期刊
JOURNAL OF PHYSIOLOGY-LONDON
卷 591, 期 3, 页码 731-744出版社
WILEY
DOI: 10.1113/jphysiol.2012.241992
关键词
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资金
- BBSRC [BB/F019521/1]
- Biotechnology and Biological Sciences Research Council [BB/F019521/1] Funding Source: researchfish
- BBSRC [BB/F019521/1] Funding Source: UKRI
The mechanisms controlling skeletal muscle oxygen consumption () during exercise are not well understood. We determined whether first-order control could explain kinetics at contractions onset () and cessation () in single skeletal muscle fibres differing in oxidative capacity, and across stimulation intensities up to . Xenopus laevis fibres (n= 21) were suspended in a sealed chamber with a fast response electrode to measure every second before, during and after stimulated isometric contractions. A first-order model did not well characterise on-transient kinetics. Including a time delay (TD) in the model provided a significantly improved characterisation than a first-order fit without TD (F-ratio; P < 0.05), and revealed separate activation' and exponential' phases in 15/21 fibres contracting at (mean +/- SD TD: 14 +/- 3 s). On-transient kinetics () was weakly and linearly related to (R2= 0.271, P= 0.015). Off-transient kinetics, however, were first-order, and was greater in low-oxidative ( < 0.05 nmol mm3 s1) than high-oxidative fibres ( > 0.10 nmol mm3 s1; 170 +/- 70 vs. 29 +/- 6 s, P < 0.001). was proportional to (R2= 0.727, P < 0.001), unlike in the on-transient. The calculated oxygen deficit was larger (P < 0.05) than the post-contraction volume of consumed oxygen at all intensities except . These data show a clear dissociation between the kinetic control of at the onset and cessation of contractions and across stimulation intensities. More complex models are therefore required to understand the activation of mitochondrial respiration in skeletal muscle at the start of exercise.
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