Low-grade inflammation is emerging as a common feature of contemporary metabolic,psychiatric,and neurodegenerative diseases.Both physical inactivity and abdominal adiposity are associated with persistent systemic low-...Low-grade inflammation is emerging as a common feature of contemporary metabolic,psychiatric,and neurodegenerative diseases.Both physical inactivity and abdominal adiposity are associated with persistent systemic low-grade inflammation.Thus,the behavioral,biological,and physiological changes that cause a predisposition to obesity and other co-morbidities could have epigenetic underpinnings in addition to various evolutionary scenarios.A key assumption involves the potential for a mismatch between the human genome molded over generations,and the issue of adapting to the modern high calorie diet and common built environments promoting inactivity.This biological mismatch appears to have dire health consequences.Therefore,the goal of this article is to provide a brief overview on the importance of inflammation as part of human survival and how physical activity(PA)and physical inactivity are critical regulators of systemic inflammation.The review will highlight antiinflammatory effects of PA and exercise training from a metabolic and systemic signaling perspective,which includes skeletal muscle to utilization of fatty acids,TLR4 signaling,and myokine/adipokine effects.The available evidence suggests that PA,regular exercise,and weight loss offer both protection against and treatment for a wide variety of chronic diseases associated with low-grade inflammation through an improved inflammatory profile.展开更多
Cancer cachexia is a progressive disorder characterized by body weight,fat,and muscle loss.Cachexia induces metabolic disruptions that can be analogous and distinct from those observed in cancer,obscuring both diagnos...Cancer cachexia is a progressive disorder characterized by body weight,fat,and muscle loss.Cachexia induces metabolic disruptions that can be analogous and distinct from those observed in cancer,obscuring both diagnosis and treatment options.Inflammation,hypogonadism,and physical inactivity are widely investigated as systemic mediators of cancer-induced muscle wasting.At the cellular level,dysregulation of protein turnover and energy metabolism can negatively impact muscle mass and function.Exercise is well known for its anti-inflammatory effects and potent stimulation of anabolic signaling.Emerging evidence suggests the potential for exercise to rescue muscle's sensitivity to anabolic stimuli,reduce wasting through protein synthesis modulation,myokine release,and subsequent downregulation of proteolytic factors.To date,there is no recommendation for exercise in the management of cachexia.Given its complex nature,a multimodal approach incorporating exercise offers promising potential for cancer cachexia treatment.This review's primary objective is to summarize the growing body of research examining exercise regulation of cancer cachexia.Furthermore,we will provide evidence for exercise interactions with established systemic and cellular regulators of cancer-induced muscle wasting.展开更多
基金This work was supported by National Institutes of Health Grants R01 CA-121249(National Cancer Institute)and R21 CA-231131 to JAC.
文摘Low-grade inflammation is emerging as a common feature of contemporary metabolic,psychiatric,and neurodegenerative diseases.Both physical inactivity and abdominal adiposity are associated with persistent systemic low-grade inflammation.Thus,the behavioral,biological,and physiological changes that cause a predisposition to obesity and other co-morbidities could have epigenetic underpinnings in addition to various evolutionary scenarios.A key assumption involves the potential for a mismatch between the human genome molded over generations,and the issue of adapting to the modern high calorie diet and common built environments promoting inactivity.This biological mismatch appears to have dire health consequences.Therefore,the goal of this article is to provide a brief overview on the importance of inflammation as part of human survival and how physical activity(PA)and physical inactivity are critical regulators of systemic inflammation.The review will highlight antiinflammatory effects of PA and exercise training from a metabolic and systemic signaling perspective,which includes skeletal muscle to utilization of fatty acids,TLR4 signaling,and myokine/adipokine effects.The available evidence suggests that PA,regular exercise,and weight loss offer both protection against and treatment for a wide variety of chronic diseases associated with low-grade inflammation through an improved inflammatory profile.
基金This work was supported by National Institutes of Health Grants R01 CA-121249(National Cancer Institute)and R21 CA-231131 to JAC.
文摘Cancer cachexia is a progressive disorder characterized by body weight,fat,and muscle loss.Cachexia induces metabolic disruptions that can be analogous and distinct from those observed in cancer,obscuring both diagnosis and treatment options.Inflammation,hypogonadism,and physical inactivity are widely investigated as systemic mediators of cancer-induced muscle wasting.At the cellular level,dysregulation of protein turnover and energy metabolism can negatively impact muscle mass and function.Exercise is well known for its anti-inflammatory effects and potent stimulation of anabolic signaling.Emerging evidence suggests the potential for exercise to rescue muscle's sensitivity to anabolic stimuli,reduce wasting through protein synthesis modulation,myokine release,and subsequent downregulation of proteolytic factors.To date,there is no recommendation for exercise in the management of cachexia.Given its complex nature,a multimodal approach incorporating exercise offers promising potential for cancer cachexia treatment.This review's primary objective is to summarize the growing body of research examining exercise regulation of cancer cachexia.Furthermore,we will provide evidence for exercise interactions with established systemic and cellular regulators of cancer-induced muscle wasting.
