Abstract:
Skeletal muscle health is influenced by many factors such as exercise and
prostaglandins (PGs) produced by the cyclooxygenase (COX) enzyme. Although aspirin
is a widely consumed COX-inhibiting drug, its impact on skeletal muscle metabolism and
potential interaction with exercise are relatively unknown. The purpose of this study was
to examine the effects of aspirin on skeletal muscle PGE2 production at rest and following
a bout of resistance exercise. Six individuals (25±1 y; 176±4 cm; 81.5±3.4 kg) performed
a whole-body resistance exercise bout (chest press; overhead press; seated row; triceps
extension; biceps curl; leg press; leg curl; knee extension) consisting of 3 sets of ~10RM.
Skeletal muscle biopsies were taken before and 3.5 h after exercise from the vastus
lateralis for measurement of ex vivo PGE2 production. Biopsied muscles were incubated
in Krebs-Henseleit buffer (Control) or supplemented with one of two aspirin
concentrations that reflected plasma levels following a standard (Oral: 1000mg; Plasma:
100μM) or low (Oral: 81mg; Plasma: 10μM) dose. Resistance exercise decreased muscle
PGE2 production (-15±5%; P<0.05 main effect). Aspirin reduced muscle PGE2 production
compared to Control (-18±5%; P<0.05) and independent of dose (P>0.05). Resistance
exercise did not alter the efficacy of aspirin to reduce PGE2 production. The effects of
resistance exercise were in contrast to a similarly designed aerobic exercise study (-
15±5% vs. +21±9%; P<0.05). These findings have important implications for
understanding the skeletal muscle adaptations to the two most common forms of exercise
promoted for overall health, especially for those individuals that regularly consume the
common COX inhibitor aspirin.
