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      Bronchodilation improves endurance but not muscular efficiency in chronic obstructive pulmonary disease

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          Abstract

          We hypothesized that bronchodilator treatment not only improves hyperinflation and endurance capacity but also muscular efficiency in stable chronic obstructive pulmonary disease (COPD). We aimed to demonstrate that tiotropium and salmeterol improve muscular efficiency compared with placebo. Twenty-five COPD patients were studied, including 20 males of mean (standard deviation) age 62 years (7 years) with baseline forced expiratory volume in 1 second of 41% (10%) predicted, and maximal workload of 101 Watt (36 Watt). Subjects were randomized for 6-week treatment with tiotropium 18 μg once daily, salmeterol 50 μg twice daily, or placebo using a double-blind, crossover design. Muscular efficiency and endurance time were measured during cycling at 50% of maximal work load. Resting energy expenditure was measured using a ventilated hood. Muscular efficiency after tiotropium, salmeterol, and placebo treatment was 14.6%, 14.4%, and 14.4%, respectively ( P > 0.05), and resting energy expenditure was 1485 kcal/24 hours, 1709 kcal/24 hours, and 1472 kcal/24 hours ( P > 0.05), respectively. Endurance time after tiotropium treatment was significantly higher than that after placebo (27.0 minutes versus 19.3 minutes [ P = 0.02]), whereas endurance time after salmeterol treatment was not higher than that after placebo (23.3 minutes [ P = 0.22]). In this small study, we were not able to demonstrate that bronchodilator therapy improved muscular efficiency. Apparently, reduced costs of breathing relative to total energy expenditure were too small to be detected.

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          Most cited references 24

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          Disorders of the respiratory muscles.

          The act of breathing depends on coordinated activity of the respiratory muscles to generate subatmospheric pressure. This action is compromised by disease states affecting anatomical sites ranging from the cerebral cortex to the alveolar sac. Weakness of the respiratory muscles can dominate the clinical manifestations in the later stages of several primary neurologic and neuromuscular disorders in a manner unique to each disease state. Structural abnormalities of the thoracic cage, such as scoliosis or flail chest, interfere with the action of the respiratory muscles-again in a manner unique to each disease state. The hyperinflation that accompanies diseases of the airways interferes with the ability of the respiratory muscles to generate subatmospheric pressure and it increases the load on the respiratory muscles. Impaired respiratory muscle function is the most severe consequence of several newly described syndromes affecting critically ill patients. Research on the respiratory muscles embraces techniques of molecular biology, integrative physiology, and controlled clinical trials. A detailed understanding of disease states affecting the respiratory muscles is necessary for every physician who practices pulmonary medicine or critical care medicine.
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            Respiratory muscle work compromises leg blood flow during maximal exercise.

            We hypothesized that during exercise at maximal O2 consumption (VO2max), high demand for respiratory muscle blood flow (Q) would elicit locomotor muscle vasoconstriction and compromise limb Q. Seven male cyclists (VO2max 64 +/- 6 ml.kg-1.min-1) each completed 14 exercise bouts of 2.5-min duration at VO2max on a cycle ergometer during two testing sessions. Inspiratory muscle work was either 1) reduced via a proportional-assist ventilator, 2) increased via graded resistive loads, or 3) was not manipulated (control). Arterial (brachial) and venous (femoral) blood samples, arterial blood pressure, leg Q (Qlegs; thermodilution), esophageal pressure, and O2 consumption (VO2) were measured. Within each subject and across all subjects, at constant maximal work rate, significant correlations existed (r = 0.74-0.90; P < 0.05) between work of breathing (Wb) and Qlegs (inverse), leg vascular resistance (LVR), and leg VO2 (VO2legs; inverse), and between LVR and norepinephrine spillover. Mean arterial pressure did not change with changes in Wb nor did tidal volume or minute ventilation. For a +/-50% change from control in Wb, Qlegs changed 2 l/min or 11% of control, LVR changed 13% of control, and O2 extraction did not change; thus VO2legs changed 0.4 l/min or 10% of control. Total VO2max was unchanged with loading but fell 9.3% with unloading; thus VO2legs as a percentage of total VO2max was 81% in control, increased to 89% with respiratory muscle unloading, and decreased to 71% with respiratory muscle loading. We conclude that Wb normally incurred during maximal exercise causes vasoconstriction in locomotor muscles and compromises locomotor muscle perfusion and VO2.
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              Muscular efficiency during steady-rate exercise: effects of speed and work rate.

              In a comparison of traditional and theoretical exercise efficiency calculations male subjects were studied during steady-rate cycle ergometer exercises of "0," 200, 400, 600, and 800 kgm/min while pedaling at 40, 60, 80, and 100 rpm. Gross (no base-line correction), net (resting metabolism as base-line correction), work (unloading cycling as base-line correction), and delta (measurable work rate as base-line correction) efficiencies were computed. The result that gross (range 7.5-20.4%) and net (9.8-24.1%) efficiencies increased with increments in work rate was considered to be an artifact of calculation. A LINEAR OR SLIGHTLY EXPONENTIAL RELATIONSHIP BETWEEN CALORIC OUTPUT AND WORK RATE DICTATES EITHER CONSTANT OR DECREASING EFFICIENCY WITH INCREMENTS IN WORK. The delta efficiency (24.4-34.0%) definition produced this result. Due to the difficulty in obtaining 0 work equivalents, the work efficiency definition proved difficult to apply. All definitions yielded the result of decreasing efficiency with increments in speed. Since the theoretical-thermodynamic computation (assuming mitochondrial P/O = 3.0 and delta G = -11.0 kcal/mol for ATP) holds only for CHO, the traditional mode of computation (based upon VO2 and R) was judged to be superior since R less than 1.0. Assuming a constant phosphorylative-coupling efficiency of 60%, the mechanical contraction-coupling efficiency appears to vary between 41 and 57%.
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                Author and article information

                Journal
                Int J Chron Obstruct Pulmon Dis
                International Journal of COPD
                International Journal of Chronic Obstructive Pulmonary Disease
                Dove Medical Press
                1176-9106
                1178-2005
                2011
                2011
                08 April 2011
                : 6
                : 229-235
                Affiliations
                [1 ]University Medical Center, Groningen, The Netherlands;
                [2 ]Boehringer Ingelheim bv, Alkmaar, The Netherlands
                Author notes
                Correspondence: Hester van der Vaart, Department of Pulmonary Diseases, University Medical Center Groningen, PO Box 30001, 9700 RB Groningen, The Netherlands, Tel +31(0)50 3612357, Fax +31(0)50 3619320, Email h.van.der.vaart@ 123456long.umcg.nl
                Article
                copd-6-229
                10.2147/COPD.S17482
                3107699
                21660300
                © 2011 van der Vaart et al, publisher and licensee Dove Medical Press Ltd.

                This is an Open Access article which permits unrestricted noncommercial use, provided the original work is properly cited.

                Categories
                Original Research

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