Muscle protein is in a state of constant renewal, which means that new proteins are constantly being produced, while old proteins are being broken down.
There is no specific definition of anabolic state, but it generally refers to the situation where the rate of muscle protein synthesis exceeds the rate of muscle protein breakdown, and the result is an increase in muscle mass.
It is traditionally believed that the anabolic state is caused by stimulation of muscle protein synthesis, but theoretically it may also be the result of inhibited muscle protein breakdown.
The primary metabolic goal of taking BCAA supplements is to maximize the anabolic state. It is generally believed that BCAA induces anabolic state by stimulating the synthesis of muscle protein. The abundant availability of all EAAs is a necessary condition for significantly stimulating muscle protein synthesis.
The lack of any EAA will limit muscle protein synthesis, and the lack of NEAA can be compensated by increasing the lack of NEAA de novo synthesis.
In the protein-containing postprandial state, all the EAA precursors required for the synthesis of new muscle protein can be obtained from the increased plasma concentration generated by the digestion of the consumed protein or the recycling after the protein breakdown.
In the case of sufficient EAA, the synthesis rate of muscle protein exceeds the decomposition rate, resulting in an anabolic state.
In the post-absorption state, the plasma EAA level is lower than the post-prandial value because the amino acid is no longer absorbed. Therefore, EAA is no longer absorbed by the muscle, but is released into the plasma by the muscle.
This catabolic state of muscle protein after absorption enables other tissues to continue to obtain EAA to maintain the rate of protein synthesis. At the expense of muscle protein, it can be considered that muscle protein plays a role in storing EAA for use by other parts of the body.
Since EAA cannot be produced in the body, and muscles will release EAA net, in the post-absorption state, the only source of EAA precursors for muscle protein synthesis is intracellular EAA produced by muscle protein decomposition.
In addition to being recombined into muscle protein through synthesis, some of the EAA released from the breakdown of muscle protein may be partially oxidized in the muscle so that they can no longer be incorporated into muscle protein.
The EAA released from the breakdown of muscle protein is not recombined into muscle protein or oxidized in muscle tissue, and released into plasma, so they can be used as precursors of protein synthesis by other tissues or be irreversibly oxidized.
Therefore, due to the net flow of EAA from protein decomposition to plasma and oxidative pathways, the synthesis rate of muscle protein is always lower than the decomposition rate of muscle protein in the post-absorption state. Expressed in different ways, when the precursor is completely derived from protein decomposition, the synthesis of muscle protein cannot exceed the decomposition rate of muscle protein. Therefore, in the absence of exogenous amino acid intake, an anabolic state will not occur.