Another target for obesity – short circuiting muscles

Not actually how muscle circuitry looks

Not actually how muscle circuitry looks

Just want to get it straight from the start; this is not something applicable to bodybuilders. At least I don’t anticipate it will be something applicable to bodybuilders. But a lot of bodybuilders do dumb things in the quest for the perfect body, so really who knows.

Ok, moving on, you may recall the title of this from a previous article, specifically the “another target for obesity…” bit. That’s right, I am going to make this a series. The original was regarding Prolylcarboxypeptidase (PRCP) and this one will be about the concept of short circuiting muscle electricity in order to waste energy and promote a lean physique. The general gist of the series is something along the lines of “new concepts, not really pertinent, but interesting none the less.”

Sarcolemmal ATP-sensitive potassium channels (K-ATP) are channels found on the membrane of muscle cells involved in muscular contraction. They are controlled by ATP, or specifically the ATP:ADP ratio (which is an energy sensor in cells, something I have discussed in a previous article). When cell energy is low i.e. low ATP:ADP ratio, the K-ATP open in order to reduce the duration of an action potential. An action potential is a quick alteration in cell voltage in order to transmit a signal. The easiest way to think of this is to literally consider your cells as batteries that power movement. Opening the K-ATP serves to reduce the duration of the signal i.e. limiting the muscle contraction, thereby saving energy. And this is important as it meant you had more chance of surviving during famines back when food supply wasn’t so luxurious. Incidentally, this may partly explain the “slow metabolism” claim a lot of people make. Their bodies may simply be better at conserving energy than others by opening K-ATP channels quicker.

But what if you short-circuit these channels, thereby prolonging the signal and essentially wasting energy? That’s exactly what researchers from the Mayo Clinic in Minnesota wanted to find out. They did this by breading mice that lacked the channel. Amazingly, these mice seemed pretty resistant to adding body weight, even when fed on a high fat diet that induces obesity in normal mice. The wasting of energy in the muscle cells seems to come directly from fat stores resulting in leaner mice. Unfortunately, and this is where it makes it non-applicable for bodybuilders, muscle efficiency is severely hampered. For the average non-gym goer, this would probably sound quite appealing as it means they could lounge around and not get fat. But for anyone who is interested in performance, activity and building muscle would not find it a welcome effect. That is, unless, researchers came up with a synthetic way to disrupt these channels in the short-term. Your workouts would be screwed up, but you would expect some pretty significant fat loss. Like I said earlier, bodybuilders have a tendency to do dumb things so this doesn’t sound completely outrageous. But this looks like something that can and should be seriously looked into in the quest to treat obesity.

Source: Alekseev AE, Reyes S, Yamada S, Hodgson-Zingman DM, Sattiraju S, Zhu Z, Sierra A, Gerbin M, Coetzee WA, Goldhamer DJ, Terzic A, Zingman LV. Sarcolemmal ATP-sensitive K(+) channels control energy expenditure determining body weight. Cell Metab. 2010 Jan;11(1):58-69.

About the Author

Matt Cahill has worked extensively in the nutritional supplement field, and is the former CEO of Designer Supplements. During his time in the field has researched and developed prohormones, testosterone boosters, and other related compounds, both for his own company and others.