Stary C M, Hogan M C
Department of Medicine, University of California San Diego, La Jolla, California 92093-0623, USA.
J Appl Physiol (1985). 1999 Jun;86(6):1812-6. doi: 10.1152/jappl.1999.86.6.1812.
The purpose of this study was to examine the development of fatigue in isolated, single skeletal muscle fibers when O2 availability was reduced but not to levels considered rate limiting to mitochondrial respiration. Tetanic force was measured in single living muscle fibers (n = 6) from Xenopus laevis while being stimulated at increasing contraction rates (0.25, 0.33, 0.5, and 1 Hz) in a sequential manner, with each stimulation frequency lasting 2 min. Muscle fatigue (determined as 75% of initial maximum force) was measured during three separate work bouts (with 45 min of rest between) as the perfusate PO2 was switched between values of 30 +/- 1.9, 76 +/- 3.0, or 159 Torr in a blocked-order design. No significant differences were found in the initial peak tensions between the high-, intermediate-, and low-PO2 treatments (323 +/- 22, 298 +/- 27, and 331 +/- 24 kPa, respectively). The time to fatigue was reached significantly sooner (P < 0.05) during the 30-Torr treatment (233 +/- 39 s) compared with the 76- (385 +/- 62 s) or 159-Torr (416 +/- 65 s) treatments. The calculated critical extracellular PO2 necessary to develop an anoxic core within these fibers was 13 +/- 1 Torr, indicating that the extracellular PO2 of 30 Torr should not have been rate limiting to mitochondrial respiration. The magnitude of an unstirred layer (243 +/- 64 micron) or an intracellular O2 diffusion coefficient (0.45 +/- 0.04 x 10(-5) cm2/s) necessary to develop an anoxic core under the conditions of the study was unlikely. The earlier initiation of fatigue during the lowest extracellular PO2 condition, at physiologically high intracellular PO2 levels, suggests that muscle performance may be O2 dependent even when mitochondrial respiration is not necessarily compromised.
本研究的目的是在氧气供应减少但未降至被认为是线粒体呼吸速率限制水平的情况下,研究分离的单根骨骼肌纤维中疲劳的发展情况。在非洲爪蟾的单根活肌纤维(n = 6)中测量强直力,同时以递增的收缩速率(0.25、0.33、0.5和1 Hz)依次刺激,每个刺激频率持续2分钟。在三个单独的工作时段(中间休息45分钟)测量肌肉疲劳(定义为初始最大力的75%),灌注液的氧分压在30±1.9、76±3.0或159 Torr之间以区组设计切换。在高、中、低氧分压处理组之间,初始峰值张力没有显著差异(分别为323±22、298±27和331±24 kPa)。与76 Torr(385±62秒)或159 Torr(416±65秒)处理相比,在30 Torr处理期间(233±39秒)达到疲劳的时间显著提前(P < 0.05)。在这些纤维内形成缺氧核心所需的计算临界细胞外氧分压为13±1 Torr,这表明30 Torr的细胞外氧分压不应是线粒体呼吸的速率限制因素。在本研究条件下形成缺氧核心所需的静止层厚度(243±64微米)或细胞内氧扩散系数(0.45±0.04×10⁻⁵ cm²/s)不太可能。在最低细胞外氧分压条件下,在生理上较高的细胞内氧分压水平时疲劳更早开始,这表明即使线粒体呼吸不一定受到损害,肌肉性能也可能依赖于氧气。