Autor: |
Miyazaki T; Joint Research Center, Tokyo Medical University Ibaraki Medical Center, Ami, Tokyo 300-0395, Japan., Nakamura-Shinya Y; Department of Immunology, Faculty of Medicine, University of Tsukuba, Tsukuba 305-8575, Japan., Ebina K; Department of Health and Nutrition, Tsukuba International University, Tsuchiura 300-0051, Japan., Komine S; Department of Acupuncture and Moxibustion, Faculty of Human Care, Teikyo Heisei University, Toshima-ku, Tokyo 170-8445, Japan.; Faculty of Medicine, University of Tsukuba, Tsukuba 305-0821, Japan., Ra SG; Institute of Liberal Arts and Sciences, Tokushima University, Tokushima 770-8502, Japan., Ishikura K; Faculty of Management, Josai University, Sakado 350-0295, Japan., Ohmori H; Faculty of Health and Sport Sciences, University of Tsukuba, Tsukuba 305-8574, Japan., Honda A; Joint Research Center, Tokyo Medical University Ibaraki Medical Center, Ami, Tokyo 300-0395, Japan.; Department of Gastroenterology and Hepatology, Tokyo Medical University Ibaraki Medical Center, Ami, Tokyo 300-0395, Japan. |
Abstrakt: |
During endurance exercises, a large amount of mitochondrial acetyl-CoA is produced in skeletal muscles from lipids, and the excess acetyl-CoA suppresses the metabolic flux from glycolysis to the TCA cycle. This study evaluated the hypothesis that taurine and carnitine act as a buffer of the acetyl moiety of mitochondrial acetyl-CoA derived from the short- and long-chain fatty acids of skeletal muscles during endurance exercises. In human subjects, the serum concentrations of acetylated forms of taurine (NAT) and carnitine (ACT), which are the metabolites of acetyl-CoA buffering, significantly increased after a full marathon. In the culture medium of primary human skeletal muscle cells, NAT and ACT concentrations significantly increased when they were cultured with taurine and acetate or with carnitine and palmitic acid, respectively. The increase in the mitochondrial acetyl-CoA/free CoA ratio induced by acetate and palmitic acid was suppressed by taurine and carnitine, respectively. Elevations of NAT and ACT in the blood of humans during endurance exercises might serve the buffering of the acetyl-moiety in mitochondria by taurine and carnitine, respectively. The results suggest that blood levels of NAT and ACT indicate energy production status from fatty acids in the skeletal muscles of humans undergoing endurance exercise. |