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Contraction and nutrition interaction promotes anabolism in cachectic muscle.
Di Girolamo, FG, Guadagni, M, Fiotti, N, Situlin, R, Biolo, G
Current opinion in clinical nutrition and metabolic care. 2019;(1):60-67
Abstract
PURPOSE OF REVIEW Cachexia is a disease-related multifactorial syndrome characterized by inflammation, massive muscle protein catabolism and carbohydrate and lipid metabolism disorder.Several studies tried to define the impact of either nutrition or physical exercise (single approach strategy) or their combination (multimodal approach strategy) on prevention and/or treatment of muscle wasting in cachectic patients. RECENT FINDINGS Single approach strategies (i.e. nutrition or physical exercise) have the potential of preventing and improving features of the cachexia syndrome possibly with a differential impact according to the underlying disease. Limited information is available on the beneficial effect of multimodal approach strategies. SUMMARY Multimodal approaches appear to be more effective than those based on single interventions in physiological condition and in cachectic patients with COPD or chronic kidney disease. Further studies, however, are required in cachexia induced by heart failure, cancer and critical illness.
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2.
Metabolic disturbance in PCOS: clinical and molecular effects on skeletal muscle tissue.
Dantas, WS, Gualano, B, Rocha, MP, Barcellos, CR, dos Reis Vieira Yance, V, Marcondes, JA
TheScientificWorldJournal. 2013;:178364
Abstract
Polycystic ovary syndrome is a complex hormonal disorder affecting the reproductive and metabolic systems with signs and symptoms related to anovulation, infertility, menstrual irregularity and hirsutism. Skeletal muscle plays a vital role in the peripheral glucose uptake. Since PCOS is associated with defects in the activation and pancreatic dysfunction of β-cell insulin, it is important to understand the molecular mechanisms of insulin resistance in PCOS. Studies of muscle tissue in patients with PCOS reveal defects in insulin signaling. Muscle biopsies performed during euglycemic hyperinsulinemic clamp showed a significant reduction in glucose uptake, and insulin-mediated IRS-2 increased significantly in skeletal muscle. It is recognized that the etiology of insulin resistance in PCOS is likely to be as complicated as in type 2 diabetes and it has an important role in metabolic and reproductive phenotypes of this syndrome. Thus, further evidence regarding the effect of nonpharmacological approaches (e.g., physical exercise) in skeletal muscle of women with PCOS is required for a better therapeutic approach in the management of various metabolic and reproductive problems caused by this syndrome.
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3.
Resistance exercise and appropriate nutrition to counteract muscle wasting and promote muscle hypertrophy.
Glover, EI, Phillips, SM
Current opinion in clinical nutrition and metabolic care. 2010;(6):630-4
Abstract
PURPOSE OF REVIEW Loss of skeletal muscle mass is a common feature of a number of clinical scenarios including limb casting, bed rest, and various disorders such as HIV-AIDS, sepsis, cancer cachexia, heart failure, and uremia. Commonly, muscle disuse (hypodynamia) is the sole reason, or a large part, of why muscle mass is lost. The reduction in strength, or dynapenia, that accompanies these conditions is also a function of the degree of hypodynamia and is related to muscle loss. RECENT FINDINGS The major and consistent finding in a number of human-based models of muscle wasting is a decline in the synthesis of new muscle proteins both in the postabsorptive and fed states. Thus, countermeasures are best suited to those that augment muscle protein synthesis and not those that attempt to counteract proteolysis. Our main thesis is that retention of muscle mass in wasting conditions will be achieved to the greatest extent by focussing on increased muscle use with moderate-to-high resistance loads as the primary countermeasure with a secondary countermeasure being to provide adequate nutritional support. Either intervention alone will alleviate some part of hypodynamia-induced muscle mass loss and dynapenia; however, together nutrition and muscular contraction will result in greater mitigation of muscle loss. SUMMARY Advances in our understanding of hypodynamia-induced muscle loss, a condition common to almost all syndromes of muscle wasting, has led to a focus on reduced basal and feeding-induced elevations in protein synthesis. Countermeasures for wasting should focus on stimulating anabolism rather than alleviating catabolism.
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4.
Sarcopenia: characteristics, mechanisms and functional significance.
Narici, MV, Maffulli, N
British medical bulletin. 2010;:139-59
Abstract
Sarcopenia reflects a progressive withdrawal of anabolism and an increased catabolism, along with a reduced muscle regeneration capacity. Muscle force and power decline more than muscle dimensions: older muscle is intrinsically weak. Sarcopenic obesity (SO) among the elderly corroborates to the loss of muscle mass increasing the risk of metabolic syndrome development. Recent studies on the musculoskeletal adaptations with ageing and key papers on the mechanisms of muscle wasting, its functional repercussions and on SO are included. Neuropathic, hormonal, immunological, nutritional and physical activity factors contribute to sarcopenia. Selective fast fibre atrophy, loss of motor units and an increase in hybrid fibres are typical findings of ageing. Satellite cell number decreases reducing muscle regeneration capacity. SO promotes further muscle wasting and increases risk of metabolic syndrome development. The proportion of fast to slow fibres seems maintained in old age. In elderly humans, nuclear domain is maintained constant. Basal protein synthesis and breakdown show little changes in old age. Instead, blunting of the anabolic response to feeding and exercise and of the antiproteolytic effect of insulin is observed. Further understanding of the mechanisms of sarcopenia requires disentangling of the effects of ageing alone from those of disuse and disease. The causes of the greater anabolic resistance to feeding and exercise of elderly women need elucidating. The enhancement of muscle regeneration via satellite cell activation via the MAPK/notch molecular pathways seems particularly promising.
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5.
Inherited conduction system abnormalities--one group of diseases, many genes.
Wolf, CM, Berul, CI
Journal of cardiovascular electrophysiology. 2006;(4):446-55
Abstract
The cardiac conduction system can be anatomically, developmentally, and molecularly distinguished from the working myocardium. Abnormalities in cardiac conduction can occur due to a variety of factors, including developmental and congenital defects, acquired injury or ischemia of portions of the conduction system, or less commonly due to inherited diseases that alter cardiac conduction system function. So called "idiopathic" conduction system degeneration may have familial clustering, and therefore is consistent with a hereditary basis. This "Molecular Perspectives" will highlight several diverse mechanisms of isolated conduction system disease as well as conduction system degeneration associated with other cardiac and non-cardiac disorders. The first part of this review focuses on channelopathies associated with conduction system disease. Human genetic studies have identified mutations in the sodium channel SCN5A gene causing tachyarrhythmia disorders, as well as progressive cardiac conduction system diseases, or overlapping syndromes. Next, the importance of embryonic developmental genes such as homeobox and T-box transcription factors are highlighted in conduction system development and function. Conduction system diseases associated with multisystem disorders, such as muscular and myotonic dystrophies, will be described. Last, a new glycogen storage cardiomyopathy associated with ventricular preexcitation and progressive conduction system degeneration will be reviewed. There are a myriad of mutations identified in genes encoding cardiac transcription factors, ion channels, gap junctions, energy metabolism regulators, lamins and other structural proteins. Understanding of the molecular and ionic mechanisms underlying cardiac conduction is essential for the appreciation of the pathogenesis of conduction abnormalities in structurally normal and altered hearts.
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6.
Mechanisms of skeletal muscle depletion in wasting syndromes: role of ATP-ubiquitin-dependent proteolysis.
Costelli, P, Baccino, FM
Current opinion in clinical nutrition and metabolic care. 2003;(4):407-12
Abstract
PURPOSE OF REVIEW Muscle protein wasting frequently complicates patient outcome in several chronic pathologies. The underlying mechanisms remain largely obscure, although studies on experimental models have clarified that a complex interplay of different factors such as nutrient supply, classical hormones, cytokines and other less well defined factors likely concur in causing muscle depletion. The aim of the present review is to highlight some crucial points in the interpretation of the data available about the contribution of the different proteolytic systems, with particular reference to the ubiquitin-proteasome system, in the onset of muscle protein wasting in disease states. RECENT FINDINGS Much effort has been directed to understanding the role of different signals, transduction pathways, and proteolytic mechanisms in the acceleration of muscle protein catabolism. Several reports propose that ATP-ubiquitin-dependent proteolysis plays a critical role in the enhancement of muscle protein catabolism observed in different pathological states. Other papers, however, suggest that the lysosomal or the calcium-dependent proteolytic pathways or both may be involved. Finally, the studies have been extended to evaluate the possibility of interfering pharmacologically with the onset of muscle protein hypercatabolism. SUMMARY As the present overview points out, several questions still remain unanswered in the issue of muscle wasting. While many different signals that have the potential to enforce the acceleration of muscle protein breakdown have been identified, it is largely unknown how they are transduced and converge into the hypercatabolic response and how the proteolytic pathways involved are activated. The concept seems to emerge that there may be a coordinated action of different proteolytic pathways in setting up muscle protein turnover towards excess catabolism.