Weavil J C, Sidhu S K, Mangum T S, Richardson R S, Amann M
Department of Exercise and Sport Science, University of Utah, Salt Lake City, Utah;
Department of Internal Medicine, University of Utah, Salt Lake City, Utah;
Am J Physiol Regul Integr Comp Physiol. 2015 Jun 15;308(12):R998-1007. doi: 10.1152/ajpregu.00021.2015. Epub 2015 Apr 15.
We investigated the role of exercise intensity and associated central motor drive in determining corticomotoneuronal excitability. Ten participants performed a series of nonfatiguing (3 s) isometric single-leg knee extensions (ISO; 10-100% of maximal voluntary contractions, MVC) and cycling bouts (30-160% peak aerobic capacity, W peak). At various exercise intensities, electrical potentials were evoked in the vastus lateralis (VL) and rectus femoris (RF) via transcranial magnetic stimulation (motor-evoked potentials, MEP), and electrical stimulation of both the cervicomedullary junction (cervicomedullary evoked potentials, CMEP) and the femoral nerve (maximal M-waves, M max). Whereas M max remained unchanged in both muscles (P > 0.40), voluntary electromyographic activity (EMG) increased in an exercise intensity-dependent manner for ISO and cycling exercise in VL and RF (both P < 0.001). During ISO exercise, MEPs and CMEPs progressively increased in VL and RF until a plateau was reached at ∼ 75% MVC; further increases in contraction intensity did not cause additional changes (P > 0.35). During cycling exercise, VL-MEPs and CMEPs progressively increased by ∼ 65% until a plateau was reached at W peak. In contrast, RF MEPs and CMEPs progressively increased by ∼ 110% throughout the tested cycling intensities without the occurrence of a plateau. Furthermore, alterations in EMG below the plateau influenced corticomotoneuronal excitability similarly between exercise modalities. In both exercise modalities, the MEP-to-CMEP ratio did not change with exercise intensity (P > 0.22). In conclusion, increases in exercise intensity and EMG facilitates the corticomotoneuronal pathway similarly in isometric knee extension and locomotor exercise until a plateau occurs at a submaximal exercise intensity. This facilitation appears to be primarily mediated by increases in excitability of the motoneuron pool.
我们研究了运动强度及相关中枢运动驱动在决定皮质脊髓运动神经元兴奋性方面的作用。10名参与者进行了一系列非疲劳性(3秒)的等长单腿膝关节伸展运动(ISO;最大自主收缩的10 - 100%,MVC)和骑行运动(峰值有氧能力的30 - 160%,W峰值)。在不同运动强度下,通过经颅磁刺激在股外侧肌(VL)和股直肌(RF)诱发电位(运动诱发电位,MEP),并对颈髓交界处进行电刺激(颈髓诱发电位,CMEP)以及对股神经进行电刺激(最大M波,M max)。虽然两块肌肉的M max均保持不变(P > 0.40),但在VL和RF中,等长运动和骑行运动的自主肌电图活动(EMG)均以运动强度依赖的方式增加(均为P < 0.001)。在等长运动期间,VL和RF中的MEP和CMEP逐渐增加,直到在约75%MVC时达到平台期;收缩强度进一步增加未引起额外变化(P > 0.35)。在骑行运动期间,VL - MEP和CMEP逐渐增加约65%,直到在W峰值时达到平台期。相比之下,在整个测试的骑行强度范围内,RF的MEP和CMEP逐渐增加约110%,未出现平台期。此外,在平台期以下,EMG的变化在不同运动方式之间对皮质脊髓运动神经元兴奋性的影响相似。在两种运动方式中,MEP与CMEP的比值均不随运动强度而变化(P > 0.22)。总之,在等长膝关节伸展运动和移动运动中,运动强度和EMG的增加以相似的方式促进皮质脊髓运动神经元通路,直到在次最大运动强度时达到平台期。这种促进作用似乎主要由运动神经元池兴奋性的增加介导。