Copyright © 2018 American Physiological Society. All rights reserved. During fatiguing voluntary contractions, the excitability of motoneurons innervating arm muscles decreases. However, the behavior of motoneurons innervating quadriceps muscles is unclear. Findings may be inconsistent because descending cortical input influences motoneuron excitability and confounds measures during exercise. To overcome this limitation, we examined effects of fatigue on quadriceps motoneuron excitability tested during brief pauses in descending cortical drive after transcranial magnetic stimulation (TMS). Participants (n = 14) performed brief (5-s) isometric knee extension contractions before and after a 10-min sustained contraction at 25% maximal electromyogram (EMG) of vastus medialis (VM) on one (n - 5) or two (n = 9) days. Electrical stimulation over thoracic spine elicited thoracic motor evoked potentials (TMEP) in quadriceps muscles during ongoing voluntary drive and 100 ms into the silent period following TMS (TMS-TMEP). Femoral nerve stimulation elicited maximal M-waves (Mmax). On the 2 days, either large (50% Mmax) or small (15% Mmax) TMS-TMEPs were elicited. During the 10-min contraction, VM EMG was maintained (P = 0.39), whereas force decreased by 52% (SD 13%) (P < 0.001). TMEP area remained unchanged (P = 0.9), whereas large TMS-TMEPs decreased by 49% (SD 28%) (P = 0.001) and small TMS-TMEPs by 71% (SD 22%) (P < 0.001). This decline was greater for small TMS-TMEPs (P = 0.019; n = 9). Therefore, without the influence of descending drive, quadriceps TMS-TMEPs decreased during fatigue. The greater reduction for smaller responses, which tested motoneurons that were most active during the contraction, suggests a mechanism related to repetitive activity contributes to reduced quadriceps motoneuron excitability during fatigue. By contrast, the unchanged TMEP suggests that ongoing drive compensates for altered motoneuron excitability. NEW & NOTEWORTHY We provide evidence tha...

For the last 35 years the central focus of acidosis has been on lactic acid or lactate as being the cause of acidosis and acidosis being the cause of fatigue during intense exercise. Unfortunately, causation has been implied from correlation. The organic chemistry of the lactate dehydrogenase reaction clearly demonstrates the error of the development of metabolic acidosis from lactate production. This is not to detract from the significant development of acidosis during intense exercise. However, the assumed negative effect of acidosis on contractile failure is also called into question. The purpose of this review and commentary is to reflect on past research that has investigated the role of acidosis in fatigue, provide extensive evidence from the record of prior and current 31P MRS research on muscle acidosis during exercise and recovery and provide further insight into proton balance during muscle energy catabolism based on computations of multiple competing cation and pH-dependent proton stoichiometry. Finally, we suggest the role of acidosis in fatigue may have a greater effect outside of the cell. © 2011 by Nova Science Publishers, Inc. All rights reserved.