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Referências sobre fadiga e overtraining do SNC (CNS fatigue e CNS overtraining)


Exercise and its effects on the central nervous system.

Anish EJ.

Division of General Internal Medicine, University of Pittsburgh School of Medicine, 5230 Centre Avenue, Pittsburgh, PA 15232, USA.

Exercise can have profound effects on numerous biologic systems within the human body, including the central nervous system (CNS). The inherent complexity of the CNS, and the methodologic difficulties in evaluating its in vivo neurochemistry in humans, provide challenges to investigators studying the impact of exercise on the CNS. As a result, our knowledge in this area of exercise science remains relatively limited. However, advances in research technology are allowing investigators to gain valuable insight into the neurobiologic mechanisms that contribute to the bidirectional communication that occurs between the periphery and the CNS during exercise. This article examines how exercise-induced alterations in the CNS contribute to central fatigue and the overtraining syndrome, and how exercise can influence psychologic wellbeing and cognitive function.

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PMID: 15659274 [PubMed - indexed for MEDLINE]

 
2: Med Sci Sports Exerc. 1997 Jan;29(1):45-57.
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Possible mechanisms of central nervous system fatigue during exercise.

Davis JM, Bailey SP.

Department of Exercise Science, School of Public Health, University of South Carolina, Columbia 29208, USA.

Fatigue of voluntary muscular effort is a complex phenomenon. To date, relatively little attention has been placed on the role of the central nervous system (CNS) in fatigue during exercise despite the fact that the unwillingness to generate and maintain adequate CNS drive to the working muscle is the most likely explanation of fatigue for most people during normal activities. Several biological mechanisms have been proposed to explain CNS fatigue. Hypotheses have been developed for several neurotransmitters including serotonin (5-HT; 5-hydroxytryptamine), dopamine, and acetylcholine. The most prominent one involves an increase in 5-HT activity in various brain regions. Good evidence suggests that increases and decreases in brain 5-HT activity during prolonged exercise hasten and delay fatigue, respectively, and nutritional manipulations designed to attenuate brain 5-HT synthesis during prolonged exercise improve endurance performance. Other neuromodulators that may influence fatigue during exercise include cytokines and ammonia. Increases in several cytokines have been associated with reduced exercise tolerance associated with acute viral or bacterial infection. Accumulation of ammonia in the blood and brain during exercise could also negatively effect the CNS function and fatigue. Clearly fatigue during prolonged exercise is influenced by multiple CNS and peripheral factors. Further elucidation of how CNS influences affect fatigue is relevant for achieving optimal muscular performance in athletics as well as everyday life.

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PMID: 9000155 [PubMed - indexed for MEDLINE]

 
3: CNS Spectr. 2007 Jan;12(1):19-22.
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Mind and muscle: the cognitive-affective neuroscience of exercise.

Stein DJ, Collins M, Daniels W, Noakes TD, Zigmond M.

Department of Mental Health and Psychiatry, University of Cape Town, South Africa.

There is growing basic-science interest in the mechanisms underpinning the positive effects of exercise on brain function and cognitive-affective performance. There is also increasing clinical evidence that exercise may prevent and treat various neuropsychiatric disorders. At the same time, there is growing awareness that athletic performance is mediated in crucial ways by central nervous system mechanisms. The relevant mechanisms in all these cases requires further exploration, but likely includes neurotrophic, neuroendocrine, and neurotransmitter systems, which in turn are crucial mediators of psychopathology and resilience. The hypothesis that Homo sapiens evolved as a specialist endurance runner provides an intriguing context against which to research the proximal mechanisms relevant to a cognitive-affective neuroscience of exercise.

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PMID: 17192760 [PubMed - indexed for MEDLINE]

 
4: Br J Sports Med. 2005 Feb;39(2):120-4.
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From catastrophe to complexity: a novel model of integrative central neural regulation of effort and fatigue during exercise in humans: summary and conclusions.

Noakes TD, St Clair Gibson A, Lambert EV.

Research Unit for Exercise Science and Sports Medicine, University of Cape Town, Sports Science of South Africa, PO Box 115, Newlands 7725, South Africa. tdnoakes@sports.uct.ac.za

It is hypothesised that physical activity is controlled by a central governor in the brain and that the human body functions as a complex system during exercise. Using feed forward control in response to afferent feedback from different physiological systems, the extent of skeletal muscle recruitment is controlled as part of a continuously altering pacing strategy, with the sensation of fatigue being the conscious interpretation of these homoeostatic, central governor control mechanisms.

PMID: 15665213 [PubMed - indexed for MEDLINE]

PMCID: PMC1725112

 
5: Obesity (Silver Spring). 2006 Mar;14(3):345-56.
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Neurobiology of exercise.

Dishman RK, Berthoud HR, Booth FW, Cotman CW, Edgerton VR, Fleshner MR, Gandevia SC, Gomez-Pinilla F, Greenwood BN, Hillman CH, Kramer AF, Levin BE, Moran TH, Russo-Neustadt AA, Salamone JD, Van Hoomissen JD, Wade CE, York DA, Zigmond MJ.

Department of Exercise Science, The University of Georgia, Ramsey Center, 330 River Road, Athens, GA 30602-6554, USA. rdishman@uga.edu

Voluntary physical activity and exercise training can favorably influence brain plasticity by facilitating neurogenerative, neuroadaptive, and neuroprotective processes. At least some of the processes are mediated by neurotrophic factors. Motor skill training and regular exercise enhance executive functions of cognition and some types of learning, including motor learning in the spinal cord. These adaptations in the central nervous system have implications for the prevention and treatment of obesity, cancer, depression, the decline in cognition associated with aging, and neurological disorders such as Parkinson's disease, Alzheimer's dementia, ischemic stroke, and head and spinal cord injury. Chronic voluntary physical activity also attenuates neural responses to stress in brain circuits responsible for regulating peripheral sympathetic activity, suggesting constraint on sympathetic responses to stress that could plausibly contribute to reductions in clinical disorders such as hypertension, heart failure, oxidative stress, and suppression of immunity. Mechanisms explaining these adaptations are not as yet known, but metabolic and neurochemical pathways among skeletal muscle, the spinal cord, and the brain offer plausible, testable mechanisms that might help explain effects of physical activity and exercise on the central nervous system.

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PMID: 16648603 [PubMed - indexed for MEDLINE]

 
6: Br J Sports Med. 2004 Aug;38(4):511-4.
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From catastrophe to complexity: a novel model of integrative central neural regulation of effort and fatigue during exercise in humans.

Noakes TD, St Clair Gibson A, Lambert EV.

Research Unit for Exercise Science and Sports Medicine, University of Cape Town, Newlands, South Africa. tdnoakes@sports.uct.ac.za <tdnoakes@sports.uct.ac.za>

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.

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PMID: 15273198 [PubMed - indexed for MEDLINE]

PMCID: PMC1724894

 
7: Exp Physiol. 2006 Jan;91(1):51-8. Epub 2005 Oct 20.
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New insights into central cardiovascular control during exercise in humans: a central command update.

Williamson JW, Fadel PJ, Mitchell JH.

Department of Kinesiology, Health Promotion & Recreation Univeristy of North Texas, Denton, TX 76203-1337, USA. jwilliamson@coe.unt.edu

The autonomic adjustments to exercise are mediated by central signals from the higher brain (central command) and by a peripheral reflex arising from working skeletal muscle (exercise pressor reflex), with further modulation provided by the arterial baroreflex. Although it is clear that central command, the exercise pressor reflex and the arterial baroreflex are all requisite for eliciting appropriate cardiovascular adjustments to exercise, this review will be limited primarily to discussion of central command. Central modulation of the cardiovascular system via descending signals from higher brain centres has been well recognized for over a century, yet the specific regions of the human brain involved in this exercise-related response have remained speculative. Brain mapping studies during exercise as well as non-exercise conditions have provided information towards establishing the cerebral cortical structures in the human brain specifically involved in cardiovascular control. The purpose of this review is to provide an update of current concepts on central command in humans, with a particular emphasis on the regions of the brain identified to alter autonomic outflow and result in cardiovascular adjustments.

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PMID: 16239250 [PubMed - indexed for MEDLINE]

 
8: Neurorehabil Neural Repair. 2005 Dec;19(4):283-95.
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License to run: exercise impacts functional plasticity in the intact and injured central nervous system by using neurotrophins.

Vaynman S, Gomez-Pinilla F.

Department of Neurosurgery and Physiological Science, and Brain Injury Research Center, UCLA School of Medicine, Los Angeles, CA 90095, USA.

Exercise has been found to impact molecular systems important for maintaining neural function and plasticity. A characteristic finding for the effects of exercise in the brain and spinal cord has been the up-regulation of brain-derived neurotrophic factor (BDNF). This review focuses on the ability of exercise to impact brain circuitry by promoting neuronal repair and enhance learning and memory by increasing neurotrophic support. A paragon for the role of activity-dependent neurotrophins in the CNS is the capacity of BDNF to facilitate synaptic function and neuronal excitability. The authors discuss the effects of exercise in the intact and injured brain and spinal cord injury and the implementation of exercise preinjury and postinjury. As the CNS displays a capacity for plasticity throughout one's lifespan, exercise may be a powerful lifestyle implementation that could be used to augment synaptic plasticity, promote behavioral rehabilitation, and counteract the deleterious effects of aging.

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PMID: 16263961 [PubMed - indexed for MEDLINE]

 
9: Clin Physiol Funct Imaging. 2007 Sep;27(5):298-304.
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Central fatigue of the first dorsal interosseous muscle during low-force and high-force sustained submaximal contractions.

Eichelberger TD, Bilodeau M.

Graduate Program in Physical Therapy and Rehabilitation Science, Carver College of Medicine, University of Iowa, IA, USA. martin.bilodeau@uottawa.ca

The aim of this study was to compare the extent of central fatigue in the first dorsal interosseous (FDI) muscle of healthy adults in low, moderate and high-force submaximal contractions. Nine healthy adults completed four experimental sessions where index finger abduction force was recorded during voluntary contractions and in response to brief trains (five pulses at 100 Hz) of electrical stimulation. The ability to maximally activate FDI under volition, or voluntary activation, and its change with sustained activity (central fatigue) was assessed using the twitch interpolation technique. The fatigue tasks consisted of continuous isometric index finger abduction contractions held until exhaustion at four target force levels: 30%, 45%, 60% and 75% of the maximal voluntary contraction. The main finding was the presence of central fatigue for the 30% task, but not for the three other fatigue tasks. The extent of central fatigue was also associated with changes in a measure reflecting the status of peripheral structures/mechanisms. It appears that central fatigue contributed to task failure for the lowest force fatigue task (30%), but not for the other (higher) contraction intensities.

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PMID: 17697026 [PubMed - indexed for MEDLINE]

 
10: J Sports Sci. 1995 Summer;13 Spec No:S49-53.
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Central and peripheral factors in fatigue.

Davis JM.

Department of Exercise Science, University of South Carolina, Columbia 29208, USA.

The causes of fatigue during muscular exercise include factors that reside in the brain (central mechanisms) as well as the muscles themselves (peripheral mechanisms). Central fatigue is largely unexplored, but there is increasing evidence that increased brain serotonin (5-HT) can lead to central (mental) fatigue, thereby causing a deterioration in sport and exercise performance. Although there are also strong theoretical grounds for a beneficial role of nutrition in delaying central fatigue, the data are much more tenuous. Dietary supplementation with branched-chain amino acids (BCAA) in low doses produces small and probably inconsequential effects on peripheral markers of brain 5-HT synthesis (plasma free tryptophan/BCAA), whereas larger doses are likely to be unpalatable, reduce the absorption of water in the gut, and may increase potentially toxic ammonia concentrations in the plasma. Alternatively, carbohydrate supplementation results in large reductions in plasma free tryptophan/BCAA and exercise time to fatigue is significantly longer, but it is difficult to distinguish between the effects of carbohydrate feedings on central fatigue mechanisms and the well-established beneficial effects of carbohydrate supplements on the contracting muscle. These data support the exciting possibility that relationships exist among nutrition, brain neurochemistry and sport performance. However, while the evidence is intriguing and makes good intuitive sense, our knowledge in this area is rudimentary at best.

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PMID: 8897320 [PubMed - indexed for MEDLINE]

 
11: Arq Bras Endocrinol Metabol. 2005 Jun;49(3):359-68. Epub 2006 Mar 16.
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[Neuroendocrine and nutritional aspects of overtraining]

[Article in Portuguese]

Rogero MM, Mendes RR, Tirapegui J.

Departamento de Alimentos e Nutrição Experimental, Faculdade de Ciências Farmacêuticas, Universidade de São Paulo, São Paulo, SP.

The overtraining syndrome is characterized by an excessive training that results in several adverse effects the main of which being the decay in performance. Its incidence among elite athletes has been experiencing a significant increase lately, which prompted a rush of interest in the search for efficient measures to prevent and treat this condition. It is necessary, however, to clarify possible mechanisms involved in the development of overtraining. Several hypothesis are being proposed, such as a greater activation of both the autonomic nervous system and the hypothalamic-pituitary-adrenal axis, and suppression of the hypothalamic-pituitary-gonadal axis. On the contrary, some studies suggest that the modulation of such systems is but a consequence of the overtraining syndrome and not its cause. Thus, recent hypothesis related to cytokine release, to central fatigue, to depletion of muscle and liver glycogen, and to a reduction in glutamine availability during physical activity are being raised.

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PMID: 16543989 [PubMed - indexed for MEDLINE]

 
12: Sports Med. 2004;34(14):967-81.
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Does overtraining exist? An analysis of overreaching and overtraining research.

Halson SL, Jeukendrup AE.

Human Performance Laboratory, School of Sport and Exercise Sciences, University of Birmingham, Edgbaston, UKDepartment of Physiology, Australian Institute of Sport, Belconnen, ACT, Australia.

Athletes experience minor fatigue and acute reductions in performance as a consequence of the normal training process. When the balance between training stress and recovery is disproportionate, it is thought that overreaching and possibly overtraining may develop. However, the majority of research that has been conducted in this area has investigated overreached and not overtrained athletes. Overreaching occurs as a result of intensified training and is often considered a normal outcome for elite athletes due to the relatively short time needed for recovery (approximately 2 weeks) and the possibility of a supercompensatory effect. As the time needed to recover from the overtraining syndrome is considered to be much longer (months to years), it may not be appropriate to compare the two states. It is presently not possible to discern acute fatigue and decreased performance experienced from isolated training sessions, from the states of overreaching and overtraining. This is partially the result of a lack of diagnostic tools, variability of results of research studies, a lack of well controlled studies and individual responses to training.The general lack of research in the area in combination with very few well controlled investigations means that it is very difficult to gain insight into the incidence, markers and possible causes of overtraining. There is currently no evidence aside from anecdotal information to suggest that overreaching precedes overtraining and that symptoms of overtraining are more severe than overreaching. It is indeed possible that the two states show different defining characteristics and the overtraining continuum may be an oversimplification. Critical analysis of relevant research suggests that overreaching and overtraining investigations should be interpreted with caution before recommendations for markers of overreaching and overtraining can be proposed. Systematically controlled and monitored studies are needed to determine if overtraining is distinguishable from overreaching, what the best indicators of these states are and the underlying mechanisms that cause fatigue and performance decrements. The available scientific and anecdotal evidence supports the existence of the overtraining syndrome; however, more research is required to state with certainty that the syndrome exists.

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PMID: 15571428 [PubMed - indexed for MEDLINE]

 
13: Curr Opin Drug Discov Devel. 2006 Sep;9(5):560-70.
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Galanin function in the central nervous system.

Walton KM, Chin JE, Duplantier AJ, Mather RJ.

Neuroscience Discovery, Pfizer Global Research and Development, Eastern Point Road, Groton, CT 06340, USA. kevin.m.wallon@pfizer.com

The peptide galanin is primarily expressed in the central nervous system (CNS) and it is active in a range of models of behavior. The identification of three galanin receptors, whose distribution of expression is distinct but overlapping, is evidence of the complexity of galanin's regulation of neuronal function. The majority of studies examining galanin have used broad methods to identify its function, employing nonselective peptide agonists and antagonists, or transgenic animal models. While these studies were informative, they provided limited insight to the specific receptors mediating the effects of galanin. The recent identification of potent, brain-permeable and selective galanin antagonists suggests it will be possible to gain greater insight into the function of each galanin receptor and their potential as therapeutic targets. This article reviews the roles identified for galanin in the CNS and how ligands of the galanin receptors, both peptidic and small-molecule, have been used to explore the behavioral models that characterize these roles.

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PMID: 17002216 [PubMed - indexed for MEDLINE]

 
14: Sports Med. 2007;37(9):737-63.
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The molecular bases of training adaptation.

Coffey VG, Hawley JA.

School of Medical Sciences, Exercise Metabolism Group, RMIT University, Melbourne, Victoria, Australia.

Skeletal muscle is a malleable tissue capable of altering the type and amount of protein in response to disruptions to cellular homeostasis. The process of exercise-induced adaptation in skeletal muscle involves a multitude of signalling mechanisms initiating replication of specific DNA genetic sequences, enabling subsequent translation of the genetic message and ultimately generating a series of amino acids that form new proteins. The functional consequences of these adaptations are determined by training volume, intensity and frequency, and the half-life of the protein. Moreover, many features of the training adaptation are specific to the type of stimulus, such as the mode of exercise. Prolonged endurance training elicits a variety of metabolic and morphological changes, including mitochondrial biogenesis, fast-to-slow fibre-type transformation and substrate metabolism. In contrast, heavy resistance exercise stimulates synthesis of contractile proteins responsible for muscle hypertrophy and increases in maximal contractile force output. Concomitant with the vastly different functional outcomes induced by these diverse exercise modes, the genetic and molecular mechanisms of adaptation are distinct. With recent advances in technology, it is now possible to study the effects of various training interventions on a variety of signalling proteins and early-response genes in skeletal muscle. Although it cannot presently be claimed that such scientific endeavours have influenced the training practices of elite athletes, these new and exciting technologies have provided insight into how current training techniques result in specific muscular adaptations, and may ultimately provide clues for future and novel training methodologies. Greater knowledge of the mechanisms and interaction of exercise-induced adaptive pathways in skeletal muscle is important for our understanding of the aetiology of disease, maintenance of metabolic and functional capacity with aging, and training for athletic performance. This article highlights the effects of exercise on molecular and genetic mechanisms of training adaptation in skeletal muscle.

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PMID: 17722947 [PubMed - indexed for MEDLINE]

 
15: Br J Hosp Med (Lond). 2007 Jul;68(7):376-9.
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Physiology of sport.

Maughan R.

Sport and Exercise Nutrition in the School of Sport and Exercise Sciences, Loughborough University, Leicestershire.

The elite athlete represents the extreme of the human gene pool, where genetic endowment is developed by an intensive training programme. Sport encompasses many different activities, calling for different physical and mental attributes. Understanding the physiology of exercise provides insights into normal physiological function.

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PMID: 17663314 [PubMed - indexed for MEDLINE]

 
16: Sports Med. 2006;36(2):133-49.
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Neural adaptations to resistive exercise: mechanisms and recommendations for training practices.

Gabriel DA, Kamen G, Frost G.

Department of Physical Education and Kinesiology, Brock University, St Catharines, Ontario, Canada. dgabriel@brocku.ca

It is generally accepted that neural factors play an important role in muscle strength gains. This article reviews the neural adaptations in strength, with the goal of laying the foundations for practical applications in sports medicine and rehabilitation.An increase in muscular strength without noticeable hypertrophy is the first line of evidence for neural involvement in acquisition of muscular strength. The use of surface electromyographic (SEMG) techniques reveal that strength gains in the early phase of a training regimen are associated with an increase in the amplitude of SEMG activity. This has been interpreted as an increase in neural drive, which denotes the magnitude of efferent neural output from the CNS to active muscle fibres. However, SEMG activity is a global measure of muscle activity. Underlying alterations in SEMG activity are changes in motor unit firing patterns as measured by indwelling (wire or needle) electrodes. Some studies have reported a transient increase in motor unit firing rate. Training-related increases in the rate of tension development have also been linked with an increased probability of doublet firing in individual motor units. A doublet is a very short interspike interval in a motor unit train, and usually occurs at the onset of a muscular contraction. Motor unit synchronisation is another possible mechanism for increases in muscle strength, but has yet to be definitely demonstrated.There are several lines of evidence for central control of training-related adaptation to resistive exercise. Mental practice using imagined contractions has been shown to increase the excitability of the cortical areas involved in movement and motion planning. However, training using imagined contractions is unlikely to be as effective as physical training, and it may be more applicable to rehabilitation.Retention of strength gains after dissipation of physiological effects demonstrates a strong practice effect. Bilateral contractions are associated with lower SEMG and strength compared with unilateral contractions of the same muscle group. SEMG magnitude is lower for eccentric contractions than for concentric contractions. However, resistive training can reverse these trends. The last line of evidence presented involves the notion that unilateral resistive exercise of a specific limb will also result in training effects in the unexercised contralateral limb (cross-transfer or cross-education). Peripheral involvement in training-related strength increases is much more uncertain. Changes in the sensory receptors (i.e. Golgi tendon organs) may lead to disinhibition and an increased expression of muscular force.Agonist muscle activity results in limb movement in the desired direction, while antagonist activity opposes that motion. Both decreases and increases in co-activation of the antagonist have been demonstrated. A reduction in antagonist co-activation would allow increased expression of agonist muscle force, while an increase in antagonist co-activation is important for maintaining the integrity of the joint. Thus far, it is not clear what the CNS will optimise: force production or joint integrity.The following recommendations are made by the authors based on the existing literature. Motor learning theory and imagined contractions should be incorporated into strength-training practice. Static contractions at greater muscle lengths will transfer across more joint angles. Submaximal eccentric contractions should be used when there are issues of muscle pain, detraining or limb immobilisation. The reversal of antagonists (antagonist-to-agonist) proprioceptive neuromuscular facilitation contraction pattern would be useful to increase the rate of tension development in older adults, thus serving as an important prophylactic in preventing falls. When evaluating the neural changes induced by strength training using EMG recording, antagonist EMG activity should always be measured and evaluated.

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PMID: 16464122 [PubMed - indexed for MEDLINE]

 
17: Br J Sports Med. 2006 Jul;40(7):573-86; discussion 586.
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Is fatigue all in your head? A critical review of the central governor model.

Weir JP, Beck TW, Cramer JT, Housh TJ.

Osteopathic Medical Center, Des Moines University, Des Moines, IA 50312, USA. joseph.weir@dmu.edu

The central governor model has recently been proposed as a general model to explain the phenomenon of fatigue. It proposes that the subconscious brain regulates power output (pacing strategy) by modulating motor unit recruitment to preserve whole body homoeostasis and prevent catastrophic physiological failure such as rigor. In this model, the word fatigue is redefined from a term that describes an exercise decline in the ability to produce force and power to one of sensation or emotion. The underpinnings of the central governor model are the refutation of what is described variously as peripheral fatigue, limitations models, and the cardiovascular/anaerobic/catastrophe model. This argument centres on the inability of lactic acid models of fatigue to adequately explain fatigue. In this review, it is argued that a variety of peripheral factors other than lactic acid are known to compromise muscle force and power and that these effects may protect against "catastrophe". Further, it is shown that a variety of studies indicate that fatigue induced decreases in performance cannot be adequately explained by the central governor model. Instead, it is suggested that the concept of task dependency, in which the mechanisms of fatigue vary depending on the specific exercise stressor, is a more comprehensive and defensible model of fatigue. This model includes aspects of both central and peripheral contributions to fatigue, and the relative importance of each probably varies with the type of exercise.

Publication Types:


PMID: 16799110 [PubMed - indexed for MEDLINE]