Seth Walsh
The man in the mirror is my only threat
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AMPK stands for AMP activated protein kinase. AMP stands for Adenosine Monophosphate. As you know, if you're familiar with creatine and ATPs, ATP stands for Adenosine Triphosphate. ATP is needed by the mitochondria for energy. AMPs are unusuable phosphates that need to bond with an ADP to make usable energy.
So, AMPK is looked at as an "energy sensor", and is activated by being in an energy deficit. How this energy deficit is measured is through the AMP:ATP ratio.
AMPK is the master regulator of energy metabolism.
Exercise activates AMPK. This should make sense now, because during exercise you are using up your ATPs. Since the AMP:ATP ratio grows bigger, AMPK gets activated.
AMPK is a negative regulator of mTOR, meaning it inhibits the mTOR pathway as AMPK itself is activated. Creatine provides more ATPs during exercise, possibly delaying or minimizing the inhibition of mTOR, which is the pathway responsible for protein synthesis. I hope this adds some insight as to why creatine is an effective supplement for keeping muscle mass and optimizing performance.
What does AMPK activate?:
ULK1 (Serine/threonine-protein kinase). ULK1 is a protein responsible for macroautophagy.
ATGL (Adipose triglyceride lipase). This is an enzyme responsible for the release of fatty acids from a triglyceride, which eventually leads to fatty acid catabolism.
What else does AMPK inhibit?:
ACC (Acetyl-CoA Corboxylase). This enzyme is responsible for fatty acid synthesis. AMPK is responsible for inhibiting fatty acid synthesis.
HMG-CoA Reductase. This enzyme is responsible for Cholesterol synthesis.
GS (Glycogen Synthase). The enzyme responsible for glycogen synthesis. In an energy deficit (with AMPK active), you won't be able to store new glycogen in your liver or muscle tissue.
What else is AMPK responsible for activating?:
TBC1D1: A very interesting channel. TBC1D1 helps insulin sensitive cells uptake glucose in the absence of insulin by recruiting GLUT4 vesicles.
GLUT4 translocalisation is an insulin mimicking process. You should not be worried about glucose not being able to enter your cells during AMPK activation during exercise, because TBC1D1 takes care of this process. (Do not buy post workout carb supplements as they're just a waste of money. You don't need an "insulin spike post workout", TBC1D1 is doing insulin's job for your cells during your exercise).
Glycolysis occurs after the GLUT4 translocalisation. Glycolysis is just the breakdown of glucose within your cells.
Summary of AMPK signalling
Increases glucose uptake and utilization
Increases fatty acid oxidation through ATGL
Increases autophagy through ULK and the negative regulation of mTOR (huge subject for another day. too extensive to even briefly explain here)
Decreases glycogen synthesis through inhibition of the GS enzyme
Decreases protein synthesis through the negative regulation of mTOR. (mTOR -> p70s6k -> s6 synthesis)
Decreases cholesterol synthesis through the enzyme HMG-CoA Reductase
Decreases fatty acid synthesis through the enzyme ACC
What you should know
AMPK signalling increases catabolism and decreases anabolism. Why is this the case? AMPK signalling aims to decrease energy expenditure and while increasing energy production, in it's own attempt to reverse the AMP:ATP ratio so our body can regain energy.
AMPK in and of itself is an energy pathway and has many many benefits which I will talk about in the future. Do not fall under the impression that AMPK signalling is bad because it promotes catabolism whilst decreasing anabolism.
Sometime soon I will go into detail about the benefits of increased catabolism (autophagy) and the benefits of decreased anabolism.
So, AMPK is looked at as an "energy sensor", and is activated by being in an energy deficit. How this energy deficit is measured is through the AMP:ATP ratio.
AMPK is the master regulator of energy metabolism.
Exercise activates AMPK. This should make sense now, because during exercise you are using up your ATPs. Since the AMP:ATP ratio grows bigger, AMPK gets activated.
AMPK is a negative regulator of mTOR, meaning it inhibits the mTOR pathway as AMPK itself is activated. Creatine provides more ATPs during exercise, possibly delaying or minimizing the inhibition of mTOR, which is the pathway responsible for protein synthesis. I hope this adds some insight as to why creatine is an effective supplement for keeping muscle mass and optimizing performance.
What does AMPK activate?:
ULK1 (Serine/threonine-protein kinase). ULK1 is a protein responsible for macroautophagy.
ATGL (Adipose triglyceride lipase). This is an enzyme responsible for the release of fatty acids from a triglyceride, which eventually leads to fatty acid catabolism.
What else does AMPK inhibit?:
ACC (Acetyl-CoA Corboxylase). This enzyme is responsible for fatty acid synthesis. AMPK is responsible for inhibiting fatty acid synthesis.
HMG-CoA Reductase. This enzyme is responsible for Cholesterol synthesis.
GS (Glycogen Synthase). The enzyme responsible for glycogen synthesis. In an energy deficit (with AMPK active), you won't be able to store new glycogen in your liver or muscle tissue.
What else is AMPK responsible for activating?:
TBC1D1: A very interesting channel. TBC1D1 helps insulin sensitive cells uptake glucose in the absence of insulin by recruiting GLUT4 vesicles.
GLUT4 translocalisation is an insulin mimicking process. You should not be worried about glucose not being able to enter your cells during AMPK activation during exercise, because TBC1D1 takes care of this process. (Do not buy post workout carb supplements as they're just a waste of money. You don't need an "insulin spike post workout", TBC1D1 is doing insulin's job for your cells during your exercise).
Glycolysis occurs after the GLUT4 translocalisation. Glycolysis is just the breakdown of glucose within your cells.
Summary of AMPK signalling
Increases glucose uptake and utilization
Increases fatty acid oxidation through ATGL
Increases autophagy through ULK and the negative regulation of mTOR (huge subject for another day. too extensive to even briefly explain here)
Decreases glycogen synthesis through inhibition of the GS enzyme
Decreases protein synthesis through the negative regulation of mTOR. (mTOR -> p70s6k -> s6 synthesis)
Decreases cholesterol synthesis through the enzyme HMG-CoA Reductase
Decreases fatty acid synthesis through the enzyme ACC
What you should know
AMPK signalling increases catabolism and decreases anabolism. Why is this the case? AMPK signalling aims to decrease energy expenditure and while increasing energy production, in it's own attempt to reverse the AMP:ATP ratio so our body can regain energy.
AMPK in and of itself is an energy pathway and has many many benefits which I will talk about in the future. Do not fall under the impression that AMPK signalling is bad because it promotes catabolism whilst decreasing anabolism.
Sometime soon I will go into detail about the benefits of increased catabolism (autophagy) and the benefits of decreased anabolism.
