Contrary to our hypothesis, the W6+BCAAs treatment resulted
in MPS rates that were less robust than with W6+High-Leu and
W25 treatments. These differences occurred despite the fact that
supplemental isoleucine and valine attenuated the decline in
concentrations of these amino acids in the blood compared with
that observed after the W6+High-Leu treatment (Table 3); how-
ever, intracellular concentrations of isoleucine and valine were
not different between these treatments (Table 4). In addition, the
W6+BCAAs treatment was associated with a lower intracellular
leucine concentration at 1.5 h, a lower mean leucine AUC pos ,
a lower leucine C max , and a greater T max than with the W6+High-
Leu treatment (Table 3). We have shown that a rapid amino-
acidemia after protein feeding stimulates greater MPS rates after
resistance exercise than a slow protracted aminoacidemia (46).
Therefore, we speculate that the greater T max for leucine, iso-
leucine, valine and SEAAs after W6+BCAAs compared with
W6+High-Leu may partially explain the observed differences in
MPS rates. Because BCAAs share a common intestinal trans-
porter, differences in amino acid appearance profiles between
W6+BCAAs and W6+High-Leu treatments likely represents
antagonism between BCAAs for uptake from the gut, which is
congruent with data showing that isoleucine and valine compete
with and can impede leucine absorption (47). The same effect
could be true for the transsarcolemmal BCAA transport because
BCAAs share the same transporter at that site (48).