Wadley A J, Chen Y W, Bennett S J, Lip G Y H, Turner J E, Fisher J P, Aldred S
School of Sport, Exercise & Rehabilitation Sciences, University of Birmingham , Edgbaston, Birmingham , UK.
Free Radic Res. 2015 Mar;49(3):290-8. doi: 10.3109/10715762.2014.1000890. Epub 2015 Feb 4.
Peroxiredoxin (PRDX) and thioredoxin (TRX) are antioxidant proteins that control cellular signalling and redox balance, although their response to exercise is unknown. This study aimed to assess key aspects of the PRDX-TRX redox cycle in response to three different modes of exercise.
Healthy males (n = 10, mean ± SD: 22 ± 3 yrs) undertook three exercise trials on separate days: two steady-state cycling trials at moderate (60% [Formula: see text]O2MAX; 27 min, MOD) and high (80% [Formula: see text]O2MAX; 20 min, HIGH) intensities, and a low-volume high-intensity interval training trial (10 × 1 min 90% [Formula: see text]O2MAX, LV-HIIT). Peripheral blood mononuclear cells were assessed for TRX-1 and over-oxidised PRDX (isoforms I-IV) protein expression before, during, and 30 min following exercise (post + 30). The activities of TRX reductase (TRX-R) and the nuclear factor kappa B (NF-κB) p65 subunit were also assessed.
TRX-1 increased during exercise in all trials (MOD, + 84.5%; HIGH, + 64.1%; LV-HIIT, + 205.7%; p < 05), whereas over-oxidised PRDX increased during HIGH only (MOD, - 28.7%; HIGH, + 202.9%; LV-HIIT, - 22.7%; p < .05). TRX-R and NF-κB p65 activity increased during exercise in all trials, with the greatest response in TRX-R activity seen in HIGH (p < 0.05).
All trials stimulated a transient increase in TRX-1 protein expression during exercise. Only HIGH induced a transient over-oxidation of PRDX, alongside the greatest change in TRX-R activity. Future studies are needed to clarify the significance of heightened peroxide exposure during continuous high-intensity exercise and the mechanisms of PRDX-regulatory control.
过氧化物酶（PRDX）和硫氧还蛋白（TRX）是控制细胞信号传导和氧化还原平衡的抗氧化蛋白，尽管它们对运动的反应尚不清楚。本研究旨在评估PRDX-TRX氧化还原循环对三种不同运动模式的关键反应。
健康男性（n = 10，平均±标准差：22±3岁）在不同日期进行了三项运动试验：两项中等强度（60%[公式：见正文]最大摄氧量；27分钟，中度）和高强度（80%[公式：见正文]最大摄氧量；20分钟，高强度）的稳态骑行试验，以及一项低容量高强度间歇训练试验（10×1分钟90%[公式：见正文]最大摄氧量，低容量高强度间歇训练）。在运动前、运动期间和运动后30分钟（运动后+30）评估外周血单个核细胞中TRX-1和过氧化PRDX（同工型I-IV）的蛋白表达。还评估了硫氧还蛋白还原酶（TRX-R）和核因子κB（NF-κB）p65亚基的活性。
在所有试验中，TRX-1在运动期间均增加（中度，+84.5%；高强度，+64.1%；低容量高强度间歇训练，+205.7%；p<0.05），而过氧化PRDX仅在高强度运动期间增加（中度，-28.7%；高强度，+202.9%；低容量高强度间歇训练，-22.7%；p<0.05）。在所有试验中，TRX-R和NF-κB p65活性在运动期间均增加，其中高强度运动中TRX-R活性的反应最大（p<0.05）。
所有试验均在运动期间刺激了TRX-1蛋白表达的短暂增加。只有高强度运动诱导了PRDX的短暂过氧化，同时TRX-R活性变化最大。未来需要进一步研究以阐明持续高强度运动期间过氧化物暴露增加的意义以及PRDX调节控制的机制。
