JASKOWSKI, M. A., A. S. JACKSON, P. B. RAVEN, and J. L. CAFFREY. Enkephalin metabolism: effect of acute exercise stress and cardiovascular fitness. Med. Sci. Sports Exerc, Vol. 21, No. 2, pp. 154–160,1989. Inhibition of enkephalin hydrolysis by catecholaminesin vitrosuggested that local and/or humoral factors released during exercise might facilitate opiate responses by reducing the rate of opiate peptide inactivation. Several measures of enkephalin hydrolysis were determined in blood samples obtained from subjects designated as trained (&OV0312;O2max, 64.3 ± 1.6 ml·min-1·kg-1) and untrained (&OV0312;O2max, 37.4 ± ml·min-1·kg-1) both at rest and after maximal exercise stress tests. Enkephalin hydrolyzing activity assessed under optimal conditions was equally distributed between plasma and intact red cells; however, hydrolysis by red cells increased dramatically following osmotic release of red cell contents. There were no apparent differences in enzyme concentration or its distribution between cells and plasma when comparing trained and untrained subjects;P> 0.05. There was also no statistical effect of maximal exercise on these measures in either group. However, when the sequential disappearance of enkephalin added to whole bloodin vitrowas evaluated, blood from trained subjects degraded the enkephalin more slowly than blood from untrained subjects and had half-livesin vitro30–50% longer both before and after the exercise test;P< 0.05. Since enzyme concentrations between the groups were similar, the longer half-lives suggest that circulating factors were responsible for moderating the rate of enkephalin metabolismin vivoand that these factors were more concentrated in trained subjects. This would facilitate opiate responses in trained subjects and perhaps provide them with added tolerance for the effort associated with elite performance levels.