Lab Anim Res.
2021 Sep;37(3):223-232. 10.1186/s42826-021-00094-0.
Comparison of intrinsic exercise capacity and response to acute exercise in ICR (Institute of Cancer Research) mice derived from three different lineages
- Affiliations
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- 1Exercise Biochemistry Laboratory, Korea National Sport University, Yangjae-daero, Songpa-gu, Seoul, Republic of Korea
- 2Department of Microbiology and Immunology, INJE University College of Medicine, Inje-ro, Gimhae-si, Gyeongsangnam-do, Republic of Korea
- 3College of Veterinary Medicine, Kyungpook National University, Daehak-ro, Buk-gu, Daegu, Republic of Korea
- 4College of Pharmacy, Pusan National University, Busandaehak-ro 63beon-gil, Geumjeong-gu, Busan, Republic of Korea
- 5Department of Biomaterials Science, College of Natural Resources and Life Science/Life and Industry Convergence Research Institute, Pusan National University, Busandaehak-ro 63beon-gil, Geumjeong-gu, Busan, Republic of Korea
- KMID: 2521037
- DOI: http://doi.org/10.1186/s42826-021-00094-0
Abstract
- Background
As a laboratory animal resource, the ICR mouse is commonly used in a variety of research fields. However, information on differences in exercise-related characteristics in ICR mice derived from different lineages and the underlying mechanisms remains to be elucidated. In this study, we investigated the intrinsic exercise capacity and a magnitude of response to acute exercise, and sought to identify mechanisms contributing to difference in Korl:ICR (a novel ICR lineage recently established by the National Institute of Food and Drug Safety Evaluation, Korea) and two commercialized ICR lineages derived from different origins (viz., A:ICR mouse from Orient Bio Com, the United States, and B:ICR mouse from Japan SLC Inc., Japan).
Results
Results showed that despite no significant difference in body weight and weight-proportioned tissue mass of heart and skeletal muscles among groups, the relatively low intrinsic exercise capacity and exaggerated response to acute exercise were identified in B:ICR comparted with Korl:ICR and A:ICR, as reflected by total work and lactate threshold (LT). Also, the mitochondrial efficiency expressed as the complex 1 and complex 1 + 2 respiratory control ratio (RCR) values for cardiac mitochondrial O 2 consumption in B:ICR was significantly lower than that in Korl:ICR with higher level of state 2 respiration by glutamate/malate and UCP3 expression in cardiac muscle.
Conclusions
Taken together, these results indicate that the intrinsic exercise capacity of ICR mouse varies according to lineages, suggesting the role of cardiac mitochondrial coupling efficiency as a possible mechanism that might contribute to differences in the intrinsic exercise capacity and magnitude of response to exercise.
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