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B J Whipp

Publications and source records attributed to B J Whipp.

At least 19 recordsLinked to original sources

Recommendations on the use of exercise testing in clinical practice.

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 (V'O(2)), V'O(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?"

Exercise Test↗

A test to establish maximum O2 uptake despite no plateau in the O2 uptake response to ramp incremental exercise.

The O2 uptake (Vo2) response to ramp incremental (RI) exercise does not consistently demonstrate plateau-like behavior at the limit of tolerance, and hence the requirements for a maximum Vo2 commonly are not met, despite apparent maximum effort. We sought to determine whether an appended step exercise (SE) test at a work rate greater than that achieved in a preceding ramp test would establish the plateau criterion. Seven healthy male adults performed RI cycle ergometry (20 W/min) to the limit of tolerance, followed by 5-min recovery (20 W) and then an SE test at 105% (RISE-105) of the final work rate (WRpeak) achieved during RI. Five of these subjects also performed an RI test followed by SE at 95% WRpeak (RISE-95). Vo2 was measured breath by breath using a turbine and mass spectrometer. The average of the final 15 s of RI or SE was used to establish respective Vo2 peaks. When Vo2 peak was approached, a constant Vo2 value (e.g., a plateau) was not discernable during any RI or SE component of the tests. Although the WRpeak [mean (SD)] was higher during the SE portion [359 W (SD 31)] than during the RI portion [341 W (SD 29)] of the RISE-105, the peak Vo2 was not different [SE, 4.30 l/min (SD 0.51); RI, 4.33 l/min (SD 0.52); P=0.49; n=7]. Similarly, in the RISE-95 test, WRpeak was 310 W (SD 31) for the SE portion and 326 W (SD 32) for the RI portion, yet the peak Vo2 values were not different [SE, 4.12 l/min (SD 0.53); RI, 4.11 l/min (SD 0.48); P=0.78; n=5]. The lack of notable difference between the Vo2 peaks established at different WRpeak values in our RISE protocols provides the plateau criterion for verification of maximum Vo2 in a single test session, even when the data response profiles do not themselves evidence a plateau.

Adult↗

Overshoot in VO2 following the onset of moderate-intensity cycle exercise in trained cyclists.

We have previously observed that following the onset of moderate intensity cycle ergometry, the pulmonary O2 uptake (VO2) in trained cyclists often does not increase towards its steady-state value with the typical mono-exponential characteristics; rather, there is a transient "overshoot". The purpose of this study was to systematically examine this phenomenon by comparing the VO2 responses to two moderate-intensity work rates and one high-intensity work rate in trained and untrained subjects. Following a ramp exercise test to the limit of tolerance for the determination of the gas exchange threshold (GET) and VO2(peak), seven trained cyclists [mean (SD); VO2(peak) 66.6 (2.5) ml x kg(-1) x min(-1)] and eight sedentary subjects [VO2(peak) 42.9 (5.1) ml x kg(-1) x min(-1)] completed six step transitions from baseline cycling to work rates requiring 60% and 80% GET and three step transitions from baseline cycling to a work rate requiring 50% of the difference between GET and VO2(peak) (50%delta). VO2 was measured breath-by-breath and modelled using standard techniques. The sedentary subjects did not overshoot the steady-state VO2 at any intensity. At 60% GET, six of the seven cyclists overshot the steady-state VO2 [by an integral volume of 164 (44) ml between approximately 45 and 125 s]. At 80% GET, four of the seven cyclists overshot the steady-state VO2 [by an integral volume of 185 (92) ml between approximately 55 and 140 s]. None of the cyclists showed an overshoot at 50%delta. These results indicate that trained cyclists evidence an overshoot in VO2 before steady-state is reached in the transition to moderate-intensity exercise. The mechanism(s) responsible for this effect remains to be elucidated, as does whether the overshoot confers any functional or performance benefit to the trained cyclist.

Adult↗

Serum cortisol reduction and abnormal prolactin and CD4+/CD8+ T-cell response as a result of controlled exercise in patients with rheumatoid arthritis and systemic lupus erythematosus despite unaltered muscle energetics.

OBJECTIVE: To investigate muscle energetics in patients with rheumatoid arthritis (RA) and systemic lupus erythematosus (SLE) and measure serum cortisol, prolactin and CD4+/CD8+ T-cell levels during and after controlled exhaustive exercise. METHODS: Patients with RA (n = 7), patients with SLE (n = 6) and healthy individuals (HI) (n = 10) performed incremental cycle ergometry to the limit of tolerance. Ventilation, oxygen uptake (VO2) and carbon dioxide output were measured and the lactate threshold (LT) was estimated. Serum cortisol, prolactin, CD4+ and CD8+ lymphocyte subset levels were determined at baseline, peak exercise and 1 h after exercise. RESULTS: Exercise tolerance was reduced in patients with RA and patients with SLE, as reflected by peak VO2 and LT, but muscle energetics were not altered. In RA and SLE, there was significant reduction in cortisol levels at peak (-10%; P = 0.03) and post-exercise times (-36%; P = 0.05). Prolactin varied significantly at peak exercise in HI only (+60%; P = 0.05). There was a significant reduction in CD4+ T cells at peak exercise in RA (-15%; P = 0.02) and SLE patients (-8%; P = 0.04) and an increase after exercise in SLE patients (+11%; P = 0.03). In HI, CD8+ T cells increased significantly (+47%; P = 0.01) at peak exercise, but this was not found in RA and SLE patients. A significant reduction in CD8+ T cells was noted after exercise in SLE patients (-6%; P = 0.05). CONCLUSION: RA and lupus patients do not have significantly altered muscle energetics, but have abnormal cortisol, prolactin and CD4+/CD8+ T-cell responses to exercise. Further studies need to be carried out to evaluate whether short bouts of strenuous exercise have detrimental clinical effects.

Adult↗

The maximally attainable VO2 during exercise in humans: the peak vs. maximum issue.

The quantification of maximum oxygen uptake (V(O2 max)), a parameter characterizing the effective integration of the neural, cardiopulmonary, and metabolic systems, requires oxygen uptake (VO2) to attain a plateau. We were interested in whether a VO2 plateau was consistently manifest during maximal incremental ramp cycle ergometry and also in ascertaining the relationship between this peak VO2 (V(O2 peak)) and that determined from one, or several, maximal constant-load tests. Ventilatory and pulmonary gas-exchange variables were measured breath by breath with a turbine and mass spectrometer. On average, V(O2 peak) [3.51 +/- 0.8 (SD) l/min] for the ramp test did not differ from that extrapolated from the linear phase of the response in 71 subjects. In 12 of these subjects, the V(O2 peak) was less than the extrapolated value by 0.1-0.4 l/min (i.e., a "plateau"), and in 19 subjects, V(O2 peak) was higher by 0.05-0.4 l/min. In the remaining 40 subjects, we could not discriminate a difference. The V(O2 peak) from the incremental test also did not differ from that of a single maximum constant-load test in 38 subjects or from the V(O2 max) in 6 subjects who undertook a range of progressively greater discontinuous constant-load tests. A plateau in the actual VO2 response is therefore not an obligatory consequence of incremental exercise. Because the peak value attained was not different from the plateau in the plot of VO2 vs. work rate (for the constant-load tests), the V(O2 peak) attained on a maximum-effort incremental test is likely to be a valid index of V(O2 max), despite no evidence of a plateau in the data themselves. However, without additional tests, one cannot be certain.

Adult↗

Negative accumulated oxygen deficit during heavy and very heavy intensity cycle ergometry in humans.

The concept of the accumulated O(2) deficit (AOD) assumes that the O(2) deficit increases monotonically with increasing work rate (WR), to plateau at the maximum AOD, and is based on linear extrapolation of the relationship between measured steady-state oxygen uptake ( VO(2)) and WR for moderate exercise. However, for high WRs, the measured VO(2) increases above that expected from such linear extrapolation, reflecting the superimposition of a "slow component" on the fundamental VO(2) mono-exponential kinetics. We were therefore interested in determining the effect of the VO(2) slow component on the computed AOD. Ten subjects [31 (12) years] performed square-wave cycle ergometry of moderate (40%, 60%, 80% and 90% ), heavy (40%Delta), very heavy (80%Delta) and severe (110% VO(2)(peak)) intensities for 10-15 min, theta(L)where is the estimated lactate threshold and Delta is the WR difference between and VO(2)(peak). VO(2) was determined breath-by-breath. Projected "steady-state" VO(2) values were determined from sub- tests. The measured VO(2) exceeded the projected value after approximately 3 min for both heavy and very heavy intensity exercise. This led to the AOD actually becoming negative. Thus, for heavy exercise, while the AOD was positive [0.63 (0.41) l] at 5 min, it was negative by 10 min [-0.61 (1.05) l], and more so by 15 min [-1.70 (1.64) l]. For the very heavy WRs, the AOD was [0.42 (0.67) l] by 5 min and reached -2.68 (2.09) l at exhaustion. For severe exercise, however, the AOD at exhaustion was positive in each case: +1.69 (0.39) l. We therefore conclude that the assumptions underlying the computation of the AOD are invalid for heavy and very heavy cycle ergometry (at least). Physiological inferences, such as the "anaerobic work capacity", are therefore prone to misinterpretation.

Adult↗

Effects of dichloroacetate on VO2 and intramuscular 31P metabolite kinetics during high-intensity exercise in humans.

Traditional control theories of muscle O2 consumption are based on an "inertial" feedback system operating through features of the ATP splitting (e.g., [ADP] feedback, where brackets denote concentration). More recently, however, it has been suggested that feedforward mechanisms (with respect to ATP utilization) may play an important role by controlling the rate of substrate provision to the electron transport chain. This has been achieved by activation of the pyruvate dehydrogenase complex via dichloroacetate (DCA) infusion before exercise. To investigate these suggestions, six men performed repeated, high-intensity, constant-load quadriceps exercise in the bore of an magnetic resonance spectrometer with each of prior DCA or saline control intravenous infusions. O2 uptake (Vo2) was measured breath by breath (by use of a turbine and mass spectrometer) simultaneously with intramuscular phosphocreatine (PCr) concentration ([PCr]), [Pi], [ATP], and pH (by 31P-MRS) and arterialized-venous blood sampling. DCA had no effect on the time constant (tau) of either Vo2 increase or PCr breakdown [tauVo2 45.5 +/- 7.9 vs. 44.3 +/- 8.2 s (means +/- SD; control vs. DCA); tauPCr 44.8 +/- 6.6 vs. 46.4 +/- 7.5 s; with 95% confidence intervals averaging < +/-2 s]. DCA, however, resulted in significant (P < 0.05) reductions in 1). end-exercise [lactate] (-1.0 +/- 0.9 mM), intramuscular acidification (pH, +0.08 +/- 0.06 units), and [Pi] (-1.7 +/- 2.1 mM); 2). the amplitude of the fundamental components for [PCr] (-1.9 +/- 1.6 mM) and Vo2 (-0.1 +/- 0.07 l/min, or 8%); and 3). the amplitude of the Vo2 slow component. Thus, although the DCA infusion lessened the buildup of potential fatigue metabolites and reduced both the aerobic and anaerobic components of the energy transfer during exercise, it did not enhance either tauVo2 or tau[PCr], suggesting that feedback, rather than feedforward, control mechanisms dominate during high-intensity exercise.

Adenosine Triphosphate↗

Dynamics of intramuscular 31P-MRS P(i) peak splitting and the slow components of PCr and O2 uptake during exercise.

The dynamics of pulmonary O(2) uptake (Vo(2)) during the on-transient of high-intensity exercise depart from monoexponentiality as a result of a "slow component" whose mechanisms remain conjectural. Progressive recruitment of glycolytic muscle fibers, with slow O(2) utilization kinetics and low efficiency, has, however, been suggested as a mechanism. The demonstration of high- and low-pH components of the exercising skeletal muscle (31)P magnetic resonance (MR) spectrum [inorganic phosphate (P(i)) peak] at high work rates (thought to be reflective of differences between oxidative and glycolytic muscle fibers) is also consistent with this conjecture. We therefore investigated the dynamics of Vo(2) (using a turbine and mass spectrometry) and intramuscular ATP, phosphocreatine (PCr), and P(i) concentrations and pH, estimated from the (31)P MR spectrum. Eleven healthy men performed prone square-wave high-intensity knee extensor exercise in the bore of a whole body MR spectrometer. A Vo(2) slow component of magnitude 15.9 +/- 6.9% of the phase II amplitude was accompanied by a similar response (11.9 +/- 7.1%) in PCr concentration. Only five subjects demonstrated a discernable splitting of the P(i) peak, however, which began from between 35 and 235 s after exercise onset and continued until cessation. As such, the dynamics of the pH distribution in intramuscular compartments did not consistently reflect the temporal features of the Vo(2) slow component, suggesting that P(i) splitting does not uniquely reflect the activity of oxidative or glycolytic muscle fibers per se.

Adenosine Triphosphate↗

Dynamic asymmetry of phosphocreatine concentration and O(2) uptake between the on- and off-transients of moderate- and high-intensity exercise in humans.

The on- and off-transient (i.e. phase II) responses of pulmonary oxygen uptake (V(O(2))) to moderate-intensity exercise (i.e. below the lactate threshold, theta;(L)) in humans has been shown to conform to both mono-exponentiality and 'on-off' symmetry, consistent with a system manifesting linear control dynamics. However above theta;(L) the V(O(2)) kinetics have been shown to be more complex: during high-intensity exercise neither mono-exponentiality nor 'on-off' symmetry have been shown to appropriately characterise the V(O(2)) response. Muscle [phosphocreatine] ([PCr]) responses to exercise, however, have been proposed to be dynamically linear with respect to work rate, and to demonstrate 'on-off' symmetry at all work intenisties. We were therefore interested in examining the kinetic characteristics of the V(O(2)) and [PCr] responses to moderate- and high-intensity knee-extensor exercise in order to improve our understanding of the factors involved in the putative phosphate-linked control of muscle oxygen consumption. We estimated the dynamics of intramuscular [PCr] simultaneously with those of V(O(2)) in nine healthy males who performed repeated bouts of both moderate- and high-intensity square-wave, knee-extension exercise for 6 min, inside a whole-body magnetic resonance spectroscopy (MRS) system. A transmit-receive surface coil placed under the right quadriceps muscle allowed estimation of intramuscular [PCr]; V(O(2)) was measured breath-by-breath using a custom-designed turbine and a mass spectrometer system. For moderate exercise, the kinetics were well described by a simple mono-exponential function (following a short cardiodynamic phase for V(O(2))), with time constants (tau) averaging: tauV(O(2))(,on) 35 +/- 14 s (+/- S.D.), tau[PCr](on) 33 +/- 12 s, tauV(O(2))(,off) 50 +/- 13 s and tau[PCr](off) 51 +/- 13 s. The kinetics for both V(O(2)) and [PCr] were more complex for high-intensity exercise. The fundamental phase expressing average tau values of tauV(O(2))(,on) 39 +/- 4 s, tau[PCr](on) 38 +/- 11 s, tauV(O(2))(,off) 51 +/- 6 s and tau[PCr](off) 47 +/- 11 s. An associated slow component was expressed in the on-transient only for both V(O(2)) and [PCr], and averaged 15.3 +/- 5.4 and 13.9 +/- 9.1 % of the fundamental amplitudes for V(O(2)) and [PCr], respectively. In conclusion, the tau values of the fundamental component of [PCr] and V(O(2)) dynamics cohere to within 10 %, during both the on- and off-transients to a constant-load work rate of both moderate- and high-intensity exercise. On average, approximately 90 % of the magnitude of the V(O(2)) slow component during high-intensity exercise is reflected within the exercising muscle by its [PCr] response.

Adult↗

Bioenergetic constraints on tactical decision making in middle distance running.

BACKGROUND: The highest velocity that a runner can sustain during middle distance races is defined by the intersection of the runner's individual velocity-time curve and the distance-time curve. The velocity-time curve is presumably fixed at the onset of a race; however, whereas the race distance is ostensibly fixed, the actual distance-time curve is not. That is, it is possible for a runner to run further than the race distance if he or she runs wide on bends in track races. In this instance, the point of intersection of the individual velocity-time curve and the distance-time curve will move downwards and to the right, reducing the best average velocity that can be sustained for the distance. METHODS: To illustrate this point, the race tactics used by the gold and silver medallists at 800 m and 5000 m in the Sydney Olympics were analysed. The paths taken by the runners were carefully tracked and the total distance they covered during the races and the average velocity they sustained over the distances they actually covered were calculated. RESULTS: In both the Olympic 800 m and 5000 m finals, for example, the winner was not the runner who ran at the highest average velocity in the race. Rather, the winners of these races were able to husband their metabolic resources to better effect by running closer to the actual race distance. CONCLUSIONS: Race results in middle distance running events are dependent not just on the energetic potential of the runners at the start of the race and their strategy for pace allocation, but also on the effect of their tactical approach to positioning on the total distance covered in the race. Middle distance runners should be conscious of minimising the distance covered in races if they wish to optimise their performance.

Decision Making↗

Effects of prior exercise on oxygen uptake and phosphocreatine kinetics during high-intensity knee-extension exercise in humans.

1. A prior bout of high-intensity square-wave exercise can increase the temporal adaptation of pulmonary oxygen uptake (.V(O2)) to a subsequent bout of high-intensity exercise. The mechanisms controlling this adaptation, however, are poorly understood. 2. We therefore determined the dynamics of intramuscular [phosphocreatine] ([PCr]) simultaneously with those of .V(O2) in seven males who performed two consecutive bouts of high-intensity square-wave, knee-extensor exercise in the prone position for 6 min with a 6 min rest interval. A magnetic resonance spectroscopy (MRS) transmit-receive surface coil under the quadriceps muscle allowed estimation of [PCr]; .V(O2) was measured breath-by-breath using a custom-designed turbine and a mass spectrometer system. 3. The .V(O2) kinetics of the second exercise bout were altered compared with the first such that (a) not only was the instantaneous rate of .V(O2) change (at a given level of .V(O2)) greater but the phase II tau was also reduced - averaging 46.6 +/- 6.0 s (bout 1) and 40.7 +/- 8.4 s (bout 2) (mean +/- S.D.) and (b) the magnitude of the later slow component was reduced. 4. This was associated with a reduction of, on average, 16.1% in the total exercise-induced [PCr] decrement over the 6 min of the exercise, of which 4.0% was due to a reduction in the slow component of [PCr]. There was no discernable alteration in the initial rate of [PCr] change. The prior exercise, therefore, changed the multi-compartment behaviour towards that of functionally first-order dynamics. 5. These observations demonstrate that the .V(O2) responses relative to the work rate input for high-intensity exercise are non-linear, as are, it appears, the putative phosphate-linked controllers for which [PCr] serves as a surrogate.

Adult↗

Reference values for dynamic responses to incremental cycle ergometry in males and females aged 20 to 80.

Interpretation of incremental cardiopulmonary exercise tests (CPET) might be enhanced by considering the simultaneous rates of change of certain key variables, e.g., Delta oxygen uptake/Delta work rate (Delta VO(2)/Delta WR), Delta heart rate/Delta VO(2) (Delta HR/Delta VO(2)), Delta ventilation/Delta carbon dioxide production (Delta VE/Delta VCO(2)), and the linearized Delta tidal volume/Delta VE (Delta VT/Delta lnVE) relationships. However, there are no published age- and sex-dependent reference values for these relationships that were appropriately obtained in randomly selected subjects. We therefore prospectively evaluated 120 sedentary individuals (60 male, 60 female, age 20 to 80 yr) who were randomly selected from more than 8,000 subjects, and submitted to standard ramp-incremental CPET on an electronically braked cycle ergometer. We found that sex and age significantly influenced several of the dynamic relationships, in addition to anthropometric attributes (p < 0.05). A comprehensive set of linear prediction equations is provided; the limits of normality (at the 95% confidence level) differed substantially from previous recommendations based on single discrete values. These data therefore provide a frame of reference for assessing the normalcy of the response profiles of four standard indices of metabolic, cardiovascular, and ventilatory function during rapidly incremental cycle ergometry in sedentary males and females up to 80 yr of age.

Adult↗

Influence of exercise intensity on the on- and off-transient kinetics of pulmonary oxygen uptake in humans.

1. The maximal oxygen uptake (V(O(2),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 V(O(2)) increases to attain this maximum (or to its submaximal requirement), and even less to the kinetic features of the response following exercise. 2. 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). 3. For moderate exercise, the V(O(2)) 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 (tau(1)); i.e. tau(1,on) averaged 33 +/- 16 s (+/- S.D.) and tau(1,off) 29 +/- 6 s. 4. The on-transient V(O(2)) 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. tau(1,on) = 32 +/- 17 s and tau(2,on) = 170 +/- 49 s. The off-transient V(O(2)) kinetics, however, remained mono-exponential (tau(1,off) = 42 +/- 11 s). 5. For very heavy exercise, the on-transient V(O(2)) kinetics were also well described by a double exponential function (tau(1,on) = 34 +/- 11 s and tau(2,on) = 163 +/- 46 s). However, a double exponential, with no delay, was required to characterise the off-transient kinetics (i.e. tau(1,off) = 33 +/- 5 s and tau(2,off) = 460 +/- 123 s). 6. At the highest intensity (severe), the on-transient V(O(2)) kinetics reverted to a mono-exponential profile (tau(1,on) = 34 +/- 7 s), while the off-transient kinetics retained a two-component form (tau(1,off) = 35 +/- 11 s and tau(2,off) = 539 +/- 379 s). 7. We therefore conclude that the kinetics of V(O(2)) 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.

Adult↗

Effect of exercise intensity on the changes in alveolar slopes of carbon dioxide and oxygen expiratory profiles in humans.

The slope of the expired alveolar partial pressure of carbon dioxide profile increases during exercise. Its relationship to metabolic rate, however, remains to be determined at high exercise intensities. We therefore determined the slope of alveolar partial pressures of carbon dioxide and oxygen (PACO2, PAO2, respectively) during incremental cycle ergometer exercise (an increment of 40 W each minute) to exhaustion in 11 normal subjects. The PACO2 and PAO2 increased as linear functions of carbon dioxide production and oxygen uptake (VO2), respectively, up to the estimated lactate threshold (thetaLa-). At higher intensities PACO2 increased disproportionately but PAO2 continued to increase at the same rate in 7 subjects but increased more rapidly in the remainder. The rate of change in PACO2 per unit rate of change in VO2 averaged 3.15 (SD 1.05) (mmHg.s(-1)). (l.min(-1))-1 while the rate of change in PAO2 per unit rate of change in VO2 averaged -3.53 (SD 0.79) (mmHg.s(-1)) (l.min(-1))-1 over this range. The more rapid increase in PACO2 above thetaLa- was consistent with an accelerated CO2 exchange, whereas the more rapid rate of change in PAO2 in 3 of the subjects may have reflected the development of an increased distribution of the ventilation perfusion ratio in addition to the effects of hyperventilation.

Adolescent↗

Is breath-hold time an objective index of exertional dyspnoea in humans?

Since dyspnoeic sensation (delta) increases progressively with work rate (WR) and the duration of a volitional breath-hold (tBH) shortens, we wished to explore whether tBH might correlate sufficiently closely with delta to provide a quantitative and descriptor-free index of respiratory sensation during dynamic exercise. Nine healthy males exercised on a cycle ergometer at a series of constant WRs, above and below the lactate threshold. Ventilatory and gas exchange variables were measured breath-by-breath. At each WR, breath-holds to the limit of tolerance were taken; delta was recorded (visual-analog scale) immediately prior to and throughout each breath-hold. During breath-holds, delta increased with time as a "break-away" monoexponential characteristic, reaching the maximum (100%) at the break-point. Despite end-tidal partial pressure of carbon dioxide at the break-point being higher and end-tidal partial pressure of oxygen being lower with increasing WR, the relationship between WR and tBH declined curvilinearly (i.e. with large falls in tBH occurring in the low WR range, but far smaller reductions at higher WRs). The tBH/minute ventilation relationship had a similar form. The relationship between pre-breath-hold delta and tBH was also complex: the large reductions in tBH in the low WR range were associated with only modest increases in pre-BH delta while, at higher WRs, the progressively smaller decrements in tBH were associated with progressively larger increases in delta. We therefore conclude that breath-hold duration is unlikely to provide a useful correlate of exertional dyspnoea during dynamic exercise. Furthermore, the relative prolongation of tBH at high WRs (accounting for the more-extreme levels of end-tidal gas tensions) may reflect the attention-diverting influence of the exercise per se.

Adult↗

Reproducibility of the parameters of the on-transient cardiopulmonary responses during moderate exercise in patients with chronic obstructive pulmonary disease.

To be clinically useful as indices reflective of altered physiological function consequent to interventions in patients with chronic obstructive pulmonary disease (COPD), the time constant (tau) and steady-state amplitude of the kinetic responses for oxygen uptake (VO2) carbon dioxide output (VCO2) ventilation (VE) and heart rate (HR) have to be appropriately differentiable and reproducible. We therefore assessed the reproducibility of tau and steady state amplitude values in 41 patients with severe COPD [mean (SD)] [forced expiratory volume in 1 s = 41 (7)% predicted], aged 64 (5) years. Of the total, 6 of the patients (15%) did not produce breath-by-breath data of sufficient quality to warrant kinetic analysis. The remaining 35 patients completed two moderate-intensity 10 min square-wave exercise tests separated by 2 h, both before and after an endurance training programme. Tests were conducted on an electromagnetically-braked cycle ergometer at an exercise intensity corresponding to 80% of the estimated lactate threshold (thetaLa) or 50% of peak oxygen uptake if thetaLa was insufficiently differentiable. Breath-by-breath measurements of VO2, VCO2, VE and HR were averaged into 10 s bins and the on-transient response kinetics were estimated using a mono-exponential model. Analysing the pre-training and the post-training test 1 and test 2 comparisons together, the test 1- test 2 differences were not significantly different from 0 for either tau or A. The standard deviation of the test 1- test 2 differences allowed us to define the magnitude of change that would reach statistical significance. For tau, this averaged some 8, 10, 11 and 8 s, for VO2, VCO2, VE and HR, respectively, for a one-tailed paired-comparisons test (i.e. appropriate for assessing hypothesised improvements resulting from an intervention); for a two-tailed comparison, the differences were approximately 2 s greater. The corresponding one-tailed values for A were 100 ml x min(-1), 95 ml x min(-1), 2.5 1 x min(-1) and 4 beats x min(-1), respectively; the two-tailed values were 10%-15% greater. We therefore conclude that both tau and A for moderate-intensity exercise can be reproducibly estimated in patients with COPD when the data set provides a sufficiently large amplitude of response and sufficiently low sample variability to allow appropriate parameter estimation.

Aged↗