Sarcopenia is the characteristic progressive loss of muscle mass and strength with age. Much like almost all other aspects of degenerative aging, sarcopenia is slowed by the practice of calorie restriction, but researchers are still debating the root causes of this process. Is sarcopenia a consequence of insulin resistance in any way, for example, or is it secondary to dietary changes that tend to happen later in life? Some researchers have compelling evidence to suggest that a progressive inability to process the essential amino acid leucine is what causes sarcopenia, and that the effect can be blunted by leucine supplementation and exercise. There is even debate as to whether the primary problem is loss of muscle mass or loss of function in the muscle fibers.
There is no shortage of other views. Here, researchers provide a convincing demonstration of their theory on sarcopenia:
Normally, [the tiny blood vessels in muscle] are closed, but when a young person eats a meal and insulin is released into the bloodstream, they open wide to allow nutrients to reach muscle cells. In elderly people, however, insulin has no such "vasodilating" effect.
"We were unsure as to whether decreased vasodilation was just one of the side effects of aging or was one of the main causes of the reduction in muscle protein synthesis in elderly people, because when nutrients and insulin get into muscle fibers, they also turn on lots of intracellular signals linked to muscle growth," said UTMB's Dr. Elena Volpi, senior author of the paper. "This research really demonstrates that vasodilation is a necessary mechanism for insulin to stimulate muscle protein synthesis."
Volpi and her collaborators reached this conclusion after an experiment in which they infused an amount of insulin equivalent to that generated by the body in response to a single meal into the thigh muscles of two sets of young volunteers. One group had been given a drug that blocked vasodilation, while the other was allowed to respond normally. Measurements of muscle protein synthesis levels where made using chemical tracers, while biopsies yielded data on specific biochemical pathways linked to muscle growth.
"We found that by blocking vasodilation, we reproduced in young people the entire response that we see in older persons - a blunting of muscle protein response and a lack of net muscle growth. In other words, from a muscle standpoint, we made young people look 50 years older," Volpi said.
The paper can be found via PubMed for those who are interested. Blood vessels are an important form of biological infrastructure in our bodies: not just tubes, but in fact complex reactive machinery. They become progressively more damaged by age, unable to adjust as they should, and this causes harm to many of our bodily systems:
The rust that causes blood vessels to degrade in performance probably has to do with increasing oxidative damage, the accumulation of AGE compounds that interfere in cell signaling, and possibly the chemistry of chronic inflammation. Blood vessels are complex little machines that rely on their structure and a coordinated set of signaling mechanisms to do their job. As the damage of aging changes that structure, interferes with signaling, and degrades the effectiveness of our blood vessels, this in turn hurts the rest of our biochemical systems.
Timmerman KL, Lee JL, Dreyer HC, Dhanani S, Glynn EL, Fry CS, Drummond MJ, Sheffield-Moore M, Rasmussen BB, & Volpi E (2010). Insulin Stimulates Human Skeletal Muscle Protein Synthesis via an Indirect Mechanism Involving Endothelial-Dependent Vasodilation and Mammalian Target of Rapamycin Complex 1 Signaling. The Journal of clinical endocrinology and metabolism PMID: 20484484