Russ David W, Lovering R M
Department of Physical Therapy and Rehabilitation Science, University of Maryland-Baltimore, School of Medicine, 100 Penn Street, Baltimore, MD 21201, USA.
Exp Physiol. 2006 Nov;91(6):957-66. doi: 10.1113/expphysiol.2006.034249. Epub 2006 Jul 20.
Activation frequency as a regulator of physiological responses in skeletal muscle, independent of contractile force, has received little attention. Here, the length-tension and force-frequency relationships were employed to keep active contractile force equal, despite a twofold difference in stimulation frequency (15 versus 30 Hz). Rat tibialis anterior muscles were tested in situ using 15 Hz stimulation at optimal length (15 Hz) and 30 Hz stimulation at shortened and lengthened positions (30 Hz(sub) and 30 Hz(supra)). Muscles were subjected to 1, 15, 30 and 80 Hz stimulation trains before and after 2 min of fatiguing stimulation. The principal findings were that the two 30 Hz protocols produced greater 38 kDa MAPK (p38) phosphorylation than the 15 Hz protocol (1.4- to 1.5-fold versus 1.1-fold), as well as greater fatigue (65-78 versus 43% decline in contraction force). In contrast, c-jun amino terminal kinase (JNK) phosphorylation appeared most responsive to total (active plus passive) tension such that the changes followed the pattern: 30 Hz(supra) > 15 Hz > 30 Hz(sub), while 44 and 42 kDa extracellular regulated kinase (ERK1/2) phosphorylation was not significantly increased in response to any of the protocols studied. Neither glycogen depletion nor myofibre damage accounted for any of the findings, but a decline in muscle excitation (m-wave) may have contributed to the greater fatigue seen at higher frequencies. These data suggest that neuromuscular activation frequency can influence certain signalling pathways in skeletal muscle, independent of force production.
作为骨骼肌生理反应调节因子的激活频率，独立于收缩力之外，一直很少受到关注。在这里，尽管刺激频率相差两倍（15赫兹与30赫兹），但采用长度-张力和力-频率关系来保持主动收缩力相等。对大鼠胫前肌进行原位测试，在最佳长度下使用15赫兹刺激（15Hz），在缩短和延长位置使用30赫兹刺激（30Hz(sub)和30Hz(supra)）。在疲劳刺激2分钟前后，对肌肉施加1、15、30和80赫兹的刺激序列。主要发现是，两种30赫兹方案比15赫兹方案产生更高的38 kDa丝裂原活化蛋白激酶（p38）磷酸化水平（分别为1.4至1.5倍和1.1倍），以及更大程度的疲劳（收缩力下降65 - 78%对43%）。相比之下，c - jun氨基末端激酶（JNK）磷酸化似乎对总（主动加被动）张力最敏感，其变化遵循以下模式：30Hz(supra) > 15Hz > 30Hz(sub)，而44和42 kDa细胞外调节激酶（ERK1/2）磷酸化在任何研究方案下均未显著增加。糖原消耗和肌纤维损伤均不能解释任何研究结果，但肌肉兴奋性（m波）下降可能是导致高频下更大疲劳的原因。这些数据表明，神经肌肉激活频率可独立于力的产生而影响骨骼肌中的某些信号通路。
