scholarly journals Genetic variants predicting aerobic capacity response to training are also associated with skeletal muscle oxidative capacity in moderate-to-severe COPD

2018 ◽  
Vol 50 (9) ◽  
pp. 688-690 ◽  
Author(s):  
Alessandra Adami ◽  
Brian D. Hobbs ◽  
Merry-Lynn N. McDonald ◽  
Richard Casaburi ◽  
Harry B. Rossiter ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Near Infrared ◽  
Oxidative Capacity ◽  
Chronic Obstructive ◽  
Obstructive Pulmonary Disease ◽  
Muscle Oxidative Capacity ◽  
Muscle Oxygen ◽  
Skeletal Muscle Dysfunction ◽  
Nominal Significance ◽  
Severe Copd

Muscle oxidative capacity is a major determinant of maximum oxygen uptake (V̇O2max). V̇O2max predicts survival in humans. Muscle oxidative capacity is low in chronic obstructive pulmonary disease (COPD) and can be assessed from the muscle oxygen consumption recovery rate constant ( k) by near-infrared spectroscopy. We hypothesized that 11 SNPs, previously associated with the increase in V̇O2max following exercise training, would correlate with k in 152 non-Hispanic White and African American smokers with and without COPD. Associations were adjusted for age, weight, FEV1% predicted, steps/day, and principal components of genetic ancestry. No SNPs were significantly associated with k. rs2792022 within BTAF1 (β = 0.130, P = 0.053) and rs24575771 within SLC22A3 (β = 0.106, P = 0.058) approached nominal significance. Case-control stratification identified three SNPs nominally associated with k in moderate-to-severe COPD ( rs6481619 within SVIL β = 0.152, P = 0.013; BTAF1 β = 0.196, P = 0.046; rs7386139 within DEPTOR β = 0.159, P = 0.047). These data support further study of the genomic contributions to skeletal muscle dysfunction in COPD.

scholarly journals A cross-validation of near-infrared spectroscopy measurements of skeletal muscle oxidative capacity with phosphorus magnetic resonance spectroscopy

2013 ◽  
Vol 115 (12) ◽  
pp. 1757-1766 ◽  
Author(s):  
Terence E. Ryan ◽  
W. Michael Southern ◽  
Mary Ann Reynolds ◽  
Kevin K. McCully
Keyword(s):  
Skeletal Muscle ◽  
Near Infrared ◽  
Plantar Flexion ◽  
Oxidative Capacity ◽  
Resonance Spectroscopy ◽  
Time Constants ◽  
Muscle Oxidative Capacity ◽  
Muscle Oxygen ◽  
Muscle Oxygen Consumption ◽  
Plantar Flexion Exercise

The purpose of this study was to cross-validate measurements of skeletal muscle oxidative capacity made with near-infrared spectroscopy (NIRS) measurements to those made with phosphorus magnetic resonance spectroscopy (31P-MRS). Sixteen young (age = 22.5 ± 3.0 yr), healthy individuals were tested with both 31P-MRS and NIRS during a single testing session. The recovery rate of phosphocreatine was measured inside the bore of a 3-Tesla MRI scanner, after short-duration (∼10 s) plantar flexion exercise as an index of skeletal muscle oxidative capacity. Using NIRS, the recovery rate of muscle oxygen consumption was also measured using repeated, transient arterial occlusions outside the MRI scanner, after short-duration (∼10 s) plantar flexion exercise as another index of skeletal muscle oxidative capacity. The average recovery time constant was 31.5 ± 8.5 s for phosphocreatine and 31.5 ± 8.9 s for muscle oxygen consumption for all participants ( P = 0.709). 31P-MRS time constants correlated well with NIRS time constants for both channel 1 (Pearson's r = 0.88, P < 0.0001) and channel 2 (Pearson's r = 0.95, P < 0.0001). Furthermore, both 31P-MRS and NIRS exhibit good repeatability between trials (coefficient of variation = 8.1, 6.9, and 7.9% for NIRS channel 1, NIRS channel 2, and 31P-MRS, respectively). The good agreement between NIRS and 31P-MRS indexes of skeletal muscle oxidative capacity suggest that NIRS is a valid method for assessing mitochondrial function, and that direct comparisons between NIRS and 31P-MRS measurements may be possible.

Oxygen delivery-utilization mismatch in contracting locomotor muscle in COPD: peripheral factors

2015 ◽  
Vol 308 (2) ◽  
pp. R105-R111 ◽  
Author(s):  
Wladimir M. Medeiros ◽  
Mari C. T. Fernandes ◽  
Diogo P. Azevedo ◽  
Flavia F. M. de Freitas ◽  
Beatriz C. Amorim ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Muscle Mass ◽  
Near Infrared ◽  
Neuromuscular Electrical Stimulation ◽  
Muscle Oxygenation ◽  
Whole Body ◽  
Chronic Obstructive ◽  
Copd Patients ◽  
Skeletal Muscle Oxygenation ◽  
Severe Copd

Central cardiorespiratory and gas exchange limitations imposed by chronic obstructive pulmonary disease (COPD) impair ambulatory skeletal muscle oxygenation during whole body exercise. This investigation tested the hypothesis that peripheral factors per se contribute to impaired contracting lower limb muscle oxygenation in COPD patients. Submaximal neuromuscular electrical stimulation (NMES; 30, 40, and 50 mA at 50 Hz) of the quadriceps femoris was employed to evaluate contracting skeletal muscle oxygenation while minimizing the influence of COPD-related central cardiorespiratory constraints. Fractional O2 extraction was estimated by near-infrared spectroscopy (deoxyhemoglobin/myoglobin concentration; deoxy-[Hb/Mb]), and torque output was measured by isokinetic dynamometry in 15 nonhypoxemic patients with moderate-to-severe COPD (SpO2 = 94 ± 2%; FEV1 = 46.4 ± 10.1%; GOLD II and III) and in 10 age- and gender-matched sedentary controls. COPD patients had lower leg muscle mass than controls (LMM = 8.0 ± 0.7 kg vs. 8.9 ± 1.0 kg, respectively; P < 0.05) and produced relatively lower absolute and LMM-normalized torque across the range of NMES intensities ( P < 0.05 for all). Despite producing less torque, COPD patients had similar deoxy-[Hb/Mb] amplitudes at 30 and 40 mA ( P > 0.05 for both) and higher deoxy-[Hb/Mb] amplitude at 50 mA ( P < 0.05). Further analysis indicated that COPD patients required greater fractional O2 extraction to produce torque (i.e., ↑Δdeoxy-[Hb/Mb]/torque) relative to controls ( P < 0.05 for 40 and 50 mA) and as a function of NMES intensity ( P < 0.05 for all). The present data obtained during submaximal NMES of small muscle mass indicate that peripheral abnormalities contribute mechanistically to impaired contracting skeletal muscle oxygenation in nonhypoxemic, moderate-to-severe COPD patients.

Pulmonary emphysema decreases hamster skeletal muscle oxidative enzyme capacity

1998 ◽  
Vol 85 (1) ◽  
pp. 210-214 ◽  
Author(s):  
John P. Mattson ◽  
David C. Poole
Keyword(s):  
Skeletal Muscle ◽  
Citrate Synthase ◽  
Vastus Lateralis ◽  
Intratracheal Instillation ◽  
Oxidative Capacity ◽  
Activity Level ◽  
Oxidative Enzyme ◽  
Chronic Obstructive ◽  
Obstructive Pulmonary Disease ◽  
Reduced Physical Activity

Skeletal muscle oxidative enzyme capacity is impaired in patients suffering from emphysema and chronic obstructive pulmonary disease. This effect may result as a consequence of the physiological derangements because of the emphysema condition or, alternatively, as a consequence of the reduced physical activity level in these patients. To explore this issue, citrate synthase (CS) activity was measured in selected hindlimb muscles and the diaphragm of Syrian Golden hamsters 6 mo after intratracheal instillation of either saline (Con, n = 7) or elastase [emphysema (Emp); 25 units/100 g body weight, n = 8]. Activity level was monitored, and no difference between groups was found. Excised lung volume increased with emphysema (Con, 1.5 ± 0.3 g; Emp, 3.0 ± 0.3 g, P < 0.002). Emphysema significantly reduced CS activity in the gastrocnemius (Con, 45.1 ± 2.0; Emp, 39.2 ± 0.8 μmol ⋅ min−1 ⋅ g wet wt−1, P < 0.05) and vastus lateralis (Con, 48.5 ± 1.5; Emp, 44.9 ± 0.8 μmol ⋅ min−1 ⋅ g wet wt−1, P < 0.05) but not in the plantaris (Con, 47.4 ± 3.9; Emp, 48.0 ± 2.1 μmol ⋅ min−1 ⋅ g wet wt−1, P < 0.05) muscle. In contrast, CS activity increased in the costal (Con, 61.1 ± 1.8; Emp, 65.1 ± 1.5 μmol ⋅ min−1 ⋅ g wet wt−1, P < 0.05) and crural (Con, 58.5 ± 2.0; Emp, 65.7 ± 2.2 μmol ⋅ min−1 ⋅ g wet wt−1, P < 0.05) regions of the diaphragm. These data indicate that emphysema per se can induce decrements in the oxidative capacity of certain nonventilatory skeletal muscles that may contribute to exercise limitations in the emphysematous patient.

scholarly journals NIRS-derived skeletal muscle oxidative capacity is correlated with aerobic fitness and independent of sex

2020 ◽  
Vol 129 (3) ◽  
pp. 558-568
Author(s):  
Austin T. Beever ◽  
Thomas R. Tripp ◽  
Jenny Zhang ◽  
Martin J. MacInnis
Keyword(s):  
Skeletal Muscle ◽  
Infrared Spectroscopy ◽  
Oxygen Uptake ◽  
Aerobic Fitness ◽  
Lactate Threshold ◽  
Near Infrared ◽  
Vastus Lateralis ◽  
Oxidative Capacity ◽  
Muscle Oxidative Capacity ◽  
Respiratory Compensation

Near-infrared spectroscopy (NIRS) can be used to measure skeletal muscle oxidative capacity. Here, we demonstrated that NIRS-derived skeletal muscle oxidative capacity of the vastus lateralis was independent of sex, reliable across and within days, and correlated with maximal and submaximal indices of aerobic fitness, including maximal oxygen uptake, lactate threshold, and respiratory compensation point. These findings highlight the utility of NIRS for investigating skeletal muscle oxidative capacity in females and males.

Skeletal muscle dysfunction in COPD: clinical and laboratory observations

2009 ◽  
Vol 117 (7) ◽  
pp. 251-264 ◽  
Author(s):  
William D.-C. Man ◽  
Paul Kemp ◽  
John Moxham ◽  
Michael I. Polkey
Keyword(s):  
Skeletal Muscle ◽  
Skeletal Muscles ◽  
Current Knowledge ◽  
Clinical Importance ◽  
Chronic Obstructive ◽  
Muscle Dysfunction ◽  
Obstructive Pulmonary Disease ◽  
Skeletal Muscle Dysfunction ◽  
Skeletal Muscle Weakness ◽  
Systemic Manifestations

COPD (chronic obstructive pulmonary disease), although primarily a disease of the lungs, exhibits secondary systemic manifestations. The skeletal muscles are of particular interest because their function (or dysfunction) not only influences the symptoms that limit exercise, but may contribute directly to poor exercise performance. Furthermore, skeletal muscle weakness is of great clinical importance in COPD as it is recognized to contribute independently to poor health status, increased healthcare utilization and even mortality. The present review describes the current knowledge of the structural and functional abnormalities of skeletal muscles in COPD and the possible aetiological factors. Increasing knowledge of the molecular pathways of muscle wasting will lead to the development of new therapeutic agents and strategies to combat COPD muscle dysfunction.

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