Dietary Apilarnil Supplementation Modulates Erythrocyte Redox Enzyme Activities in Rats Subjected to Repeated Swimming Exercise

Background: Exercise-induced reactive oxygen species (ROS) participate in both oxidative stress and physiological adaptation. Erythrocytes rely on NADPH-generating and thiol-related antioxidant systems to maintain redox homeostasis during exercise. Apilarnil, a drone brood-derived bee product containing diverse bioactive compounds, may influence redox-related enzymatic responses; however, its effects on erythrocyte NADPH-dependent and thiol-related enzyme activities during repeated exercise remain unclear. Methods: Forty adult male Wistar rats were randomly assigned to five groups (n = 8/group): control (CN), acute exhaustive swimming (AES), short-term repeated swimming with vehicle (ST), repeated swimming plus apilarnil 0.2 g·kg−1·day−1 (ST + AP0.2), and repeated swimming plus apilarnil 0.4 g·kg−1·day−1 (ST + AP0.4). Repeated-swimming groups swam for 30 min/day for 14 consecutive days. Apilarnil was administered orally throughout the intervention. On Day 15, the AES and repeated-swimming groups underwent a terminal exhaustive swimming challenge. Erythrocyte G6PD, 6PGD, GST, GR, and TrxR activities were determined spectrophotometrically. Results: Acute exhaustive swimming alone did not significantly alter erythrocyte enzyme activities. In contrast, repeated swimming exposure followed by the terminal exhaustive challenge was associated with higher G6PD, 6PGD, GST, GR, and TrxR activities compared with sedentary controls. Compared with ST, the higher apilarnil dose was associated with lower GST activity, and both doses were associated with lower GR and TrxR activities. G6PD and 6PGD activities did not differ significantly between apilarnil-treated and ST groups. Conclusions: Within the context of short-term repeated swimming, apilarnil-supplemented rats showed lower activities of selected erythrocyte redox enzymes than vehicle-treated rats. Because direct oxidative stress markers, hemolysis-related outcomes, and upstream molecular pathways were not assessed, these findings should be interpreted as evidence of enzymatic modulation rather than definitive evidence of oxidative protection or enhanced antioxidant adaptation.