Chronic resistance training activates autophagy and reduces apoptosis of muscle cells by modulating IGF-1 and its receptors, Akt/mTOR and Akt/FOXO3a signaling in aged rats

Luo, Li; Lu, Aming; Wang, Yan; Hong, An; Chen, Yulan; Hu, Juan; Li, Xiaoning; Qin, Zheng‐Hong

doi:10.1016/j.exger.2013.02.009

Cited by 149 publications

(140 citation statements)

References 67 publications

Supporting

Mentioning

129

Contrasting

Unclassified

Order By: Relevance

“…Kim et al reported lower expression of beclin-1 and Atg7 in skeletal muscle of old compared with young animals, but these factors were upregulated in old mice after an 8-week aerobic training program (Kim et al 2013). In addition, 9 weeks of resistance exercise training prevented the loss of muscle mass and improved muscle strength, accompanied by reduced LC3-II/LC3-I ratio, reduced p62 protein levels, and increased levels of autophagy regulatory proteins, including Beclin 1, Atg5/12, and Atg7 in skeletal muscles from aged rats (Luo et al 2013). In any case, the present work is the first investigation addressing the effects of exercise training on the decline of the autophagy machinery in older human subjects.…”

Section: Discussionmentioning

confidence: 99%

“…Thus, selective autophagic elimination of flawed mitochondria (i.e., mitophagy pathway) may be involved in the removal and recycling of defective mitochondria during exercise, improving the resistance to oxidative stress, and potentially the inflammation Peeri and Amiri 2015;Li et al 2016). Nevertheless, resistance training, which has minimum impact on mitochondrial function, is also capable of reversing the undesirable effects of age on the autophagy regulatory proteins (Luo et al 2013). These results support previous investigations showing increased mRNA levels of LC3B and Atg7, and a tendency for LAMP2, in vastus lateralis muscle from older and obese women after an intervention of caloric restriction and moderate-intensity combined resistance and endurance exercise (Wohlgemuth et al 2011).…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Effects of aerobic training on markers of autophagy in the elderly

Mejías-Peña

Rodriguez‐Miguelez

Fernandez‐Gonzalo

et al. 2016

AGE

View full text Add to dashboard Cite

Autophagy is a molecular process essential for the maintenance of cellular homeostasis, which appears to (i) decline with age and (ii) respond to physical exercise. In addition, recent evidence suggests a crosstalk between autophagy and toll-like receptor (TLR)-associated inflammatory responses. This study assessed the effects of aerobic exercise training on autophagy and TLR signaling in older subjects. Twentynine healthy women and men (age, 69.7 ± 1.0 year) were randomized to a training (TG) or a control (CG) group. TG performed an 8-week aerobic training program, while CG followed their daily routines. Peripheral blood mononuclear cells were isolated from blood samples obtained before and after the intervention, and protein levels of protein 1 light chain 3 (LC3), sequestosome 1 (p62/SQSTM1), beclin-1, phosphorylated unc-51-like kinase (ULK-1), ubiquitin-like autophagy-related (Atg)12, Atg16, and lysosome-associated membrane protein (LAMP)-2 were measured. TLR2 and TLR4 signaling pathways were also analyzed. Peak oxygen uptake increased in TG after the intervention. Protein expression of beclin-1, Atg12, Atg16, and the LC3II/I ratio increased following the training program (p < 0.05), while expression of p62/SQSTM1 and phosphorylation of ULK-1 at Ser 757 were lower (p < 0.05). Protein content of TLR2, TLR4, myeloid differentiation primary response gen 88 (MyD88), and TIR domaincontaining adaptor-inducing interferon (TRIF) were not significantly modified by exercise. The current data indicate that aerobic exercise training induces alterations in multiple markers of autophagy, which seem to be unrelated to changes in TLR2 and TLR4 signaling pathways. These results expand knowledge on exerciseinduced autophagy adaptations in humans and suggest that the exercise type employed may be a key factor explaining the potential relationship between autophagy and TLR pathways.

show abstract

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Effects of aerobic training on markers of autophagy in the elderly

Mejías-Peña

Rodriguez‐Miguelez

Fernandez‐Gonzalo

et al. 2016

AGE

View full text Add to dashboard Cite

show abstract

“…177 Long-term resistance training (9 wk) prevents age-related muscle atrophy and is associated with increased autophagy levels in rat gastrocnemius muscles. 190 Similarly, regular aerobic exercise prevents an age-related decrease in autophagy proteins (BECN1 and ATG7), suggesting that exercise plays an important role in skeletal muscle remodeling through the modulation of the degradation of the crucial muscle proteins. 191,192 Taken together, these studies demonstrate the requirement of autophagy in exercise-mediated development of skeletal muscle adaptation and physical endurance.…”

Section: Exercise Modulates Autophagy In Animalsmentioning

confidence: 99%

Heat shock response and autophagy—cooperation and control

2015

View full text Add to dashboard Cite

Abbreviations: AKT, v-akt murine thymoma viral oncogene homolog 1; AMPK, adenosine monophosphate-activated protein kinase; ATG, autophagy-related; BECN1, Beclin 1, autophagy related; EIF4EBP1, eukaryotic translation initiation factor 4E binding protein 1; ER, endoplasmic reticulum; FOXO, forkhead box O; HSF1, heat shock transcription factor 1; HSP, heat shock protein; HSPA8/ HSC70, heat shock 70kDa protein 8; IL, interleukin; LC3, MAP1LC3, microtubule-associated protein 1 light chain 3; MTMR14/ hJumpy, myotubularin related protein 14; MTOR, mechanistic target of rapamycin; NR1D1/Rev-Erb-a, nuclear receptor subfamily 1, group D, member 1; PBMC, peripheral blood mononuclear cell; PPARGC1A/PGC-1a, peroxisome proliferator-activated receptor, gamma, coactivator 1 a; RHEB, Ras homolog enriched in brain; SOD, superoxide dismutase; SQSTM1/p62, sequestosome 1; TPR, translocated promoter region, nuclear basket protein; TSC, tuberous sclerosis complex; ULK1, unc-51 like autophagy activating kinase 1.Protein quality control (proteostasis) depends on constant protein degradation and resynthesis, and is essential for proper homeostasis in systems from single cells to whole organisms. Cells possess several mechanisms and processes to maintain proteostasis. At one end of the spectrum, the heat shock proteins modulate protein folding and repair. At the other end, the proteasome and autophagy as well as other lysosome-dependent systems, function in the degradation of dysfunctional proteins. In this review, we examine how these systems interact to maintain proteostasis. Both the direct cellular data on heat shock control over autophagy and the time course of exercise-associated changes in humans support the model that heat shock response and autophagy are tightly linked. Studying the links between exercise stress and molecular control of proteostasis provides evidence that the heat shock response and autophagy coordinate and undergo sequential activation and downregulation, and that this is essential for proper proteostasis in eukaryotic systems.

show abstract

“…Thus, we aimed to establish a protocol applicable to subjects with muscle disease in our previous test. Referencing existing protocols [39][40][41][42], our modified method was accomplished successfully. The workout equipment consisting of climbing ladders (20 × 115 cm) with 4 cm grids inclined at 85 degrees were made in our laboratory.…”

Section: Long-term Effects Of Resistance Exercise Trainingmentioning

confidence: 99%

Effects of long-term resistance exercise training on autophagy in rat skeletal muscle of chloroquine-induced sporadic inclusion body myositis

Kwon¹,

Lee²,

Lima³

et al. 2015

J. Exerc. Nutr, Biochem.

View full text Add to dashboard Cite

Insu Kwon, Youngil Lee, Ludmila M. Cosio-Lima, Joon-Yong Cho and Dong-Chul Yeom. Effects of long-term resistance exercise training on autophagy in rat skeletal muscle of chloroquine-induced sporadic inclusion body myositis. JENB., Vol. 19, No. 3, pp.225-234, 2015 [Purpose] We examined whether resistance exercise training restores impaired autophagy functions caused by Chloroquine (CQ)-induced Sporadic Inclusion Body Myositis (sIBM) in rat skeletal muscle.[Methods] Male wistar rats were randomly assigned into three groups: Sham (n = 6), CQ (n = 6), and CQ + Exercise (CE, n = 6). To create a rat model of sIBM, rats in the CQ and CE group were intraperitoneally injected with CQ 5 days a week for 16 weeks. Rats in the CE group performed resistance exercise training 3 times a week for 8 weeks in conjunction with CQ starting from week 9 to week 16. During the training period, maximal carrying load, body weight, muscle weight, and relative muscle weight were measured. Autophagy responses were examined by measuring specific markers.[Results] While maximal carrying capacity for resistance exercise training was dramatically increased in the CE group, no significant changes occurred in the skeletal muscle weight as well as in the relative muscle weight of CE compared to the other groups. CQ treatment caused significant increases in the levels of Beclin-1 and p62, and decreases in the levels of LAMP-2 proteins. Interestingly, no significant differences in the LC3-II/I ratio or the LC3-II protein levels were observed. Although CQ-treatment groups suppressed the levels of the potent autophagy inducer, BNIP3, p62 levels were decreased in only the CE group.[Conclusion] Our findings demonstrate that sIBM induced by CQ treatment results in muscle degeneration via impaired autophagy and that resistance exercise training improves movable loading activity. Finally, regular exercise training may provide protection against sIBM by enhancing the autophagy flux through p62 protein.

show abstract

Chronic resistance training activates autophagy and reduces apoptosis of muscle cells by modulating IGF-1 and its receptors, Akt/mTOR and Akt/FOXO3a signaling in aged rats

Cited by 149 publications

References 67 publications

Effects of aerobic training on markers of autophagy in the elderly

Effects of aerobic training on markers of autophagy in the elderly

Heat shock response and autophagy—cooperation and control

Effects of long-term resistance exercise training on autophagy in rat skeletal muscle of chloroquine-induced sporadic inclusion body myositis

Contact Info

Product

Resources

About