Ultra‐endurance exercise differentially affects highly unsaturated fatty acid composition in cheek cells and serum phospholipids

Abstract

The Western States Endurance Run is a 100‐mile trail footrace through the Sierra Nevada Mountains. We hypothesized that the event would generate enough reactive oxygen species (ROS) in runners to cause ‘membrane damage’ as evidenced by degradation of highly unsaturated fatty acids, primarily arachidonate (AA) and docosahexaenoate (DHA). Ten runners (7M/3F, aged 27 to 60 yr) with a completion time of 22.83±4.26 hours provided buccal (cheek) cell and serum phospholipid (PL) samples for determination of fatty acid composition at baseline, immediately post‐race, and days 1 and 2 post‐race. Consistent with our hypothesis, cheek cell AA decreased by 19% (P = 0.003) and DHA by 23% (P = 0.002) immediately post‐race. In contrast, serum PL AA increased by 15% (P = 0.005) and DHA increased by 8% (NS). The implications of a decrease in cheek cell AA and DHA remain unclear, but they could reflect a failure of cellular antioxidant defenses to manage the cumulative ROS burden associated with ultra‐endurance exercise. The increase in serum PL AA may reflect release from other pools such as adipose tissue or damaged skeletal muscle, or alternatively it could represent an attempt to deliver AA to aid in repair and regeneration of ROS‐mediated tissue damage. The speed of fatty acid changes suggest that cheek cells can be used to assess acute systemic oxidative stress.