Muscle Release of Amino Acids Is Related to Reduced Glucose and Amino Acid Uptake

The postabsorptive decline in the serum insulin concentration has a twofold effect on muscle: the entry of amino acids from the serum into the intracellular amino acid pool is dimin­ished, and the entry of glucose into muscle cells for energy production declines.

The pattern of utilization of amino acids for energy by muscle may at first seem unnecessarily complex, involving selective use and extensive transformation of amino acids. BCAAs serve as primary sources of energy in muscle cells during the postabsorptive phase because these amino acids account for approximately one third of all muscle amino acid. Catabolism of BCAAs begins with deamination and the forma­tion of the α-keto-acid of the BCAA. The α-keto-acids then enter the Krebs cycle for energy production. Deamination of the BCAA requires that some acceptor be available to receive the amino group, and this acceptor is ultimately pyruvate, resulting in the formation of alanine. The source of pyruvate can be muscle glycogen, blood glucose, or the metabolic products of BCAA α-keto-acids. When metabolism of BCAA α-keto-acids serves as the supply of pyruvate for alanine synthesis, the net reaction is conversion of BCAA to alanine (Figure 32-13). Thus the overall metabolic activity in muscle during the postabsorptive phase is the destruction of BCAAs and the formation of alanine. The alanine formed is released from the muscle cells into the blood, from which it may be taken up by the liver for gluconeogenesis.

FIGURE 32-13 Catabolism of branch-chain amino acids (BCAAs) by muscle cells. The pyruvate for export of amino groups may be derived from glucose or the amino acids themselves.