Written by Samuel Biesack
Losing body fat while maintaining muscle has been an area of interest for bodybuilders and scientists for years. Typical conjecture states that in order to lose body fat, a calorie deficit is necessary. While that is certainly true, as you become leaner the ability to maintain lean mass as well becomes just as important. Being leaner requires pinpointing exactly how to target fat loss so that you can optimize your body composition. AMPK is theoretically one such target.
Before rushing into specifics, let’s get some important information out of the way beginning with ATP. ATP or Adenosine triphosphate is a molecule that is comprised of an adenosine and three phosphates, hence the name. When energy is required (which is always), ATP donates one of its three phosphates to some component in the body. This phosphorylates whatever the phosphate was donated to, which in turn causes some sort of action in the body.
The second term we need to be familiar with is enzyme. Enzymes are present in pretty much every cell in the body and they have the distinct role of catalyzing or accelerating chemical reactions in the body. In essence, an enzyme causes something to occur within the cell.
Now that is settled, let’s discuss what AMPK is. 5′-adenosine monophosphate-activated protein kinase – or AMPK for short – is a type of enzyme that acts in two different ways depending on location (in muscle or fat tissue) and how it is activated (exercise or calorie restriction). This enzyme is an energy sensor of cells, specifically when energy is low.
More accurately, AMPK measures the amount of ADP (Adenosine diphosphate, meaning two phosphate) and AMP (adenosine monophosphate, meaning one phosphate). As ATP is used (thus donating a phosphate) the level of ADP and AMP rises in the cell, indicating energy usage. As ADP and AMP levels rise, AMPK is “turned on.” Phosphorylation (activation) of AMPK has a myriad of benefits when it comes to dropping body fat. Further, when it is stimulated by exercises as we will touch on shortly, it won’t compete with anabolic processes. In essence, promoting fat loss without effecting the ability to grow muscle.
For fat loss, this is extremely beneficial because AMPK associates with other enzymes that either directly aid in “fat burning” or directly inhibit the genesis and size increase of fat cells. In essence, phosphorylation of AMPK increases the chance of “burning fat” while reducing the chance of gaining fat.
What are ways to target AMPK and reap the benefits?
Muscle contraction is one of the easiest ways to increase AMPK activity. This is primarily because contraction requires energy to occur, thus the level of ADP and AMP in the muscle cell increases. In addition, by elevating AMPK as a result of muscle contraction, the ability of the muscle cell to absorb glucose (carbohydrate is converted to glucose when consumed) is increased substantially. Without going on a tangent, this is a very beneficial side effect due to shuttling the glucose into the muscle to be stored as glycogen rather than (potentially) being stored and converted to fat.
Carbohydrate restriction and glycogen depletion
Some studies (1) have indicated that having low muscle glycogen (glucose stored in the muscle) may be a key to activating AMPK. Chronic carbohydrate restriction is one potential route to achieve this state. However, if carbohydrate restriction is not a road you are willing to go down, depletion workouts can achieve a similar result for short durations. For an in-depth summary of what depletion workouts are, read this.
In addition, some supplements have been shown to have a positive benefit on AMPK. Supplements such as Alpha-Lipoic Acid (ALA) and Rhodiola Rosea have been shown to have a positive impact on AMPK levels. However, it should be noted that as mentioned prior, there are different types of AMPK, which can have different actions. One type of AMPK will directly compete with muscle growth pathways thus, as a precaution supplements such as these should be taken at times that are not around your training sessions.
About the Author
Sam is currently a student in the Master’s of Exercise and Nutrition Science program at the University of Tampa. In addition, he holds a B.S. in Behavioral Neuroscience the CSCS certification through the NSCA.
1. Taylor, C., Bartlett, J. D., van de Graaf, C. S., Louhelainen, J., Coyne, V., Iqbal, Z., … Morton, J. P. (2013). Protein ingestion does not impair exercise-induced AMPK signalling when in a glycogen-depleted state: implications for train-low compete-high. European Journal of Applied Physiology, 113(6), 1457–1468. http://doi.org/10.1007/s00421-012-2574-7