Changing stroke rehab and research worldwide now.Time is Brain! trillions and trillions of neurons that DIE each day because there are NO effective hyperacute therapies besides tPA(only 12% effective). I have 523 posts on hyperacute therapy, enough for researchers to spend decades proving them out. These are my personal ideas and blog on stroke rehabilitation and stroke research. Do not attempt any of these without checking with your medical provider. Unless you join me in agitating, when you need these therapies they won't be there.

What this blog is for:

My blog is not to help survivors recover, it is to have the 10 million yearly stroke survivors light fires underneath their doctors, stroke hospitals and stroke researchers to get stroke solved. 100% recovery. The stroke medical world is completely failing at that goal, they don't even have it as a goal. Shortly after getting out of the hospital and getting NO information on the process or protocols of stroke rehabilitation and recovery I started searching on the internet and found that no other survivor received useful information. This is an attempt to cover all stroke rehabilitation information that should be readily available to survivors so they can talk with informed knowledge to their medical staff. It lays out what needs to be done to get stroke survivors closer to 100% recovery. It's quite disgusting that this information is not available from every stroke association and doctors group.

Thursday, December 17, 2020

Osteocalcin Signaling in Myofibers Is Necessary and Sufficient for Optimum Adaptation to Exercise

Your doctors and stroke hospital have had 4 years to get this tested in humans. HAVE THEY DONE ONE DAMN THING? 

You do want your exercise decline reversed?

The latest here: 

 Osteocalcin Signaling in Myofibers Is Necessary andSufficient for Optimum Adaptation to Exercise

Mera et al., 2016, Cell Metabolism 23, 1078–1092
Authors Paula Mera, Kathrin Laue, Mathieu Ferron, ..., Michelle Puchowicz, Irwin Kurland, Gerard Karsenty Correspondence gk2172@cumc.columbia.edu 
In Brief 
Mera et al. show that the bone-derived hormone osteocalcin is necessary for optimum exercise capacity and that this hormone decreases with aging in mice, monkeys, and humans of both genders. Osteocalcin promotes muscle uptake and utilization of glucose and lipids during exercise and greatly improves the exercise capacity of old mice.
Graphical Abstract 
Highlights 
 Bone via the hormone osteocalcin improves muscle function during exercise 
Circulating osteocalcin levels decrease in aging mice, monkeys, and humans 
Osteocalcin promotes muscle uptake and utilization of glucose and fatty acids 
Osteocalcin promotes muscle IL-6 secretion during exercise  
 

SUMMARY 

Circulating levels of undercarboxylated and bioactive osteocalcin double during aerobic exercise at the time levels of insulin decrease. In contrast, circulating levels of osteocalcin plummet early during adulthood in mice, monkeys, and humans of both genders. Exploring these observations revealed that osteocalcin signaling in myofibers is necessary for adaptation to exercise by favoring uptake and catabolism of glucose and fatty acids, the main nutrients of myofibers. Osteocalcin signaling in myofibers also accounts for most of the exercise-induced release of interleukin-6, a myokine that promotes adaptation to exercise in part by driving the generation of bioactive osteocalcin. We further show that exogenous osteocalcin is sufficient to enhance the exercise capacity of young mice and to restore to 15-month-old mice the exercise capacity of 3-month-old mice. This study uncovers a bone-tomuscle feedforward endocrine axis that favors adaptation to exercise and can reverse the age-induced decline in exercise capacity.

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