EXERCISE CAUSES OXIDATIVE DAMAGE TO RAT SKELETAL-MUSCLE MICROSOMES WHILE INCREASING CELLULAR SULFHYDRYLS

The physiological and biochemical demands on contracting muscle make t his tissue particularly susceptible to molecular and cellular damage. We looked at membrane structures in cardiac and skeletal muscle and in erythrocytes for exercise-induced lipid peroxidation. These tissues w ere removed from each of the rats used in this study. We also examined and compared the effects of exercise on the redox status of blood pla sma, erythrocytes and cardiac and skeletal muscle from the same rats. We used a swim stress protocol to exercise the rats to exhaustion. Som e form of chemical modification or oxidative damage to membranes was o bserved in all of the tissues tested. Cardiac muscle microsomes from e xercised rats exhibited increased malondialdehyde and decreased phosph olipid (control, 249.1 vs exercised, 120.6 nmols phospholipid/mg prote in). Skeletal muscle microsomes showed decreased sulfhydryls, decrease d phospholipid (control, 1,276.9 vs exercised, 137.7 nmols phospholipi d/mg protein), increased malondialdehyde and greater protein crosslink ing after exercise. Erythrocyte membranes also exhibited exercised-ind uced protein oxidation. However, the total cellular sulfhydryl content remained the same in erythrocytes and cardiac tissue but increased in blood plasma (control, 10.8 vs exercised, 24.7 mumols SH/dl plasma) a nd skeletal muscle after exercise. We conclude that exercise profoundl y effects membrane structures. The body compensates for this lipid per oxidation and protein damage by increasing total cellular sulfhydryls in blood plasma and skeletal muscle which would aid in repair of the d amaged membranes.