myosin
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- May 27, 2011
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Understanding Fat-Loss, Part One: Physiology
I mentioned in another thread that I was going to discuss supplementation and fat loss. I decided to break it into two parts. I don’t want to just tell someone “do this, do that”, etc (though there is a time and place for that of course). Rather, I want the person to understand the “why” and the “how” of what’s happening behind the “what” we are doing. And, to be honest, I’m breaking this in two parts also b/c we are in the middle of moving from our home to another and have a few other projects going on, so I’m trying to manage my time effectively
Now, these two parts are dealing with fat-loss and supplementation. So, before anyone starts to chime in with the parroted-response, “The best choice for fat-loss is diet!”, let me say, yes, I wholeheartedly agree. As the saying goes, “Abs are made in the kitchen.”
Also, this is not an “exhaustive explanation” behind fat loss but does cover the major key points that we need. This topic could actually become a VERY involved one eventually drawing upon cortisol:testosterone ratio’s, etc. I’m keeping this short, sweet, and to the point. Like putting on muscle and utilizing the different mechanisms behind it, in part two, I will address the supplements that address these different mechanisms in fat loss.
Once it all gets broken down, fat loss comes down to two main components- lipolysis (break down, mobilization) and oxidation (utilization).
Lipolysis- There are two different receptors located on fat cells that can promote or inhibit the release of fat from the cell: alpha (a) and beta (b). These two are further broken down: a1, a2 and b1, b2 and b3. The b1 receptor is really located only in the heart and when stimulated affects heart rate only, not fat loss, so we won’t be concerned with this guy. The b2 receptors are primarily found on the fat cells. The b3 receptors are found primarily on “brown fat.” “Brown fat?” Yes, sounds like a contradiction, but brown fat is actually VERY metabolically active in burning fat for fuel/energy. More on this later down.
When the b2 receptors are stimulated by catecholamines (adrenaline, nor-adrenaline) they cause the release of free fatty acids (FFA’s) from the fat cell. I will address the b3 receptors under the “oxidation” portion of this post. When the a1 and a2 cells are stimulated by catecholamines, they can actually INHIBIT the release of FFA’s (how to correct that will be addressed in part two).
Lipolysis can also be stimulated by thermogenesis (increase in body heat or metabolism). By increasing the temperature of the body, FFA’s are released for energy.
While this section is about stimulating lipolysis, we should also address the other side of the equation… how lipolysis can be inhibited as well. A main factor that can cause lipolysis to be inhibited is by too high of insulin levels in the bloodstream. When insulin is present at too high of levels it can promote the storage the fat. Note that I used the phrase “too high of levels” a couple of times… this is key. Insulin is NOT your “enemy”. Fat loss can occur if insulin is present as it aids in the promotion of amino acid and glucose entry into the muscle cell (some competitive bodybuilders will even use insulin in their pre-contest prep and still come in at single digit bodyfat levels). It’s about how much is present and how sensitive are the insulin receptors on the muscle cell.
Oxidation- So, we get the fat cell to release its FFA’s into the bloodstream… OK, so then what? We need to do something with these FFA’s, otherwise, they just end up back in the fat cell. So then, they need to be utilized. This is done in two ways.
The first, is that inside the muscle cell is the mitochondria, typically called “the powerhouse” of the cell. FFAs need to enter the mitochondria where they are then burned for energy.
The second, is for the b3 receptors of the brown fat to be stimulated. When they are activated, they increase the activity of the brown fat mitochondria to burn the FFA’s from the “white fat.”
So, the questions we address in part two are: What supplements stimulate b2 and b3 receptors? What supplements prevent the a-receptors from inhibiting lipolysis? How can we increase the utilization of the FFAs to be burned for energy? What supplements help with increasing muscle cell insulin sensitivity?
Hope to be back in a day or two.
I mentioned in another thread that I was going to discuss supplementation and fat loss. I decided to break it into two parts. I don’t want to just tell someone “do this, do that”, etc (though there is a time and place for that of course). Rather, I want the person to understand the “why” and the “how” of what’s happening behind the “what” we are doing. And, to be honest, I’m breaking this in two parts also b/c we are in the middle of moving from our home to another and have a few other projects going on, so I’m trying to manage my time effectively
Now, these two parts are dealing with fat-loss and supplementation. So, before anyone starts to chime in with the parroted-response, “The best choice for fat-loss is diet!”, let me say, yes, I wholeheartedly agree. As the saying goes, “Abs are made in the kitchen.”
Also, this is not an “exhaustive explanation” behind fat loss but does cover the major key points that we need. This topic could actually become a VERY involved one eventually drawing upon cortisol:testosterone ratio’s, etc. I’m keeping this short, sweet, and to the point. Like putting on muscle and utilizing the different mechanisms behind it, in part two, I will address the supplements that address these different mechanisms in fat loss.
Once it all gets broken down, fat loss comes down to two main components- lipolysis (break down, mobilization) and oxidation (utilization).
Lipolysis- There are two different receptors located on fat cells that can promote or inhibit the release of fat from the cell: alpha (a) and beta (b). These two are further broken down: a1, a2 and b1, b2 and b3. The b1 receptor is really located only in the heart and when stimulated affects heart rate only, not fat loss, so we won’t be concerned with this guy. The b2 receptors are primarily found on the fat cells. The b3 receptors are found primarily on “brown fat.” “Brown fat?” Yes, sounds like a contradiction, but brown fat is actually VERY metabolically active in burning fat for fuel/energy. More on this later down.
When the b2 receptors are stimulated by catecholamines (adrenaline, nor-adrenaline) they cause the release of free fatty acids (FFA’s) from the fat cell. I will address the b3 receptors under the “oxidation” portion of this post. When the a1 and a2 cells are stimulated by catecholamines, they can actually INHIBIT the release of FFA’s (how to correct that will be addressed in part two).
Lipolysis can also be stimulated by thermogenesis (increase in body heat or metabolism). By increasing the temperature of the body, FFA’s are released for energy.
While this section is about stimulating lipolysis, we should also address the other side of the equation… how lipolysis can be inhibited as well. A main factor that can cause lipolysis to be inhibited is by too high of insulin levels in the bloodstream. When insulin is present at too high of levels it can promote the storage the fat. Note that I used the phrase “too high of levels” a couple of times… this is key. Insulin is NOT your “enemy”. Fat loss can occur if insulin is present as it aids in the promotion of amino acid and glucose entry into the muscle cell (some competitive bodybuilders will even use insulin in their pre-contest prep and still come in at single digit bodyfat levels). It’s about how much is present and how sensitive are the insulin receptors on the muscle cell.
Oxidation- So, we get the fat cell to release its FFA’s into the bloodstream… OK, so then what? We need to do something with these FFA’s, otherwise, they just end up back in the fat cell. So then, they need to be utilized. This is done in two ways.
The first, is that inside the muscle cell is the mitochondria, typically called “the powerhouse” of the cell. FFAs need to enter the mitochondria where they are then burned for energy.
The second, is for the b3 receptors of the brown fat to be stimulated. When they are activated, they increase the activity of the brown fat mitochondria to burn the FFA’s from the “white fat.”
So, the questions we address in part two are: What supplements stimulate b2 and b3 receptors? What supplements prevent the a-receptors from inhibiting lipolysis? How can we increase the utilization of the FFAs to be burned for energy? What supplements help with increasing muscle cell insulin sensitivity?
Hope to be back in a day or two.
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