緒論：研究指出天然的辣椒素酯類物質 (capsinoids, CSN) 增加人體的能量消耗與脂 肪氧化作用。當運動的能量來源偏向脂肪利用，有助於延緩疲勞與降低肝醣的分解，並 促進運動表現。因此，本研究欲探討運動前攝取辣椒素酯類物質是否有利後續運動期間 的脂肪氧化作用、延遲肌肉肝醣耗竭與運動疲勞的產生。方法：十名健康男性受試者 (年 齡：20.6 ± 0.3 歲；身高：171.3 ± 2.4 公分；體重：67.0 ± 3.4 kg；BMI：21. 1 ± 0.6 kg/m2； O2 max：46.4 ± 2.4 ml/kg/min) 分別完成安慰劑 (placebo) 試驗或辣椒素酯類物質 (CSN)，試驗兩種試驗至少間隔七天。受試者在試驗當天先食用輕熱量早餐，接著口服 30 mg 的辣椒素酯類物質或安慰劑膠囊後，在原地腳踏車上進行單次70 分鐘的肌肉肝醣 耗竭運動。在餐前、運動前與運動期間每20 分鐘進行採血；運動期間全程採集氣體間接 分析能量代謝；肌肉樣本在運動前、後進行採樣。結果：CSN 試驗在運動期間第40 與 60 分之甘油與非酯化脂肪酸濃度低於placebo (p < .05)；CSN 試驗的血氨與尿素濃度在運 動期間第40、60 分與運動結束明顯低於placebo (p < .05)；CSN 試驗的肌酸激酶在第60 分與運動結束的濃度顯著較低 (p < .05)。兩種試驗在運動後的肌肉肝醣濃度顯著低於運 動前 (p < .05)。CSN 試驗沒有改變肌肉肝醣、血糖與乳酸等濃度，顯示單次補充CSN 不 會降低運動誘發的疲勞。結論：人體在運動前補充辣椒素酯類物質不會改變運動期間的 脂肪氧化作用、延遲肌肉肝醣耗竭與運動疲勞的產生。

Introduction: In previous study, a capsinoids intake would enhance the energy expenditure and fat oxidation in humans. If a capsinoids (CSN) can stimulate fat oxidation and spare glycogen stores following exercise resulting in delaying exercise-induced fatigue. The purpose of the study was to investigate the effect of acute oral CNS supplementation on fat oxidation, muscle glycogen and fatigue during exercise. Methods: Ten healthy subjects (age 20.6 ± 0.3 years; height 171.3 ± 2.4 cm; weight 67.0 ± 3.4 kg; BMI 21.1 ± 0.6 kg/m2; V ‧ O2 max 46.4 ± 2.4 ml/kg/min) completed a crossover study design with CNS and placebo trials and performed a single bout of cycling exercise challenge with glycogen depletion protocol for 70 minutes, separated a 7-d washout period. All subjects consumed 30 mg CSN or placebo with light breakfast before exercise challenge. Blood samples were measured before meal and during exercise. Expired gas samples were collected during exercise. Simultaneously, muscle biopsy samples were obtained from vastus lateralis before and immediately after exercise. Results: Plasma glycerol and non-esterified fatty acid, at 40 and 60 min during exercise were significantly lower after CSN consumption compared to placebo (p < .05). Plasma ammonia and urea at 40th, 60th and the end of the exercise in the CSN trial were elevated compared with placebo (p < .05). Lower response in creatine kinase at 60 min during exercise and immediately after exercise was found after CSN supplementation (p < .05). Muscle glycogen content after exercise was reduced significantly in both CSN and placebo trials (p < .05). No effect was found in this study after acute oral CSN supplementation on attenuating exercise-induced fatigue, based on no significant difference responses in muscle glycogen, blood glucose and lactate. Conclusion: Oral CSN supplementation could not change lipolysis during exercise, delay muscle glycogen depletion and attenuate subsequence exercise-induced fatigue.