Fat Loss Hypertrophy Uncategorized

Master your metabolism to torch fat and add muscle

Aaron Deere is a sports nutritionist, functional medicine consultant and advanced personal trainer. He is based in London.

What is AMPK?
Adenosine monophosphate-activated protein kinase (AMPK) is an enzyme that plays a central role in cellular energy homeostasis. It is expressed in tissues throughout the body, including the liver, brain and skeletal muscle, and has been shown to exhibit multiple functions, acting a metabolic ‘master switch’, regulating cellular functions, such as the cellular uptake of glucose, beta-oxidation of fatty acids and the biogenesis of mitochondria.

In relation to strength and conditioning training, the key function revolves around fatty acid oxidation.
The net effect of AMPK activation is to halt energy-consuming (anabolic) pathways and promote energy-conserving (catabolic) cellular pathways, which results in increased rates of fatty acid oxidation and adaptations which will further facilitate fat oxidation. Levels of AMPK are therefore of great importance in programmes designed to reduce body-fat levels.

How is it activated?
AMPK plays a role in cellular energy homeostasis, acting as the cell fuel gauge. It is sensitive to the ratio between adenosine monophosphate (AMP) and adenosine triphosphate (ATP), and is activated by any cellular process which decreases ATP levels, or increases AMP concentrations, with glucose deprivation within the cell the key activator of AMPK. When the cell energy level drops below a predetermined level AMPK is activated, with research suggesting a decrease in cellular energy levels of 30% being sufficient to increase AMPK levels to a threshold which promotes fat oxidation adaptations. AMPK fundamentally acts to conserve energy by turning off energy-consuming anabolism and switches on catabolism, which ultimately aims to improve energy efficiency and the ‘fitness’ of cell.

How does it influence muscle building?
AMPK exhibits an inverse relationship with a protein called mTOR, which regulates cell growth, cell proliferation, protein synthesis and transcription. Fundamentally it acts as the anabolic switch within the cell and is responsible for muscular hypertrophy and strength gains from resistance training. mTOR is inhibited by AMPK. Therefore, when AMPK levels are high and the body is in more of a ‘catabolic’ state, the anabolic pathways involving mTOR are down-regulated.

How does it influence fat loss?
The relationship between AMPK and mTOR is best thought of as an inverse relationship, where by when one is high the other is low. Therefore, greater rates of fat loss are seen when AMPK levels are high and signal to the body to improve energy efficiency. As mentioned above a decrease in cellular energy levels of 30% has been shown to be sufficient to increase AMPK levels to a threshold which promotes fat oxidation adaptations.

The energy level of cell (glycogen) is directly affected by exercise and dietary intake of carbohydrates. Limiting carbohydrate intake, especially in the two-hour post-exercise window, will increase AMPK levels within the body and promote adaptations related to fat oxidation.

What does all this mean?
If the goal of training is to increase muscle size or strength then high levels of AMPK are not optimal.
The elevated levels of AMPK will inhibit mTOR, one of the key proteins that are responsible for cell growth and cell proliferation. In animal models, increased AMPK activity has been suggested as a potential cause for Huntington’s disease, via brain atrophy and facilitated neuronal loss, with chronic increased activity also being suggested to have a link to Alzheimer’s disease in humans, but results of current research are equivocal on both these outcomes.

Lee, Woo Je, et al. “AMPK activation increases fatty acid oxidation in skeletal muscle by activating PPAR and PGC-1.” Biochemical and biophysical research communications 340.1 (2006): 291-295.
Hardie DG. AMP-activated/SNF1 protein kinases: conserved guardians of cellular energy. Nat Rev Mol Cell Biol 2007; 8: 774–85.
Carling D, Clarke PR, Zammit VA, Hardie DG. Purification and characterization of the AMP-activated protein kinase. Copurification of acetyl-CoA carboxylase kinase and 3-hydroxy-3-methylglutaryl-CoA reductase kinase activities. Eur J Biochem 1989; 186: 129–36.
Steinberg GR, Kemp BE. AMPK in Health and Disease. Physiol Rev 2009; 89: 1025–78.
Towler MC, Hardie DG. AMP-activated protein kinase in metabolic control and insulin signaling. Circ Res 2007; 100: 328–41.
Lopez-Lopez C, Dietrich MO, Metzger F, Loetscher H, Torres-Aleman I. Disturbed cross talk between insulin-like growth factor I and AMP-activated protein kinase as a possible cause of vascular dysfunction in the amyloid precursor protein/presenilin 2 mouse model of Alzheimer’s disease. J Neurosci 27: 824–831, 2007.
Ju, Tz-Chuen, et al. “Nuclear translocation of AMPK-1 potentiates striatal neurodegeneration in Huntington’s disease.” The Journal of cell biology 194.2 (2011): 209-227.



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