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...

Mental fatigue impairs physical performance in humans

Fatigue is commonly reported in many neurologic illnesses, including multiple sclerosis, Parkinson disease, myasthenia gravis, traumatic brain injury, and stroke. Fatigue contributes substantially to decrements in quality of life and disability in these illnesses. Despite the clear impact of fatigue as a disabling symptom, our understanding of fatigue pathophysiology is limited and current treatment options rarely lead to meaningful improvements in fatigue. Progress continues to be hampered by issues related to terminology and assessment. In this article, we propose a unified taxonomy and a novel assessment approach to addressing distinct aspects of fatigue and fatigability in clinical and research settings. This taxonomy is based on our current knowledge of the pathophysiology and phenomenology of fatigue and fatigability. Application of our approach indicates that the assessment and reporting of fatigue can be clarified and improved by utilizing this taxonomy and creating measures to address distinct aspects of fatigue and fatigability. We review the strengths and weaknesses of several common measures of fatigue and suggest, based on our model, that many research questions may be better addressed by using multiple measures. We also provide examples of how to apply and validate the taxonomy and suggest directions for future research.

Fatigue and fatigability in neurologic illnesses: Proposal for a unified taxonomy

Short-duration sprints (<10 seconds), interspersed with brief recoveries (<60 seconds), are common during most team and racket sports. Therefore, the ability to recover and to reproduce performance in subsequent sprints is probably an important fitness requirement of athletes engaged in these disciplines, and has been termed repeated-sprint ability (RSA). This review (Part I) examines how fatigue manifests during repeated-sprint exercise (RSE), and discusses the potential underpinning muscular and neural mechanisms. A subsequent companion review to this article will explain a better understanding of the training interventions that could eventually improve RSA. Using laboratory and field-based protocols, performance analyses have consistently shown that fatigue during RSE typically manifests as a decline in maximal/mean sprint speed (i.e. running) or a decrease in peak power or total work (i.e. cycling) over sprint repetitions. A consistent result among these studies is that performance decrements (i.e. fatigue) during successive bouts are inversely correlated to initial sprint performance. To date, there is no doubt that the details of the task (e.g. changes in the nature of the work/recovery bouts) alter the time course/magnitude of fatigue development during RSE (i.e. task dependency) and potentially the contribution of the underlying mechanisms. At the muscle level, limitations in energy supply, which include energy available from phosphocreatine hydrolysis, anaerobic glycolysis and oxidative metabolism, and the intramuscular accumulation of metabolic by-products, such as hydrogen ions, emerge as key factors responsible for fatigue. Although not as extensively studied, the use of surface electromyography techniques has revealed that failure to fully activate the contracting musculature and/or changes in inter-muscle recruitment strategies (i.e. neural factors) are also associated with fatigue outcomes. Pending confirmatory research, other factors such as stiffness regulation, hypoglycaemia, muscle damage and hostile environments (e.g. heat, hypoxia) are also likely to compromise fatigue resistance during repeated-sprint protocols.

Repeated-Sprint Ability – Part I: Factors Contributing to Fatigue

Mental health symptoms and disorders are common among elite athletes, may have sport related manifestations within this population and impair performance. Mental health cannot be separated from physical health, as evidenced by mental health symptoms and disorders increasing the risk of physical injury and delaying subsequent recovery. There are no evidence or consensus based guidelines for diagnosis and management of mental health symptoms and disorders in elite athletes. Diagnosis must differentiate character traits particular to elite athletes from psychosocial maladaptations.Management strategies should address all contributors to mental health symptoms and consider biopsychosocial factors relevant to athletes to maximise benefit and minimise harm. Management must involve both treatment of affected individual athletes and optimising environments in which all elite athletes train and compete. To advance a more standardised, evidence based approach to mental health symptoms and disorders in elite athletes, an International Olympic Committee Consensus Work Group critically evaluated the current state of science and provided recommendations.

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Mental health in elite athletes: International Olympic Committee consensus statement (2019).

Position Statement: The position of The Society regarding caffeine supplementation and sport performance is summarized by the following seven points: 1.) Caffeine is effective for enhancing sport performance in trained athletes when consumed in low-to-moderate dosages (~3-6 mg/kg) and overall does not result in further enhancement in performance when consumed in higher dosages (≥ 9 mg/kg). 2.) Caffeine exerts a greater ergogenic effect when consumed in an anhydrous state as compared to coffee. 3.) It has been shown that caffeine can enhance vigilance during bouts of extended exhaustive exercise, as well as periods of sustained sleep deprivation. 4.) Caffeine is ergogenic for sustained maximal endurance exercise, and has been shown to be highly effective for time-trial performance. 5.) Caffeine supplementation is beneficial for high-intensity exercise, including team sports such as soccer and rugby, both of which are categorized by intermittent activity within a period of prolonged duration. 6.) The literature is equivocal when considering the effects of caffeine supplementation on strength-power performance, and additional research in this area is warranted. 7.) The scientific literature does not support caffeine-induced diuresis during exercise, or any harmful change in fluid balance that would negatively affect performance.

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International society of sports nutrition position stand: caffeine and performance

The original central fatigue hypothesis suggested that an exercise-induced increase in extracellular serotonin concentrations in several brain regions contributed to the development of fatigue during prolonged exercise. Serotonin has been linked to fatigue because of its well known effects on sleep, lethargy and drowsiness and loss of motivation. Several nutritional and pharmacological studies have attempted to manipulate central serotonergic activity during exercise, but this work has yet to provide robust evidence for a significant role of serotonin in the fatigue process. However, it is important to note that brain function is not determined by a single neurotransmitter system and the interaction between brain serotonin and dopamine during prolonged exercise has also been explored as having a regulative role in the development of fatigue. This revised central fatigue hypothesis suggests that an increase in central ratio of serotonin to dopamine is associated with feelings of tiredness and lethargy, accelerating the onset of fatigue, whereas a low ratio favours improved performance through the maintenance of motivation and arousal. Convincing evidence for a role of dopamine in the development of fatigue comes from work investigating the physiological responses to amphetamine use, but other strategies to manipulate central catecholamines have yet to influence exercise capacity during exercise in temperate conditions. Recent findings have, however, provided support for a significant role of dopamine and noradrenaline (norepinephrine) in performance during exercise in the heat. As serotonergic and catecholaminergic projections innervate areas of the hypothalamus, the thermoregulatory centre, a change in the activity of these neurons may be expected to contribute to the control of body temperature whilst at rest and during exercise. Fatigue during prolonged exercise clearly is influenced by a complex interaction between peripheral and central factors.

Central fatigue : The serotonin hypothesis and beyond

Since the publication of the serotonin hypothesis, numerous theories involving the accumulation or depletion of different substances in the brain have been proposed to explain central fatigue. Alth...

Brain neurotransmitters in fatigue and overtraining.

The combination of acute dopamine/noradrenaline reuptake inhibition (bupropion; BUP) and heat stress (30°C) significantly improves performance (9%). Furthermore the maintenance of a higher power output resulted in the attainment of significantly higher heart rates and rectal temperatures—above 40°C—in the BUP trial compared to the placebo trial. Since BUP is an aid to cease smoking that is taken for longer periods, question remains if similar performance and thermoregulatory effects are found following administration of BUP over several days (10 days). The purpose of the present study was to examine the effects of chronic BUP on exercise performance, thermoregulation and hormonal variables in the heat. Eight trained male cyclists participated in the study. Subjects completed two trials consisting of 60 min fixed intensity exercise (55% W
 max) followed by a time trial (TT) in a double-blind randomized crossover design. Exercise was performed in 30°C. Subjects took either placebo (PLAC) or BUP (Zyban™) for 3 days (150 mg), followed by 300 mg for 7 days. Chronic BUP did not influence TT performance (BUP 40′42″ ± 4′18″; PLAC 41′36″ ± 5′12″), but significantly increased core temperature (P = 0.030). BUP significantly increased circulating growth hormone levels (PLAC: 9.8 ± 5.8 ng L−1; BUP: 13 ± 6.8 ng L−1; P < 0.008). Discussion/conclusion: Chronic BUP did not influence TT performance in 30°C and subjects did not reach core temperature values as high as observed during the acute BUP study. It seems that chronic administration results in an adaptation of central neurotransmitter homeostasis, resulting in a different response to the drug.

Performance and thermoregulatory effects of chronic bupropion administration in the heat.

A maximal dose of bupropion has enabled subjects to maintain a higher power output than reported during the placebo session in the heat. Because this drug is taken in different doses it is important to know if there is a dose-response relationship with regard to exercise at high ambient temperature. Ten well-trained male cyclists ingested placebo (pla; 200 mg) or bupropion (50%, 75%, 100% of maximal dose: bup50: 150 mg; bup75: 225 mg; bup100: 300 mg) the evening before and morning of the experimental trial. Trials were conducted in 30 °C (humidity 48%). Subjects cycled for 60 min at 55% W (max) , immediately followed by a time trial to measure performance. Bup100 improved performance (pla: 33'42" ± 2'06"; bup100: 32'06" ± 1'54"; P = 0.035). Bupropion increased core temperature at the end of exercise, while heart rate was higher only in the bup100 trial (P < 0.05). No changes in rating of perceived exertion (RPE) or thermal sensation were found. Lower doses of bupropion were not ergogenic, indicating there was no dose-response effect. Interestingly, despite an increase in core temperature and improved performance in the maximal dose, there was no change in RPE and thermal sensation, suggesting an altered motivation or drive to continue exercise.

A dopamine/noradrenaline reuptake inhibitor improves performance in the heat, but only at the maximum therapeutic dose.

The following is the abstract of the article discussed in the subsequent letter:

This study examined neurohumoral alterations during prolonged exercise with and without hyperthermia. The cerebral oxygen-to-carbohydrate uptake ratio (O2/CHO = arteriovenous oxygen difference divided by arteriovenous

P. Watson

Papers

Central fatigue : The serotonin hypothesis and beyond

Brain neurotransmitters in fatigue and overtraining.

Performance and thermoregulatory effects of chronic bupropion administration in the heat.

A dopamine/noradrenaline reuptake inhibitor improves performance in the heat, but only at the maximum therapeutic dose.

A spurious correlation