Exercise against tumor- and chemotherapy-induced muscle wasting

Coletti, Dario

doi:10.15761/bem.1000s1004

Cited by 2 publications

(2 citation statements)

References 62 publications

(67 reference statements)

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“…Thus, resistance training leads to the induction of myofibrillar protein synthesis and increased anaerobic capacity, whereas endurance exercise sessions mainly lead to improved mitochondrial density and function, oxygen delivery and uptake, anti-oxidant defenses and resistance to fatigue [25] . The beneficial effects of exercise have been tested in different chronic conditions, including coronary heart disease, type 2 diabetes mellitus, obesity and aging [24,27] . Notably, both exercise types exert beneficial effects in cachectic animals.…”

Section: Exercise As a Modulator Of Muscle Metabolismmentioning

confidence: 99%

Muscle mitochondria and oxidative metabolism as targets against cancer cachexia

Ballarò¹,

Penna²,

Ferraro³

et al. 2019

JCMT

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Cancer cachexia is a debilitating syndrome mainly characterized by muscle and fat wasting, leading to the progressive loss of body weight and complicating the management of cancer patient. In particular, the loss of muscle weight is a negative prognostic factor, being associated with chemotherapy toxicity and reduced survival. Increased inflammation and protein dysmetabolism are some of the impairments that lead to muscle wasting in cancer patients. Together with these alterations, tumor growth and chemotherapy administration may affect mitochondrial function, impinging on the muscle energy metabolism. Indeed, therapeutic approaches poised to correct both hypercatabolism and mitochondrial alterations could be effective in preventing cancer-induced muscle wasting. Among the non-pharmacological approaches, exercise training is one of the best modulator of muscle physiology able to impinge on both protein and energy metabolism. However, the wasting phenotype that characterizes cancer patients could be not compatible with physical training, prompting the development of different strategies to improve muscle metabolism. The aim of this mini-review is to discuss both the beneficial effects and the limitations of exercise training in cancer cachexia and the adoption of drugs able to modulate exercise-induced pathways.

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Section: Exercise As a Modulator Of Muscle Metabolismmentioning

confidence: 99%

Muscle mitochondria and oxidative metabolism as targets against cancer cachexia

Ballarò¹,

Penna²,

Ferraro³

et al. 2019

JCMT

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“…Until specific molecular and/or biochemical characteristics are determined, the efforts to develop effective treatments for CFS will continue to be not conclusive.On the other hand, the clinical benefits of physiotherapy approaches developed for other similar clinical cases of early aging and aging per se (whether traumatic, metabolic, genetic or equally unknown), justify the option to apply them to CFS. 14-16 In summary, to date, the number of studies performed to define the clinical aspects of the disease is still not adequate to clearly indicate onset and prognosis. 17 Probably, its persistence may involve complex interactions of immune, autonomic and neuroendocrine regulation but these studies remain poorly understood.…”

mentioning

confidence: 99%

Old muscle in young body: an aphorism describing the Chronic Fatigue Syndrome

Pietrangelo

Fulle

Coscia³

et al. 2018

Eur J Transl Myol

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The chronic fatigue syndrome (CFS) otherwise known as myalgic encephalomyelitis (ME), is a debilitating syndrome whose identification is very complex due to lack of precise diagnostic criteria. This pathology begins with limitations in duration and intensity of exercise and rapid onset of pain during physical activity. Its etiology is unknown, and symptoms are not limited to the muscles. Epidemiology is rather difficult to delimit, even if it affects mainly young (20-40 years), female subjects. The results of muscular research show some peculiarities that can justify what has been observed in vivo. In particular, 1. presence of oxidative damage of lipid component of biological membranes and DNA not compensated by the increase of the scavenger activity; 2. Excitation-Contraction (E-C) alteration with modification of Ca2+ transport; 3. passage from slow to fast fiber phenotype; 4. inability to increase glucose uptake; 5. presence of mitochondrial dysfunction; and 6. genes expressed differentially (particularly those involved in energy production). The skeletal muscles of CFS / ME patients show a significant alteration of the oxidative balance due to mitochondrial alteration and of the fiber phenotype composition as shown in sarcopenic muscles of the elderly. Vice versa, the muscle catabolism does not appear to be involved in the onset of this syndrome. The data support the hypothesis that patients with CFS are subjected to some of the problems typical for muscle aging, which is probably related to disorders of muscle protein synthesis and biogenesis of mitochondria. Patients with CFS can benefit from an appropriate training program because no evidence suggests that physical exercise worsens symptoms. Type, intensity and duration of any physical activity that activates muscle contraction (including Electrical Stimulation) require further investigation even if it is known that non-exhaustive physical activity decreases painful symptomatology.

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Exercise against tumor- and chemotherapy-induced muscle wasting

Cited by 2 publications

References 62 publications

Muscle mitochondria and oxidative metabolism as targets against cancer cachexia

Muscle mitochondria and oxidative metabolism as targets against cancer cachexia

Old muscle in young body: an aphorism describing the Chronic Fatigue Syndrome

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