本研究目的是為了解運動造成的肌肉損傷，對於選手在恢復期間之血糖代謝能力、肌酸激酶及細胞激素變化的影響。本研究以十名大專甲組男子游泳代表隊為受試對象（年紀20.5±1.2歲；身高176.2±5.0公分；體重68.2±6.2公斤），經10天停止運動後，接受單次高強度運動。於運動前及運動後一天、三天及五天採血，以取得血糖、胰島素、肌酸激酶、介白質－6(IL-6)及α-腫瘤壞死因子(TNF-α)等指標之基礎值及恢復期間變化。本研究結果：空腹血糖、胰島素及HOMA-IR index（胰島素抗性指標）在運動後一天的數值，皆明顯高於運動前測值(p<.05)，但隨即在運動後第三天及第五天恢復至前測水準。以肌酸激酶評估肌肉損傷現象，運動後第一天，肌酸激酶即明顯較前測值高(p<.05)，並且在第三天及第五天仍明顯高於前測水準(p<.05)。細胞激素IL-6在運動後第一天即顯著高於前測值(p<.05)，並且持續至少5天，TNF-α與IL-6呈現相同趨勢，即運動後第一天、第三天及第五天皆明顯高於前測值(p<.05)。本研究結論發現，單次高強度運動造成的肌肉損傷，會產生短暫的抗胰島素現象（胰島素抗性現象），而肌酸激酶、IL-6及TNF-α等肌肉損傷相關指標持續明顯升高至第五天，顯示發炎反應及組織修補過程尚未完成，此時胰島素阻抗已消失，代表細胞能源運送系統已優先修復。建議未來遇肌肉損傷時，初期應以高質量蛋白質補充為主，待肌肉修復數日後再補充高碳水化物以利肝醣回補。

This study was aimed to investigate the effects of exercise-induced muscle damage on the changes in blood glucose, serum insulin, creatine kinase (CK) and cytokines during five days post recovery period. Ten male elite swimmers of a school team were recruited as subjects in this study. All the subjects were under detraining for ten days, and the blood samples were collected before the single training as baseline levels. Subjects were asked to be trained under a designed program with an experienced trainer and the blood samples were collected after training and also one day, three days and five days after training. Blood glucose metabolism, bio-indicators such as CK, interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α) were analyzed as the indexes in post recovery period. One-way ANOVA has been used to determine the significance between baseline and different recovery time periods. In the analysis of glucose metabolism test, fasting blood glucose, serum insulin, and HOMAIR which were seen as insulin resistance indexes were significantly higher (p<.05) on the first day of the post recovery period. But the insulin resistance status was not continuously found in the third and fifth day after training. Meanwhile, the CK levels were truly higher (p<.05) from the first day to the fifth day of recovery period. The pro-inflammatory cytokine IL-6 known as energy sensor in muscle was elevated significantly (p<.05) from the first day to the end of the recovery period, and TNF-α was increased significantly (p<.05) as IL-6 after single bout of high intensity training. These results conclude that acute intense training-induced muscle damage causes a short term of insulin resistance from exhausting of muscle glycogen. Monitoring of cytokines such as IL-6 and TNF-α could be biomarkers that indicated the recovery status of during the post training period. In the beginning of the muscle damage, high quality protein intakes should promote the muscle repairing, and then high carbohydrate consumption could help with glycogen replenish in the recovery period.