Study on the Correlation Between NF-κB and Central Fatigue

In recent years, the World Health Organization (WHO) has included fatigue as a major risk factor for human life and health. The incidence rate of fatigue is high. In Europe and America, nearly 1/3 of the population is suffering from fatigue. Due to the acceleration of modern people’s life rhythm and the increase of work pressure, more and more attention has been paid to central fatigue. The activation of NF-κB is related to central fatigue, which has been paid little attention by previous studies. At the same time, previous studies have mostly focused on the immune regulation function of NF-κB, while the NF-κB pathway plays an equally important role in regulating nerve function. NF-κB can participate in the occurrence and development of central fatigue by mediating immune inflammatory response, regulating central excitability and inhibitory transmitters, regulating synaptic plasticity and regulating central nervous system (CNS) functional genes. In addition to neuroprotective effects, NF-κB also has nerve damage effects, which is also closely related to the occurrence and development of central fatigue. In this review, we focus on the relationship between NF-κB pathway and central fatigue and further explore the biological mechanism of central fatigue. At the same time, the clinical application and potential of typical NF-κB inhibitors in the treatment of fatigue were analyzed to provide reference for the clinical treatment of central fatigue.

The effect of rolling massage on the excitability of the corticospinal pathway

The aim of the present study was to investigate the alterations of corticospinal excitability (motor evoked potential, MEP) and inhibition (silent period, SP) following rolling massage of the quadriceps muscles. Transcranial magnetic and femoral nerve electrical stimuli were used to elicit MEPs and compound muscle action potential (Mmax) in the vastus lateralis and vastus medialis muscles prior to and following either (i) 4 sets of 90-s rolling massage (ROLLING) or (ii) rest (CONTROL). One series of neuromuscular evaluations, performed after each set of ROLLING or CONTROL, included 3 MEPs and 1 Mmax elicited every 4 s during 15-s submaximal contractions at 10% (experiment 1, n = 16) and 50% (experiment 2, n = 10) of maximal voluntary knee extensions (MVC). The MEP/Mmax ratio and electromyographic activity recorded from vastus lateralis at 10% MVC demonstrated significantly lower values during ROLLING than CONTROL (P < 0.05). The ROLLING did not elicit any significant changes in muscle excitability (Mmax area) and duration of transcranial magnetic stimulation-induced SP recorded from any muscle or level of contraction (P > 0.05). The findings suggest that rolling massage can modulate the central excitability of the circuitries innervating the knee extensors; however, the observed effects are dependent on the background contraction intensity during which the neuromuscular measurements are recorded.

Central excitability does not limit postfatigue voluntary activation of quadriceps femoris

After fatigue, motor evoked potentials (MEP) elicited by transcranial magnetic stimulation and cervicomedullary evoked potentials elicited by stimulation of the corticospinal tract are depressed. These reductions in corticomotor excitability and corticospinal transmission are accompanied by voluntary activation failure, but this may not reflect a causal relationship. Our purpose was to determine whether a decline in central excitability contributes to central fatigue. We hypothesized that, if central excitability limits voluntary activation, then a caffeine-induced increase in central excitability should offset voluntary activation failure. In this repeated-measures study, eight men each attended two sessions. Baseline measures of knee extension torque, maximal voluntary activation, peripheral transmission, contractile properties, and central excitability were made before administration of caffeine (6 mg/kg) or placebo. The amplitude of vastus lateralis MEPs elicited during minimal muscle activation provided a measure of central excitability. After a 1-h rest, baseline measures were repeated before, during, and after a fatigue protocol that ended when maximal voluntary torque declined by 35% (Tlim). Increased prefatigue MEP amplitude ( P = 0.055) and cortically evoked twitch ( P < 0.05) in the caffeine trial indicate that the drug increased central excitability. In the caffeine trial, increased MEP amplitude was correlated with time to task failure ( r = 0.74, P < 0.05). Caffeine potentiated the MEP early in the fatigue protocol ( P < 0.05) and offset the 40% decline in placebo MEP ( P < 0.05) at Tlim. However, this was not associated with enhanced maximal voluntary activation during fatigue or recovery, demonstrating that voluntary activation is not limited by central excitability.