單次口服辣椒素酯類物質無法減緩後續運動產生疲勞之產生

Acute oral capsinoids supplementation could not attenuate exercise induced fatigue in human study

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；VO2 max：46.4 ± 2.4 ml/kg/min) 分別完成安慰劑試驗 (placebo) 或辣椒素試驗 (CSN)，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 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 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；VO2 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.