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Biomedical subjects

P LeBlanc

Publications and source records attributed to P LeBlanc.

At least 19 recordsLinked to original sources
PubMed2005

Hypoxaemia enhances peripheral muscle oxidative stress in chronic obstructive pulmonary disease.

BACKGROUND: Because oxidative stress affects muscle function, the underlying mechanism to explain exercise induced peripheral muscle oxidative stress in patients with chronic obstructive pulmonary disease (COPD) is clinically relevant. This study investigated whether chronic hypoxaemia in COPD worsens peripheral muscle oxidative stress and whether an abnormal muscle inflammatory process is associated with it. METHODS: Nine chronically hypoxaemic and nine non-hypoxaemic patients performed repeated knee extensions until exhaustion. Biopsy specimens were taken from the vastus lateralis muscle before and 48 hours after exercise. Muscle oxidative stress was evaluated by lipid peroxidation (lipofuscin and thiobarbituric acid reactive substances (TBARs)) and oxidised proteins. Inflammation was evaluated by quantifying muscle neutrophil and tumour necrosis factor (TNF)-alpha levels. RESULTS: When both groups were taken together, arterial oxygen pressure was positively correlated with quadriceps endurance time (n = 18, r = 0.57; p < 0.05). At rest, quadriceps lipofuscin inclusions were significantly greater in hypoxaemic patients than in non-hypoxaemic patients (2.9 (0.2) v 2.0 (0.3) inclusions/fibre; p < 0.05). Exercise induced a greater increase in muscle TBARs and oxidised proteins in hypoxaemic patients than in non-hypoxaemic patients (40.6 (9.1)% v 10.1 (5.8)% and 51.2 (11.9)% v 3.7 (12.2)%, respectively, both p = 0.01). Neutrophil levels were significantly higher in hypoxaemic patients than in non-hypoxaemic patients (53.1 (11.6) v 21.5 (11.2) counts per fibre x 10(-3); p < 0.05). Exercise did not alter muscle neutrophil levels in either group. Muscle TNF-alpha was not detected at baseline or after exercise. CONCLUSION: Chronic hypoxaemia was associated with lower quadriceps endurance time and worsened muscle oxidative stress at rest and after exercise. Increased muscle neutrophil levels could be a source of the increased baseline oxidative damage. The involvement of a muscle inflammatory process in the exercise induced oxidative stress of patients with COPD remains to be shown.

Aged↗
PubMed2004

Peripheral muscle endurance and the oxidative profile of the quadriceps in patients with COPD.

BACKGROUND: Based on previously reported changes in muscle metabolism that could increase susceptibility to fatigue, we speculated that patients with chronic obstructive pulmonary disease (COPD) have reduced quadriceps endurance and that this will be correlated with the proportion of type I muscle fibres and with the activity of oxidative enzymes. METHODS: The endurance of the quadriceps was evaluated during an isometric contraction in 29 patients with COPD (mean (SE) age 65 (1) years; forced expiratory volume in 1 second 37 (3)% predicted) and 18 healthy subjects of similar age. The electrical activity of the quadriceps was recorded during muscle contraction as an objective index of fatigue. The time at which the isometric contraction at 60% of maximal voluntary capacity could no longer be sustained was used to define time to fatigue (Tf). Needle biopsies of the quadriceps were performed in 16 subjects in both groups to evaluate possible relationships between Tf and markers of muscle oxidative metabolism (type I fibre proportion and citrate synthase activity). RESULTS: Tf was lower in patients with COPD than in controls (42 (3) v 80 (7) seconds; mean difference 38 seconds (95% CI 25 to 50), p<0.001). Subjects in both groups had evidence of electrical muscle fatigue at the end of the endurance test. In both groups significant correlations were found between Tf and the proportion of type I fibres and citrate synthase activity. CONCLUSION: Isometric endurance of the quadriceps muscle is reduced in patients with COPD and the muscle oxidative profile is significantly correlated with muscle endurance.

Aged↗
PubMed2004

The influence of lung volume reduction surgery on exercise in patients with COPD.

Although the influence of lung volume reduction surgery (LVRS) on incremental- and constant-power exercise is important in the evaluation of this procedure for patients with chronic obstructive pulmonary disease (COPD), it is rarely reported even in large randomised controlled trials. This report describes 39 patients with severe COPD ((mean +/- SE) forced expiratory volume in one second 32 +/- 2% pred, functional residual capacity 195 +/- 6% pred) who participated in a randomised controlled trial of LVRS and who completed incremental exercise tests at 6 months as well as endurance tests (constant power of 25 +/- 1 W) at 3, 9 and 12 months. Peak oxygen uptake (V'O2,pk) was similar between the treatment (n = 19) and control groups (n = 20) at baseline. After LVRS, the treatment group had a significantly greater V'O2,pk (mean difference (95% CI) 1.28 (0.07-2.50) mL x kg x min(-1)) and power (13 (6-20) W). The treatment group achieved a significantly greater minute ventilation (7.1 (2.9-11.3) L x min(-1)) with a greater tidal volume (0.16 (0.04-0.28) L). Baseline endurance was similar between groups. After surgery, there were significant between-group differences in endurance time, which were maintained at 12 months (7.3 (3.9-10.8) min). Lung volume reduction surgery is associated with an increase in exercise capacity and endurance, as compared with conventional medical treatment.

Aged↗
PubMed2003

Influence of lung volume reduction surgery (LVRS) on health related quality of life in patients with chronic obstructive pulmonary disease.

BACKGROUND: The clinical value of LVRS has been questioned in the absence of trials comparing it with pulmonary rehabilitation, the prevailing standard of care in COPD. Patients with heterogeneous emphysema are more likely to benefit from volume reduction than those with homogeneous disease. Disease specific quality of life is a responsive interpretable outcome that enables health professionals to identify the magnitude of the effect of an intervention across several domains. METHODS: Non-smoking patients aged <75 years with severe COPD (FEV(1) <40% predicted, FEV(1)/FVC <0.7), hyperinflation, and evidence of heterogeneity were randomised to surgical or control groups after pulmonary rehabilitation and monitored at 3 month intervals for 12 months with no crossover between the groups. The primary outcome was disease specific quality of life as measured by the Chronic Respiratory Questionnaire (CRQ). Treatment failure was defined as death or functional decline (fall of 1 unit in any two domains of the CRQ). Secondary outcomes included pulmonary function and exercise capacity. RESULTS: LVRS resulted in significant between group differences in each domain of the CRQ at 12 months (change of 0.5 represents a small but important difference): dyspnoea 1.9 (95% confidence interval (CI) 1.3 to 2.6; p<0.0001); emotional function 1.5 (95% CI 0.9 to 2.1; p<0.0001); fatigue 2.0 (95% CI 1.4 to 2.6; p<0.0001); mastery 1.8 (95% CI 1.2 to 2.5; p<0.0001). In the control group one of 27 patients died and 16 experienced functional decline over 12 months. In the surgical group four of 28 patients died and three experienced functional decline (hazard ratio = 3.1 (95% CI 1.3 to 7.6; p=0.01). Between group improvements (p<0.05) in lung volumes, flow rates, and exercise were sustained at 12 months (RV -47% predicted (95% CI -71 to -23; p=0.0002); FEV(1) 0.3 l (95% CI 0.1 to 0. 5; p=0.0003); submaximal exercise 7.3 min (95% CI 3.9 to 10.8; p<0.0001); 6 minute walk 66 metres (95% CI 32 to 101; p=0.0002). CONCLUSIONS: In COPD patients with heterogeneous emphysema, LVRS resulted in important benefits in disease specific quality of life compared with medical management, which were sustained at 12 months after treatment.

Female↗
PubMed2003

In vitro and in vivo contractile properties of the vastus lateralis muscle in males with COPD.

Peripheral muscle weakness is common in chronic obstructive pulmonary disease (COPD) but it is still under debate whether weakness is due to atrophy or contractile dysfunction. In vitro and in vivo contractile properties of the vastus lateralis muscle were studied in 16 patients with stable COPD (forced expiratory volume in one second 39 +/- 16% of predicted, age 67 +/- 4 yrs (mean +/- sD)) and nine sedentary control subjects. Isometric knee extensor strength was measured while mid-thigh muscle cross-sectional area (MTMCSA) was obtained using computed tomography. Muscle strips from the vastus lateralis obtained through open biopsy were rapidly suspended in an oxygenated Krebs-Ringer solution that was maintained at 35 degrees C with a pH of 7.40 to study their contractile properties. The isometric knee extensors strength/MTMCSA ratio was 0.50 +/- 0.08 versus 0.58 +/- 0.06 kg x cm(-2) for COPD and control subjects, respectively. The muscle bundle cross-sectional area (CSA) was 4.6 +/- 2.1 and 4.4 +/- 3.1 mm(-2), the length at which active tension was maximum was 15 +/- 4 and 15 +/- 3 mm, and maximal isometric peak forces normalised for CSA were 4.3 +/- 2.7 and 4.8 +/- 2.6 N x cm(-2) for COPD and control subjects, respectively. The force/frequency relationship tended to be shifted to the right in patients with COPD, meaning that a higher stimulation frequency was necessary to produce the same relative force. Patients with COPD had a lower proportion of type I fibre than controls (26 +/- 12% versus 39 +/- 11%) with reciprocal significant increase in type IIb fibre proportion (20+/-16% versus 8 +/- 4%). The proportion of type IIa fibres was similar between the two groups. These results suggest that the contractile properties of the vastus lateralis are preserved in patients with chronic obstructive pulmonary disease. Therefore, the reduction in the quadriceps strength in patients with chronic obstructive pulmonary disease cannot be explained on the basis of an alteration of the contractile apparatus.

Aged↗
PubMed2001

Limitation of lower limb VO(2) during cycling exercise in COPD patients.

Patients with chronic obstructive pulmonary disease (COPD) usually stop exercise before reaching physiological limits in terms of O(2) delivery and extraction. A plateau in lower limb O(2) uptake (VO(2)) and blood flow occurs despite progression of the imposed workload during cycling in some patients with COPD, suggesting that maximal capacity to transport O(2) had been reached and that it had been extracted in the peripheral exercising muscles. This study addresses this observation. Symptom-limited incremental cycle exercise was performed by 14 men [62 +/- 11 (SD) yr] with severe COPD (forced expiratory volume in 1 s = 35 +/- 7% of predicted value). Leg blood flow was measured at each exercise step with a thermodilution catheter inserted in the femoral vein. This value was multiplied by two to account for both working legs (Q(LEGS)). Arterial and femoral venous blood was sampled at each exercise step to measure blood gases. Leg O(2) consumption (VO(2LEGS)) was calculated according to the Fick equation. Total body VO(2) (VO(2TOT)) was measured from expired gas analysis, and tidal volume (VT) and minute ventilation (VE) were derived from the flow signal. In eight patients, VO(2LEGS) kept increasing in parallel with VO(2TOT) as external work rate was increasing. In six subjects, a plateau in VO(2LEGS) and Q(LEGS) occurred during exercise (increment of <3% between 2 consecutive increasing workloads) despite the increase in workload and VO(2TOT) [corresponding mean was 110 +/- 38 ml (11 +/- 4%)]. These six patients also exhibited a plateau in O(2) extraction during exercise. Peak exercise work rate was higher in the eight patients without a plateau than in the six with a plateau (51 +/- 10 vs. 40 +/- 13 W, P = 0.043). VT, VE, and dyspnea were significantly greater at submaximal exercise in patients of the plateau group compared with those of the nonplateau group. These results show that, in some patients with COPD, blood flow directed to peripheral muscles and O(2) extraction during exercise may be limited. We speculate that redistribution of cardiac output and O(2) from the lower limb exercising muscles to the ventilatory muscles is a possible mechanism.

Aged↗
PubMed2000

Peripheral muscle dysfunction in chronic obstructive pulmonary disease.

Peripheral muscle dysfunction is a common systemic complication of moderate to severe COPD and may contribute to disability, handicap, and premature mortality. In contrast to the lung impairment, which is largely irreversible, peripheral muscle dysfunction is potentially remediable with exercise training, nutritional intervention, oxygen, and anabolic drugs. Therapeutic success is often incomplete, however, and a better understanding of the mechanisms involved in the development of peripheral muscle dysfunction in COPD is needed to help develop innovative and more effective therapeutic strategies.

Aging↗
PubMed2000

Influence of work rate incremental rate on the exercise responses in patients with COPD.

PURPOSE: The peak work rate (Wpeak) measured during a progressive stepwise exercise test is commonly used to select the target training intensity for an exercise training program. In healthy subjects, a greater Wpeak is achieved when a faster rate of increase in work rate is used, whereas VO2 peak is independent of the rate of increase in work rate. This effect might be even more pronounced in chronic obstructive pulmonary disease (COPD) patients, in whom the VO2 kinetics during exercise are slower compared with healthy subjects. METHODS: To investigate this, we studied 10 COPD patients (9 M/1 F, age: 65+/-5 yr [mean +/- SD], FEV1: 33+/-8%). They underwent, on separate days, three stepwise exercise tests on an ergocycle. For each test, increments of 5, 10, or 20 W x min(-1) were used in random order; the investigator was blinded as to which increment was used. VO2, VCO2, heart rate (HR), minute ventilation (VE), breathlessness and leg fatigue at rest, at each work rate, and at maximal capacity were obtained. RESULTS: Wpeak averaged 40+/-13, 53+/-14, and 66+/-19 W for the 5-, 10-, and 20-W protocol, respectively (P < 0.001), whereas VO2 peak was comparable at 0.96+/-0.16, 1.02+/-0.18, and 1.03+/-0.20 L x min(-1). As the rate of increase in work rate became faster, the VO2/work rate relationship shifted to the right. This is exemplified by the VO2 at 40 W, which averaged 0.98+/-0.06, 0.90+/-0.09, and 0.83+/-0.10 L x min(-1) for the 5-, 10-, and 20-W protocol, respectively (P < 0.05). Similar observations were made for the relationship between HR, VE, and symptom scores, and work rate. There was no significant differences in peak values for HR and VE, and symptoms scores. CONCLUSIONS: We conclude that the work rate incremental rate influences the Wpeak achieved, whereas the peak values for VO2, HR, VE, and symptom scores remain comparable. These findings have practical implications for the exercise evaluation of patients with COPD.

Adaptation, Physiological↗
PubMed2000

Oxidative enzyme activities of the vastus lateralis muscle and the functional status in patients with COPD.

BACKGROUND: Enzymatic and histochemical abnormalities of the peripheral muscle may play a role in exercise intolerance in patients with chronic obstructive pulmonary disease (COPD). A study was undertaken to measure the mitochondrial enzyme activity of the vastus lateralis muscle in patients with COPD and to evaluate the relationship between enzyme activities and functional status. METHODS: Fifty seven patients with COPD of mean (SD) age 66 (7) years with forced expiratory volume in one second (FEV(1)) 39 (15)% predicted and peak oxygen uptake (VO(2)) of 14 (4) ml/min/kg and 15 normal subjects of similar age were included in the study. Each subject performed a stepwise exercise test up to maximal capacity during which five-breath averages of VO(2) were measured. Muscle specimens were obtained by percutaneous needle biopsy of the vastus lateralis muscle and the activity of two mitochondrial enzymes (citrate synthase (CS) and 3-hydroxyacyl CoA dehydrogenase (HADH)) was measured. The functional status of the patients was classified according to peak VO(2). RESULTS: CS and HADH activities were markedly reduced in patients with COPD compared with normal subjects (22.3 (2.7) versus 29.5 (7.3) micromol/min/g muscle (p<0.0001) and 5. 1 (2.0) versus 6.7 (1.9) micromol/min/g muscle (p<0.005), respectively). The activity of CS decreased progressively with the deterioration in the functional status while that of HADH was not related to functional status. Using a stepwise regression analysis, percentage predicted functional residual capacity (FRC), the activity of CS, oxygen desaturation during exercise, age, and inspiratory capacity (% pred) were found to be significant determinants of peak VO(2). The regression model explained 59% of the variance in peak VO(2) (p<0.0001). CONCLUSIONS: The oxidative capacity of the vastus lateralis muscle is reduced in patients with moderate to severe COPD compared with normal subjects of similar age. In these individuals the activity of CS correlated significantly with peak exercise capacity and independently of lung function impairment.

3-Hydroxyacyl CoA Dehydrogenases↗
PubMed1999

Altered expression of myosin heavy chain in the vastus lateralis muscle in patients with COPD.

This study was designed to further characterize peripheral skeletal muscle alterations in patients with chronic obstructive pulmonary disease (COPD) and to evaluate the possible relationship between myosin heavy chain (MyoHC) isoform expression and exercise tolerance in these individuals. MyoHC composition from biopsy of the vastus lateralis muscle was examined in 12 COPD patients (forced expiratory volume in one second (FEV1)=31+/-9% predicted, peak oxygen consumption (V'O2)=15+/-4 mL x kg(-1) x min(-1)) and 10 age-matched normal male subjects (peak V'O2=20+/-5 mL x kg(-1) x min(-1)). The proportion of MyoHC type I was smaller in COPD than in normals (27+/-17% versus 41+/-9%, p<0.05) with an increase in MyoHC type IIa (51+/-15% versus 39+/-9%, p<0.05) and the proportion of MyoHC type IIx being comparable between both groups. A significant relationship was found between peak V'Oo2 mL x kg(-1) x min(-1) and FEV1 % pred (r=0.91, p<0.0001) and the percentage of MyoHC type I (r=0.61, p=0.016). In stepwise multiple regression, only FEV1 % pred was found to be a significant determinant of peak V'O2 (p<0.0001). This variable explained 83% of the total variance of peak V'O2. In summary, this study showed considerable modifications in the phenotypic expression of the myosin heavy chain in the vastus lateralis muscle in patients with chronic obstructive pulmonary disease. An independent effect of myosin heavy chain expression on exercise capacity was not found. These results suggest that chronic inactivity and muscle deconditioning may not be the sole factors explaining peripheral muscle dysfunction in patients with chronic obstructive pulmonary disease.

Aged↗
PubMed1998

Metabolic and hemodynamic responses of lower limb during exercise in patients with COPD.

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 blood lactate concentrations. COPD patients had lower arterial and venous pH at submaximal exercise, and there was a significant positive correlation between venous pH at 40 W and the peak O2 uptake (r = 0.91, P < 0.0001). The correlation between venous pH and peak O2 uptake suggests that early muscle acidosis may be involved in early exercise termination in COPD patients. The early lactate release from the lower limb during exercise could not be accounted for by changes in peripheral O2. The present results point to skeletal muscle dysfunction as being responsible for the early onset of lactic acidosis in COPD.

Acidosis, Lactic↗
PubMed1998

Peripheral muscle weakness in patients with chronic obstructive pulmonary disease.

Peripheral muscle weakness is commonly found in patients with chronic obstructive pulmonary disease (COPD) and may play a role in reducing exercise capacity. The purposes of this study were to evaluate, in patients with COPD: (1) the relationship between muscle strength and cross-sectional area (CSA), (2) the distribution of peripheral muscle weakness, and (3) the relationship between muscle strength and the severity of lung disease. Thirty-four patients with COPD and 16 normal subjects of similar age and body mass index were evaluated. Compared with normal subjects, the strength of three muscle groups (p < 0.05) and the right thigh muscle CSA, evaluated by computed tomography (83.4 +/- 16.4 versus 109.6 +/- 15.6 cm2, p < 0.0001), were reduced in COPD. The quadriceps strength/thigh muscle CSA ratio was similar for the two groups. The reduction in quadriceps strength was proportionally greater than that of the shoulder girdle muscles (p < 0.05). Similar observations were made whether or not patients had been exposed to systemic corticosteroids in the 6-mo period preceding the study, although there was a tendency for the quadriceps strength/thigh muscle CSA ratio to be lower in patients who had received corticosteroids. In COPD, quadriceps strength and muscle CSA correlated positively with the FEV1 expressed in percentage of predicted value (r = 0.55 and r = 0. 66, respectively, p < 0.0005). In summary, the strength/muscle cross-sectional area ratio was not different between the two groups, suggesting that weakness in COPD is due to muscle atrophy. In COPD, the distribution of peripheral muscle weakness and the correlation between quadriceps strength and the degree of airflow obstruction suggests that chronic inactivity and muscle deconditioning are important factors in the loss in muscle mass and strength.

Aged↗
PubMed1997

Intensity of training and physiologic adaptation in patients with chronic obstructive pulmonary disease.

The applicability of high-intensity training and the possibility of inducing physiologic adaptation to training are still uncertain in patients with severe chronic obstructive pulmonary disease (COPD). The purposes of this study were to evaluate the proportion of patients with moderate to severe COPD in whom high-intensity exercise training (30-min exercise session at 80% of baseline maximal power output [Wmax]) is feasible, and the response to training in these patients. We also sought to evaluate the possible influence of disease severity on the training intensity achieved and on the development of physiologic adaptation following endurance training. Forty-two patients with COPD (age = 66 +/- 7 yr, FEV1 = 38 +/- 13% predicted, [mean +/- SD]) were evaluated at baseline and after a 12-wk endurance training program. Each evaluation included a stepwise exercise test on an ergocycle up to the individual maximal capacity during which minute ventilation (VE), oxygen consumption (VO2), carbon dioxide production (VCO2), and arterial lactic acid concentrations were measured. The training consisted of 25 to 30-min exercise sessions on a calibrated ergocycle three times a week, with a target training intensity at 80% of Wmax. The training intensity was adjusted with the objective of reaching the target intensity, but also to ensure that the cycling exercise could be maintained for the specified duration. The training intensity sustained for the duration of each exercise session averaged 24.5 +/- 12.6, 51.7 +/- 17.4, 63.8 +/- 22.4, and 60.4 +/- 22.7% of Wmax at Weeks 2, 4, 10, and 12, respectively. High-intensity training was achieved in zero, three, five, and five patients at Weeks 2, 4, 10, and 12, respectively. A significant increase in VO2max and Wmax occurred with training (p < 0.0002). This improvement in exercise capacity was accompanied by a 6% and 17% reduction in VE and in arterial lactic acid concentration for a given work rate, respectively (p < 0.0001), suggesting that physiologic adaptation to training occurred. The intensity of training achieved, in % Wmax, was not influenced by the initial VO2max, age, or FEV1. The effects of training were compared in patients with an FEV1 > or = 40% or < 40% predicted. Percent changes in VO2max, Wmax, and VE, were significant and of similar magnitude for both groups, whereas the decrease in arterial lactic acid for a given work rate reached statistical significance only in those patients with an FEV1 > or = 40% predicted. We conclude that although most patients were unable to achieve high-intensity training as defined in this study, significant improvement in their exercise capacity was obtained and physiologic adaptation to endurance training occurred. The training intensity expressed as a percent of the individual maximum exercise capacity, and the relative effectiveness of training, were not influenced by the severity of airflow obstruction.

Adaptation, Physiological↗
PubMed1996

Oxidative capacity of the skeletal muscle and lactic acid kinetics during exercise in normal subjects and in patients with COPD.

Early lactic acidosis during exercise and abnormal skeletal muscle function have been reported in chronic obstructive pulmonary disease (COPD) but a possible relationship between these two abnormalities has not been evaluated. The purpose of this study was to compare and correlate the increase in arterial lactic acid (La) during exercise and the oxidative capacity of the skeletal muscle in nine COPD patients (age = 62 +/- 5 yr, mean +/- SD, FEV1 40 +/- 9% of predicted) and in nine normal subjects of similar age (54 +/- 3 yr). Following a transcutaneous biopsy of the vastus laterialis, each subject performed a stepwise exercise test on an ergocycle up to his or her maximal capacity during which 5-breath averages of oxygen consumption (Vo2), and serial La concentration measurements were obtained. From the muscle biopsy specimen, the activity of two oxidative enzymes, citrate synthase (CS) and 3-hydroxyacyl CoA dehydrogenase (HADH), and of three glycolytic enzymes, lactate dehydrogenase, hexokinase, and phosphofructokinase were determined. The La/Vo2 relationship during exercise was fitted by an exponential function in the form La = a + bvo2, where be represents the shape of the relationship. The activity of the oxidative enzymes was significantly lower in COPD than in control subjects (22.8 +/- 3.3 versus 36.8 +/- 8.6 mumol/min/g muscle for CS, and 3.1 +/- 1.1 versus 5.5 +/- 1.4 mumol/min/g for HADH, p < 0.0005) and the increase in lactic acid was steeper in COPD (b = 4.3 +/- 2.0 versus 2.1 +/- 0.2 for normal subjects, p = 0.0005). A significant inverse relationship was found between CS, HADH, and b. No difference was found between the two groups for the glycolytic enzymes. We conclude that in COPD the increase in arterial La during exercise is excessive, the oxidative capacity of the skeletal muscle is reduced, and that these two results are interrelated.

3-Hydroxyacyl CoA Dehydrogenases↗
PubMed1996

Skeletal muscle adaptation to endurance training in patients with chronic obstructive pulmonary disease.

The purpose of this study was to evaluate the physiologic responses to endurance training in patients with moderate to severe airflow obstruction by specifically looking at changes in skeletal muscle enzymatic activities. Eleven patients (age = 65 +/- 7 yr, mean +/- SD, FEV1 = 36 +/- 11% of predicted value, range = 24 to 54%) were evaluated before and after an endurance training program. Each evaluation included a percutaneous biopsy of the vastus lateralis and a stepwise exercise test on an ergocycle up to his/her maximal capacity. VE, VO2, VcO2, and serial arterial lactic acid concentration were measured during the exercise test. The activity of two oxidative enzymes, citrate synthase (CS) and 3-hydroxyacyl-CoA dehydrogenase (HADH), and of three glycolytic enzymes, lactate dehydrogenase, hexokinase, and phosphofructokinase was determined. The training consisted of 30-min exercise sessions on a calibrated ergocycle, 3 times a week for 12 wk. The aerobic capacity was severely reduced at baseline (VO2max = 54 +/- 12% of predicted) and increased by 14% after training (p < 0.05). For an identical exercise workload, there was a significant reduction in VE (34.5 +/- 10.0 versus 31.9 +/- 9.0 L/min, p < 0.05) and in arterial lactic acid concentration (3.4 +/- 1.3 versus 2.8 +/- 0.9 mmol/L, p < 0.01) after training. The lactate threshold also increased after training (p < 0.01) while the activity of the three glycolytic enzymes was similar at the two evaluations. In contrast, the activity of CS and HADH increased significantly after training (22.3 +/- 3.5 versus 25.8 +/- 3.8 mumol/min/g muscle for CS, p < 0.05, and 5.5 +/- 2.9 versus 7.7 +/- 2.5 mumol/min/g for HADH, p < 0.01). A significant inverse relationship was found between the percent changes in the activity of CS and HADH, and the percent changes in arterial lactic acid during exercise (p = 0.01). We conclude that endurance training can reduce exercise-induced lactic acidosis and improve skeletal muscle oxidative capacity in patients with moderate to severe chronic obstructive pulmonary disease (COPD).

3-Hydroxyacyl CoA Dehydrogenases↗
PubMed1995

Functional outcome of patients with chronic obstructive pulmonary disease and exercise hypercapnia.

Chronic hypercapnia is associated with a poor prognosis in chronic obstructive pulmonary disease (COPD). Some patients are normocapnic at rest but retain CO2 during exercise. The significance of this abnormality on the course of the disease is unknown. Sixteen stable COPD patients (13 males and 3 females, aged 60 +/- 5 yrs, mean +/- SD) who had previously undergone pulmonary function tests and progressive exercise testing with arterial blood sampling at rest and maximal capacity, entered the study. At first evaluation (E1), subjects were normocapnic at rest (arterial carbon dioxide tension (Pa,CO2): 4.9-5.7 kPa, (37-43 mmHg)) and all presented exercise-induced hypercapnia (end-exercise Pa,CO2 > 5.7 kPa (43 mmHg) with a minimal 0.5 kPa (4 mmHg) increase from resting value). The subjects were re-evaluated 24-54 months later (34 +/- 8 months) (second evaluation (E2)). At E2, forced expiratory volume in one second (FEV1) had decreased from 42 +/- 13 to 38 +/- 15% of predicted values, and mean resting Pa,CO2 had increased from 5.2 +/- 0.3 to 5.7 + 0.4 kPa. Maximal exercise capacity (Wmax) decreased between E1 and E2 from 76 +/- 30 to 56 +/- 22 W. Even if Wmax was lower at E2, end-exercise, Pa,CO2 was higher than at E1 (6.6 +/- 0.8 vs 6.4 +/- 0.5 kPa). At E2, eight subjects presented resting hypercapnia (group H), whilst the others remained normocapnic (Group N). Group H subjects had higher Pa,CO2, at Wmax than Group N and lower Wmax than Group N at E2.(ABSTRACT TRUNCATED AT 250 WORDS)

Female↗
PubMed1995

Evaluation of the emphysematous patient.

Most of the patients with emphysema complain of dyspnea and become limited in their activities during the course of the disease. Dyspnea is probably due to the change in the configuration of the thorax which is secondary to hyperinflation. The investigation should include the radiologic quantification of the structural abnormalities of the lungs and the functional consequences of these changes. When volume reduction of the lung is considered, the effects of hyperinflation on the mechanic of breathing and the ventilatory response to exercise has to be investigated rigorously.

Humans↗