Barbell Training is Big Medicine

[Jonathon Sullivan]

Hi. My name is Luchezar, and I am from Bulgaria. I want to share with you that in our National Sports Academy we have professor Pavel Dobrev who is using barbell training to help people of old age, up to ninety years old for their quality of life with big results. He has free trainings in the mornings in 7:30-8:30 am for all who desire to participate.

Outstanding. Thank you for this.

Very inspirational article Dr. Sullivan.
(snip)

I started Benching, Squatting, Pressing, Rowing, and doing Chins and Dips on an assistance machine. After about 3 months of heavy compound exercises, at my last Dr appointment, I was 255 lbs, had a fasting BG of 105 and an a1C of 6.3%...he was so impressed he said I dont have to come back until August, and at that point we will take a look at discontinuing the Metformin.

You're the one who's inspirational, Bill. Thank you for sharing this. Don't stop now.

It's really sad the state of diabetes education in the US. Resistance training wasn't even discussed, when it is the best thing you can do.

We're working on it.

[billb7581]

Dont worry, I am not going anywhere. My goals are to get everything to non diabetic levels and be off of medication...although Metformin seems relatively safe from everything I have read.

[Jonathon Sullivan]

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
Li Luoa, b, A-Ming Lua, Yan Wangb, An Honga, Yulan Chena, Juan Hua, Xiaoning Lic, Zheng-Hong Qinb

Experimental Gerontology 2013; 48(4)427–436

Abstract

Resistance exercise training (RET) remains the most effective treatment for the loss of muscle mass and strength in elderly people. However, the underlying cellular and molecular mechanisms are not well understood. Recent evidence suggests that autophagic signaling is altered in aged skeletal muscles. This study aimed to investigate if RET affects IGF-1 and its receptors, the Akt/mTOR, and Akt/FOXO3a signaling pathways and regulates autophagy and apoptosis in the gastrocnemius muscles of 18–20 month old rats. The results showed that 9 weeks of RET 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, Atg7, and the lysosomal enzyme cathepsin L. RET also reduced cytochrome c level in the cytosol but increased its level in mitochondrial fraction, and inhibited cleaved caspase 3 production and apoptosis. Furthermore, RET upregulated the expression of IGF-1 and its receptors but downregulated the phosphorylation of Akt and mTOR. In addition, RET upregulated the expression of total AMPK, phosphorylated AMPK, and FOXO3a. Taken together, these results suggest that the benefits of RET are associated with increased autophagy activity and reduced apoptosis of muscle cells by modulating IGF-1 and its receptors, the Akt/mTOR and Akt/FOXO3a signaling pathways in aged skeletal muscles.