Therdyothin Atiporn, Phiphopthatsanee Nacharin
Orthopedics, Police General Hospital, Bangkok, THA.
Psychiatry, Faculty of Medicine, King Mongkut's Institute of Technology Ladkrabang, Bangkok, THA.
Cureus. 2025 Apr 1;17(4):e81559. doi: 10.7759/cureus.81559. eCollection 2025 Apr.
Exercise-induced muscle damage (EIMD) refers to muscle injuries following exercises involving repetitive eccentric muscle contractions. The resultant inflammation and muscle protein leakage into the circulation lead to muscle pain and strength deficit, compromising athletic performance. This narrative review summarizes the current evidence on the effect and mechanism of omega-3 polyunsaturated fatty acids (n-3 PUFA) in potentially mitigating EIMD. Several studies suggested n-3 PUFA's role in alleviating delayed-onset muscle soreness, particularly in untrained individuals and those receiving higher doses of continuous supplementation. However, its impact on muscle strength attenuation and the reduction of performance post-exercise remains inconclusive. Also unclear are n-3 PUFA's effects on the reduction of circulating pro-inflammatory substances and muscle proteins. One of the possible mechanisms is its anti-inflammatory property, which involves its ability to incorporate into cell membranes and displace prostaglandin precursor. n-3 PUFA also decreases cyclooxygenase production and can be converted into specialized pro-resolving mediators (SPMs), further reducing inflammation. Moreover, n-3 PUFA's incorporation into cell membranes alters cell membrane properties, diminishing protein release during muscle breakdown. n-3 PUFA exhibits analgesic effects through SPM-induced modulation of receptors and ion channels, reducing both peripheral and central sensitization. n-3 PUFA also diminishes mitochondrial free radical production and accelerates nerve conduction, thereby improving voluntary muscle activation.
运动诱导的肌肉损伤(EIMD)是指在涉及重复性离心肌肉收缩的运动后发生的肌肉损伤。由此产生的炎症和肌肉蛋白渗漏到循环系统中会导致肌肉疼痛和力量不足,从而影响运动表现。这篇叙述性综述总结了目前关于ω-3多不饱和脂肪酸(n-3 PUFA)在潜在减轻EIMD方面的作用和机制的证据。几项研究表明,n-3 PUFA在减轻延迟性肌肉酸痛方面具有作用,特别是在未经训练的个体和接受较高剂量持续补充的个体中。然而,其对运动后肌肉力量衰减和运动表现下降的影响仍无定论。n-3 PUFA对减少循环中的促炎物质和肌肉蛋白的影响也尚不清楚。一种可能的机制是其抗炎特性,这涉及到它能够融入细胞膜并取代前列腺素前体的能力。n-3 PUFA还会减少环氧化酶的产生,并可转化为专门的促解决介质(SPM),进一步减轻炎症。此外,n-3 PUFA融入细胞膜会改变细胞膜特性,减少肌肉分解过程中的蛋白质释放。n-3 PUFA通过SPM诱导的受体和离子通道调节表现出镇痛作用,减少外周和中枢敏化。n-3 PUFA还会减少线粒体自由基的产生并加速神经传导,从而改善随意肌激活。