Fatigue is a Brain-Derived Emotion that Regulates the Exercise Behavior to Ensure the Protection of Whole Body Homeostasis

An influential book written by A. Mosso in the late nineteenth century proposed that fatigue that “at first sight might appear an imperfection of our body, is on the contrary one of its most marvelous perfections. The fatigue increasing more rapidly than the amount of work done saves us from the injury which lesser sensibility would involve for the organism” so that “muscular fatigue also is at bottom an exhaustion of the nervous system.” It has taken more than a century to confirm Mosso’s idea that both the brain and the muscles alter their function during exercise and that fatigue is predominantly an emotion, part of a complex regulation, the goal of which is to protect the body from harm. Mosso’s ideas were supplanted in the English literature by those of A. V. Hill who believed that fatigue was the result of biochemical changes in the exercising limb muscles – “peripheral fatigue” – to which the central nervous system makes no contribution. The past decade has witnessed the growing realization that this brainless model cannot explain exercise performance. This article traces the evolution of our modern understanding of how the CNS regulates exercise specifically to insure that each exercise bout terminates whilst homeostasis is retained in all bodily systems. The brain uses the symptoms of fatigue as key regulators to insure that the exercise is completed before harm develops. These sensations of fatigue are unique to each individual and are illusionary since their generation is largely independent of the real biological state of the athlete at the time they develop. The model predicts that attempts to understand fatigue and to explain superior human athletic performance purely on the basis of the body’s known physiological and metabolic responses to exercise must fail since subconscious and conscious mental decisions made by winners and losers, in both training and competition, are the ultimate determinants of both fatigue and athletic performance

Evidence for complex integration and dynamic neural regulation of skeletal muscle recruitment during exercise in humans

A model is proposed in which the development of physical exhaustion is a relative rather than an absolute event and the sensation of fatigue is the sensory representation of the underlying neural integrative processes. Furthermore, activity is controlled as part of a pacing strategy involving active neural calculations in a “governor” region of the brain, which integrates internal sensory signals and information from the environment to produce a homoeostatically acceptable exercise intensity. The end point of the exercise bout is the controlling variable. This is an example of a complex, non-linear, dynamic system in which physiological systems interact to regulate activity before, during, and after the exercise bout

From catastrophe to complexity: a novel model of integrative central neural regulation of effort and fatigue during exercise in humans

It is a popular belief that exercise performance is limited by metabolic changes in the exercising muscles, so called peripheral fatigue. Exercise terminates when there is a catastrophic failure of homoeostasis in the exercising muscles. A revolutionary theory is presented that proposes that exercise performance is regulated by the central nervous system specifically to ensure that catastrophic physiological failure does not occur during normal exercise in humans

A high rate of injury during the 1995 Rugby World Cup

Objective. To determine the frequency and nature of injuries sustained by the 416 players from 16 countries participating in the 1995 Rugby World Cup played in South Africa in May/June 1995.Methods. The study was a prospective analysis of all injuries requiring medical attention during that competition. Data were collected by the match doctors on duty at each of the venues at which the matches were played. Data were collated and analysed.Results. There were 48 preliminary and 7 final-round matches. Of a total of 70 injuries during the tournament, 58 occurred during the preliminary matches (frequency 30 injuries per 1 000 player hours); the frequency was somewhat higher during the 7 final-round matches (43 injuries per 1 000 player hours). Overall injury frequency was 1 injury every 0.8 matches during the preliminary and 1 every 0.6 matches during the final-round matches. Thirty per cent of injuries were to ligaments, 27% were lacerations and 14% were muscle strains. The lower limb accounted for 42% of all injuries, the upper limb for 29% and the face for 17%. Fifty-six per cent of injuries occurred during the tackle phase of play, 23% during the ruck and maul, 11 % during open play and 9% during foul play. The scrum and line-out together contributed only 1% of all injuries. Loose forwards suffered 25% of all injuries; centres and wings 20%; prop forwards and half-backs 16% each; locks 14%; hookers 7% and fullbacks 3%. One player suffered a paralysing spinal cord injury during a preliminary match. The incidence of catastrophic neck injuries in the tournament was therefore 4.6 per 10 000 player hours.Conclusions. The frequency of injury in this competition is the highest yet recorded in any group of rugby players. The risk of rugby injury is therefore greatest in the best players in the game, challenging the view that superior fitness, skill and experience can reduce the risk of rugby injury. In contrast, the larger size, greater speed and superior competitiveness and commitment of the best rugby players in the world would explain why they are at the highest risk of injury. The high frequency of injury in international rugby has implications for: (I) the frequency with which such matches should be played; and (il) the number of players needed to complete a season of international rugby

Spinal cord injuries in South African Rugby Union (1980-2007)

Objectives and design. To address an apparent increase in the number of rugby-related spinal cord injuries (SCIs) in South Africa, a retrospective case-series study was conducted on injuries that occurred between 1980 and 2007. We aimed to identify preventable causes to reduce the overall rate of SCIs in South African rugby. Methods. We identified 264 rugby-related SCIs. A structured questionnaire was used, and it was possible to obtain information on a total of 183 players, including 30 who had died. Results. SCIs increased in number in the 1980s and in 2006. Forwards sustained 76% of all SCIs, and club players 60%. Players aged 17 had the highest number of SCIs. In only 50% of cases were medical personnel present at the time of injury, and 49% of injured players waited longer than 6 hours for acute management. Of players with an SCI, 61% had a catastrophic outcome after 12 months, including 8% who died during that time; 65% received no financial compensation; and only 29% of players had medical aid or health insurance. Conclusion. A register of all rugby-related SCIs in South Africa is essential to monitor the magnitude of the problem, identify potential risk factors, and formulate appropriate preventive interventions. The lack of reliable denominator data limits calculation of incident rates. Players from previously disadvantaged communities in particular suffered the consequences of limited public health care resources and no financial compensation

Low-carbohydrate and high-fat intake can manage obesity and associated conditions: Occasional survey

This study analyses 127 communications from individuals self-reporting their weight change following adoption of a low-carbohydrate, high-fat (LCHF) eating plan. Total combined self-reported weight loss was 1 900 kg (range 5 kg gain to 84 kg loss). The mean ± standard deviation weight loss of 15 (±12) kg is among the largest yet described. Sixteen subjects reported the LCHF ‘cured’ (i.e. medications no longer required) one or more of their medical conditions, most commonly type 2 diabetes mellitus (T2DM) (n=14), hypertension (n=8) and hypercholesterolaemia (n=7). Another 9 subjects with either type 1 diabetes mellitus or T2DM reduced medications as did 7 patients with hypertension; 8 no longer suffered from irritable bowel syndrome. These data show that significant and rapid weight loss is possible on an unsupervised eating plan that severely restricts daily carbohydrate intake to approximately <75 g/day. Better weight loss on a carbohydrate-restricted LCHF eating plan than on an iso-caloric high-carbohydrate, low-fat (HCLF) diet is well described in the literature, probably due to a paradoxical reduction of hunger by carbohydrate restriction. A randomised controlled clinical trial is urgently required to disprove the hypothesis that the LCHF eating plan can reverse cases of T2DM, metabolic syndrome and hypertension without pharmacotherapy.

Exercise and the heart : effects of exercise training on coronary artery disease and on myocardial function, metabolism and vulnerability to ventricular fibrillation

There is epidemiological and experimental evidence suggesting that exercise training may reduce the mortality rate from coronary heart disease, in particular the sudden death rate, and that it may improve the peak functional capacity of the heart. This thesis includes experimental work that is relevant to both these questions