scholarly journals Exercising D. melanogaster Modulates the Mitochondrial Proteome and Physiology. The Effect on Lifespan Depends upon Age and Sex

2021 ◽  
Vol 22 (21) ◽  
pp. 11606
Author(s):  
Brad Ebanks ◽  
Ying Wang ◽  
Gunjan Katyal ◽  
Chloe Sargent ◽  
Thomas L. Ingram ◽  
...  

Ageing is a major risk factor for many of the most prevalent diseases, including neurodegenerative diseases, cancer, and heart disease. As the global population continues to age, behavioural interventions that can promote healthy ageing will improve quality of life and relieve the socioeconomic burden that comes with an aged society. Exercise is recognised as an effective intervention against many diseases of ageing, but we do not know the stage in an individual’s lifetime at which exercise is most effective at promoting healthy ageing, and whether or not it has a direct effect on lifespan. We exercised w1118 Drosophila melanogaster, investigating the effects of sex and group size at different stages of their lifetime, and recorded their lifespan. Climbing scores at 30 days were measured to record differences in fitness in response to exercise. We also assessed the mitochondrial proteome of w1118 Drosophila that had been exercised for one week, alongside mitochondrial respiration measured using high-resolution respirometry, to determine changes in mitochondrial physiology in response to exercise. We found that age-targeted exercise interventions improved the lifespan of both male and female Drosophila, and grouped males exercised in late life had improved climbing scores when compared with those exercised throughout their entire lifespan. The proteins of the electron transport chain were significantly upregulated in expression after one week of exercise, and complex-II-linked respiration was significantly increased in exercised Drosophila. Taken together, our findings provide a basis to test specific proteins, and complex II of the respiratory chain, as important effectors of exercise-induced healthy ageing.

Author(s):  
Brad Ebanks ◽  
Ying Wang ◽  
Gunjan Katyal ◽  
Chloe Sargent ◽  
Thomas L Ingram ◽  
...  

Ageing is a major risk factor for many of the most prevalent diseases, including neurodegenerative disease, cancer and heart disease. As the global population continues to age, behavioural interventions that can promote healthy ageing will improve quality of life and relieve the socio-economic burden that comes with an aged society. Exercise is recognised as an effective intervention against many diseases of ageing, but we don’t know the stage in an individual’s lifetime in which exercise is most effective at promoting healthy ageing and whether it has a direct effect on lifespan. We exercised w1118 Drosophila melanogaster, interrogating effects of sex and group size, at different stages of their lifetime and recorded their lifespan. Climbing scores at 30 days were measured to record differences in fitness in response to exercise. We also assessed the mitochondrial proteome of w1118 Drosophila that had been exercised for one week, alongside mitochondrial respiration measured using High-Resolution Respirometry, to determine changes in mitochondrial physiology in response to exercise. We found that age-targeted exercise interventions improve lifespan in male and female Drosophila, and grouped males exercised in late life had improved climbing scores, when compared with those exercised throughout their entire lifespan. The proteins of the electron transport chain were significantly upregulated in expression after one week of exercise, and complex II linked respiration was significantly increased in exercised -Drosophila. Taken together our study provides a basis to test specific proteins and complex II of the respiratory chain as important effectors of exercise induced healthy ageing.


Antioxidants ◽  
2021 ◽  
Vol 10 (2) ◽  
pp. 153
Author(s):  
Aslı Devrim-Lanpir ◽  
Lee Hill ◽  
Beat Knechtle

Exercise frequently alters the metabolic processes of oxidative metabolism in athletes, including exposure to extreme reactive oxygen species impairing exercise performance. Therefore, both researchers and athletes have been consistently investigating the possible strategies to improve metabolic adaptations to exercise-induced oxidative stress. N-acetylcysteine (NAC) has been applied as a therapeutic agent in treating many diseases in humans due to its precursory role in the production of hepatic glutathione, a natural antioxidant. Several studies have investigated NAC’s possible therapeutic role in oxidative metabolism and adaptive response to exercise in the athletic population. However, still conflicting questions regarding NAC supplementation need to be clarified. This narrative review aims to re-evaluate the metabolic effects of NAC on exercise-induced oxidative stress and adaptive response developed by athletes against the exercise, especially mitohormetic and sarcohormetic response.


2004 ◽  
Vol 63 (2) ◽  
pp. 227-232 ◽  
Author(s):  
Yun Chau Long ◽  
Ulrika Widegren ◽  
Juleen R. Zierath

Exercise training improves glucose homeostasis through enhanced insulin sensitivity in skeletal muscle. Muscle contraction through physical exercise is a physiological stimulus that elicits multiple biochemical and biophysical responses and therefore requires an appropriate control network. Mitogen-activated protein kinase (MAPK) signalling pathways constitute a network of phosphorylation cascades that link cellular stress to changes in transcriptional activity. MAPK cascades are divided into four major subfamilies, including extracellular signal-regulated kinases 1 and 2, p38 MAPK, c-Jun NH2-terminal kinase and extracellular signal-regulated kinase 5. The present review will present the current understanding of parallel MAPK signalling in human skeletal muscle in response to exercise and muscle contraction, with an emphasis on identifying potential signalling mechanisms responsible for changes in gene expression.


2004 ◽  
Vol 287 (6) ◽  
pp. E1189-E1194 ◽  
Author(s):  
Christian P. Fischer ◽  
Peter Plomgaard ◽  
Anne K. Hansen ◽  
Henriette Pilegaard ◽  
Bengt Saltin ◽  
...  

Contracting skeletal muscle expresses large amounts of IL-6. Because 1) IL-6 mRNA expression in contracting skeletal muscle is enhanced by low muscle glycogen content, and 2) IL-6 increases lipolysis and oxidation of fatty acids, we hypothesized that regular exercise training, associated with increased levels of resting muscle glycogen and enhanced capacity to oxidize fatty acids, would lead to a less-pronounced increase of skeletal muscle IL-6 mRNA in response to acute exercise. Thus, before and after 10 wk of knee extensor endurance training, skeletal muscle IL-6 mRNA expression was determined in young healthy men ( n = 7) in response to 3 h of dynamic knee extensor exercise, using the same relative workload. Maximal power output, time to exhaustion during submaximal exercise, resting muscle glycogen content, and citrate synthase and 3-hydroxyacyl-CoA dehydrogenase enzyme activity were all significantly enhanced by training. IL-6 mRNA expression in resting skeletal muscle did not change in response to training. However, although absolute workload during acute exercise was 44% higher ( P < 0.05) after the training period, skeletal muscle IL-6 mRNA content increased 76-fold ( P < 0.05) in response to exercise before the training period, but only 8-fold ( P < 0.05, relative to rest and pretraining) in response to exercise after training. Furthermore, the exercise-induced increase of plasma IL-6 ( P < 0.05, pre- and posttraining) was not higher after training despite higher absolute work intensity. In conclusion, the magnitude of the exercise-induced IL-6 mRNA expression in contracting human skeletal muscle was markedly reduced by 10 wk of training.


2008 ◽  
Vol 36 (2) ◽  
pp. 369-374 ◽  
Author(s):  
Panagiotis Baltopoulos ◽  
Charalampos Tsintzos ◽  
George Prionas ◽  
Maria Tsironi

Background Thoracic outlet syndrome is described as a group of distinct disorders producing signs and symptoms attributed to compression of nerves and blood vessels in the thoracic outlet region. Purpose To describe the exercise-induced scalenus anticus syndrome attributed to the anterior scalenus hypertrophy as a thoracic outlet syndrome underlying mechanism and to give recommendations for a safe and effective surgical treatment. Study Design Case series; Level of evidence, 4. Methods Twelve young professional athletes admitted for thoracic outlet syndrome (8 cases of neurologic thoracic outlet syndrome, 4 cases of mixed neurologic and vascular thoracic outlet syndrome) who reported numbness, tingling, early fatigue, muscle weakness, and pain were enrolled in the study. Scalenus hypertrophy was suspected to be the causative factor. Scalenectomy was performed in all cases. Results All patients had moderate to severe hypertrophy of the anterior scalenus muscle. Scalenectomy was performed, and there were no intraoperative or postoperative complications. Full activity was quickly achieved, and no recurrence of symptoms was documented. Conclusion Surgical intervention for scalenus anticus syndrome can allow an athlete to return to full activity and improve quality of life. Surgical intervention seems to be the treatment of choice in terms of restoring quality of life and physical activity.


PLoS ONE ◽  
2016 ◽  
Vol 11 (6) ◽  
pp. e0157704 ◽  
Author(s):  
Laurence Bal-Theoleyre ◽  
Alain Lalande ◽  
Frank Kober ◽  
Roch Giorgi ◽  
Frederic Collart ◽  
...  

2021 ◽  
Vol 22 (1) ◽  
Author(s):  
Aloka B. Bandara ◽  
Joshua C. Drake ◽  
David A. Brown

Abstract Background Succinate dehydrogenase (Complex II) plays a dual role in respiration by catalyzing the oxidation of succinate to fumarate in the mitochondrial Krebs cycle and transferring electrons from succinate to ubiquinone in the mitochondrial electron transport chain (ETC). Mutations in Complex II are associated with a number of pathologies. SDHD, one of the four subunits of Complex II, serves by anchoring the complex to the inner-membrane and transferring electrons from the complex to ubiquinone. Thus, modeling SDHD dysfunction could be a valuable tool for understanding its importance in metabolism and developing novel therapeutics, however no suitable models exist. Results Via CRISPR/Cas9, we mutated SDHD in HEK293 cells and investigated the in vitro role of SDHD in metabolism. Compared to the parent HEK293, the knockout mutant HEK293ΔSDHD produced significantly less number of cells in culture. The mutant cells predictably had suppressed Complex II-mediated mitochondrial respiration, but also Complex I-mediated respiration. SDHD mutation also adversely affected glycolytic capacity and ATP synthesis. Mutant cells were more apoptotic and susceptible to necrosis. Treatment with the mitochondrial therapeutic idebenone partially improved oxygen consumption and growth of mutant cells. Conclusions Overall, our results suggest that SDHD is vital for growth and metabolism of mammalian cells, and that respiratory and growth defects can be partially restored with treatment of a ubiquinone analog. This is the first report to use CRISPR/Cas9 approach to construct a knockout SDHD cell line and evaluate the efficacy of an established mitochondrial therapeutic candidate to improve bioenergetic capacity.


Author(s):  
Naina Vishwakarma

Geriatric problems are arising much and more in the present Era. With the increase in average life-span due to medical facilities it resulted in large number of people with old age Worldwide. To overcome this Ayurved advocates healthy ageing through Rasayan Chikitsa. By proper administration of Rasayan Therapy as a preventive tool one can prevent Jarajanit(Geriatic) vyadhis. Many herbs and techniques which provide solution to ageing and their complications are described in Ayurved. The Herbs with their properties slows down the natural process of aging and help in managing geriatric problem and improving the quality of life. Here   Amalaki an Rasayan Dravya in Geriatric diseases is brought in focus.


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