乳酸迷思：乳酸是導致運動疲勞的原因嗎？

Lactate Myth: Is Lactate a Cause of Fatigue During Exercise?

郭家驊(Chia-Hua Kuo)

《大專體育學刊》 24卷4期 (2022/12) Pp. i-iv

https://doi.org/10.5297/ser.202212_24(4).0000

摘要

自1920到1970年代，乳酸堆積導致運動疲勞與延遲性肌肉酸痛（delayed onset muscle soreness, DOMS）是運動學術領域很流行的理論。然而，這個理論在現代科學已逐漸被證明是錯誤的。這個理論的起 源主要是來自於錯誤解讀德國科學家Otto Meyerhof在青蛙肌肉收縮離體實驗的發現（Kresge et al., 2005）。Otto Meyerhof在1922年，因對於醣解作用的知識貢獻與英國科學家Archibald V. Hill共同獲得諾貝爾奬。在他的研究中發現沒有氧氣供應的狀況下反覆肌肉收縮無法持續太久，同時觀察到肌肉肝醣減少、乳酸增加、酸度增加的現象（Kresge et al., 2005）。後人將乳酸增加與肌肉疲勞發生兩者的相關性錯誤推論為因果關係，忽略了肌肉肝醣耗盡才是主要導致疲勞的原因。這個乳酸疲勞理論被類似研究設計的肌肉收縮離體實驗證明為錯誤 （Kristensen et al., 2005）。在實驗中，爲證明因果關係，肌肉乳酸濃度與酸度增加下比較肌肉收縮表現，發現乳酸與酸度增加均不影響肌肉收縮能力。而且在鉀離子濃度較高的實驗條件下，加入乳酸甚至可提高肌肉收縮力。這個研究更近一步證明，如果肌肉無法在收縮過程產生乳酸，在肌肉酸度增加的狀況下持續收縮的時間將更短（Kristensen et al., 2005）。這個研究證明了乳酸不但不是導致疲勞的原因，他反而是肌肉收縮過程需要的快速能源。在1967年，Hermansen et al.（1967）的人體實驗的結果也不支持乳酸是疲勞的導因。在他的實驗中，年輕人進行長達90min的耐力試驗（強度為77%最大有氧功率），發現乳酸堆積的尖峰時間在前20min，隨後因肌肉中的肝醣逐漸耗盡，乳酸濃度也隨之下降。疲勞的發生時間在接近90min，並非發生在乳酸最高峰的前20min。這個研究突顯肌肉肝醣消耗度對運動疲勞的重要性，而非乳酸堆積。同時期的研究也證明肌肉肝醣與耐力之間的因果關係（Bergström et al., 1967）。乳酸的主要來源是肌肉中所儲存的肝醣，並非脂肪與氨基酸。因此，飲食內容可改變血乳酸濃度，進而改變耐力。在人體耐力試驗運動前3h與運動過程中給予三種不同的營養補充選擇，發現補充品葡萄糖比例較高者，運動導致相對較高的乳酸堆積，然而耐力表現愈好（Chryssanthopoulos et al., 2002）。脂肪占比高的食物最不容易導致乳酸堆積，但耐力表現相對最差（Rowlands & Hopkins, 2002）。對於缺乏運動訓練者，運動完後大約1～2天開始有DOMS發生，這個酸痛感也不是來自乳酸，而是典型的發炎反應後期肌肉再生過程導致的疼痛。乳酸在運動後90 min內已恢復到運動前的低點（Hsu et al., 2005），乳酸堆積顯然無法合理解釋訓練後DOMS的原因。總結來說，乳酸是肌肉收縮的重要快速能源（Gladden, 2000）。乳酸堆積並不會導致肌肉疲勞。此外，增加乳酸較多的高醣飲食，反而是提高運動耐力表現的營養選擇。

並列摘要

From 1920s to 1970s, lactate accumulation as a cause of fatigue during exercise and delay onset muscle soreness (DOMS) is a popular theory. However, the modern science has proven that lactate is unlikely the cause of fatigue during endurance exercise and DOMS. The origin of this false theory comes from a misinterpretation of the scientific results from a German scientist, Otto Meyerhof, the Nobel laurate together with Archibald V. Hill in 1922. This study showed that electrically stimulated contracting muscle of frog legs produced lactate from glycogen in absence of oxygen (Kresge et al., 2005). The muscle gets fatigue quickly (stopped contracting) together with increased acidity after repeated stimulations. This correlational result leads to misinterpretations of the causal relationship by forming an erroneous theory that lactic acid is responsible for muscle fatigue during muscle contraction. This theory has been proven wrong by a similar ex vivo muscle contraction study (Kristensen et al., 2005), in which increasing lactate concentrations do not inhibit the ability of skeletal muscles to contract. In addition, improved muscle force was observed with incubating of muscle with lactate at different pH: 20 mm Na-lactate (which acidifies internal pH), 12 mm Na-lactate + 8 mm lactic acid (which mimics the pH changes during muscle activity), and 20 mm lactic acid (which acidifies external pH more than internal pH) in normal and potassium-depressed muscles. In vivo evidence against the lactate-fatigue theory was already available before the 1970. In 1967, Hermansen et al. (1967) has found lactate peaking during the first 20 min of endurance exercise maintaining the same exercise intensity at 77% maximal workload, and declined thereafter during the remaining 70 min. If lactate accumulation is the cause of fatigue, exercise should no longer persisted during the first 20 min. In the same group, they demonstrated that muscle glycogen depletion is the main cause of fatigue during endurance exercise (Bergström et al., 1967). In this context, we need to keep in mind that glycogen is the main source of lactate, not fatty acid and amino acids. Another study compared 3 dietary supplement conditions, supplemented 3 h before exercise performance test: A) carbohydrate meal + glucose drink, B) carbohydrate meal + water drink, and C) No meal + water drink. This study demonstrated that carbohydrate-containing meal boosted blood lactate levels during exercise but resulted in longer exercise time (meal A: 125 min, meal B: 111 min, meal C: 103 min) (Chryssanthopoulos et al., 2002). In particular, the supplement produces the lowest blood lactate is the high-fat low carbohydrate supplements, which produces the poorest endurance performance (Rowlands & Hopkins, 2002). DOMS is a cause of muscle inflammation, not due to lactate accumulation. DOMS typically occurs 48 h after exercise. However, exercise induced lactate increase returns to pre-exercise baseline in 90 min (Hsu et al., 2005). Apparently, lactate cannot be the cause of muscle soreness 2 days later exercise. In conclusion, lactate is an important fuel for muscle contraction (Gladden, 2000) and that the accumulation of lactate does not inhibit skeletal muscle contractility. Instead, the lactate-boosting nutritional supplements can improve the endurance performance.

參考文獻

Bergström, J., Hermansen, L., Hultman, E., & Saltin, B. (1967). Diet, muscle glycogen and physical performance. Acta Physiologica Scandinavica, 71(2–3), 140-150. https://doi.org/10.1111/j.1748-1716.1967.tb03720.x

Chryssanthopoulos, C., Williams, C., Nowitz, A., Kotsiopoulou, C., & Vleck, V. (2002). The effect of a high carbohydrate meal on endurance running capacity. International Journal of Sport Nutrition and Exercise Metabolism, 12(2), 157-171. https://doi.org/10.1123/ijsnem.12.2.157

Gladden, L. B. (2000). Muscle as a consumer of lactate. Medicine & Science in Sports & Exercise, 32(4), 764-771. https://doi.org/10.1097/00005768-200004000-00008

Hermansen, L., Hultman, E., & Saltin, B. (1967). Muscle glycogen during prolonged severe exercise. Acta Physiologica Scandinavica, 71(2–3), 129-139. https://doi.org/10.1111/j.1748-1716.1967.tb03719.x

Hsu, A. R., Hagobian, T. A., Jacobs, K. A., Attallah, H., & Friedlander, A. L. (2005). Effects of heat removal through the hand on metabolism and performance during cycling exercise in the heat. Canadian Journal of Applied Physiology, 30(1), 87-104. https://doi.org/10.1139/h05-107