consequent to the residual metabolic acidemia from the high-intensity warm-up.

Breathing has inherent irregularities that produce breath-to-breath fluctuations ("noise") in pulmonary gas exchange. These impair the precision of characterizing nonsteady-state gas exchange kinetics during exercise. We quantified the effects of this noise on the confidence of estimating kinetic parameters of the underlying physiological responses and hence of model discrimination. Five subjects each performed eight transitions from 0 to 100 W on a cycle ergometer. Ventilation, CO2 output, and O2 uptake were computed breath by breath. The eight responses were interpolated uniformly, time aligned, and averaged for each subject; and the kinetic parameters of a first-order model (i.e., the time constant and time delay) were then estimated using three methods: linear least squares, nonlinear least squares, and maximum likelihood. The breath-by-breath noise approximated an uncorrelated Gaussian stochastic process, with a standard deviation that was largely independent of metabolic rate. An expression has therefore been derived for the number of square-wave repetitions required for a specified parameter confidence using methods b and c; method a being less appropriate for parameter estimation of noisy gas exchange kinetics.

Evidence-based recommendations on the clinical use of cardiopulmonary exercise testing (CPET) in lung and heart disease are presented, with reference to the assessment of exercise intolerance, prognostic assessment and the evaluation of therapeutic interventions (e.g. drugs, supplemental oxygen, exercise training). A commonly used grading system for recommendations in evidence-based guidelines was applied, with the grade of recommendation ranging from A, the highest, to D, the lowest.For symptom-limited incremental exercise, CPET indices, such as peak O 2 uptake (V9O 2 ), V9O 2 at lactate threshold, the slope of the ventilation-CO 2 output relationship and the presence of arterial O 2 desaturation, have all been shown to have power in prognostic evaluation. In addition, for assessment of interventions, the tolerable duration of symptom-limited high-intensity constant-load exercise often provides greater sensitivity to discriminate change than the classical incremental test. Field-testing paradigms (e.g. timed and shuttle walking tests) also prove valuable.In turn, these considerations allow the resolution of practical questions that often confront the clinician, such as: 1) ''When should an evaluation of exercise intolerance be sought?''; 2) ''Which particular form of test should be asked for?''; and 3) ''What cluster of variables should be selected when evaluating prognosis for a particular disease or the effect of a particular intervention?''

The maximal oxygen uptake (V̇O2,peak) during dynamic muscular exercise is commonly taken as a crucial determinant of the ability to sustain high‐intensity exercise. Considerably less attention, however, has been given to the rate at which V̇O2 increases to attain this maximum (or to its submaximal requirement), and even less to the kinetic features of the response following exercise. Six, healthy, male volunteers (aged 22 to 58 years), each performed 13 exercise tests: initial ramp‐incremental cycle ergometry to the limit of tolerance and subsequently, on different days, three bouts of square‐wave exercise each at moderate, heavy, very heavy and severe intensities. Pulmonary gas exchange variables were determined breath by breath throughout exercise and recovery from the continuous monitoring of respired volumes (turbine) and gas concentrations (mass spectrometer). For moderate exercise, the V̇O2 kinetics were well described by a simple mono‐exponential function, following a short cardiodynamic phase, with the on‐ and off‐transients having similar time constants (τ1); i.e. τ1,on averaged 33 ± 16 s (± S.D.) and τ1,off 29 ± 6 s. The on‐transient V̇O2 kinetics were more complex for heavy exercise. The inclusion of a second slow and delayed exponential component provided an adequate description of the response; i.e. τ1,on= 32 ± 17 s and τ2,on= 170 ± 49 s. The off‐transient V̇O2 kinetics, however, remained mono‐exponential (τ1,off= 42 ± 11 s). For very heavy exercise, the on‐transient V̇O2 kinetics were also well described by a double exponential function (τ1,on= 34 ± 11 s and τ2,on= 163 ± 46 s). However, a double exponential, with no delay, was required to characterise the off‐transient kinetics (i.e. τ1,off= 33 ± 5 s and τ2,off= 460 ± 123 s). At the highest intensity (severe), the on‐transient V̇O2 kinetics reverted to a mono‐exponential profile (τ1,on= 34 ± 7 s), while the off‐transient kinetics retained a two‐component form (τ1,off= 35 ± 11 s and τ2,off= 539 ± 379 s). We therefore conclude that the kinetics of V̇O2 during dynamic muscular exercise are strikingly influenced by the exercise intensity, both with respect to model order and to dynamic asymmetries between the on‐ and off‐transient responses.

This document reviews 1) the measurement properties of commonly used exercise tests in patients with chronic respiratory diseases and 2) published studies on their utilty and/or evaluation obtained from MEDLINE and Cochrane Library searches between 1990 and March 2015.Exercise tests are reliable and consistently responsive to rehabilitative and pharmacological interventions. Thresholds for clinically important changes in performance are available for several tests. In pulmonary arterial hypertension, the 6-min walk test (6MWT), peak oxygen uptake and ventilation/carbon dioxide output indices appear to be the variables most responsive to vasodilators. While bronchodilators do not always show clinically relevant effects in chronic obstructive pulmonary disease, high-intensity constant work-rate (endurance) tests (CWRET) are considerably more responsive than incremental exercise tests and 6MWTs. High-intensity CWRETs need to be standardised to reduce interindividual variability. Additional physiological information and responsiveness can be obtained from isotime measurements, particularly of inspiratory capacity and dyspnoea. Less evidence is available for the endurance shuttle walk test. Although the incremental shuttle walk test and 6MWT are reliable and less expensive than cardiopulmonary exercise testing, two repetitions are needed at baseline. All exercise tests are safe when recommended precautions are followed, with evidence suggesting that no test is safer than others. @ERSpublications A review of exercise testing to evaluate interventions aimed to improve exercise tolerance in respiratory patients

In the non‐steady state of moderate intensity exercise, pulmonary O2 uptake (V̇p,O2) is temporally dissociated from muscle O2 consumption (V̇m,O2) due to the influence of the intervening venous blood volume and the contribution of body O2 stores to ATP synthesis. A monoexponential model of V̇p,O2 without a delay term, therefore, implies an obligatory slowing of V̇p,O2 kinetics in comparison to V̇m,O2. During moderate exercise, an association of V̇m,O2 and [phosphocreatine] ([PCr]) kinetics is a necessary consequence of the control of muscular oxidative phosphorylation mediated by some function of [PCr]. It has also been suggested that the kinetics of V̇p,O2 will be expressed with a time constant within 10 % of that of V̇m,O2. V̇p,O2 and intramuscular [PCr] kinetics were investigated simultaneously during moderate exercise of a large muscle mass in a whole‐body NMR spectrometer. Six healthy males performed prone constant‐load quadriceps exercise. A transmit‐receive coil under the right quadriceps allowed determination of intramuscular [PCr]; V̇p,O2 was measured breath‐by‐breath, in concert with [PCr], using a turbine and a mass spectrometer system. Intramuscular [PCr] decreased monoexponentially with no delay in response to exercise. The mean of the time constants (τPCr) was 35 s (range, 20–64 s) for the six subjects. Two temporal phases were evident in the V̇p,O2 response. When the entire V̇p,O2 response was modelled to be exponential with no delay, its time constant (τ′V̇p,O2) was longer in all subjects (group mean = 62 s; range, 52–92 s) than that of [PCr], reflecting the energy contribution of the O2 stores. Restricting the V̇p,O2 model fit to phase II resulted in matching kinetics for V̇p,O2 (group mean τV̇p,O2= 36 s; range, 20–68 s) and [PCr], for all subjects. We conclude that during moderate intensity exercise the phase II τV̇p,O2 provides a good estimate of τPCr and by implication that of V̇m,O2 (τV̇m,O2).