1.
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.
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.
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.
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.