Otis Jeffrey S, Roy Roland R, Edgerton V Reggie, Talmadge Robert J
Muscle Function Laboratory, Virginia Polytechnic Institute and State University, Blacksburg 24061, USA.
J Appl Physiol (1985). 2004 Feb;96(2):584-96. doi: 10.1152/japplphysiol.00724.2003. Epub 2003 Oct 17.
To determine whether long-term reductions in neuromuscular activity result in alterations in metabolic capacity, the activities of oxidative, i.e., succinate dehydrogenase (SDH) and citrate synthase (CS), and glycolytic, i.e., alpha-glycerophosphate dehydrogenase (GPD), enzyme markers were quantified in rat soleus muscles 1, 3, and 6 mo after a complete spinal cord transection (ST). In addition, the proportional content of lactate dehydrogenase (LDH) isozymes was used as a marker for oxidative and glycolytic capacities. The myosin heavy chain (MHC) isoform content of a fiber served as a marker of phenotype. In general, MHC isoforms shifted from MHC1 toward MHC2, particularly MHC2x, after ST. Mean SDH and CS activities were higher in ST than control at all time points. The elevated SDH and CS activities were indicative of an enhanced oxidative capacity. GPD activities were higher in ST than control rats at all time points. The increase in activity of SDH was larger than GPD. Thus the GPD-to-SDH (glycolytic-to-oxidative) ratio was decreased after ST. Compared with controls, total LDH activity increased transiently, and the LDH isozyme profile shifted from LDH-1 toward LDH-5, indicative of an enhanced glycolytic capacity. Combined, these results indicate that 1) the metabolic capacities of soleus fibers were not compromised, but the interrelationships among oxidative and glycolytic capacity and MHC content were apparently dissociated after ST; 2) enhancements in oxidative and glycolytic enzyme activities are not mutually exclusive; and 3) chronic reductions in skeletal muscle activity do not necessarily result in a reduced oxidative capacity.
为了确定神经肌肉活动的长期减少是否会导致代谢能力的改变，在大鼠脊髓完全横断（ST）后1、3和6个月，对其比目鱼肌中氧化酶（即琥珀酸脱氢酶（SDH）和柠檬酸合酶（CS））以及糖酵解酶（即α-甘油磷酸脱氢酶（GPD））的活性进行了定量分析。此外，乳酸脱氢酶（LDH）同工酶的比例含量被用作氧化和糖酵解能力的标志物。纤维的肌球蛋白重链（MHC）亚型含量作为表型的标志物。一般来说，脊髓横断后，MHC亚型从MHC1向MHC2转变，尤其是MHC2x。在所有时间点，脊髓横断组的SDH和CS平均活性均高于对照组。SDH和CS活性的升高表明氧化能力增强。在所有时间点，脊髓横断组的GPD活性均高于对照大鼠。SDH活性的增加大于GPD。因此，脊髓横断后GPD与SDH（糖酵解与氧化）的比值降低。与对照组相比，总LDH活性短暂增加，LDH同工酶谱从LDH-1向LDH-5转变，表明糖酵解能力增强。综合这些结果表明：1）比目鱼肌纤维的代谢能力没有受损，但脊髓横断后氧化和糖酵解能力以及MHC含量之间的相互关系明显解离；2）氧化酶和糖酵解酶活性的增强并非相互排斥；3）骨骼肌活动的长期减少不一定会导致氧化能力降低。
