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      Early-Phase Recovery of Cardiorespiratory Measurements after Maximal Cardiopulmonary Exercise Testing in Patients with Chronic Obstructive Pulmonary Disease

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          Abstract

          Background. This study investigated respiratory gas exchanges and heart rate (HR) kinetics during early-phase recovery after a maximal cardiopulmonary exercise test (CPET) in patients with chronic obstructive pulmonary disease (COPD) grouped according to airflow limitation. Methods. Thirty control individuals (control group: CG) and 81 COPD patients (45 with “mild” or “moderate” airflow limitation, COPD I-II, versus 36 with “severe” or “very severe” COPD, COPD III-IV) performed a maximal CPET. The first 3 min of recovery kinetics was investigated for oxygen uptake ( V ˙ O 2), minute ventilation ( V ˙ E ), respiratory equivalence, and HR. The time for V ˙ O 2 to reach 25% (T 1/4 V ˙ O 2) of peak value was also determined and compared. Results. The V ˙ O 2, V ˙ E , and HR recovery kinetics were significantly slower in both COPD groups than CG ( p < 0.05). Moreover, COPD III-IV group had significantly higher V ˙ O 2 and V ˙ E during recovery than COPD I-II group ( p < 0.05). T 1/4 V ˙ O 2 significantly differed between groups ( p < 0.01; 58 ± 18 s in CG, 79 ± 26 s in COPD I-II group, and 121 ± 34 s in COPD III-IV) and was significantly correlated with forced expiratory volume in one second in COPD patients ( p < 0.001, r = 0.53) and with peak power output ( p < 0.001, r = 0.59). Conclusion. The COPD groups showed slower kinetics in the early recovery period than CG, and the kinetics varied with severity of airflow obstruction.

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          Contractile properties of the human diaphragm during chronic hyperinflation.

          In patients with chronic obstructive pulmonary disease (COPD) and hyperinflation of the lungs, dysfunction of the diaphragm may contribute to respiratory decompensation. We evaluated the contractile function of the diaphragm in well-nourished patients with stable COPD, using supramaximal, bilateral phrenic-nerve stimulation, which provides information about the strength and inspiratory action of the diaphragm. In eight patients with COPD and five control subjects of similar age, the transdiaphragmatic pressure generated by the twitch response to phrenic-nerve stimulation was recorded at various base-line lung volumes, from functional residual capacity to total lung capacity, and during relaxation and graded voluntary efforts at functional residual capacity (twitch occlusion). At functional residual capacity, the twitch transdiaphragmatic pressure ranged from 10.9 to 26.6 cm of water (1.07 to 2.60 kPa) in the patients and from 19.8 to 37.1 cm of water (1.94 to 3.64 kPa) in the controls, indicating considerable overlap between the two groups. The ratio of esophageal pressure to twitch transdiaphragmatic pressure, an index of the inspiratory action of the diaphragm, was -0.50 +/- 0.05 in the patients, as compared with -0.43 +/- 0.02 in the controls (indicating more efficient inspiratory action in the patients than in the controls). At comparable volumes, the twitch transdiaphragmatic pressure and esophageal-to-transdiaphragmatic pressure ratio were higher in the patients than in normal subjects, indicating that the strength and inspiratory action of the diaphragm in the patients were actually better than in the controls. Twitch occlusion (a measure of the maximal activation of the diaphragm) indicated near-maximal activation in the patients with COPD, and the maximal transdiaphragmatic pressure was 106.9 +/- 13.8 cm of water (10.48 +/- 1.35 kPa). The functioning of the diaphragms of the patients with stable COPD is as good as in normal subjects at the same lung volume. Compensatory phenomena appear to counterbalance the deleterious effects of hyperinflation on the contractility and inspiratory action of the diaphragm in patients with COPD. Our findings cast doubt on the existence of chronic fatigue of the diaphragm in such patients and therefore on the need for therapeutic interventions aimed at improving diaphragm function.
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            Metabolic bases of excess post-exercise oxygen consumption: a review.

            The classical "oxygen debt" hypothesis formulated by Hill and associates in the 1920s was an attempt to link the metabolism of lactic acid with the O2 consumption in excess of resting that occurs after exercise. The O2 debt was hypothesized to represent the oxidation of a minor fraction (1/5) of the lactate formed during exercise, to provide the energy to reconvert the remainder (4/5) of the lactate to glycogen during recovery. In 1933 Margaria et al. modified this hypothesis by distinguishing between initial, fast ("alactacid"), and second, slow ("lactacid"), O2-debt curve components. They hypothesized that the fast phase of the post-exercise O2 consumption curve was due to the restoration of phosphagen (ATP + CP). It is now probable that the original lactic acid explanation of the O2 debt was too simplistic. Numerous studies on several species have provided evidence demonstrating a dissociation between the kinetics of lactate removal and the slow component of the post-exercise VO2. The metabolism of lactate, a readily oxidizable substrate, following exercise appears to be directed primarily toward energy production in mitochondria. The elevated concentration of lactate present at the end of exercise may be viewed as a "reservoir of carbon," which may serve as a source of oxidative ATP production or as a source of carbon skeletons for the synthesis of glucose, glycogen, amino acids, and TCA cycle intermediates. The metabolic basis of the elevated post-exercise VO2 may be understood in terms of those factors which directly or indirectly influence mitochondrial O2 consumption. Included among these factors are catecholamines, thyroxine, glucocorticoids, fatty acids, calcium ions, and temperature. Of these, elevated temperature is perhaps the most important. As no complete explanation of the post-exercise metabolism exists, it is recommended that the term "O2 debt" be used to describe a set of phenomena during recovery from exercise. The terms "alactacid debt" and "lactacid debt," which suggest a mechanism, are inappropriate. Use of alternative terms, e.g., "excess post-exercise oxygen consumption" (EPOC) and "recovery O2," will avoid implication of causality in describing the elevation in metabolic rate above resting levels after exercise.
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              Respiratory and Limb Muscle Dysfunction in COPD.

              In the next decade, Chronic Obstructive Pulmonary Disease (COPD) will be a major leading cause of death worldwide. Impaired muscle function and mass are common systemic manifestations in COPD patients and negatively influence survival. Respiratory and limb muscles are usually affected in these patients, thus contributing to poor exercise tolerance and reduced quality of life (QoL). Muscles from the lower limbs are more severely affected than those of the upper limbs and the respiratory muscles. Several epidemiological features of COPD muscle dysfunction are being reviewed. Moreover, the most relevant etiologic factors and biological mechanisms contributing to impaired muscle function and mass loss in respiratory and limb muscles of COPD patients are also being discussed. Currently available therapeutic strategies such as different modalities of exercise training, neuromuscular electrical and magnetic stimulation, respiratory muscle training, pharmacological interventions, nutritional support, and lung volume reduction surgery are also being reviewed, all applied to COPD patients. We claim that body composition and quadriceps muscle strength should be routinely explored in COPD patients in clinical settings, even at early stages of their disease. Despite the progress achieved over the last decade in the description of this relevant systemic manifestation in COPD, much remains to be investigated. Further elucidation of the molecular mechanisms involved in muscle dysfunction, muscle mass loss and poor anabolism will help design novel therapeutic targets. Exercise and muscle training, alone or in combination with nutritional support, is undoubtedly the best treatment option to improve muscle mass and function and QoL in COPD patients.
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                Author and article information

                Journal
                Pulm Med
                Pulm Med
                PM
                Pulmonary Medicine
                Hindawi Publishing Corporation
                2090-1836
                2090-1844
                2016
                27 November 2016
                : 2016
                : 9160781
                Affiliations
                1Service de Pneumologie, Hôpital de Bois-Guillaume, CHU de Rouen, 76031 Rouen Cedex, France
                2Service de Physiologie Digestive, Urinaire, Respiratoire et Sportive, CHU de Rouen, 76000 Rouen, France
                3UPRES EA 3830, GRHV, 76000 Rouen, France
                4CETAPS, EA 3832, UFR STAPS, Université de Rouen, 76821 Mont Saint Aignan, France
                Author notes

                Academic Editor: Stefano Centanni

                Author information
                http://orcid.org/0000-0001-6515-7736
                Article
                10.1155/2016/9160781
                5149691
                28018674
                ec35103b-47ea-4257-b6a8-349ec77e8558
                Copyright © 2016 Marie Bellefleur et al.

                This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                : 28 July 2016
                : 18 October 2016
                : 27 October 2016
                Categories
                Clinical Study

                Respiratory medicine
                Respiratory medicine

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