The mechanisms of central fatigue are largely unexplored, but the central fatigue hypothesis suggests that increased brain serotonin (5-HT) can cause a deterioration in sport and exercise performance. There is now convincing evidence that exercise-induced increases in the plasma free tryptophan (f-TRP)/branched-chain amino acids (BCCA) ratio are associated with increased brain 5-HT and the onset of fatigue during prolonged exercise. Furthermore, when drugs are administered to alter brain 5-HT, they have the predicted effects on exercise performance. The influence of nutritional manipulations of f-TRP/BCCA on performance is less well established. The effects of BCCA supplementation on exercise performance are mixed, and the published studies often suffer from methodological flaws. Alternatively, dramatic reductions in f-TRP/BCCA and enhanced performance accompany carbohydrate feedings during prolonged exercise. However, it is difficult to distinguish between the effects of carbohydrate feedings on mechanisms that reside in the brain versus the muscles themselves.
Rihab Borji, Firas Zghal, Nidhal Zarrouk, Sonia Sahli, and Haithem Rebai
the maximal voluntary force or power of a muscle or a muscle group ( Enoka & Stuart, 1992 ). The origin of neuromuscular fatigue is generally related to central and/or peripheral factors ( Allen, Lamb, & Westerblad, 2008 ). Central fatigue can be defined as a progressive exercise-induced failure of
Katja Tomazin, Jean-Benoit Morin, and Guillaume Y. Millet
To compare neuromuscular fatigue induced by repeated-sprint running vs cycling.
Eleven active male participants performed 2 repeated-maximal-sprint protocols (5×6 s, 24-s rest periods, 4 sets, 3 min between sets), 1 in running (treadmill) and 1 in cycling (cycle ergometer). Neuromuscular function, evaluated before (PRE); 30 s after the first (S1), the second (S2), and the last set (LAST); and 5 min after the last set (POST5) determined the knee-extensor maximal voluntary torque (MVC); voluntary activation (VA); single-twitch (Tw), high- (Db100), and low- (Db10) frequency torque; and maximal muscle compound action potential (M-wave) amplitude and duration of vastus lateralis.
Peak power output decreased from 14.6 ± 2.2 to 12.4 ± 2.5 W/kg in cycling (P < .01) and from 21.4 ± 2.6 to 15.2 ± 2.6 W/kg in running (P < .001). MVC declined significantly from S1 in running but only from LAST in cycling. VA decreased after S2 (~–7%, P < .05) and LAST (~–9%, P < .01) set in repeated-sprint running and did not change in cycling. Tw, Db100, and Db10/Db100 decreased to a similar extent in both protocols (all P < .001 post-LAST). Both protocols induced a similar level of peripheral fatigue (ie, low-frequency peripheral fatigue, no changes in M-wave characteristics), while underlying mechanisms probably differed. Central fatigue was found only after running.
Findings about neuromuscular fatigue resulting from RS cycling cannot be transferred to RS running.
Romain Meeusen and Phil Watson
It is clear that the cause of fatigue is complex, infuenced by both events occurring in the periphery and the central nervous system (CNS). It has been suggested that exercise-induced changes in serotonin (5-HT), dopamine (DA), and noradrenaline (NA) concentrations contribute to the onset of fatigue during prolonged exercise. Serotonin has been linked to fatigue because of its documented role in sleep, feelings of lethargy and drowsiness, and loss of motivation, whereas increased DA and NA neurotransmission favors feelings of motivation, arousal, and reward. 5-HT has been shown to increase during acute exercise in running rats and to remain high at the point of fatigue. DA release is also elevated during exercise but appears to fall at exhaustion, a response that may be important in the fatigue process. The rates of 5-HT and DA/NA synthesis largely depend on the peripheral availability of the amino acids tryptophan (TRP) and tyrosine (TYR), with increased brain delivery increasing serotonergic and DA/NA activity, respectively. TRP, TYR, and the branched-chained amino acids (BCAAs) use the same transporter to pass through the blood-brain barrier, meaning that the plasma concentration ratio of these amino acids is thought to be a very important marker of neurotransmitter synthesis. Pharmacological manipulation of these neurotransmitter systems has provided support for an important role of the CNS in the development of fatigue. Work conducted over the last 20 y has focused on the possibility that manipulation of neurotransmitter precursors may delay the onset of fatigue. Although there is evidence that BCAA (to limit 5-HT synthesis) and TYR (to elevate brain DA/NA) ingestion can influence perceived exertion and some measures of mental performance, the results of several apparently well-controlled laboratory studies have yet to demonstrate a clear positive effect on exercise capacity or performance. There is good evidence that brain neurotransmitters can play a role in the development of fatigue during prolonged exercise, but nutritional manipulation of these systems through the provision of amino acids has proven largely unsuccessful.
Pedro L. Valenzuela, Carlos Amo, Guillermo Sánchez-Martínez, Elaia Torrontegi, Javier Vázquez-Carrión, Zigor Montalvo, Alejandro Lucia, and Pedro de la Villa
-paced exercise is duration-dependent. Thomas et al 29 observed a greater and lower peripheral and central fatigue, respectively, with short-duration cycling exercise (∼6 min) than with more prolonged bouts (>30 min). Thus, we hypothesize that tDCS could provide greater benefits on those exercise tasks where
Anthony Birat, Yoann M. Garnier, Pierre Bourdier, Alexis Dupuy, Alexandre Dodu, Claire Grossoeuvre, Anne-Charlotte Dupont, Anthony J. Blazevich, Mélanie Rance, Claire Morel, Stéphane Nottin, and Sébastien Ratel
. This impairment in neuromuscular function is a strong indicator of central fatigue, which could be ascribed to an inability of the central nervous system to voluntarily activate the muscles ( 41 ). At the peripheral level, long-duration running could also impair several steps in the excitation
Inge K. Stoter, Brian R. MacIntosh, Jared R. Fletcher, Spencer Pootz, Inge Zijdewind, and Florentina J. Hettinga
To evaluate pacing behavior and peripheral and central contributions to muscle fatigue in 1500-m speed-skating and cycling time trials when a faster or slower start is instructed.
Nine speed skaters and 9 cyclists, all competing at regional or national level, performed two 1500-m time trials in their sport. Athletes were instructed to start faster than usual in 1 trial and slower in the other. Mean velocity was measured per 100 m. Blood lactate concentrations were measured. Maximal voluntary contraction (MVC), voluntary activation (VA), and potentiated twitch (PT) of the quadriceps muscles were measured to estimate central and peripheral contributions to muscle fatigue. In speed skating, knee, hip, and trunk angles were measured to evaluate technique.
Cyclists showed a more explosive start than speed skaters in the fast-start time trial (cyclists performed first 300 m in 24.70 ± 1.73 s, speed skaters in 26.18 ± 0.79 s). Both trials resulted in reduced MVC (12.0% ± 14.5%), VA (2.4% ± 5.0%), and PT (25.4% ± 15.2%). Blood lactate concentrations after the time trial and the decrease in PT were greater in the fast-start than in the slow-start trial. Speed skaters showed higher trunk angles in the fast-start than in the slow-start trial, while knee angles remained similar.
Despite similar instructions, behavioral adaptations in pacing differed between the 2 sports, resulting in equal central and peripheral contributions to muscle fatigue in both sports. This provides evidence for the importance of neurophysiological aspects in the regulation of pacing. It also stresses the notion that optimal pacing needs to be studied sport specifically, and coaches should be aware of this.
Sebastian Ludyga, Thomas Gronwald, and Kuno Hottenrott
Although men and women are suggested to vary in resistance to fatigue, possible sex difference in its central component have rarely been investigated via electroencephalography (EEG). Therefore, we examined differences in cortical activity between male and female cyclists (n = 26) during cycling exercise. Participants performed an incremental test to derive the anaerobic threshold from the lactate power curve. In addition, cyclists’ cortical activity was recorded with EEG before and during cycling exercise. Whereas women showed higher frontal alpha and beta activity at rest, no sex-specific differences of relative EEG spectral power occurred during cycling at higher intensity. Women and men’s brains respond similarly during submaximal cycling, as both sexes show an inverted U-shaped curve of alpha power. Therefore, sex differences observable at rest vanish after the onset of exercise.
Tom R. Eaton, Aaron Potter, François Billaut, Derek Panchuk, David B. Pyne, Christopher J. Gore, Ting-Ting Chen, Leon McQuade, and Nigel K. Stepto
Heat and hypoxia exacerbate central nervous system (CNS) fatigue. We therefore investigated whether essential amino acid (EAA) and caffeine ingestion attenuates CNS fatigue in a simulated team sport–specific running protocol in a hot, hypoxic environment. Subelite male team sport athletes (n = 8) performed a repeat sprint running protocol on a nonmotorized treadmill in an extreme environment on 4 separate occasions. Participants ingested one of four supplements: a double placebo, 3 mg.kg-1 body mass of caffeine + placebo, 2 × 7 g EAA (Musashi Create)+placebo, or caffeine + EAA before each exercise session using a randomized, double-blind crossover design. Electromyography (EMG) activity and quadriceps evoked responses to magnetic stimulation were assessed from the dominant leg at preexercise, halftime, and postexercise. Central activation ratio (CAR) was used to quantify completeness of quadriceps activation. Oxygenation of the prefrontal cortex was measured via near-infrared spectroscopy. Mean sprint work was higher (M = 174 J, 95% CI [23, 324], p < .05, d = 0.30; effect size, likely beneficial) in the caffeine + EAA condition versus EAAs alone. The decline in EMG activity was less (M = 13%, 95% CI [0, 26]; p < .01, d = 0.58, likely beneficial) in caffeine + EAA versus EAA alone. Similarly, the pre- to postexercise decrement in CAR was significantly less (M = −2.7%, 95% CI [0.4, 5.4]; p < .05, d = 0.50, likely beneficial) when caffeine + EAA were ingested compared with placebo. Cerebral oxygenation was lower (M = −5.6%, 95% CI [1.0, 10.1]; p < .01, d = 0.60, very likely beneficial) in the caffeine + EAA condition compared with LNAA alone. Coingestion of caffeine and EAA appears to maintain muscle activation and central drive, with a small improvement in running performance.
Sofia I. Lampropoulou and Alexander V. Nowicky
The way psychometric and neurophysiological measurements of fatigue are connected is not well understood. Thus, the time course of perceived effort changes due to fatigue, as well as the peripheral and central neurophysiological changes accompanying fatigue, were evaluated. Twelve healthy participants (35 ± 9 years old) undertook 10 min intermittent isometric fatiguing exercise of elbow flexors at 50% of maximum voluntary contraction (MVC). Perceived effort ratings, using the 0–10 numeric rating scale (NRS), were recorded at midrange of MVC. Single pulse TMS of the left motor cortex and electrical stimulation over the biceps muscle was used for the assessment of voluntary activation and peripheral fatigue. The fatiguing exercise caused a 44% reduction in the MVC (p < .001) accompanied by an 18% nonsignificant reduction of the biceps MEP amplitude. The resting twitch force decreased (p < .001) while the superimposed twitches increased (p < .001) causing a decrease (19%) of the voluntary activation (p < .001). The perceived effort ratings increased by 1 point at 30%, by 2 points at 50% MVC respectively on the NRS (p < .001) and were accompanied by an increase in mean biceps EMG. A substantial role of the perceived effort in the voluntary motor control system was revealed.