Antarctic krill oil alleviates exercise-induced muscle inflammation by modulating TLR4/MyD88/NF-κB signaling in mice.

Abstract

Exercise-induced fatigue and inflammation can significantly impair athletic performance and recovery. Effective strategies to mitigate these effects are critical for athletes and those engaged in high-intensity physical activities. Anti-inflammatory properties have been associated with Antarctic krill oil (AKO), which contains n-3 polyunsaturated fatty acids (n-3 PUFA) such as eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA). After exhaustive exercise, this study examined how 4-week AKO supplementation affected skeletal muscle inflammation and the TLR4/MyD88/NF-κB signaling pathways in mice. Sixty male SPF-grade 8-week-old C57BL/6J mice were randomly assigned to four groups: soybean oil control (BO-C), AKO control (KO-C), soybean oil exercise (BO-E), and AKO exercise (KO-E). The KO groups received 200 mg/kg/BW AKO intragastrically for four weeks, while the BO groups received an equivalent volume of soybean oil. After the supplementation period, the exercise groups underwent a strenuous treadmill exercise. Grasping force was measured at 0 h, 6 h, 24 h, 48 h, and 72 h post-exercise, and tissue samples were analyzed histologically and biochemically. Results showed that AKO significantly reduced body weight and enhanced exercise endurance and recovery. Furthermore, serum CK, LDH and CRP levels, as well as muscle TNF-α concentrations, and TLR4 and MyD88 protein expressions were lower in the KO-E group than in the BO-E group. As a result of modulating the TLR4/MyD88/NF-κB signaling pathway through AKO supplementation, it decreases inflammation after exhaustive exercise and promotes recovery.