Prior to this post there was a few post that covered the freeing of stored fatty acids. Those post can be found here:
http://anabolicminds.com/forum/weight-loss/260687-norepinephrine-mediated-lipolysis.html
http://anabolicminds.com/forum/weight-loss/260799-adrenergic-regulation-lipolysis.html
To briefly recap what was covered in those post,
First, catecholamines are released from the adrenal glands. The 2 we are concerned with are epinephrine and norepinephrine. These will bind to adrenoceptors, which are found all over the body. There are 2 main types of adrenorecptors the catecholamines can bind to. Those are beta-adrenorecptors and alpha-adrenoreceptors. Each type with their own subtype. The main ones we are concerned with with regards to fat loss are the alpha-2 receptors and the beta-2 receptors. When a catecholamine binds to a beta2 receptor we get a increased cAMP levels. Conversely, when a catecholamine binds to a alpha2 receptor, cAMP levels are decreased. This is important because cAMP is the regulator of Hormone Sensitive Lipase (HSL) and HSL determines how quickly or slowly fat is mobilized. If HSL activity is low then fat mobilization will also be low and if HSL is high than so will fat mobilization. So the goal is to increase HSL. We accomplish this by increasing cAMP in the fat cell. Now back to the catecholamines, so what we want is to increase increase beta receptor stimulation AND decrease alpha receptor stimulation. Remember the goal is to increase cAMP and this is accomplished by beta2 activation but can also be inhibited by alpha2 activation. In this post (http://anabolicminds.com/forum/supplements/260916-targeting-a2-receptors.html) I address how yohimbine or rauwolscine supplementation can help inhibit alpha adrenergic activity thus increasing beta receptor stimulation.
But now that the fatty acids have been free’d, what happens next?
Well a few things can happen next. Some of the now free’d fatty acids (FFA) will remain in the fat cell and turn back into triglycerides and some will be carried across the membrane into the extracellular fluid where it will either pass into the bloodstream or be taken up by surrounding fat cells and turn back into triglycerides. The goal here is to get the FFA away from the cell and into the bloodstream. To do this the FFA needs to bind to a transport protein called albumin and there needs to be increased bloodflow, specifically blood flow through the adipose tissue.
Blood flow is affected by several things. One of those things is the adrenoreceptors. These receptors affect blood flow similarly to how they affect lipolysis. Beta receptors increase blood flow while alpha receptors inhibit it. This is good for us because we can then manipulate blood flow the same way we manipulate lipolysis.
Another thing that affects blood flow is, the type of fat it is (mainly because different kinds of fat have different ratios of these receptors.) Ultimately there are 2 kinds of fat in your body, visceral and adipose. The one kind of fat, visceral fat or “deep” fat, is the fat around the inner organs. Large amounts of this fat poses a serious risk to health. It is speculated that visceral fat plays a large role in insulin resistance but we have yet to fully understand what the role is. Luckily for us, visceral fat has very high blood flow and is very sensitive to catecholamines. As a result, this kind of fat is mobilized and burned fairly easily.
Now the other kind of fat, adipose, is a different story. Adipose cells can vary quite a bit. There are 2 kinds of adipose tissue, white and brown. Brown fat (BAT) is a bit different from white fat (WAT). BAT has a relatively high amount of mitochondria compared to WAT. As a result of this, BAT actually burns other types of fat. This oxidation in this fat releases heat and thus is responsible for the phenomenon known as nonshivering thermogenesis and for utilization of excess caloric intake via diet-induced-thermogenesis.. Sounds great right? Unfortunately, humans have very little of this fat. This kind of fat is predominantly found in hibernating animals and used for regulating body temperature. This fat is of little concern to us.
The other kind of fat, WAT, is the one we are concerned with. This is the fat that is found directly under the skin (subcutaneous fat). This kind of fat serves 3 main functions, heat insulation, as a mechanical cushion, and also as a source of energy. The last function is the one we will focus on. In scenarios where energy intake is less than energy output, the body can turn to several different sources of energy. The one we want the body to turn to is fat, specifically WAT. Unfortunately WAT is not as vascularized as BAT. Because of this, WAT has a lot less blood flow. In addition to this, it is also less sensitive to the catecholamines and the most sensitive to insulin.
So now comes the question, how do we improve blood flow to our adipose? Adipose blood flow varies depending on several factors such as body weight and nutritional state but there appears to be 2 ways we can improve blood flow here.
Back to FFA metabolism, once the FFA has moved out of the cell it will bind to a transport protein and if blood flow is sufficient, it will be carried away from the cell and into the bloodstream where it will be taken to tissues so that it can be used for energy. Several types of tissue are capable of using fat to fulfil energy needs. It accomplishes this via beta-oxidation.
At the tissue site, the albumin-FFA complex releases the FFA for transport into the tissue. Fatty acids are taken up to the muscle tissue or the liver via a mitochondrial enzyme called carnitine palmityl transferase (CPT). SIDE NOTE: Here aerobic exercise can also help. The more aerobically trained you are, the more CPT activity. Glycogen levels also contribute towards the regulation of CPT. There is an inverse relationship between the two, meaning when glycogen is high, CPT activity is low. The way we can use this to our advantage is by including intensive glycogen depleting training strategies. Back to the inside of the muscle fiber, the FFA can do one of two things. It can re-esterfiy and be stored or it can bind with proteins and enter the mitochondria. Some fats are able to enter freely via diffusion but some need to be carried across the membrane.
Once inside, several biochemical changes take place. During beta-oxidation, the fatty acid molecules transform into acetyl-CoA. Then it enters into the citric acid cycle. Several reactions occur during this but ultimately the end result is the formation of ATP.
http://anabolicminds.com/forum/weight-loss/260687-norepinephrine-mediated-lipolysis.html
http://anabolicminds.com/forum/weight-loss/260799-adrenergic-regulation-lipolysis.html
To briefly recap what was covered in those post,
First, catecholamines are released from the adrenal glands. The 2 we are concerned with are epinephrine and norepinephrine. These will bind to adrenoceptors, which are found all over the body. There are 2 main types of adrenorecptors the catecholamines can bind to. Those are beta-adrenorecptors and alpha-adrenoreceptors. Each type with their own subtype. The main ones we are concerned with with regards to fat loss are the alpha-2 receptors and the beta-2 receptors. When a catecholamine binds to a beta2 receptor we get a increased cAMP levels. Conversely, when a catecholamine binds to a alpha2 receptor, cAMP levels are decreased. This is important because cAMP is the regulator of Hormone Sensitive Lipase (HSL) and HSL determines how quickly or slowly fat is mobilized. If HSL activity is low then fat mobilization will also be low and if HSL is high than so will fat mobilization. So the goal is to increase HSL. We accomplish this by increasing cAMP in the fat cell. Now back to the catecholamines, so what we want is to increase increase beta receptor stimulation AND decrease alpha receptor stimulation. Remember the goal is to increase cAMP and this is accomplished by beta2 activation but can also be inhibited by alpha2 activation. In this post (http://anabolicminds.com/forum/supplements/260916-targeting-a2-receptors.html) I address how yohimbine or rauwolscine supplementation can help inhibit alpha adrenergic activity thus increasing beta receptor stimulation.
But now that the fatty acids have been free’d, what happens next?
Well a few things can happen next. Some of the now free’d fatty acids (FFA) will remain in the fat cell and turn back into triglycerides and some will be carried across the membrane into the extracellular fluid where it will either pass into the bloodstream or be taken up by surrounding fat cells and turn back into triglycerides. The goal here is to get the FFA away from the cell and into the bloodstream. To do this the FFA needs to bind to a transport protein called albumin and there needs to be increased bloodflow, specifically blood flow through the adipose tissue.
Blood flow is affected by several things. One of those things is the adrenoreceptors. These receptors affect blood flow similarly to how they affect lipolysis. Beta receptors increase blood flow while alpha receptors inhibit it. This is good for us because we can then manipulate blood flow the same way we manipulate lipolysis.
Another thing that affects blood flow is, the type of fat it is (mainly because different kinds of fat have different ratios of these receptors.) Ultimately there are 2 kinds of fat in your body, visceral and adipose. The one kind of fat, visceral fat or “deep” fat, is the fat around the inner organs. Large amounts of this fat poses a serious risk to health. It is speculated that visceral fat plays a large role in insulin resistance but we have yet to fully understand what the role is. Luckily for us, visceral fat has very high blood flow and is very sensitive to catecholamines. As a result, this kind of fat is mobilized and burned fairly easily.
Now the other kind of fat, adipose, is a different story. Adipose cells can vary quite a bit. There are 2 kinds of adipose tissue, white and brown. Brown fat (BAT) is a bit different from white fat (WAT). BAT has a relatively high amount of mitochondria compared to WAT. As a result of this, BAT actually burns other types of fat. This oxidation in this fat releases heat and thus is responsible for the phenomenon known as nonshivering thermogenesis and for utilization of excess caloric intake via diet-induced-thermogenesis.. Sounds great right? Unfortunately, humans have very little of this fat. This kind of fat is predominantly found in hibernating animals and used for regulating body temperature. This fat is of little concern to us.
The other kind of fat, WAT, is the one we are concerned with. This is the fat that is found directly under the skin (subcutaneous fat). This kind of fat serves 3 main functions, heat insulation, as a mechanical cushion, and also as a source of energy. The last function is the one we will focus on. In scenarios where energy intake is less than energy output, the body can turn to several different sources of energy. The one we want the body to turn to is fat, specifically WAT. Unfortunately WAT is not as vascularized as BAT. Because of this, WAT has a lot less blood flow. In addition to this, it is also less sensitive to the catecholamines and the most sensitive to insulin.
So now comes the question, how do we improve blood flow to our adipose? Adipose blood flow varies depending on several factors such as body weight and nutritional state but there appears to be 2 ways we can improve blood flow here.
- Fasting
- Aerobic exercise
Back to FFA metabolism, once the FFA has moved out of the cell it will bind to a transport protein and if blood flow is sufficient, it will be carried away from the cell and into the bloodstream where it will be taken to tissues so that it can be used for energy. Several types of tissue are capable of using fat to fulfil energy needs. It accomplishes this via beta-oxidation.
At the tissue site, the albumin-FFA complex releases the FFA for transport into the tissue. Fatty acids are taken up to the muscle tissue or the liver via a mitochondrial enzyme called carnitine palmityl transferase (CPT). SIDE NOTE: Here aerobic exercise can also help. The more aerobically trained you are, the more CPT activity. Glycogen levels also contribute towards the regulation of CPT. There is an inverse relationship between the two, meaning when glycogen is high, CPT activity is low. The way we can use this to our advantage is by including intensive glycogen depleting training strategies. Back to the inside of the muscle fiber, the FFA can do one of two things. It can re-esterfiy and be stored or it can bind with proteins and enter the mitochondria. Some fats are able to enter freely via diffusion but some need to be carried across the membrane.
Once inside, several biochemical changes take place. During beta-oxidation, the fatty acid molecules transform into acetyl-CoA. Then it enters into the citric acid cycle. Several reactions occur during this but ultimately the end result is the formation of ATP.