Walter Staiano

Mental fatigue impairs physical performance in humans

Mental fatigue is a psychobiological state caused by prolonged periods of demanding cognitive activity. Although the impact of mental fatigue on cognitive and skilled performance is well known, its effect on physical performance has not been thoroughly investigated. In this randomized crossover study, 16 subjects cycled to exhaustion at 80% of their peak power output after 90 min of a demanding cognitive task (mental fatigue) or 90 min of watching emotionally neutral documentaries (control). After experimental treatment, a mood questionnaire revealed a state of mental fatigue (P = 0.005) that significantly reduced time to exhaustion (640 +/- 316 s) compared with the control condition (754 +/- 339 s) (P = 0.003). This negative effect was not mediated by cardiorespiratory and musculoenergetic factors as physiological responses to intense exercise remained largely unaffected. Self-reported success and intrinsic motivation related to the physical task were also unaffected by prior cognitive activity. However, mentally fatigued subjects rated perception of effort during exercise to be significantly higher compared with the control condition (P = 0.007). As ratings of perceived exertion increased similarly over time in both conditions (P < 0.001), mentally fatigued subjects reached their maximal level of perceived exertion and disengaged from the physical task earlier than in the control condition. In conclusion, our study provides experimental evidence that mental fatigue limits exercise tolerance in humans through higher perception of effort rather than cardiorespiratory and musculoenergetic mechanisms. Future research in this area should investigate the common neurocognitive resources shared by physical and mental activity.

Talking yourself out of exhaustion: the effects of self-talk on endurance performance

PURPOSE The psychobiological model of endurance performance proposes that the perception of effort is the ultimate determinant of endurance performance. Therefore, any physiological or psychological factor affecting the perception of effort will affect endurance performance. Accordingly, this novel study investigated the effects of a frequently used psychological strategy, motivational self-talk (ST), on RPE and endurance performance. METHODS In a randomized between-group pretest-posttest design, 24 participants (mean ± SD age = 24.6 ± 7.5 yr, VO2max = 52.3 ± 8.7 mL·kg·min) performed two constant-load (80% peak power output) cycling time-to-exhaustion (TTE) tests, punctuated by a 2-wk ST intervention or a control phase. RESULTS A group (ST vs Control) × test (pretest vs posttest) mixed-model ANOVA revealed that ST significantly enhanced TTE test from pretest to posttest (637 ± 210 vs 750 ± 295 s, P < 0.05) with no change in the control group (486 ± 157 vs 474 ± 169 s). Moreover, a group × test × isotime (0%, 50%, and 100%) mixed-model ANOVA revealed a significant interaction for RPE, with follow-up tests showing that motivational self-talk significantly reduced RPE at 50% isotime (7.3 ± 0.6 vs 6.4 ± 0.8, P < 0.05), with no significant difference in the control group (6.9 ± 1.9 vs 7.0 ± 1.7). CONCLUSIONS This study is the first to demonstrate that ST significantly reduces RPE and enhances endurance performance. The findings support the psychobiological model of endurance performance and illustrate that psychobiological interventions designed to specifically target favorable changes in the perception of effort are beneficial to endurance performance. Consequently, this psychobiological model offers an important and novel perspective for future research investigations.

Superior Inhibitory Control and Resistance to Mental Fatigue in Professional Road Cyclists.

Purpose Given the important role of the brain in regulating endurance performance, this comparative study sought to determine whether professional road cyclists have superior inhibitory control and resistance to mental fatigue compared to recreational road cyclists. Methods After preliminary testing and familiarization, eleven professional and nine recreational road cyclists visited the lab on two occasions to complete a modified incongruent colour-word Stroop task (a cognitive task requiring inhibitory control) for 30 min (mental exertion condition), or an easy cognitive task for 10 min (control condition) in a randomized, counterbalanced cross-over order. After each cognitive task, participants completed a 20-min time trial on a cycle ergometer. During the time trial, heart rate, blood lactate concentration, and rating of perceived exertion (RPE) were recorded. Results The professional cyclists completed more correct responses during the Stroop task than the recreational cyclists (705±68 vs 576±74, p = 0.001). During the time trial, the recreational cyclists produced a lower mean power output in the mental exertion condition compared to the control condition (216±33 vs 226±25 W, p = 0.014). There was no difference between conditions for the professional cyclists (323±42 vs 326±35 W, p = 0.502). Heart rate, blood lactate concentration, and RPE were not significantly different between the mental exertion and control conditions in both groups. Conclusion The professional cyclists exhibited superior performance during the Stroop task which is indicative of stronger inhibitory control than the recreational cyclists. The professional cyclists also displayed a greater resistance to the negative effects of mental fatigue as demonstrated by no significant differences in perception of effort and time trial performance between the mental exertion and control conditions. These findings suggest that inhibitory control and resistance to mental fatigue may contribute to successful road cycling performance. These psychobiological characteristics may be either genetic and/or developed through the training and lifestyle of professional road cyclists.

The parabolic power-velocity relationship does not apply to fatigued states

It is traditionally assumed that submaximal exercise stops when fatigue mechanisms reduce maximal force/power to the point that muscles are no longer able to produce the required force/power (exhaustion) (Allen et al. 2008). If this assumption was true, maximal force/power measured immediately after exhaustion should be very close to the force/power required by the submaximal exercise task. We tested this hypothesis by measuring maximal voluntary cycling power (MVCP) immediately after exhaustive cycling exercise at 80% of peak aerobic power. Contrary to the traditional assumption, MVCP immediately after exhaustion (731 W) was three times the power output required by the time to exhaustion test (242 W). Therefore, we concluded that muscle fatigue does not cause exhaustion during high-intensity aerobic exercise (Marcora and Staiano 2010). In his Letter to the Editor, Burnley argues that this conclusion is not valid because we failed to account for the crucial influence of the parabolic power–velocity relationship in our study design (Burnley 2010). The power– velocity relationship postulates that, on its ascending arm, an increase in cadence results in a large increase in MVCP. According to Burnley, our fatigued subjects stopped the time to exhaustion test because, after 10.5 min, they were no longer able to produce 242 W at 40 RPM. The very high power output measured immediately after exhaustion (731 W) does not disprove this traditional assumption because the final MVCP test was performed at a much higher cadence (108 RPM), thus increasing our subjects’ ability to produce power. This argument has two main weaknesses. First, it applies only to unfatigued states (Fig. 1, open circles). In fatigued states, cadence has a small effect on MVCP, and the power–velocity relationship is quite flat rather than parabolic (Fig. 1, filled circles) (Beelen and Sargeant 1991). Therefore, the effect of cadence on MVCP in unfatigued states (Burnley’s mechanical explanation) does not invalidate our conclusion that muscle fatigue does not cause exhaustion during high-intensity aerobic exercise. Because of the effect of fatigue on the power–velocity relationship, if we performed the final MVCP test at exactly the same cadence as the time to exhaustion test, MVCP would have not been much lower than 731 W and certainly higher than 242 W. In our opinion, our highly motivated subjects decided to stop the time to exhaustion test because they believed they were not capable of cycling for much longer (psychological explanation). This belief is based on the high perception of effort experienced near exhaustion (Garcin and Billat 2001). In further support to our hypothesis, similar results have been obtained using isometric exercise tasks (Hunter et al. 2004) where the power– velocity relationship does not apply at all! The second major weakness of Burnley’s argument is that, during the time to exhaustion test, the Lode ergometer was set in hyperbolic mode. This setting means that our subjects were free to choose a cadence between 40 and 120 RPM whilst cycling at a constant power of 242 W. However, they chose to cycle, on average, at 75 RPM. According to Burnley’s argument, they could have increased their physiological ability to produce power and avoided exhaustion at 10.5 min simply by choosing a Communicated by Susan Ward.

Reply to: The parabolic power-velocity relationship does apply to fatigued states

We thank MacIntosh and Fletcher (2010) for sharing thesepreviously unpublished power–cadence data. We concedethat, on the basis of the only power–cadence data (Beelenand Sargeant 1991) available at the time of writing ourreply to Burnley (2010), we may have underestimated theeffect of cadence on the ability to produce maximal vol-untary cycling power (MVCP) in a fatigued state (Marcoraand Staiano 2010b). Nevertheless, the power–cadence dataprovided by MacIntosh and Fletcher (2010) strengthen,rather than weaken, our conclusion that muscle fatiguedoes not cause exhaustion during high-intensity aerobicexercise (Marcora and Staiano 2010a). In fact, according tothe fatigued power–cadence relationship shown in Fig. 1(open squares) (MacIntosh and Fletcher 2010), fatiguedsubjects that can produce 600 W at 108 RPM are able toproduce 400 W at 40 RPM. Therefore, the fact that oursubjects were able to produce 731 W at 108 RPM in thefinal MVCP test suggests that they were able to produce[400 W at exhaustion (40 RPM).Whether our subjects were able to produce [400 or731 W at exhaustion is totally irrelevant. What is relevantto our conclusion is that, despite significant muscle fatigue,they were able to produce more than 242 W at exhaustion.This finding goes against one of the most fundamentalassumptions in exercise physiology: submaximal exerciseterminates at the point commonly called exhaustionbecause central and/or peripheral fatigue mechanismsreduce muscle function to the point that subjects are nolonger capable of producing the force/power required bythe task despite their maximal voluntary effort (task fail-ure) (Allen et al. 2008; Jones and Burnley 2009).We argue that exhaustion is a form of task disengage-ment, i.e. a conscious decision to withdraw effort when theeffort required by exercise is beyond the maximal effortsubjects are willing to produce in order to succeed in thetask (potential motivation) (Marcora 2008; Marcora et al.2008, 2009, Marcora and Staiano 2010a). Therefore, inwell-motivated subjects, the main factor causing exhaus-tion is perception of effort, not muscle fatigue. In otherwords, it is mind over muscle. Accordingly, future researchon what limits exercise tolerance should investigate thepsychobiology of perceived exertion using appropriatepsychophysical and neurophysiologic methods (Marcora2009) rather than the central and peripheral mechanisms ofmuscle fatigue (Decorte et al. 2010; Jones and Burnley2009).References

Reply to: What limits exercise during high-intensity aerobic exercise?

We thank Professors Allen and Westerblad (2010) for their interest in our study (Marcora and Staiano 2010a) which is stirring an interesting discussion on what causes exhaustion during intense aerobic exercise. Although the various cardiorespiratory, central and peripheral mechanisms of muscle fatigue are still being debated (McKenna and Hargreaves 2008), most exercise physiologists agree that exhaustion during intense aerobic exercise is caused by muscle fatigue deWned as any exercise-induced decrease in maximal voluntary force or power produced by a muscle or muscle group (Taylor and Gandevia 2008). In other words, it is assumed that well-motivated subjects stop intense aerobic exercise when fatigue reduces muscle function to the point (commonly called exhaustion or task failure) that they are no longer able to produce the required power output despite their maximal voluntary eVort (Figure 9 in Allen et al. 2008). Because we could not Wnd any experimental evidence that this assumption is valid, we conducted a simple study to Wnd out ourselves (Marcora and Staiano 2010a). The data show that, 3–4 s after exhaustive aerobic exercise at 242 W, subjects can produce a maximal voluntary cycling power (MVCP) of 741 W. Because of the massive diVerence in power output (489 W), we concluded that well-motivated subjects stop intense aerobic exercise even if their fatigued neuromuscular system is still able to produce the required power output. Albeit straightforward, this conclusion is contrary to the traditional belief that muscle fatigue causes exhaustion during intense aerobic exercise. Therefore, it is not surprising that scientists adopting the muscle fatigue model of exercise tolerance are now questioning the validity of our conclusion (Allen and Westerblad 2010; Burnley 2010). We have already rebutted the argument that diVerences in pedal frequency between exhaustion and the Wnal MVCP test can invalidate our conclusion that muscle fatigue does not cause task failure during intense aerobic exercise (Marcora and Staiano 2010b). Therefore, in this Reply, we focus on the issue of recovery. Allen and Westerblad (2010) argue that our subjects may have been severely fatigued at exhaustion and that much of the diVerence in power output observed between intense aerobic exercise and the Wnal MVCP test may simply be rapidly occurring recovery processes. Quantitatively, this argument implies that fatigued subjects stopped cycling because they were no longer able to produce 242 W and then, in 3–4 s of partial recovery, their MVCP increased by 300% to 731 W. Of course, we agree that some recovery of muscle function may have occurred during the 3–4 s of partial recovery between exhaustion and the loaded phase of the Wnal MVCP test. However, the magnitude of the changes implied by Allen and Westerblad’s argument are not biologically plausible. Firstly, their argument implies that intense aerobic exercise can reduce MVCP by 77% (from 1,075 to 242 W). However, this extreme level of muscle fatigue has never been demonstrated in vivo. In humans, aerobic exercise reduces muscle function by 7–34% (Sargeant and Dolan 1987; Millet and Lepers 2004). Secondly, their argument implies that, after fatiguing contractions, muscle function can increase by 300% in 3–4 s of partial recovery. However, MVCP increases by 25% in 5 s of full recovery (Sargeant and Dolan 1987); maximal force increases by 100% in 10 s of full recovery (Westerblad and Communicated by Susan Ward.

The cardinal exercise stopper: Muscle fatigue, muscle pain or perception of effort?

The capacity to sustain high-intensity aerobic exercise is essential for endurance performance. Therefore, it is important to understand what is the factor limiting time to exhaustion (TTE) in healthy and fit adults. In Study 1, maximal voluntary cycling power (MVCP) was measured in 11 volunteers before and immediately after a high-intensity TTE test on cycle ergometer. Cadence was 60 rpm in both the MVCP and TTE tests. Despite a 35% loss in MVCP, power produced during the final MVCP test (mean ± SD 469 ± 111 W) was significantly higher than the power required by the TTE test (269 ± 55 W) (P < 0.001). In Study 2, 12 participants performed a cold pressor test (CPT) to the limit of tolerance followed by a high-intensity TTE test on cycle ergometer. Ratings of pain unpleasantness (RPU) during the TTE test were anchored to the unpleasantness of pain experienced during the CPT. On average, the RPU was 9.7 ± 0.4 at completion of the CPT and 5.0 ± 0.9 at exhaustion during the TTE test. The difference between these two ratings of pain unpleasantness was statistically significant (P < 0.001). In both Studies 1 and 2, the slope of the rating of perceived exertion (RPE) during the TTE test correlated significantly with TTE (r = -0.75 and -0.83, P < 0.01). Results of this two-part investigation suggest that perception of effort, rather than severe locomotor muscle fatigue or intolerably unpleasant muscle pain, is the cardinal exercise stopper during high-intensity aerobic exercise.

Erratum to: The limit to exercise tolerance in humans: mind over muscle?

The recent publication by Samuele Maria Marcora and Walter Staiano entitled ‘‘The limit to exercise tolerance in humans: mind over muscle?’’ (Eur J Appl Physiol 109(4):763–770, 2010; published online on March 11, 2010; published in print in July 2010) has provoked considerable discussion. This includes a Letter to the Editor by Mark Burnley entitled ‘‘The limit to exercise tolerance in humans: validity compromised by failing to account for the power–velocity relationship’’ (Eur J Appl Physiol 109(6):1225–1226, 2010; published online on April 7, 2010; published in print in August 2010). We regret to note, however, that due to an oversight in the publication process, the Authors’ response to this Letter was actually published prior to Dr Burnley’s Letter. This Response can be found in Eur J Appl Physiol 109(4):787–788, 2010; published online on May 5, 2010; published in print in July 2010). We apologise to both Dr Marcora and Dr Staiano and also to Dr Burnley for any confusion that has resulted.