The younger drinker’s illusion of superhuman strength known as “beer muscles” acquires new meaning after decades of alcohol abuse, as cellular damage weakens muscle strength over time.
In a new study published Monday in The Journal of Cell Biology, researchers from Thomas Jefferson University say such muscle weakness has long been a common symptom of alcoholics and people with mitochondrial disease — and now they know why. As the body ages, cellular organelles called mitochondria self-repair damage by fusing with other mitochondria and exchanging contents.
Yet that mitochondrial repair process breaks down within the cells of someone who’s abused alcohol for years, says Gyorgy Hajnoczky, a pathologist who directs the hospital’s MitoCare Center.
Researchers had previously questioned whether mitochondria in skeletal muscle used fusion to repair themselves, given the density of those organelles packed tightly among fibers of muscle cell — something some saw as impossible. In the study, Hajnoczky and his colleagues demonstrated that mitofusin fusion proteins (Mfn1) were most important for the task in skeletal muscle tissue cells. To do so, they devised a system whereby they tagged the mitochondria of skeletal muscle in laboratory rats with two different colors, looking for signs of fusion. In rats whose mitochondria cells displayed the color red, the researchers programmed mitochondrial cells, through genetic engineering, to turn green when hit with a laser. Surprisingly, the mitochondria not only fused in those cells but ranged within the intracellular body much further than previously thought.
Researcher Veronica Eisner said in a press release they’d showed “for the first time that mitochondrial fusion occurs in muscle cells.”
After IDing these Mfn1 proteins, the researchers found that levels fell by as much as half when tested on laboratory rats simulating the adult alcoholic. And as suspected, muscle strength dropped with attendant losses of the protein used in fusion, the researchers said.
"That alcohol can have a specific effect on this one gene involved in mitochondrial fusion suggests that other environmental factors may also specifically alter mitochondrial fusion and repair," Hajnoczky said. "The work provides more evidence to support the concept that fission and fusion — or mitochondrial dynamics — may be responsible for more than just a subset of mitochondrial diseases we know of."
Researchers first suspected mitochondrial fusion as the problem when investigating Autosomal Dominant Optical Atropy disease and a specific type of Charcot-Marie-Tooth disease, both of which are mitochondrial diseases.
In the meantime, researchers may soon begin researching a possible drug therapy for muscle strength lost to alcoholism and various mitochondrial diseases.
Source: Eisner V, Lenaers G, Hajnoczky G. Mitochondrial fusion is frequent in skeletal muscle and supports excitation–contraction coupling. Cell Biology. 2014.