Resistance exercise reduced the expression of fibroblast growth factor-2 in skeletal muscle of aged mice

Yoon, Dong Hyun; Kim, Hee-jae; Choi, Mi‐Jung; Song, Wook

doi:10.1016/j.imr.2016.05.001

Cited by 19 publications

(20 citation statements)

References 20 publications

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“…We found exercise did not change food intake in both WT and OXGR1KO mice (Fig. 7D), consistent with the previous observations in the adult and aged male mice following the same ladder-climbing resistance exercise (Kim et al, 2016). Exercise effectively decreased body weight gain in WT control mice, while deletion of OXGR1 attenuated the bodyweight decrease induced by resistance exercise (Fig.…”

Section: Resultssupporting

confidence: 92%

“…Ten-week-old C57BL/6 male mice were divided into four groups: resistance exercise group, endurance exercise group, running wheel exercise group, or a control group without exercise. For resistance exercise group, resistance ladder-climbing exercise was performed as described previously (Kim et al, 2016). Ladder climbing exercise was conducted by using a 1 m ladder with 1.5 cm grids.…”

Section: Methodsmentioning

confidence: 99%

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α-ketoglutaric acid stimulates muscle hypertrophy and fat loss through OXGR1-dependent adrenal activation

Yuan

Jiang

et al. 2019

Preprint

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Running title: α-ketoglutaric acid stimulates lipolysis through OXGR1 31 32 Conflict of interest statement 33The authors have declared that no conflict of interest exists. 34 35 36 37 38 39 40 41 42 43 44 3 Summary: Beneficial effects of resistance exercise on metabolic health and particularly muscle 45hypertrophy and fat loss are well established, but the underlying chemical and physiological 46 mechanisms are not fully understood. Here we identified a myometabolite-mediated metabolic 47 pathway that is essential for the beneficial metabolic effects of resistance exercise in vivo. We showed 48 that substantial accumulation of the tricarboxylic acid cycle intermediate α-ketoglutaric acid (AKG) is 49 a metabolic signature of resistance exercise performance. Interestingly, human plasma AKG level is 50 also negatively correlated with BMI. Pharmacological elevation of circulating AKG induces muscle 51 hypertrophy, brown adipose tissue (BAT) thermogenesis, and white adipose tissue (WAT) lipolysis in 52 vivo. We further found that AKG stimulates the adrenal release of adrenaline through 2-oxoglutarate 53 receptor 1 (OXGR1) expressed in adrenal glands. Finally, by using both loss-of-function and 54 gain-of-function mouse models, we showed that OXGR1 is essential for AKG-mediated 55 exercise-induced beneficial metabolic effects. These findings reveal an unappreciated mechanism for 56 the salutary effects of resistance exercise, using AKG as a systemically-derived molecule for adrenal 57 stimulation of muscle hypertrophy and fat loss. 58 59 Keywords: AKG/lipolysis /obesity/OXGR1/thermogenesis. 60 61 62 63 64 5 provide signatures of endurance exercise performance and cardiovascular disease susceptibility, and 88also identify molecular pathways that may modulate the salutary effects on cardiovascular function. 89However, very few metabolomics data is available for resistance exercise (Berton et al, 2017; Li et al, 90 2012), and the underlying chemical and physiological mechanisms for the stimulatory effects of 91 resistance exercise on fat loss and muscle hypertrophy are not fully understood. Our goal is to identify 92 the essential mediator for the beneficial metabolic effects of resistance exercise and provide potential 93 therapeutic strategies to mimic the health effects of resistance exercise to combat obesity. 94 95Emerging evidence has identified skeletal muscle as secretory organs in regulating energy 96 homeostasis and obesity progression in other tissues (Ibrahim et al, 2017; Rai & Demontis, 2016). 97Exercise can induce systemic metabolic effects either via changes in the mass and metabolic demand 98 of muscle or via the release of muscle-derived cytokines (myokines) and metabolites (myometabolites) 99

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Section: Resultssupporting

confidence: 92%

Section: Methodsmentioning

confidence: 99%

α-ketoglutaric acid stimulates muscle hypertrophy and fat loss through OXGR1-dependent adrenal activation

Yuan

Jiang

et al. 2019

Preprint

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“…ACVA, a homodimeric glycoprotein produced by the decidua, placenta and fetal membranes, is involved in cellular differentiation, proliferation, remodelling and morphogenesis (31) . FGF-2 is a heparin-binding protein that regulates cellular functions, including muscle regeneration, maintenance and skeletal muscle growth by increasing the proliferation of satellite cells (32) . Moreover, TGF-β1 is known as a multifunctional protein that acts as a skeletal muscle regenerator since it contributes to extracellular matrix reconstitution as well as muscle tissue remodelling (33) .…”

Section: Discussionmentioning

confidence: 99%

Comparison of whole egg v. egg white ingestion during 12 weeks of resistance training on skeletal muscle regulatory markers in resistance-trained men

Bagheri

Moghadam

et al. 2020

Br J Nutr

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Eggs are considered a high-quality protein source for its complete amino acid profile and digestibility. Therefore, this study aimed to compare the effects of the whole egg (WE) vs. egg white (EW) ingestion during 12 weeks of resistance training (RT) on skeletal muscle regulatory markers and body composition in resistance-trained men. Thirty resistance-trained men (24.6 ± 2.7 years) were randomly assigned into a WE + RT (WER; n=15) or EW + RT (EWR; n=15) groups. The WER group ingested three WE while the EWR group ingested an isonitrogenous quantity of six EW per day immediately after the RT session. Serum concentrations of regulatory markers and body composition were measured at baseline and after 12 weeks. Significant main effects of time were observed for bodyweight [WER = 1.7 kg and EWR= 1.8 kg], skeletal muscle mass [WER = 2.9 kg and EWR= 2.7 kg], Fibroblast growth factor 2 [WER = 116.1 pg.ml and EWR= 83.2 pg.ml], and follistatin [WER = 0.05 ng.ml and EWR= 0.04 ng.ml], which significantly increased (p ˂ 0.05); and for fat mass [WER = -1.9 kg and EWR= -1.1 kg], Transforming growth factor-β1 [WER = -0.5 ng.ml and EWR= -0.1 ng.ml], Activin A [WER = -6.2 pg.ml and EWR= -4.5 pg.ml], and myostatin [WER = -0.1 ng.ml and EWR= -0.06 ng.ml], which significantly decreased (p ˂ 0.05) in both the WER and EWR groups. Consumption of eggs absent of yolk during chronic RT results in similar body composition and functional outcomes as WE of equal protein value. EW or WE may be used interchangeably for the dietary support of RT-induced muscular hypertrophy when protein intake is maintained.

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“…Aerobic exercise was performed on a motor-driven rodent treadmill (20 m/min, 60 min) for 3 d (Monday, Wednesday, Friday) a week (24). Resistance exercise were performed on a ladder (90˚) for 3 d (Tuesday, Thursday, and Saturday) every week, with no load, and the mice in the 4 groups climbed from the bottom of the ladder to the top 1 time or 4 times/group (25).…”

Section: Animalsmentioning

confidence: 99%

AMPKα2 Deficiency Does Not Affect the Exercise-Induced Improvements in Glucose Tolerance and Metabolic Disorders in Mice Fed a High-Fat Diet

Sun

Tian²,

Zheng

et al. 2019

J Nutr Sci Vitaminol

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Exercise can improve obesity and metabolic disorders in mice fed a high-fat diet (HFD), but the role of AMPKa2 in the process remains unclear. The aim of this study was to investigate the role of AMPKa2 in the exercise-induced improvements in glucose tolerance and metabolic turnover in obesity mice. Male wild-type mice (n512) and AMPKa2 knockout (AMPKa2 KO) mice (n512) were fed a HFD for 16 wk and were then randomly divided into four groups: WT HFD group (WT HF), AMPKa2 KO HFD group (AMPKa2 KO HF), WT HFD exercise group (WT HE), and AMPK HFD exercise group (AMPKa2 KO HE). The HF groups continue to be fed a HFD from 16 wk to 24 wk, and the HE groups were fed a HFD and performed exercise training. After 8 wk of exercise, all mice were placed in an energy metabolism chamber to test their metabolic turnover, include locomotor activity, food intake, oxygen consumption (VO2), carbon dioxide production (VCO2), energy expenditure (EE) and respiratory exchange ratio (RER), over a period of 3 d. Exercise improved glucose tolerance, VO2, VCO2 and EE in mice fed a HFD (p,0.05). The VO2, VCO2 and EE in AMPKa2 KO HE group were lower than these in WT HE group (p,0.05). Our findings revealed exercise improved glucose tolerance and metabolic disorders in C57 and AMPKa2 KO mice fed a HFD. AMPKa2 is not essential for exercise-induced improvements in glucose tolerance and metabolic disorders.

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Resistance exercise reduced the expression of fibroblast growth factor-2 in skeletal muscle of aged mice

Cited by 19 publications

References 20 publications

α-ketoglutaric acid stimulates muscle hypertrophy and fat loss through OXGR1-dependent adrenal activation

α-ketoglutaric acid stimulates muscle hypertrophy and fat loss through OXGR1-dependent adrenal activation

Comparison of whole egg v. egg white ingestion during 12 weeks of resistance training on skeletal muscle regulatory markers in resistance-trained men

AMPKα2 Deficiency Does Not Affect the Exercise-Induced Improvements in Glucose Tolerance and Metabolic Disorders in Mice Fed a High-Fat Diet

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