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Effects of high-intensity training on lipid metabolism in Thoroughbreds

Yu Kitaoka PhD1, Kazutaka Mukai DVM, PhD2, Hiroko Aida DVM, PhD3, Atsushi Hiraga DVM, PhD4, Hiroyuki Masuda MSc5, Tohru Takemasa PhD6, and Hideo Hatta PhD7
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  • 1 Graduate School of Comprehensive Human Sciences, University of Tsukuba, Tennodai 1-1-1 Tsukuba, Ibaraki 305-8574, Japan.
  • | 2 Equine Research Institute, Japan Racing Association, 321-4 Tokami-cho, Utsunomiya, Tochigi 320-0856, Japan.
  • | 3 Equine Research Institute, Japan Racing Association, 321-4 Tokami-cho, Utsunomiya, Tochigi 320-0856, Japan.
  • | 4 Equine Research Institute, Japan Racing Association, 321-4 Tokami-cho, Utsunomiya, Tochigi 320-0856, Japan.
  • | 5 Department of Sports Sciences, Graduate School of Arts and Sciences, The University of Tokyo, 3-8-1 Komaba, Meguro-ku, Tokyo 153-8902, Japan.
  • | 6 Graduate School of Comprehensive Human Sciences, University of Tsukuba, Tennodai 1-1-1 Tsukuba, Ibaraki 305-8574, Japan.
  • | 7 Department of Sports Sciences, Graduate School of Arts and Sciences, The University of Tokyo, 3-8-1 Komaba, Meguro-ku, Tokyo 153-8902, Japan.

Abstract

Objective—To investigate the effects of high-intensity training (HIT) on carbohydrate and fat metabolism in Thoroughbreds.

Animals—12 Thoroughbreds (3 to 4 years old; 6 males and 6 females).

Procedures—Horses performed HIT for 18 weeks. They ran at 90% or 110% of maximal oxygen consumption (o2max) for 3 minutes (5 d/wk) and were subjected to incremental exercise testing (IET) before and after training. Blood samples were collected during IET, and muscle samples were obtained from the gluteus medius muscle immediately after IET. Phosphofructokinase, citrate synthase, and β-3-hydroxyacyl CoA dehydrogenase (β-HAD) activities were measured to determine glycolytic and oxidative capacities. Peroxisome proliferator-activated receptor-γ coactivator-1α (PGC-1α) and fatty acid translocase (FAT/CD36) protein contents were detected via western blotting. Metabolome analysis was performed via capillary electrophoresis–electrospray ionization mass spectrometry to measure substrate concentrations related to carbohydrate metabolism.

Results—Peak speed during IET and o2max increased after HIT. Activities of citrate synthase and β-HAD increased after HIT, whereas phosphofructokinase activity remained unchanged. The PGC-1α and FAT/CD36 protein contents increased after HIT, but plasma lactate concentration and the respiratory exchange ratio decreased after HIT. The plasma free fatty acid concentration increased after HIT, whereas the glucose concentration was not altered. Fructose 1,6-diphosphate, phosphoenolpyruvate, and pyruvate concentrations decreased after HIT.

Conclusions and Clinical Relevance—HIT caused an increase in oxidative capacity in equine muscle, which suggested that there was a decreased reliance on carbohydrate utilization and a concomitant shift toward fatty acid utilization during intensive exercise.

Abstract

Objective—To investigate the effects of high-intensity training (HIT) on carbohydrate and fat metabolism in Thoroughbreds.

Animals—12 Thoroughbreds (3 to 4 years old; 6 males and 6 females).

Procedures—Horses performed HIT for 18 weeks. They ran at 90% or 110% of maximal oxygen consumption (o2max) for 3 minutes (5 d/wk) and were subjected to incremental exercise testing (IET) before and after training. Blood samples were collected during IET, and muscle samples were obtained from the gluteus medius muscle immediately after IET. Phosphofructokinase, citrate synthase, and β-3-hydroxyacyl CoA dehydrogenase (β-HAD) activities were measured to determine glycolytic and oxidative capacities. Peroxisome proliferator-activated receptor-γ coactivator-1α (PGC-1α) and fatty acid translocase (FAT/CD36) protein contents were detected via western blotting. Metabolome analysis was performed via capillary electrophoresis–electrospray ionization mass spectrometry to measure substrate concentrations related to carbohydrate metabolism.

Results—Peak speed during IET and o2max increased after HIT. Activities of citrate synthase and β-HAD increased after HIT, whereas phosphofructokinase activity remained unchanged. The PGC-1α and FAT/CD36 protein contents increased after HIT, but plasma lactate concentration and the respiratory exchange ratio decreased after HIT. The plasma free fatty acid concentration increased after HIT, whereas the glucose concentration was not altered. Fructose 1,6-diphosphate, phosphoenolpyruvate, and pyruvate concentrations decreased after HIT.

Conclusions and Clinical Relevance—HIT caused an increase in oxidative capacity in equine muscle, which suggested that there was a decreased reliance on carbohydrate utilization and a concomitant shift toward fatty acid utilization during intensive exercise.

Contributor Notes

Supported by the Japan Racing Association.

Dr. Kitaoka was supported in part by a grant-in-aid for JSPS Fellows from the Japan Society for the Promotion of Science.

Address correspondence to Dr. Hatta (hatta@idaten.c.u-tokyo.ac.jp).