scholarly journals Mitochondrial Bioenergetics and Turnover during Chronic Muscle Disuse

2021 ◽  
Vol 22 (10) ◽  
pp. 5179
Author(s):  
Jonathan M. Memme ◽  
Mikhaela Slavin ◽  
Neushaw Moradi ◽  
David A. Hood
Keyword(s):  
Bed Rest ◽  
Metabolic Health ◽  
Muscle Quality ◽  
Whole Body ◽  
Oxygen Species ◽  
Mitochondrial Quality Control ◽  
Muscle Disuse ◽  
Mitochondrial Alterations ◽  
And Function ◽  
Limb Immobilization

Periods of muscle disuse promote marked mitochondrial alterations that contribute to the impaired metabolic health and degree of atrophy in the muscle. Thus, understanding the molecular underpinnings of muscle mitochondrial decline with prolonged inactivity is of considerable interest. There are translational applications to patients subjected to limb immobilization following injury, illness-induced bed rest, neuropathies, and even microgravity. Studies in these patients, as well as on various pre-clinical rodent models have elucidated the pathways involved in mitochondrial quality control, such as mitochondrial biogenesis, mitophagy, fission and fusion, and the corresponding mitochondrial derangements that underlie the muscle atrophy that ensues from inactivity. Defective organelles display altered respiratory function concurrent with increased accumulation of reactive oxygen species, which exacerbate myofiber atrophy via degradative pathways. The preservation of muscle quality and function is critical for maintaining mobility throughout the lifespan, and for the prevention of inactivity-related diseases. Exercise training is effective in preserving muscle mass by promoting favourable mitochondrial adaptations that offset the mitochondrial dysfunction, which contributes to the declines in muscle and whole-body metabolic health. This highlights the need for further investigation of the mechanisms in which mitochondria contribute to disuse-induced atrophy, as well as the specific molecular targets that can be exploited therapeutically.

Unravelling the mechanisms regulating muscle mitochondrial biogenesis

2016 ◽  
Vol 473 (15) ◽  
pp. 2295-2314 ◽  
Author(s):  
David A. Hood ◽  
Liam D. Tryon ◽  
Heather N. Carter ◽  
Yuho Kim ◽  
Chris C.W. Chen
Keyword(s):  
Contractile Activity ◽  
Activity Patterns ◽  
Metabolic Health ◽  
Whole Body ◽  
Mitochondrial Content ◽  
Compensatory Response ◽  
Pharmacological Agents ◽  
Regulatory Pathways ◽  
Muscle Disuse ◽  
Biogenesis Of Mitochondria

Skeletal muscle is a tissue with a low mitochondrial content under basal conditions, but it is responsive to acute increases in contractile activity patterns (i.e. exercise) which initiate the signalling of a compensatory response, leading to the biogenesis of mitochondria and improved organelle function. Exercise also promotes the degradation of poorly functioning mitochondria (i.e. mitophagy), thereby accelerating mitochondrial turnover, and preserving a pool of healthy organelles. In contrast, muscle disuse, as well as the aging process, are associated with reduced mitochondrial quality and quantity in muscle. This has strong negative implications for whole-body metabolic health and the preservation of muscle mass. A number of traditional, as well as novel regulatory pathways exist in muscle that control both biogenesis and mitophagy. Interestingly, although the ablation of single regulatory transcription factors within these pathways often leads to a reduction in the basal mitochondrial content of muscle, this can invariably be overcome with exercise, signifying that exercise activates a multitude of pathways which can respond to restore mitochondrial health. This knowledge, along with growing realization that pharmacological agents can also promote mitochondrial health independently of exercise, leads to an optimistic outlook in which the maintenance of mitochondrial and whole-body metabolic health can be achieved by taking advantage of the broad benefits of exercise, along with the potential specificity of drug action.

scholarly journals Physical Exercise: A Novel Tool to Protect Mitochondrial Health

2021 ◽  
Vol 12 ◽  
Author(s):  
Daniela Sorriento ◽  
Eugenio Di Vaia ◽  
Guido Iaccarino
Keyword(s):  
Physical Exercise ◽  
Heart Diseases ◽  
Oxygen Species ◽  
Metabolic Abnormalities ◽  
Energetic Metabolism ◽  
Potential Therapeutic Target ◽  
Mitochondrial Quality Control ◽  
Factors Associated ◽  
And Function ◽  
Critical Process

Mitochondrial dysfunction is a crucial contributor to heart diseases. Alterations in energetic metabolism affect crucial homeostatic processes, such asATP production, the generation of reactive oxygen species, and the release of pro-apoptotic factors, associated with metabolic abnormalities. In response to energetic deficiency, the cardiomyocytes activate the Mitochondrial Quality Control (MQC), a critical process in maintaining mitochondrial health. This process is compromised in cardiovascular diseases depending on the pathology’s severity and represents, therefore, a potential therapeutic target. Several potential targeting molecules within this process have been identified in the last years, and therapeutic strategies have been proposed to ameliorate mitochondria monitoring and function. In this context, physical exercise is considered a non-pharmacological strategy to protect mitochondrial health. Physical exercise regulates MQC allowing the repair/elimination of damaged mitochondria and synthesizing new ones, thus recovering the metabolic state. In this review, we will deal with the effect of physical exercise on cardiac mitochondrial function tracing its ability to modulate specific steps in MQC both in physiologic and pathologic conditions.

scholarly journals Mitochondrial Impairment in Sarcopenia

Biology ◽  
2021 ◽  
Vol 10 (1) ◽  
pp. 31
Author(s):  
Francesco Bellanti ◽  
Aurelio Lo Buglio ◽  
Gianluigi Vendemiale
Keyword(s):  
Skeletal Muscle ◽  
Muscle Quality ◽  
Protein Homeostasis ◽  
Related Condition ◽  
Selective Autophagy ◽  
Mitochondrial Homeostasis ◽  
Mitochondrial Alterations ◽  
Mitochondrial Impairment ◽  
Age Related ◽  
And Function

Sarcopenia is defined by the age-related loss of skeletal muscle quality, which relies on mitochondrial homeostasis. During aging, several mitochondrial features such as bioenergetics, dynamics, biogenesis, and selective autophagy (mitophagy) are altered and impinge on protein homeostasis, resulting in loss of muscle mass and function. Thus, mitochondrial dysfunction contributes significantly to the complex pathogenesis of sarcopenia, and mitochondria are indicated as potential targets to prevent and treat this age-related condition. After a concise presentation of the age-related modifications in skeletal muscle quality and mitochondrial homeostasis, the present review summarizes the most relevant findings related to mitochondrial alterations in sarcopenia.

Effect of dietary protein on bed-rest-related changes in whole-body-protein synthesis

1990 ◽  
Vol 52 (3) ◽  
pp. 509-514 ◽  
Author(s):  
C A Stuart ◽  
R E Shangraw ◽  
E J Peters ◽  
R R Wolfe
Keyword(s):  
Protein Synthesis ◽  
Dietary Protein ◽  
Bed Rest ◽  
Whole Body ◽  
Body Protein

scholarly journals The Interplay between Mitochondrial Morphology and Myomitokines in Aging Sarcopenia

2020 ◽  
Vol 22 (1) ◽  
pp. 91
Author(s):  
Vanina Romanello
Keyword(s):  
Mitochondrial Dysfunction ◽  
Poor Quality ◽  
Whole Body ◽  
Fibroblast Growth Factor 21 ◽  
Mitochondrial Morphology ◽  
Mass Force ◽  
Major Mechanism ◽  
Muscle Aging ◽  
And Function

Sarcopenia is a chronic disease characterized by the progressive loss of skeletal muscle mass, force, and function during aging. It is an emerging public problem associated with poor quality of life, disability, frailty, and high mortality. A decline in mitochondria quality control pathways constitutes a major mechanism driving aging sarcopenia, causing abnormal organelle accumulation over a lifetime. The resulting mitochondrial dysfunction in sarcopenic muscles feedbacks systemically by releasing the myomitokines fibroblast growth factor 21 (FGF21) and growth and differentiation factor 15 (GDF15), influencing the whole-body homeostasis and dictating healthy or unhealthy aging. This review describes the principal pathways controlling mitochondrial quality, many of which are potential therapeutic targets against muscle aging, and the connection between mitochondrial dysfunction and the myomitokines FGF21 and GDF15 in the pathogenesis of aging sarcopenia.

scholarly journals Processed By-Products from Soy Beverage (Okara) as Sustainable Ingredients for Nile Tilapia (O. niloticus) Juveniles: Effects on Nutrient Utilization and Muscle Quality

Animals ◽  
2021 ◽  
Vol 11 (3) ◽  
pp. 590
Author(s):  
Glenise B. Voss ◽  
Vera Sousa ◽  
Paulo Rema ◽  
Manuela. E. Pintado ◽  
Luísa M. P. Valente
Keyword(s):  
Nile Tilapia ◽  
Lactobacillus Rhamnosus ◽  
Protein Digestibility ◽  
Nutrient Utilization ◽  
Nutrient Digestibility ◽  
Fish Growth ◽  
Muscle Quality ◽  
Whole Body ◽  
Hypertrophic Growth ◽  
Bifidobacterium Animalis

The apparent digestibility coefficients (ADCs) of differently processed okara meals were assessed in Nile tilapia diets: dried okara not autoclaved (FOK), dried okara autoclaved (AOK), okara hydrolyzed with Alcalase (ALOK) or Cynara cardunculus proteases (CYOK), and hydrolyzed okara fermented with lactic bacteria: Lactobacillus rhamnosus R11 (CYR11OK) or Bifidobacterium animalis ssp. lactis Bb12 (CYB12OK). Okara processing significantly affected nutrient digestibility: dry matter ADC was highest in CYR11OK (80%) and lowest in FOK (40%). The lowest protein digestibility was observed in CYR11OK (72%), and the highest in AOK (97%) and CYOK (91%), evidencing the effectiveness of the autoclave and the use of C. cardunculus proteases to increase okara protein bioavailability. The inclusion of up to 20% of AOK or CYOK did not affect fish growth, nutrient utilization, or whole body composition of Nile tilapia. The flesh quality (color, pH, water activity, cohesiveness, elasticity and resilience) was not affected by the dietary incorporation of AOK or CYOK. Fish fed with AOK diets stand out for their high density of muscle fibers, particularly in AOK20, which can explain their high muscle firmness and may result in further hypertrophic growth. Altogether, results suggest that hydrolyzed or autoclaved okara are valuable ingredients for Nile tilapia diets.

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