Exercise physiology in COPD (original) (raw)
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Metabolic derangements in COPD muscle dysfunction
Journal of Applied Physiology, 2013
Puente-Maestu L, Lázaro A, Humanes B. Metabolic derangements in COPD muscle dysfunction. Mitochondrial muscle alterations are common in patients with chronic obstructive pulmonary disease (COPD) and manifest mainly as decreased oxidative capacity and excessive production of reactive oxygen species (ROS). The significant loss of oxidative capacity observed in the quadriceps of COPD patients is mainly due to reduced mitochondrial content in the fibers, a finding consistent with the characteristic loss of type I fibers observed in that muscle. Decreased oxidative capacity does not directly limit maximum performance; however, it is associated with increased lactate production at lower exercise intensity and reduced endurance. Since type I fiber atrophy does not occur in respiratory muscles, the loss of such fibers in the quadriceps could be to the result of disuse. In contrast, excessive production of ROS and oxidative stress are observed in both the respiratory muscles and the quadriceps of COPD patients. The causes of increased ROS production are not clear, and a number of different mechanisms can play a role. Several mitochondrial alterations in the quadriceps of COPD patients are similar to those observed in diabetic patients, thus suggesting a role for muscle alterations in this comorbidity. Amino acid metabolism is also altered. Expression of peroxisome proliferator-activated receptor-␥ coactivator-1␣ mRNA is low in the quadriceps of COPD patients, which could also be a consequence of type I fiber loss; nevertheless, its response to exercise is not altered. Patterns of muscle cytochrome oxidase gene activation after training differ between COPD patients and healthy subjects, and the profile is consistent with hypoxic stress, even in nonhypoxic patients. electron transport chain; bioenergetics; mitochondria; permeability transition pore; reactive oxygen species; oxidative enzymes; magnetic resonance spectroscopy THE MITOCHONDRION IS A membrane-enclosed organelle found in most eukaryotic cells (37). It ranges in diameter from 0.5 to 1.0 m. Mitochondria generate most of the cell's supply of adenosine triphosphate (ATP), the source of chemical energy (62), and are involved in a range of other processes, such as signaling, cellular differentiation, apoptosis, and control of the cell cycle and cell growth (62). Mitochondrial dysfunction has been implicated in a number of human diseases, including chronic obstructive pulmonary disease (COPD) .
Acta Physiologica, 2012
To study the effects of physical training at mild intensities on skeletal muscle energy metabolism in eight patients with chronic obstructive pulmonary disease (COPD) and eight paired healthy sedentary subjects. Methods: Energy metabolism of patients and controls vastus lateralis muscle was studied before and after 3 months of cycling training at mild exercises intensities. Results: The total amount of work accomplished was about 4059 AE 336 kJ in patients with COPD and 7531 AE 1693 kJ in control subjects. This work corresponds to a mechanical power set at 65.2 AE 7.5% of the maximum power for patients with COPD and 52 AE 3.3% of the maximum power in control group. Despite this low level of exercise intensities, we observed an improvement in mitochondrial oxidative phosphorylation through the creatine kinase system revealed by the increased apparent K m for ADP (from 105.5 AE 16.1 to 176.9 AE 26.5 lm, P < 0.05 in the COPD group and from 126.9 AE 16.8 to 177.7 AE 17.0, P > 0.05 in the control group). Meanwhile, maximal mechanical and metabolic power increased significantly from 83.1 AE 7.1 to 91.3 AE 7.4 Watts (P < 0.05) and from 16 AE 0.8 to 18.7 AE 0.98 mL O 2 kg)1 min)1 (P < 0.05) only in the COPD group. Conclusion: This study shows that physical training at mild intensity is able to induce comparable changes in skeletal muscles oxidative energy metabolism in patients with COPD and sedentary healthy subjects, but different changes of maximal mechanical and metabolic power.
Peripheral muscle weakness contributes to exercise limitation in COPD
American Journal of Respiratory and Critical Care Medicine, 1996
Recently, it was suggested that fatigue of peripheral muscles could contribute to exercise limitation in patients with chronic obstructive pulmonary disease (COPO). In order to quantify the role of peripheral muscle force, we restudied potential determinants of exercise capacity (6-min walking distance [6 MWO] and maximal oxygen consumption [Vo2max]) in 41 consecutive COPO patients (FEV1, 43 ± 19% of predicted, TLco, 56 ± 25% of predicted) admitted to our pulmonary rehabilitation program.
Journal of Applied Physiology, 2013
Louvaris Z, Kortianou EA, Spetsioti S, Vasilopoulou M, Nasis I, Asimakos A, Zakynthinos S, Vogiatzis I. Intensity of daily physical activity is associated with central hemodynamic and leg muscle oxygen availability in COPD. In chronic obstructive pulmonary disease (COPD), daily physical activity is reported to be adversely associated with the magnitude of exerciseinduced dynamic hyperinflation and peripheral muscle weakness. There is limited evidence whether central hemodynamic, oxygen transport, and peripheral muscle oxygenation capacities also contribute to reduced daily physical activity. Nineteen patients with COPD (FEV1, 48 Ϯ 14% predicted) underwent a treadmill walking test at a speed corresponding to the individual patient's mean walking intensity, captured by a triaxial accelerometer during a preceding 7-day period. During the indoor treadmill test, the individual patient mean walking intensity (range, 1.5 to 2.3 m/s 2 ) was significantly correlated with changes from baseline in cardiac output recorded by impedance cardiography (range, 1.2 to 4.2 L/min; r ϭ 0.73), systemic vascular conductance (range, 7.9 to 33.7 ml·min Ϫ1 ·mmHg Ϫ1 ; r ϭ 0.77), systemic oxygen delivery estimated from cardiac output and arterial pulse-oxymetry saturation (range, 0.15 to 0.99 L/min; r ϭ 0.70), arterio-venous oxygen content difference calculated from oxygen uptake and cardiac output (range, 3.7 to 11.8 mlO 2/100 ml; r ϭ Ϫ0.73), and quadriceps muscle fractional oxygen saturation assessed by near-infrared spectrometry (range, Ϫ6 to 23%; r ϭ 0.77). In addition, mean walking intensity significantly correlated with the quadriceps muscle force adjusted for body weight (range, 0.28 to 0.60; r ϭ 0.74) and the ratio of minute ventilation over maximal voluntary ventilation (range, 38 to 89%, r ϭ Ϫ0.58). In COPD, in addition to ventilatory limitations and peripheral muscle weakness, intensity of daily physical activity is associated with both central hemodynamic and peripheral muscle oxygenation capacities regulating the adequacy of matching peripheral muscle oxygen availability by systemic oxygen transport. activity monitoring; chronic obstructive pulmonary disease; nearinfrared spectroscopy; quadriceps muscle oxygenation; walking intensity IN PATIENTS WITH CHRONIC OBSTRUCTIVE pulmonary disease (COPD), daily physical activity is reduced compared with that in healthy age-matched individuals (6). Furthermore, it is well documented that reduced levels of physical activity in patients with COPD are associated with a faster rate of disease progression, * Z. Louvaris and E. A. Kortianou contributed equally to this work.
Journal of Applied Physiology, 2008
dynamics COPD: relationship to central cardiovascular onset of heavy-intensity exercise in patients with Kinetics of muscle deoxygenation are accelerated at the You might find this additional info useful... 53 articles, 34 of which can be accessed free at: This article cites /content/104/5/1341.full.html#ref-list-1 9 other HighWire hosted articles, the first 5 are: This article has been cited by [PDF] [Full Text] , July , 2010; 65 (7): 573-575. Thorax Peter Calverley Better lungs for better legs: novel bronchodilator effects in COPD [PDF] [Full Text] [Abstract] , August , 2010; 109 (2): 388-395. J Appl Physiol Charis Roussos, Spyros Zakynthinos and Ioannis Vogiatzis Dimitris Athanasopoulos, Zafeiris Louvaris, Evgenia Cherouveim, Vasilis Andrianopoulos, healthy humans Expiratory muscle loading increases intercostal muscle blood flow during leg exercise in [PDF] [Full Text] [Abstract] , October , 2012; 57 (10): 1602-1610. Respir Care During Exercise in Subjects With COPD: A Preliminary Study The Relationship Between Skeletal Muscle Oxygenation and Systemic Oxygen Uptake [PDF] [Full Text] [Abstract] , September 15, 2013; 115 (6): 794-802. oxygen availability in COPD Intensity of daily physical activity is associated with central hemodynamic and leg muscle [PDF] [Full Text] [Abstract] , January 15, 2015; 308 (2): R105-R111. Am J Physiol Regul Integr Comp Physiol
Metabolic and hemodynamic responses of lower limb during exercise in patients with COPD
Journal of applied physiology (Bethesda, Md. : 1985), 1998
Premature lactic acidosis during exercise in patients with chronic obstructive pulmonary disease (COPD) may play a role in exercise intolerance. In this study, we evaluated whether the early exercise-induced lactic acidosis in these individuals can be explained by changes in peripheral O2 delivery (O2). Measurements of leg blood flow by thermodilution and of arterial and femoral venous blood gases, pH, and lactate were obtained during a standard incremental exercise test to capacity in eight patients with severe COPD and in eight age-matched controls. No significant difference was found between the two groups in leg blood flow at rest or during exercise at the same power outputs. Blood lactate concentrations and lactate release from the lower limb were greater in COPD patients at all submaximal exercise levels (all P < 0.05). Leg D02 at a given power output was not significantly different between the two groups, and no significant correlation was found between this parameter and ...
Exercise-induced quadriceps oxidative stress and peripheral muscle dysfunction in COPD patients
activities is often quoted as being one of the main reasons why myopathy associated with chronic obstructive pulmonary disease patients with COPD have peripheral myopathy (5). Recent (COPD). This study was designed to look at whether local exercise studies, however, have suggested that other factors such as induces muscle oxidative stress and whether this oxidative stress exposure to systemic corticosteroids (6), malnutrition , may be associated with the reduced muscle endurance in patients hypoxia (8), and apoptosis may also contribute to the with COPD. Quadriceps endurance was measured in 12 patients alteration in peripheral muscle function. Oxidative stress, with COPD (FEV 1 ϭ 0.96 Ϯ 0.14 SEM) and 10 healthy sedentary resulting from an inability of the antioxidant systems to cope subjects by repeated knee extensions of the dominant leg. Biopsies with elevated oxidant production, is also believed to play of the vastus lateralis muscle were obtained before and 48 hours an important role in altering peripheral muscle function in after exercise. Muscle oxidative stress was measured by lipid peroxipatients with COPD (10, 11). Indeed, our group has recently dation and oxidized proteins. Muscle antioxidant was evaluated by documented evidences of lipid peroxidation, a marker of peroxidase glutathion activity. Quadriceps endurance was signifioxidative stress, in the plasma of patients with COPD but cantly reduced in patients with COPD when compared with the not in healthy subjects after local quadriceps exercise perhealthy control subjects (p Ͻ 0.01). Forty-eight hours postexercise, formed to exhaustion (2). Although we hypothesized that only patients with COPD had a significant increase in muscle lipid the contracting quadriceps was the source of this oxidative peroxidation (p Ͻ 0.05) and oxidized proteins (p Ͻ 0.05), whereas stress, it was not confirmed because no muscle biopsies were increased peroxidase glutathion activity was only observed in condone. This is an important question because muscle oxidative trol subjects (p Ͻ 0.05). Both increases in muscle lipid peroxidation stress causes noticeable myocyte damage (12, 13) and may and oxidized proteins were significantly and inversely correlated potentially be detrimental to muscle function, thus contributwith quadriceps endurance capacity in COPD (p Ͻ 0.05). In suming to muscle fatigue (14) and reduced endurance (13). On mary, local exercise induced muscle oxidative stress in patients the basis of this observation, we hypothesized that muscle with COPD, whereas it failed to raise antioxidant activity. In these oxidative stress could be associated with reduced peripheral individuals, muscle oxidative stress was associated with a reduced muscle endurance in patients with COPD. quadriceps endurance.
Exercise capacity and quadriceps muscle metabolism following training in subjects with COPD
Respiratory Medicine, 2006
The aim of the study was to determine whether 16 sessions of exercise training, completed twice weekly, alters exercise capacity, quadriceps muscle metabolism, cross-sectional area (CSA) and strength in subjects with chronic obstructive pulmonary disease (COPD). We studied (a) 10 COPD subjects (mean age7SEM ¼ 7172 years; FEV 1 ¼ 0.9970.1 L) before and after 16 sessions of exercise training, and (b) 10 healthy subjects (age ¼ 6873 years). The COPD subjects underwent an incremental peak exercise test using a cycle ergometer and a 6-min walk test: both improved following exercise training (Po0:05). Magnetic resonance spectroscopy measurements, in quadriceps muscle, of post-exercise phosphocreatinine (PCr) recovery kinetics were used to assess mitochondrial function in vivo: in the COPD subjects pre-training this was 1978% lower than in healthy subjects (P ¼ 0:03), but a 38712% increase was seen in the COPD subjects following training (P ¼ 0:003). Magnetic resonance imaging was used to assess quadriceps CSA: after training in the COPD subjects this showed a 772% increase (P ¼ 0:03). Quadriceps strength, measured by the best of five maximum voluntary contractions, also showed a 32711% increase in the COPD subjects (P ¼ 0:007). Sixteen sessions of exercise ARTICLE IN PRESS (Z.J. McKeough).
Ventilatory and metabolic changes as a result of exercise training in COPD patients
Chest, 1992
Patients with COPD feel better and are able to sustain a given level of activity longer after a program of exercise training, but the underlying physiologic mechanisms have not been completely elucidated. Since the physical performance of patients with COPD is limited mainly by pathophysiologic derangements of the ventilatory system, the exercise performance can be ameliorated by increasing the level of ventilation that they can sustain or by reducing the ventilatory requirement for a given level of activity. Almost all studies have yielded negative results in patients with COPD in terms of exercise training having the ability to improve VEmax. The only way to reduce the ventilatory requirement is to reduce CO, output. Lower levels of lactate result in less nonmetabolic CO, produced by bicarbonate buffering and this is the likely mechanism responsible for a lower ventilatory requirement for work rates above the pretraining anaerobic threshold. We specifically wished to determine whether a program of intensity, frequency, and duration known capable of producing a physiologic training effect in healthy subjects would do so in patients with COPD. Further, we sought to determine whether exercise training at a work rate associated with lactic acidosis is more effective in inducing a training effect in patients with COPD than a work rate not associated with lactic acidosis. Nineteen patients with COPD were selected and performed an incremental test as well as 2 square wave tests at a low and a high work rate. Identical tests were performed after an 8-week program of cycle ergometer training either for 45 mm/day at a high work rate or for a proportionally longer time at a low work rate. For the high work rate training group, identical work rates engendered less lactate (4.5 vs 7.2 mEqfL) and less VE (48 vs 55 L/min) after training; the low work rate training group had significantly less lactate and VE decrease (p<O.Ol). Further, in the first group, there was an increase in exercise tolerance averaging 71% in the high constant work rate test. There was a good correlation (r 0.73, p<O.005) between the decrease in blood lactate and the decrease in ventilation. The major findings of this study are that patients with COPD who experience lactic acidosis during exercise can achieve physiologic training responses from a program of endurance training and that training work rates engendering high levels of blood lactate are more effective than work rates eliciting low lactate levels.