Hypothermia Decreases O2 Cost for ex vivo Contraction in Mouse Skeletal Muscle

Introduction Evidence suggests that the energy efficiency of key ATPases involved in skeletal muscle contractile activity are improved in a hypothermic condition. However, it is unclear how a decrease in temperature affects skeletal muscle O2 consumption (mVO2) induced by muscle contraction. Methods Isolated mouse extensor digitorum longus (EDL) muscles were incubated in a temperature-controlled (37°C or 25°C) bath that included an O2 probe. EDL muscles from one limb were subjected to the measurement of resting mVO2, and the contralateral EDL muscles were used for the measurement of mVO2 with electrically-stimulated contraction. For the resting protocol, muscles were suspended at resting tension for 15 mins with continuous O2 recordings. For the contraction protocol, EDL muscles underwent ten electrically-stimulated isometric contractions with continuous O2 recordings for 15 mins. The rate of O2 disappearance was quantified as μmole O2 per minute and normalized to the wet weight of the muscle. Results Resting mVO2 was greater at 37°C than at 25°C, consistent with the idea that lower temperature reduces basal metabolic rate. Electrically-stimulated contraction robustly increased mVO2 at both 37°C and 25°C, which was sustained for ~3 min post-contraction. During that period, mVO2 was elevated ~5-fold at both 37°C and 25°C. Greater contraction-induced mVO2 at 37°C compared to 25°C occurred despite lower force generated at 37°C than at 25°C. Conclusion Together, O2 cost for muscle contraction (force-time integral per O2 consumed) was greater at 37°C than at 25°C. Levels of high-energy phosphates were consistent with greater energy demand at 37°C compared to 25°C. In conclusion, these results indicate that muscle contraction that occurs at subnormal temperature requires less O2 than at 37°C. These authors contributed equally for the study. Patrick J. Ferrara and Anthony R.P. Verkerke. Corresponding Author: Katsuhiko Funai, Ph.D. University of Utah, 15 North 2030 East, EIHG 3145, Salt Lake City, UT 84112, USA. Email: kfunai@health.utah.edu This work was funded by NIH grants DK095774, DK107397, and DK109888 to KF and AR070200 to JJB, and by American Heart Association grant 18PRE33960491 to ARPV. Conflict of Interest: We have no conflict of interest to report. The results of the present study do not constitute endorsement by ACSM and are presented clearly, honestly, and without fabrication, falsification, or inappropriate data manipulation. Accepted for Publication: 14 May 2018 © 2018 American College of Sports Medicine

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