Those who have used creatine products such as creatine monohydrate or creatine phosphate realize the effects that more creatine can provide. When anabolic/androgenic steroids (AAS) are administered they cause an increase in Phosphocreatine (CP) synthesis. Let me explain why this creatine stuff is such a cool thing.
ATP (Adenosine Triphosphate) is the fuel that your muscles use to actuate contractions. For this to happen ATP must be changed into ADP (Adenosine Diphosphate) so that energy can be released. This in turn allows for muscular contractions. In order to convert ADP back into the energy source ATP phospcreatine (CP) is needed. So the more CP that is available, the greater the regeneration of ADP to ATP and the greater the work capacity of the muscle at an accelerated rate. There was once a belief that elevated cellular CP levels added strength but not size. Obviously this belief was crushed when creatine products hit the supplement market. Increased CP levels also increase cellular glycogen and protein stores (amino acids) in muscle tissue. This action of course AAS do quite well and so do creatine products. So CP also increases cellular size, due to an increase in intercellular nutrient volume.
STEROIDS POSITIVELY EFFECT FAT
AAS have a positive effect upon fat distribution and storage. There are 3 reasons for this. The first reason is that AAS reduce the amount of insulin released in response to nutrient intake and improved insulin sensitivity. This is in part due to an improved CP synthesis rate and other metabolic factors resulting in an athlete's muscle cells becoming better able to absorb nutrients such as carbohydrates in the form of glucose and glycogen and proteins in the form of amino acids. Insulin is anti-catabolic and anabolic. Great for muscle cells, but it also causes the conversion of glucose into glycerol and then into triglycerides. Insulin can therefore increase fat stores and growth of fat cells. A decrease in insulin release and an increase in insulin sensitivity means better utilization of nutrients for muscle growth.
The second reason AAS effect fat is because testosterone blocks the activity of a fat-synthesizing hormone called lipoprotein lipase. Since lipoprotein lipase is blocked, less can be produced and stored. GH also has this effect.
The third way testosterone affects fat synthesis is not positive. When testosterone levels are elevated, more is converted into estrogens by way of the conversion enzyme aromatase. This is called aromatization. Estrogen in turn increases female pattern fat deposits and suppresses HPT A function. At least estrogen can increase GH production.
ATP (Adenosine Triphosphate) is the fuel that your muscles use to actuate contractions. For this to happen ATP must be changed into ADP (Adenosine Diphosphate) so that energy can be released. This in turn allows for muscular contractions. In order to convert ADP back into the energy source ATP phospcreatine (CP) is needed. So the more CP that is available, the greater the regeneration of ADP to ATP and the greater the work capacity of the muscle at an accelerated rate. There was once a belief that elevated cellular CP levels added strength but not size. Obviously this belief was crushed when creatine products hit the supplement market. Increased CP levels also increase cellular glycogen and protein stores (amino acids) in muscle tissue. This action of course AAS do quite well and so do creatine products. So CP also increases cellular size, due to an increase in intercellular nutrient volume.
STEROIDS POSITIVELY EFFECT FAT
AAS have a positive effect upon fat distribution and storage. There are 3 reasons for this. The first reason is that AAS reduce the amount of insulin released in response to nutrient intake and improved insulin sensitivity. This is in part due to an improved CP synthesis rate and other metabolic factors resulting in an athlete's muscle cells becoming better able to absorb nutrients such as carbohydrates in the form of glucose and glycogen and proteins in the form of amino acids. Insulin is anti-catabolic and anabolic. Great for muscle cells, but it also causes the conversion of glucose into glycerol and then into triglycerides. Insulin can therefore increase fat stores and growth of fat cells. A decrease in insulin release and an increase in insulin sensitivity means better utilization of nutrients for muscle growth.
The second reason AAS effect fat is because testosterone blocks the activity of a fat-synthesizing hormone called lipoprotein lipase. Since lipoprotein lipase is blocked, less can be produced and stored. GH also has this effect.
The third way testosterone affects fat synthesis is not positive. When testosterone levels are elevated, more is converted into estrogens by way of the conversion enzyme aromatase. This is called aromatization. Estrogen in turn increases female pattern fat deposits and suppresses HPT A function. At least estrogen can increase GH production.
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