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Biomedical subjects

A M Schols

Publications and source records attributed to A M Schols.

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↗

Increased leptin concentrations correlate with increased concentrations of inflammatory markers in morbidly obese individuals.

OBJECTIVE: To study whether an increase of plasma leptin concentrations, as observed in the case of increased body weight, is associated with an inflammatory state. SUBJECTS: Sixty-three healthy subjects with body mass index (BMI) ranging from 20 to 61 kg/m2. MEASUREMENTS: Plasma concentrations of leptin, the inflammatory parameter soluble TNF-alpha receptors (TNFR55 and TNFR75), the acute phase proteins lipopolysaccharide binding protein (LBP), serum amyloid A (SAA), alpha-acid glycoprotein (AGP), C-reactive protein (CRP), plasminogen activator inhibitor-1 (PAI-1) and the anti-inflammatory soluble Interleukin-1 decoy receptor (sIL-1RII) were measured. RESULTS: As expected, BMI correlated significantly with leptin (r=0.823, P<0.001), but also with all acute phase proteins, both soluble TNF receptors and PAI concentrations. After correction for BMI and sex, no significant correlation between leptin and the acute phase proteins was seen. Interestingly, however, leptin strongly correlated with both TNF receptors (r=0.523, P<0.001 for TNFR55 and r=0.438, P<0.001 for TNFR75). CONCLUSIONS: This study shows the development of a pro-inflammatory state with increasing body weight. The BMI independent relationship between leptin and both soluble TNF-receptors is consistent with a regulatory role for leptin in the inflammatory state in morbidly obese subjects.

Acute-Phase Proteins↗

Acute effects of different nutritional supplements on symptoms and functional capacity in patients with chronic obstructive pulmonary disease.

BACKGROUND: Use of nutritional supplements in depleted patients with chronic obstructive pulmonary disease (COPD) requires optimization between positive effects on outcome and potential acute adverse effects on metabolism and exercise performance. OBJECTIVE: The aim of this study was to investigate the acute effects of nutritional supplements on metabolism and exercise capacity in stable COPD patients. DESIGN: In part 1, the effects of 3 different energy loads (placebo, 1046 kJ, and 2092 kJ) with a normal distribution of macronutrients were investigated in 14 COPD patients. In part 2, the effects of a fat-rich compared with a carbohydrate-rich supplement (both 1046 kJ) were studied in 11 COPD patients. The study was performed in a randomized, double-blind, crossover fashion. Metabolic and ventilatory variables were measured postprandially and during a submaximal cycle endurance exercise test. RESULTS: Overall, no immediate negative effects of the supplements were found in part 1. A slight but significant postprandial increase in respiratory quotient was found after the 1046-kJ and 2092-kJ supplements compared with placebo. There was no significant difference in metabolism or exercise capacity after a fat-rich or carbohydrate-rich supplement. Surprisingly, the change in shortness of breath (postprandial compared with preprandial) was significantly greater after the fat-rich supplement. CONCLUSIONS: An energy load up to 2092 kJ had no adverse immediate effect in COPD patients compared with placebo. The subjects who consumed the fat-rich supplement experienced more shortness of breath than did the subjects who consumed the carbohydrate-rich supplement.

Aged↗

Inflammatory cytokines inhibit myogenic differentiation through activation of nuclear factor-kappaB.

Muscle wasting is often associated with chronic inflammation. Because tumor necrosis factor alpha (TNF-alpha) has been implicated as a major mediator of cachexia, its effects on C2C12 myocytes were examined. TNF-alpha activated nuclear factor-kappaB (NF-kappaB) and interfered with the expression of muscle proteins in differentiating myoblasts. Introduction of a mutant form of inhibitory protein kappaBalpha (IkappaBalpha) restored myogenic differentiation in myoblasts treated with TNF-alpha or interleukin 1beta. Conversely, activation of NF-kappaB by overexpression of IkappaB kinase was sufficient to block myogenesis, illustrating the causal link between NF-kappaB activation and inhibition of myogenic differentiation. The inhibitory effects of TNF-alpha on myogenic differentiation were reversible, indicating that the effects of the cytokine were not due to nonspecific toxicity. Treatment of differentiated myotubes with TNF-alpha did not result in a striking loss of muscle-specific proteins, which shows that myogenesis was selectively affected in the myoblast stage by TNF-alpha. An important finding was that NF-kappaB was activated to the same extent in differentiating and differentiated cells, illustrating that once myocytes have differentiated they become refractory to the effects of NF-kappaB activation. These results demonstrate that inflammatory cytokines may contribute to muscle wasting through the inhibition of myogenic differentiation via a NF-kappaB-dependent pathway.

Analysis of Variance↗

Systemic anti-inflammatory mediators in COPD: increase in soluble interleukin 1 receptor II during treatment of exacerbations.

BACKGROUND: The aim of this study was to test the hypothesis that the chronic inflammatory process present in chronic obstructive pulmonary disease (COPD) is due to a defective endogenous anti-inflammatory mechanism. METHODS: Systemic levels of the anti-inflammatory mediators soluble interleukin 1 receptor II (sIL-1RII), soluble tumour necrosis factor receptor p55 (sTNF-R55) and sTNF-R75, and of C reactive protein (CRP) and lipopolysaccharide binding protein (LBP) were analysed in 55 patients with stable COPD (median forced expiratory volume in one second (FEV(1)) 34% predicted (range 15-78)) and compared with levels in 23 control subjects. In addition, changes in these mediators were studied in 13 patients with COPD (median FEV(1) 34% predicted (range 19-51)) during the first 7 days in hospital with an exacerbation of the disease. RESULTS: Patients with stable COPD were characterised by a systemic inflammatory process indicated by an increased leucocyte count (7.2 (4.7-16.4) v 4.8 (3.5-8.3) x 10(9)/l), raised levels of CRP (11.8 (1.1-75.0) v 4.1 (0.6-75.0) microg/ml) and LBP (45.6 (8.1-200.0) v 27.9 (14.1-71.5) microg/ml), and moderate increases in both sTNF-Rs. In contrast, the sIL-1RII level did not differ between patients and controls (4.53 (2.09-7.60) v 4.63 (3.80-5.93) ng/ml). During treatment of disease exacerbations, systemic levels of both CRP (at day 3) and LBP (at day 7) were significantly reduced compared with day 1, whereas sIL-1RII levels increased. CONCLUSIONS: These data suggest an imbalance in systemic levels of pro- and anti-inflammatory mediators in patients with stable COPD. The increase in the anti-inflammatory mediator sIL-1RII during treatment of exacerbations may contribute to the clinical improvement.

Adult↗

beta-Adrenoceptor-mediated thermogenesis and lipolysis in patients with chronic obstructive pulmonary disease.

The present study investigated whether development or maintenance of a relatively increased fat mass in normal-weight patients with chronic obstructive pulmonary disease (COPD), despite periods of weight loss, may be related to impaired beta-adrenoceptor-mediated responses in lipid utilization and thermogenesis. Nine COPD patients and nine healthy controls (body mass index: 23.0 +/- 1.3 vs. 23.8 +/- 0.6 kg/m2, not significant; fat mass: 19.0 +/- 2.1 vs. 11.9 +/- 1.5 kg, P < 0.01) received consecutive 30-min infusions of 6, 12, and 24 ng x kg fat free mass(-1) x min(-1) isoproterenol. During beta-adrenergic stimulation, nonesterified fatty acid levels increased significantly less in COPD patients (P < 0.001). Respiratory exchange ratio decreased similarly in both groups, indicating a similar change in the rate of lipid to carbohydrate oxidation. Energy expenditure increased similarly in both groups during beta-adrenergic stimulation. However, because plasma isoproterenol concentrations were significantly higher in COPD patients, thermogenesis related to isoproterenol concentration was significantly reduced in this group (P < 0.05). In conclusion, beta-adrenoceptor-mediated lipolysis and thermogenesis are impaired in COPD patients. This may play a role in the development or maintenance of their relatively increased fat mass.

Adrenergic beta-Agonists↗

Effects of exercise on amino acid metabolism in patients with chronic obstructive pulmonary disease.

Depletion of fat-free mass (FFM) significantly contributes to decreased skeletal muscle weakness and impaired exercise capacity in patients with chronic obstructive pulmonary disease (COPD). FFM wasting suggests disturbances in intermediary metabolism, confirmed by data showing profound alterations in the skeletal muscle amino acid (AA) status in COPD at rest. To unravel whether there is a role for AAs in the mechanisms for skeletal muscle dysfunction in COPD, basic knowledge of AA metabolism in the muscle during exercise is important. We examined the effects of 20 min of exercise on AA metabolism in 14 patients with COPD and eight control subjects. Arterialized venous blood and a quadriceps femoris muscle biopsy were obtained before and immediately after exercise. FFM was not significantly different between the groups. In COPD, a significant reduction of most muscle AAs was present postexercise, whereas several plasma AAs were increased (p < 0.05). Consequently, sum AAs was reduced in muscle (20%; p < 0.01) and increased in plasma (16%, p < 0.05), suggesting an enhanced AA release from muscle in COPD during exercise. In the COPD group, the increase in plasma alanine and glutamine was even higher postexercise (61%, p < 0.01 and 21%, p < 0.01, respectively), suggesting enhanced nitrogen efflux. This study shows that exercise alters amino acid (intermediary) metabolism in patients with COPD and independent of the presence of FFM wasting.

Aged↗

Dose dependent increased mortality risk in COPD patients treated with oral glucocorticoids.

Systemic corticosteroids are often administered in COPD patients. The relationship between systemic glucocorticoids and mortality in patients with moderate to severe chronic obstructive pulmonary disease (COPD) was retrospectively analysed. Baseline characteristics of the patients, in stable clinical condition, were collected on admission to a pulmonary rehabilitation centre. Overall mortality was asessed at the end of follow-up. The Cox proportional hazards model was used to quantify the relationship between glucocorticoid use, distinguishing administration route (oral/inhalation) and oral dose, and overall mortality, adjusted for the influence of age, sex, smoking, lung function, resting arterial blood gases and body mass index. On multivariate analysis, oral glucocorticoid use at a (prednisone equivalent) dose of 10 mg x day(-1) without inhaled glucocorticoids, was associated with an increased risk (RR=2.34, 95% confidence interval (CI) 1.24-4.44) while 15 mg x day(-1) carried a relative risk of 4.03, CI = 1.99-8.15). A significant interaction was observed between inhaled and oral glucocorticoid use. Combined with inhaled glucocorticoids, the relative risk of oral glucocorticoid use appeared to be significantly smaller. It is concluded that in severe chronic obstructive pulmonary disease, maintenance treatment with oral glucocorticoids is associated with increased mortality in a dose-dependent manner. Since the present study design cannot exclude the possibility of bias by indication, further prospective studies are indicated using a broader patient characterization.

Administration, Oral↗

Different effects of corticosteroid-induced muscle wasting compared with undernutrition on rat diaphragm energy metabolism.

An important adverse effect of corticosteroid treatment is respiratory muscle weakness with diaphragm muscle wasting, but little is known about the underlying pathophysiological processes involved. In order to differentiate between the effects of nutrition depletion and corticosteroids on diaphragm muscle metabolism, a study was performed to investigate the effects of triamcinolone (TR) for 2 weeks and of chronic undernutrition in a pair-weight (PW) group on the structure and energy metabolism of the diaphragm in male Wistar rats compared with a free-fed (FF) group. Diaphragm mass was reduced in TR and PW rats to a similar degree, but the extent of type-IIx/b atrophy was more pronounced in TR rats than in PW rats. No myopathic features were observed after either treatment. ATP in absolute terms as well as the ATP/ADP ratio, total adenine nucleotides, the phosphocreatine (PCr) level and the ratio between PCr and creatine (PCr/Cr) were decreased in the diaphragm of both TR and PW rats. In contrast to the PW group, the total Cr pool was reduced and pyruvate and lactate levels were elevated in the diaphragm of the TR group compared with the FF group. In conclusion, the results of this study indicate that severe undernutrition causes a decrease in muscle energy status resulting in a new metabolic equilibrium, while chronic low-dose TR treatment (0.25 mg/kg per day i.m.) causes a decrease in muscle energy status together with a mismatch between glycolysis and oxidative metabolism.

Adrenal Cortex Hormones↗

Nutritional abnormalities and supplementation in chronic obstructive pulmonary disease.

Weight loss and muscle wasting commonly occur in patients with chronic obstructive pulmonary disease (COPD). A decreased dietary intake and elevated energy requirements underlie weight loss in these patients. Disturbances in intermediary metabolism caused by altered anabolic and catabolic mediators such as hormones, cytokines, and growth factors, and resulting in disproportionate muscle wasting have been described. Nutritional supplementation in combination with an anabolic stimulus (e.g. exercise) has been shown effective in improving functional capacity, health status, and mortality in most depleted patients. Nutritional or pharmacologic modulation of the catabolic response may further enhance the response in the near future.

Algorithms↗

Muscle metabolic status in patients with severe COPD with and without long-term prednisolone.

Both abnormalities in high energy phosphate metabolism and a decreased oxidative enzyme capacity have been reported in skeletal muscle of stable chronic obstructive pulmonary disease (COPD) patients. The first aim of this study was to investigate whether these findings are present in anterior tibialis muscle and whether or not they are associated. Abnormalities in mitochondrial structure and function as well as signs of myopathy have been found during corticosteroid treatment. The second aim of this study, therefore, was to investigate whether in COPD patients prolonged use of low dose prednisolone has effects on muscle energy metabolism and qualitative morphology. In a cross-sectional study 15 COPD patients (forced expiratory volume in one second (FEV1) 33+/-9 (mean+/-SD) % predicted) who were steroid-naive (CORT-) were compared with 10 healthy control subjects (HC) and with 14 COPD patients (FEV1 30+/-11 % pred), who had been using oral prednisolone for at least 1 yr (CORT+). It was found that adenosine triphosphate (ATP)/adenosine diphosphate was lower in CORT- compared to HC (5.7 versus 6.2, p=0.03). Inosine monophosphate was detected in 13 of 15 CORT- compared to 3 of 10 HC (p=0.004). However, although indications were found for an imbalance in production and utilization of ATP, comparing CORT- and HC, no differences in oxidative (citrate synthase and 3-hydroxy-acyl-coenzyme A dehydrogenase) and glycolytic (hexokinase, lactate dehydrogenase and phosphofructokinase) enzyme capacities were found. When, comparing steroid-treated and steroid-naive patient subgroups, no differences in the above mentioned parameters of muscle energy metabolism and of muscle qualitative morphology were found.

Aged↗

Tissue depletion and health related quality of life in patients with chronic obstructive pulmonary disease.

The relationship between tissue depletion and decreased exercise performance has been well established in patients with COPD. In this study we investigated the influence of the pattern of tissue depletion on health related quality of life (HRQL) and their mutual relationship with exercise capacity and dyspnoea. Patients with low body weight and/or low fat-free mass (FFM; using bioelectrical impedance) were categorized in three groups according to type of tissue depletion: loss of both FFM and fat mass (FM), and loss of FFM or FM only. Handgrip strength (HGS) was used as a functional outcome measure of tissue depletion. Exercise performance was assessed by 12 min walking distance (12MWD) and dyspnoea by visual analogue scale (VAS). HRQL was measured with the St George's Respiratory Questionnaire (SGRQ) and the Medical Psychological Questionnaire for Lung diseases (MPQL). Patients with depletion of FFM irrespective of body weight showed greater impairment in 12MWD, HGS, the 'activity' and 'impact' scores of the SGRQ and the domain 'invalidity' of the MPQL, in comparison with depleted patients with relative preservation of FFM. Exercise performance and dyspnoea were also significantly related to these subscores of HRQL. In addition, dyspnoea related significantly to the domain 'symptoms' of the SGRQ. Tissue depletion pattern remained significantly related to SGRQ-scores and the domain 'invalidity' of the MPQL when dyspnoea and walking distance were added to the model as a covariates. Tissue depletion is an important determinant of HRQL independent of exercise capacity and dyspnoea.

Aged↗

Early non-elective readmission for chronic obstructive pulmonary disease is associated with weight loss.

AIM: To identify risk factors for early nonelective readmission in patients with chronic obstructive pulmonary disease, previously admitted for an exacerbation of their disease. Clinical characteristics were analysed with special emphasis on body weight on admission and weight changes during hospitalization. METHODS: The computerized hospital database was used to select all hospital admissions in 1994 and 1995 with exacerbation of chronic obstructive pulmonary disease as main discharge diagnosis. Cases were retained if they were nonselectively readmitted within 14 days after prior discharge, and if they had no oedema. Controls were randomly selected from the discharge listing and were not readmitted within 3 months. Cases and controls were matched on several parameters including FEV(1)% predicted obtained during a stable phase of the disease. Hospital charts were reviewed for clinical parameters on admission, discharge and readmission. RESULTS: Fourteen cases were retained in the study. On admission, lung function, blood gases and parameters describing morbidity and social factors, were not different in cases and controls. The discharge procedure was adequate. During hospitalization the cases lost weight (mean+/-SD) (-1.6+/-1.9 kg, P= 0.01), while controls remained weight stable. Using a matched pairs logistic regression analysis, weight loss during hospitalization (P= 0.011) and low BMI on admission (P= 0. 046) were related to the increased risk of unplanned readmission. CONCLUSION: These findings provide further support for the concept that nutritional status is related to morbidity in COPD.

Aged↗

Skeletal muscle weakness is associated with wasting of extremity fat-free mass but not with airflow obstruction in patients with chronic obstructive pulmonary disease.

BACKGROUND: Skeletal muscle weakness is a prominent problem in many patients with chronic obstructive pulmonary disease (COPD). OBJECTIVE: The aim of the study was to determine the relation between skeletal muscle function, body composition, and lung function in COPD (emphysema and chronic bronchitis) patients and healthy volunteers. DESIGN: In 50 patients with chronic bronchitis, 49 patients with emphysema, and 28 healthy volunteers, skeletal muscle function was assessed by handgrip and linear isokinetic dynamometry. Whole-body and subregional fat-free mass (FFM) were assessed by dual-energy X-ray absorptiometry. RESULTS: Whole-body and extremity FFM were significantly lower in patients with emphysema (P < 0.001) and chronic bronchitis (P < 0.05) than in healthy volunteers, but trunk FFM was significantly lower only in patients with emphysema (P < 0.001). Extremity FFM was not significantly different between the COPD subtype groups, despite significantly lower values for whole-body and trunk FFM (P < 0.05) in patients with emphysema. Absolute skeletal muscle function (P < 0. 001) and muscle function per kilogram of whole-body FFM were significantly lower in both COPD subtype groups than in healthy volunteers (P < 0.05), but no significant difference was found between patients with chronic bronchitis and those with emphysema. Muscle function per kilogram of extremity FFM was not significantly different between the 3 groups and was not associated with forced expiratory volume in 1 s. CONCLUSION: Skeletal muscle weakness is associated with wasting of extremity FFM in COPD patients, independent of airflow obstruction and COPD subtype.

Absorptiometry, Photon↗

Skeletal muscle dysfunction in chronic obstructive pulmonary disease and chronic heart failure: underlying mechanisms and therapy perspectives.

Low exercise tolerance has a large influence on health status in chronic obstructive pulmonary disease and chronic heart failure. In addition to primary organ dysfunction, impaired skeletal muscle performance is a strong predictor of low exercise capacity. There are striking similarities between both disorders with respect to the muscular alterations underlying the impairment. However, different alterations occur in different muscle types. Histologic and metabolic data show that peripheral muscles undergo a shift from oxidative to glycolytic energy metabolism, whereas the opposite is observed in the diaphragm. These findings are in line with the notion that peripheral and diaphragm muscle are limited mainly by endurance and strength capacity, respectively. In both diseases, muscular impairment is multifactorially determined; hypoxia, oxidative stress, disuse, medication, nutritional depletion, and systemic inflammation may contribute to the observed muscle abnormalities and each factor has its own potential for innovative treatment approaches.

Adrenal Cortex Hormones↗

Factors contributing to alterations in skeletal muscle and plasma amino acid profiles in patients with chronic obstructive pulmonary disease.

BACKGROUND: There is increasing evidence of abnormal protein metabolism in patients with chronic obstructive pulmonary disease (COPD), as reflected by lower plasma branched-chain amino acid (BCAA) concentrations and different muscle amino acid (AA) patterns than in age-matched control subjects. OBJECTIVE: We examined whether the low plasma BCAA concentrations in COPD reflect an imbalance between anabolic and catabolic processes as evidenced by a low fat-free mass (FFM) and alterations in the anabolic hormone insulin and whether discrepancies in muscle AA concentrations between studies are related to different patient characteristics. DESIGN: AA profiles in arterial plasma and quadriceps femoris muscle and insulin concentrations in venous plasma were analyzed in 28 postabsorptive COPD patients (14 with and 14 without macroscopic emphysema) and in 28 control subjects. FFM was measured by dual-energy X-ray absorptiometry. RESULTS: The lower sum of plasma BCAAs in the COPD group than in the control subjects was the result of a lower leucine concentration (P: < 0.001); no significant difference in valine and isoleucine was found between the groups. In the COPD group, the lower leucine concentrations were associated with low FFM (P: < 0.01). Compared with the control group, the muscle-to-plasma leucine gradient was higher in the COPD group (P: < 0.001) and was associated with a higher insulin concentration (P: < 0.01). Several muscle AA concentrations were higher or tended to be higher in the group without emphysema than in the control group, whereas nearly all AA concentrations were lower in the group with emphysema. CONCLUSIONS: Leucine metabolism is altered in COPD patients and is associated with low FFM and high insulin concentrations. There were striking differences in the skeletal muscle AA profile between the COPD subtypes.

Absorptiometry, Photon↗

Nutrition in chronic obstructive pulmonary disease.

Weight loss is a frequently occurring complication in patients with chronic obstructive pulmonary disease (COPD) and is a determining factor of functional capacity, health status, and mortality. Weight loss in COPD is a consequence of increased energy requirements unbalanced by dietary intake. Both metabolic and mechanical inefficiency contribute to the elevated energy expenditure. A disbalance between protein synthesis and protein breakdown may cause a disproportionate depletion of fat-free mass in some patients. Nutritional support is indicated for depleted patients with COPD because it provides not only supportive care, but direct intervention through improvement in respiratory and peripheral skeletal muscle function and in exercise performance. A combination of oral nutritional supplements and exercise or anabolic stimulus appears to be the best treatment approach to obtaining significant functional improvement. Patients responding to this treatment even demonstrated a decreased mortality. Poor response was related to the effects of systemic inflammation on dietary intake and catabolism. The effectiveness of anticatabolic modulation requires further investigation.

Anabolic Agents↗

Altered glutamate metabolism is associated with reduced muscle glutathione levels in patients with emphysema.

Chronic obstructive pulmonary disease (COPD) is often characterized by an impaired skeletal muscle energy metabolism, which is at least partly related to chronic hypoxia and a reduced diffusing capacity. We have found that muscle glutamate (Glu), which is negatively influenced by these conditions, was reduced in patients with severe COPD. The aim of this study was to investigate whether the reduced intracellular Glu level in patients with emphysema is associated with an increased muscle glycolytic metabolism. Since Glu is an important substrate in the synthesis of glutamine (Gln) and glutathione (GSH), the influence of Glu status on muscle GSH and Gln was also examined. In 13 patients with emphysema and 25 control patients, arterial blood and biopsies from the vastus lateralis muscle were obtained. Expressed as a percentage of the control values, the patients with emphysema had reduced values for muscle Glu (64 +/- 12%; p < 0.001), GSH (76 +/- 23%; p < 0.01), and Gln (93 +/- 5%; p < 0.01), and higher values for lactate (p < 0.01) and pyruvate (p < 0.05). No differences were found in plasma values. Muscle Glu was highly associated with GSH (R(2) = 0.61; p < 0.001), but not with Gln. This study illustrates that reduced Glu levels in skeletal muscle of patients with emphysema are possibly related to an enhanced glycolytic activity and associated with decreased GSH levels.

Biomarkers↗