Paap, Davy; Takken, Tim.
Expert Review of Cardiovascular Therapy, December 2014, Vol. 12 Issue: Number 12 p1439-1453, 15p
Abstract: Reference values (RV) for cardiopulmonary exercise testing (CPET) provide the comparative basis for answering
important questions concerning the normality of exercise response in
patients and significantly impacts the clinical decision-making
process. The aim of this study is to systematically review the
literature on RV for CPET in healthy adults. A secondary aim is to make
appropriate recommendations for the practical use of RV for CPET.
Systematic searches of MEDLINE, EMBASE and PEDro databases up to March
2014 were performed. In the last 30 years, 35 studies with CPET RV were
published. There is no single set of ideal RV; characteristics of each
population are too diverse to pool the data in a single equation.
Therefore, each exercise laboratory must select appropriate sets of RV
that best reflect the characteristics of the population/patient tested,
and equipment and methodology utilized.
Horsley, Alex; Siddiqui, Salman
Respirology, January 2015, Vol. 20 Issue: Number 1 p33-45, 13p
Abstract: Adult cystic fibrosis (CF) is notable for the wide heterogeneity in severity
of disease expression, both between patients and within the lungs of
individuals. Although CFairways disease appears to start in the small
airways, in adults there is typically widespread bronchiectasis,
increased airway secretions, and extensive obstruction and inflammation
of the small airways. The complexity and heterogeneity of airways
disease in CFmeans that although there are many different methods of
assessing and describing lung ‘function’, none of these
single‐dimensional tests is able to provide a comprehensive assessment
of lung physiology across the spectrum seen in adult CF. The most
widely described measure, the forced expiratory volume in 1 s, remains
a useful and simple clinical tool, but is insensitive to early changes
and may be dissociated from other more detailed assessments of disease
severity such as computed tomography. In this review, we also discuss
the use of more sensitive novel assessments such as multiple breath
washout tests and impulse oscillometry, as well as the role of
cardiopulmonary exercise testing. In the future, hyperpolarized gas
magnetic resonance imaging techniques that combine regional structural
and functional information may help us to better understand these
measures, their applications and limitations.;
Ninaber, M.K.; Hamersma,
W.B.G.J.; Schouffoer, A.A.; van t Wout, E.F.A.; Stolk, J.. QJM:
An International Journal of Medicine, January 2015, Vol. 108 Issue: Number
1 p33-33, 1p;
Background: Exercise intolerance (EI) in
systemic sclerosis (SSc) is difficult to manage by the clinician. The
peripheral chemoreflex drive compensates for metabolic acidosis during
exercise and may be related to EI. Aim: To assess the global peripheral
chemoreflex drive (GPCD) in patients with SSc at rest and during
Methods: Consecutively tested SSc patients (n = 49) were
evaluated by pulmonary function tests, carbon dioxide (CO2)
rebreathing studies and non-invasive cardiopulmonary exercise testing
(CPET). Results of their CO2 rebreathing tests were compared
with those of controls (n = 32). Respiratory compensation for
metabolic acidosis during CPET was defined by the occurrence of a sharp
increase in minute ventilation (VdotE) and the ventilatory equivalent
for CO2 (V’E and V’CO2) at the end of the
isocapnic buffer phase. Euoxic (eVHR) and hyperoxic (hVHR) ventilatory
responses to hypercapnia were measured and its difference (eVHR − hVHR)
was considered to reflect the GPCD. Results: In 45 patients with SSc,
CPET results showed respiratory compensation at the occurrence of
metabolic acidosis. eVHR − hVHR in patients with diffuse cutaneous SSc
(dcSSc) differed significantly from that in patients with limited
cutaneous SSc (lcSSc) and from that in controls (0.47 ± 0.38 (dcSSc)
vs. 0.90 ± 0.77 (lcSSc) and 0.90 ± 0.49 (controls) l/min/mmHg; P =
0.04 and P = 0.03, respectively).
compensation for metabolic acidosis occurred in all patients. However,
the GPCD was diminished in dcSSc patients, suggesting an altered
control of breathing. Its assessment may help the clinician to better
understand reported EI and exertional dyspnea in dcSSc patients.;
Karlman Wasserman, William L Beaver, Xing-Guo Sun, William Stringer
Resting arterial H+ concentration ([H+]a) is in the nanomolar range (40+/-2 nm/L) while its production is in the millimolar range/min, with little variation from subject to subject. To determin the precision with which [H+]a is regulated during exercise, [H+]a, PaCO2 and ventilation (Ve) were measured during progressively increasing work rate exercise in 16 normal subjects. (Ve) increased with [H+]a, the latter attributable to PaCO2 increase below the lactic acidosis threshold (LAT) (DVe/D[H+]a ~15 L min-1 nanomol-1). [H+]a and PaCO2 increased, simultaneously, as work rate was increased below LAT. PaCO2 reversed direction of change between LAT and ventilatory compensation point (VCP). Above LAT, [H+]a increase relative to (Ve) increase was greater than below LAT. PaCO2 decreased above the LAT, while [H+]a continued to increase. Thus the exercise acidosis was converted from respiratory, below, to a metabolic, above the LAT. We conclude that [H+]a is increased and regulated over the full range of exercise, but with less sensitivity above the LAT.
Respiratory Physiology & Neurobiology 178 (2011) 191-195
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Brian J. Whipp, Susan A. Ward, and Harry B. Rossiter
Med. Sci. Sports Exerc., Vol. 37, No. 9, pp. 1574-1585, 2005
For moderate-intensity exercise (below lactate threshold, thetaL), muscle O(2) consumption (VO(2)) kinetics are expressed in a first-order phase 2 (or fundamental) pulmonary O(2) uptake (VO(2)) response: dVO(2)/dt . tau + DeltaVO(2)((t)) = DeltaVO(2)((ss)); where DeltaVO(2)(ss) is the steady-state VO(2) increment, and tau the VO(2) time constant (which is within approximately 10% of tauQVO(2)). A likely source of VO(2) control in this intensity domain is ADP-mediated, for which intramuscular phosphocreatine (PCr) may serve as a proxy variable. Whether, in reality, this behavior reflects the operation of a single homogeneous compartment is unclear, however; a multicompartment structure comprised of units having a similar DeltaVO(2)((ss)) but with widely varying tau can also yield a “well-fit” exponential response with an apparent single tau. In support of this is the inverse (although poorly predictive) correlation between tau and both theta(L) and VO(2max). Above theta(L), the fundamental VO(2) kinetics are supplemented with a delayed, slowly developing component that can set VO(2) on a trajectory towards VO(2max), and that has complex temporal- and intensity-related kinetics. This VO(2) slow component is also demonstrable in [PCr], suggesting that the decreased efficiency above theta(L) predominantly reflects a high phosphate cost of force production rather than a high O(2) cost of phosphate production. In addition, the oxygen deficit for the slow component is more likely to reflect a progressive shifting of DeltaVO(2)((ss)) rather than a single DeltaVO(2)((ss)) having a single tau.
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Hean-Yee Ong, Conor S. O’Dochartaigh, Sharon Lovell, Victor H. Patterson, Karlman Wasserman, D. Paul Nicholls, and Marshall S. Riley
Am J Respir Crit Care Med, Vol 169. pp 1238-1244, 2004
During constant work-rate exercise above the lactic acidosis threshold, oxygen consumption fails to plateau by 3 minutes, but continues to rise slowly. This slow component correlates closely with the rise in lactate in normal subjects. We investigated if oxygen consumption during constant work-rate exercise could rise after 3 minutes in the absence of a rise in lactate. We studied five patients with McArdle’s disease, one patient with phosphofructokinase deficiency and six normal subjects. Subjects performed two 6-minute duration constant work-rate exercise tests at 40 and 70% of peak oxygen consumption. During low-intensity exercise, oxygen consumption reached steady state by 3 minutes in both groups. Lactate rose slightly in control subjects but not in patients. During high-intensity exercise, oxygen consumption rose from the third to the sixth minute by 144 (21-607) ml/minute (median and range) in control subjects and by 142 (73-306) ml/minute in patients (p = not significant, Mann-Whitney U test). Over the same period, lactate (geometric mean and range) rose from 2.68 (1.10-5.00) to 5.39 (2.70-10.00) mmol/L in control subjects, but did not rise in patients (1.20 [0.64-1.60] to 0.70 [0.57-1.20] mmol/L). We conclude that the slow component of oxygen consumption during heavy exercise is not dependent on lactic acidosis.
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Chuang, M. L. Ting, H. Otsuka, T. et al
J Appl Physiol 87:1087-1097; 1999
Previous studies have shown that a metabolic alkalosis develops in the muscle during early exercise. This has been linked to phosphocreatine hydrolysis. Over a similar time frame, the femoral vein blood pH and plasma K(+) and HCO(-)(3) concentrations increase without an increase in PCO(2). Thus CO(2) from aerobic metabolism is converted to HCO(-)(3) rather than being eliminated by the lungs. The purpose of this study was to quantify the increase in early CO(2) stores and the component due to the exercise-induced metabolic alkalosis (E-I Alk). To avoid masking the increase in CO(2) stores by CO(2) released as HCO(-)(3) buffers lactic acid, the transient increase in CO(2) stores was measured only for work rates (WRs) below the lactic acidosis threshold (LAT). The increase in CO(2) stores was evident at the airway starting at approximately 15 s; the increase reached a peak at approximately 60 s and was complete by approximately 3 min of exercise. The increase in CO(2) stores was greater, but the kinetics were unaffected at the higher WR. Three components of the change in aerobically generated CO(2) stores were considered relevant: the carbamate component of the Haldane effect, the increase in CO(2) stores due to increase in tissue PCO(2), and the E-I Alk. The Haldane effect was calculated to be approximately 5%. Physically dissolved CO(2) in the tissues was approximately 30% of the store increase. The remaining E-I Alk CO(2) stores averaged 61 and 68% for 60 and 80% LAT WRs, respectively. The kinetics of O(2) uptake correlated with the time course of the increase in CO(2) stores; the size of the O(2) deficit correlated with the size of the E-I Alk component of the CO(2) stores. We conclude that a major component of the aerobically generated increase in CO(2) stores is the new HCO(-)(3) generated as phosphocreatine is converted to creatine.
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Karlman Wasserman, MD, PhD, FCCP
Chest 1997; 112: 1091-1101
No abstract available. A classic paper describing diagnosis of cardio-pulmonary pathophysiology from CPET.
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Paolo Palange, Gabriele Valli, Paolo Onorati, Rosa Antonucci, Patrizia Paoletti, Alessia Rosato, Felice Manfredi, and Pietro Serra
J Appl Physiol 97: 1637–1642, 2004.
We tested the hypothesis that heliox breathing, by reducing lung dynamic hyperinflation (DH) and dyspnea (Dys) sensation, may significantly improve exercise endurance capacity in patients with chronic obstructive pulmonary disease [n = 12, forced expiratory volume in 1 s = 1.15 (SD 0.32) liters]. Each subject underwent two cycle ergometer high-intensity constant work rate exercises to exhaustion, one on room air and one on heliox (79% He-21% O2). Minute ventilation (VE), carbon dioxide output, heart rate, inspiratory capacity (IC), Dys, and arterial partial pressure of CO2 were measured. Exercise endurance time increased significantly with heliox [9.0 (SD 4.5) vs. 4.2 (SD 2.0) min; P < 0.001]. This was associated with a significant reduction in lung DH at isotime (Iso), as reflected by the increase in IC [1.97 (SD 0.40) vs. 1.77 (SD 0.41) liters; P < 0.001] and a decrease in Dys [6 (SD 1) vs. 8 (SD 1) score; P < 0.001]. Heliox induced a state of relative hyperventilation, as reflected by the increase in VE [38.3 (SD 7.7) vs. 35.5 (SD 8.8) l/min; P < 0.01] and VE/carbon dioxide output [36.3 (SD 6.0) vs. 33.9 (SD 5.6); P < 0.01] at peak exercise and by the reduction in arterial partial pressure of CO2 at Iso [44 (SD 6) vs. 48 (SD 6) Torr; P < 0.05] and at peak exercise [46 (SD 6) vs. 48 (SD 6) Torr; P < 0.05]. The reduction in Dys at Iso correlated significantly (R = -0.75; P < 0.01) with the increase in IC induced by heliox. The increment induced by heliox in exercise endurance time correlated significantly with resting increment in resting forced expiratory in 1 s (R = 0.88; P < 0.01), increase in IC at Iso (R = 0.70; P < 0.02), and reduction in Dys at Iso (R = -0.71; P < 0.01). In chronic obstructive pulmonary disease, heliox breathing improves high-intensity exercise endurance capacity by increasing maximal ventilatory capacity and by reducing lung DH and Dys.
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Janos Porszasz, Richard Casaburi, Attila Somfay, Linda J. Woodhouse, and Brian J. Whipp
Med. Sci. Sports Exerc., Vol. 35, No. 9, pp. 1596-1602, 2003
INTRODUCTION: A treadmill exercise test requiring a low initial metabolic rate that then increments the work rate linearly to reach the subject’s limit of tolerance in approximately 10 min would have significant advantages for exercise testing and rehabilitation of subjects with impaired exercise tolerance. METHODS: We developed such a treadmill protocol that uses a linear increase in walking speed coupled with a curvilinear increase in treadmill grade to yield a linear increase in work rate. RESULTS: Twenty-two healthy, sedentary subjects performed both this new treadmill protocol and a standard cycle ergometry ramp protocol eliciting similar work rate profiles. The low initial treadmill speed and grade resulted in a low initial metabolic rate, commensurate with unloaded pedaling on a cycle ergometer (average [OV0312]O2 = 0.54 +/- 0.16 vs 46 +/- 0.12 l x min(-1)). This combination of simultaneous increase in speed and grade yielded a linear work rate and its oxygen uptake response (R2 = 0.96 +/- 0.03) with a slope of 11.4 +/- 2.4 ml x min(-1) x W(-1)-slightly, but significantly, higher than on the cycle (9.6 +/- 2.0 ml x min(-1) x W(-1)). This difference was attributed to unmeasured work associated, for example, with additional limb movements and frictional losses. As previously demonstrated, both the peak oxygen uptake and the estimated lactate threshold were higher on the treadmill than for cycle ergometry (averaging 23% and 27%, respectively, in these subjects). CONCLUSION: This treadmill protocol provides a linear profile of work rate as is currently standard for cycle ergometry and is appropriate for testing of subjects with low exercise tolerance.
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