Pyruvate is a keystone molecule critical for numerous aspects of eukaryotic and human metabolism. Pyruvate is the end-product of glycolysis, is derived from additional sources in the cellular cytoplasm, and is ultimately destined for transport into mitochondria as a master fuel input undergirding citric acid cycle carbon flux. In mitochondria, pyruvate drives ATP production by oxidative phosphorylation and multiple biosynthetic pathways intersecting the citric acid cycle. Mitochondrial pyruvate metabolism is regulated by many enzymes, including the recently discovered mitochondria pyruvate carrier, pyruvate dehydrogenase, and pyruvate carboxylase, to modulate overall pyruvate carbon flux. Mutations in any of the genes encoding for proteins regulating pyruvate metabolism may lead to disease. Numerous cases have been described. Aberrant pyruvate metabolism plays an especially prominent role in cancer, heart failure, and neurodegeneration. Because most major diseases involve aberrant metabolism, understanding and exploiting pyruvate carbon flux may yield novel treatments that enhance human health.

/pdf/regulation-of-pyruvate-metabolism-and-human-disease-2vflael6v2.pdf

Regulation of pyruvate metabolism and human disease.

Pulmonary rehabilitation, a multidisciplinary and structured intervention for patients with chronic pulmonary diseases, has been shown to improve exercise tolerance, reduce dyspnea and improve health-related quality of life. Pulmonary rehabilitation appears to be cost-effective, since it reduces health care utilization. Exercise training represents the cornerstone of every pulmonary rehabilitation program. To obtain clinically relevant effects, training should closely supervised, of high intensity, lasting 30-45 min for at least 3 days/week. Patients should undertake a minimum of 20 sessions, but longer programs result in larger and more long-lasting effects. Education and self-management programs have been shown to result in a substantial reduction in hospital admissions. Nutritional intervention should be considered for patients who are underweight or those with body composition abnormalities. Patients reporting fear and anxiety may benefit from psychosocial support, and the integration of occupational therapy in a pulmonary rehabilitation program can improve independence in activity. Multidisciplinary pulmonary rehabilitation is preferably implemented in an outpatient hospital- or community-based setting. Inpatient programs are suited for patients with limited transportation capabilities or severe deconditioning. The most convincing effects of home-based rehabilitation are in maintaining the improvements obtained in an outpatient setting.

Pulmonary Rehabilitation in Chronic Obstructive Pulmonary Disease

The aim of this review was to examine the mechanisms by which physical activity and inactivity modify muscle fatigue It is well known that acute or chronic increases in physical activity result in structural, metabolic, hormonal, neural and molecular adaptations that increase the level of force or power that can be sustained by a muscle These adaptations depend on the type, intensity and volume of the exercise stimulus, but recent studies have highlighted the role of high intensity, short duration exercise as a time-efficient method to achieve both anaerobic and aerobic/endurance type adaptations The factors that determine the fatigue profile of a muscle during intense exercise include muscle fibre composition, neuromuscular characteristics high energy metabolite stores, buffering capacity, ionic regulation, capillarization and mitochondrial density Muscle fiber type transformation during exercise training is usually towards the intermediate type IIA at the expense of both type I and type IIx myosin heavy chain isoforms High intensity training results in increases of both glycolyic and oxidative enzymes, muscle capilarization, improved phosphocreatine resynthesis and regulation of K+, H+ and lactate ions Decreases of the habitual activity level due to injury or sedentary lifestyle result in partial or even compete reversal of the adaptations due to previous training, manifested by reductions in fibre cross-sectional area, decreased oxidative capacity and capillarization Complete immobilization due to injury results in markedly decreased force output and fatigue resistance Muscle unloading reduces electromyographic activity and causes muscle atrophy and significant decreases in capillarization and oxidative enzymes activity The last part of the review discusses the beneficial effects of intermittent high intensity exercise training in patients with different health conditions to demonstrate the powerful effect exercise on health and well being

/pdf/effects-of-physical-activity-and-inactivity-on-muscle-a623m5oyn2.pdf

Effects of physical activity and inactivity on muscle fatigue

Skeletal Muscle Adaptations to Interval Training in Patients With Advanced COPD

Evidence has been accumulating that chronic inactivity leading to muscle disuse is unlikely to be the only explanation for the peripheral muscle dysfunction of chronic obstructive pulmonary disease (COPD) patients. Although a new concept of myopathy was recently proposed, the question of disuse and/or a form of myopathy is still being debated. This review proposes definitions for the terms used in this debate, discusses the relevant studies and concludes that the evidence points to a myopathy associated with muscle disuse in COPD. COPD myopathy implies pharmacological and/or pathophysiological mechanisms that need to be identified in order to optimally orient therapeutic strategies. The literature indicates that corticosteroids, inflammation, hypoxaemia and oxidative stress are among the factors contributing to COPD muscle dysfunction, but their relative contributions have not been fully elucidated. This review presents the advances in understanding each of these mechanisms, especially the data showing that muscle oxidative stress occurs and contributes to muscle dysfunction in chronic obstructive pulmonary disease. The current review also reports the studies that have elucidated the molecular mechanisms underlying this stress in chronic obstructive pulmonary disease by demonstrating alterations in oxidant and/or antioxidant systems. Finally, the review considers how inflammation and hypoxaemia may trigger oxidative stress in chronic obstructive pulmonary disease muscles and presents the therapeutic modalities that should be proposed to prevent it.

https://erj.ersjournals.com/content/erj/26/4/703.full.pdf

From muscle disuse to myopathy in COPD: potential contribution of oxidative stress.

The aim of this study was to examine the nature of fibre-type redistribution in relation to fibre metabolic profile in the vastus lateralis in chronic obstructive pulmonary disease (COPD) and COPD subtypes. Fifteen COPD patients (eight with emphysema stratified by high-resolution computed tomography) and 15 healthy control subjects were studied. A combination of myofibrillar adenosine triphosphatase staining and immunohistochemistry was used to identify pure, as well as hybrid fibre types. For oxidative capacity, fibres were stained for cytochrome c oxidase and succinate dehydrogenase activities, and glycogen phosphorylase for glycolytic capacity. The proportion of type-I fibres in COPD patients was markedly lower (16% versus 42%), especially in emphysema, and the proportion of hybrid fibres was higher (29% versus 16%) compared to controls. The proportion of fibres staining positive for oxidative enzymes was lower in COPD patients, which correlated with the proportion of type-I fibres. In COPD oxidative capacity was lower within IIA fibres. The authors conclude that fibre-type transitions are involved in the fibre-type redistribution in chronic obstructive pulmonary disease. Low oxidative capacity is closely related to the proportion of type-I fibres, but an additional reduction of oxidative enzyme activity is present within IIA fibres. Fibre-type abnormalities may be aggravated in emphysema.

https://erj.ersjournals.com/content/erj/19/4/617.full.pdf

Skeletal muscle fibre-type shifting and metabolic profile in patients with chronic obstructive pulmonary disease

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Skeletal muscle fibre-type shifting and metabolic profile in patients with chronic obstructive pulmonary disease