γ‐Oryzanol improves exercise endurance and muscle strength by upregulating PPARδ and ERRγ activity in aged mice

2021 ◽  
pp. 2000652
Author(s):  
Jisong Ahn ◽  
Hyo Jeong Son ◽  
Hyo Deok Seo ◽  
Tae Youl Ha ◽  
Jiyun Ahn ◽  
...  
2021 ◽  
Vol 21 ◽  
Author(s):  
Johanna Abrigo ◽  
Felipe Simon ◽  
Daniel Cabrera ◽  
Cristian Vilos ◽  
Claudio Cabello-Verrugio

Background: Sarcopenia is a progressive and generalized skeletal muscle disorder characterized by muscle weakness, loss of muscle mass, and decline in the capacity of force generation. Aging can cause sarcopenia. Several therapeutic strategies have been evaluated to prevent or alleviate this disorder. One of them is angiotensin 1-7 [Ang-(1-7)], an anti-atrophic peptide for skeletal muscles that regulates decreased muscle mass for several causes, including aging. Another regulator of muscle mass and function is andrographolide, a bicyclic diterpenoid lactone that decreases the nuclear factor kappa B (NF-κB) signaling and attenuates the severity of some muscle diseases. Objective: Evaluate the effect of combined administration of Ang-(1-7) with andrographolide on the physical performance, muscle strength, and fiber´s diameter in a murine model of sarcopenia by aging. Methods: Aged male mice of the C57BL/6J strain were treated with Andrographolide, Ang-(1-7), or combined for three months. The physical performance, muscle strength, and fiber´s diameter were measured. Results: The results showed that aged mice (24 months old) treated with Ang-(1-7) or Andrographolide improved their performance on a treadmill test, muscle strength, and their fiber´s diameter compared to aged mice without treatment. The combined administration of Ang-(1-7) with andrographolide to aged mice has an enhanced synergically effect on physical performance, muscle strength, and fiber´s diameter. Conclusion: Our results indicated that in aged mice, the effects of andrographolide and Ang-(1-7) on muscle function, strength, and fiber´s diameter are potentiated.


2018 ◽  
Vol 67 ◽  
pp. 128-136 ◽  
Author(s):  
Kajri A. Sheth ◽  
Chitra C. Iyer ◽  
Christopher G. Wier ◽  
Alexander E. Crum ◽  
Anna Bratasz ◽  
...  
Keyword(s):  

2018 ◽  
Vol 125 (2) ◽  
pp. 381-392 ◽  
Author(s):  
Daniel Langer ◽  
Casey Ciavaglia ◽  
Azmy Faisal ◽  
Katherine A. Webb ◽  
J. Alberto Neder ◽  
...  

Among patients with chronic obstructive pulmonary disease (COPD), those with the lowest maximal inspiratory pressures experience greater breathing discomfort (dyspnea) during exercise. In such individuals, inspiratory muscle training (IMT) may be associated with improvement of dyspnea, but the mechanisms for this are poorly understood. Therefore, we aimed to identify physiological mechanisms of improvement in dyspnea and exercise endurance following inspiratory muscle training (IMT) in patients with COPD and low maximal inspiratory pressure (Pimax). The effects of 8 wk of controlled IMT on respiratory muscle function, dyspnea, respiratory mechanics, and diaphragm electromyography (EMGdi) during constant work rate cycle exercise were evaluated in patients with activity-related dyspnea (baseline dyspnea index <9). Subjects were randomized to either IMT or a sham training control group ( n = 10 each). Twenty subjects (FEV1 = 47 ± 19% predicted; Pimax  = −59 ± 14 cmH2O; cycle ergometer peak work rate = 47 ± 21% predicted) completed the study; groups had comparable baseline lung function, respiratory muscle strength, activity-related dyspnea, and exercise capacity. IMT, compared with control, was associated with greater increases in inspiratory muscle strength and endurance, with attendant improvements in exertional dyspnea and exercise endurance time (all P < 0.05). After IMT, EMGdi expressed relative to its maximum (EMGdi/EMGdimax) decreased ( P < 0.05) with no significant change in ventilation, tidal inspiratory pressures, breathing pattern, or operating lung volumes during exercise. In conclusion, IMT improved inspiratory muscle strength and endurance in mechanically compromised patients with COPD and low Pimax. The attendant reduction in EMGdi/EMGdimax helped explain the decrease in perceived respiratory discomfort despite sustained high ventilation and intrinsic mechanical loading over a longer exercise duration. NEW & NOTEWORTHY In patients with COPD and low maximal inspiratory pressures, inspiratory muscle training (IMT) may be associated with improvement of dyspnea, but the mechanisms for this are poorly understood. This study showed that 8 wk of home-based, partially supervised IMT improved respiratory muscle strength and endurance, dyspnea, and exercise endurance. Dyspnea relief occurred in conjunction with a reduced activation of the diaphragm relative to maximum in the absence of significant changes in ventilation, breathing pattern, and operating lung volumes.


2021 ◽  
Vol 4 (1) ◽  
Author(s):  
Masashi Fukuoka ◽  
Hiromi Fujita ◽  
Kosumo Numao ◽  
Yasuko Nakamura ◽  
Hideo Shimizu ◽  
...  

AbstractParabiosis experiments suggest that molecular factors related to rejuvenation and aging circulate in the blood. Here, we show that miR-199-3p, which circulates in the blood as a cell-free miRNA, is significantly decreased in the blood of aged mice compared to young mice; and miR-199-3p has the ability to enhance myogenic differentiation and muscle regeneration. Administration of miR-199 mimics, which supply miR-199-3p, to aged mice resulted in muscle fiber hypertrophy and delayed loss of muscle strength. Systemic administration of miR-199 mimics to mdx mice, a well-known animal model of Duchenne muscular dystrophy (DMD), markedly improved the muscle strength of mice. Taken together, cell-free miR-199-3p in the blood may have an anti-aging effect such as a hypertrophic effect in aged muscle fibers and could have potential as a novel RNA therapeutic for DMD as well as age-related diseases. The findings provide us with new insights into blood-circulating miRNAs as age-related molecules.


Pneumologie ◽  
2017 ◽  
Vol 71 (S 01) ◽  
pp. S1-S125
Author(s):  
T Troosters ◽  
J Bourbeau ◽  
F Maltais ◽  
N Leidy ◽  
D Erzen ◽  
...  

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