|
|
CNS fatigue and how to overcome it is being researched by Dedicated Athlete through the control of real world testing environments, clinical studies with independent universities and feedback from our consumers.
Central nervous system fatigue describes when muscle contractions become limited by inability to recruit motor neurons. CNS fatigue manifests when the effort is intense and is associated with reduced strength and an inability to maintain the contraction. The inability for contractions mainly affect slow twitch muscle fibers; mainly endurance athletes. Research suggests that CNS fatigue plays a role in the reduction of the ratio between the brain's uptake of oxygen relative to carbohydrate, changes in plasma tryptophan/branched chain amino acid ratio in responses to training volume variation, failure at axon branch points and/or alterations in muscle membrane properties and other unknown causes.
Research on CNS fatigue during exercise:
Exercise and its effects on the central nervous system.
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.
PMID: 15659274 [PubMed - in process]
Cerebral perturbations provoked by prolonged exercise.
Department of Human Physiology, Institute of Exercise and Sport Sciences, August Krogh Institute, Universitetsparken 13, DK-2100 Copenhagen, Denmark.
This review addresses cerebral metabolic and neurohumoral alterations during prolonged exercise in humans with special focus on associations with fatigue. Global energy turnover in the brain is unaltered by the transition from rest to moderately intense exercise, apparently because exercise-induced activation of some brain regions including cortical motor areas is compensated for by reduced activity in other regions of the brain. However, strenuous exercise is associated with cerebral metabolic and neurohumoral alterations that may relate to central fatigue. Fatigue should be acknowledged as a complex phenomenon influenced by both peripheral and central factors. However, failure to drive the motorneurons adequately as a consequence of neurophysiological alterations seems to play a dominant role under some circumstances. During exercise with hyperthermia excessive accumulation of heat in the brain due to impeded heat removal by the cerebral circulation may elevate the brain temperature to >40 degrees C and impair the ability to sustain maximal motor activation. Also, when prolonged exercise results in hypoglycaemia, perceived exertion increases at the same time as the cerebral glucose uptake becomes low, and centrally mediated fatigue appears to arise as the cerebral energy turnover becomes restricted by the availability of substrates for the brain. Changes in serotonergic activity, inhibitory feed-back from the exercising muscles, elevated ammonia levels, and alterations in regional dopaminergic activity may also contribute to the impaired voluntary activation of the motorneurons after prolonged and strenuous exercise. Furthermore, central fatigue may involve depletion of cerebral glycogen stores, as signified by the observation that following exhaustive exercise the cerebral glucose uptake increases out of proportion to that of oxygen. In summary, prolonged exercise may induce homeostatic disturbances within the central nervous system (CNS) that subsequently attenuates motor activation. Therefore, strenuous exercise is a challenge not only to the cardiorespiratory and locomotive systems but also to the brain. Copyright 2004 Elsevier Ltd
PMID: 15142684 [PubMed - indexed for MEDLINE]
The brain and fatigue: new opportunities for nutritional interventions?
Department of Human Physiology and Sports Medicine, Faculty of Physical Education and Physiotherapy, Vrije Universiteit Brussel, Belgium.
It is clear that the cause of fatigue is complex, influenced by events occurring in both the periphery and the central nervous system. Work conducted over the last 20 years has focused on the role of brain serotonin and catecholamines in the development of fatigue, and the possibility that manipulation of neurotransmitter precursors may delay the onset of fatigue. While there is some evidence that branched-chain amino acid and tyrosine ingestion can influence perceived exertion and some measures of mental performance, the results of several apparently well-controlled laboratory studies have not demonstrated a positive effect on exercise capacity or performance under temperate conditions. As football is highly reliant upon the successful execution of motor skills and tactics, the possibility that amino acid ingestion may help to attenuate a loss in cognitive function during the later stages of a game would be desirable, even in the absence of no apparent benefit to physical performance. There are several reports of enhanced performance of high-intensity intermittent exercise with carbohydrate ingestion, but at present it is difficult to separate the peripheral effects from any potential impact on the central nervous system. The possibility that changes in central neurotransmission play a role in the aetiology of fatigue when exercise is performed in high ambient temperatures has recently been examined, although the significance of this in relation to the pattern of activity associated with football has yet to be determined.
Lactic Acid and exercise performance : culprit or friend?
Institute of Sport and Recreation Research New Zealand, Faculty of Health and Environmental Sciences, Auckland University of Technology, Auckland, New Zealand.
This article critically discusses whether accumulation of lactic acid, or in reality lactate and/or hydrogen (H(+)) ions, is a major cause of skeletal muscle fatigue, i.e. decline of muscle force or power output leading to impaired exercise performance. There exists a long history of studies on the effects of increased lactate/H(+) concentrations in muscle or plasma on contractile performance of skeletal muscle. Evidence suggesting that lactate/H(+) is a culprit has been based on correlation-type studies, which reveal close temporal relationships between intramuscular lactate or H(+) accumulation and the decline of force during fatiguing stimulation in frog, rodent or human muscle. In addition, an induced acidosis can impair muscle contractility in non-fatigued humans or in isolated muscle preparations, and several mechanisms to explain such effects have been provided. However, a number of recent high-profile papers have seriously challenged the 'lactic acid hypothesis'. In the 1990s, these findings mainly involved diminished negative effects of an induced acidosis in skinned or intact muscle fibres, at higher more physiological experimental temperatures. In the early 2000s, it was conclusively shown that lactate has little detrimental effect on mechanically skinned fibres activated by artificial stimulation. Perhaps more remarkably, there are now several reports of protective effects of lactate exposure or induced acidosis on potassium-depressed muscle contractions in isolated rodent muscles. In addition, sodium-lactate exposure can attenuate severe fatigue in rat muscle stimulated in situ, and sodium lactate ingestion can increase time to exhaustion during sprinting in humans. Taken together, these latest findings have led to the idea that lactate/H(+) is ergogenic during exercise.It should not be taken as fact that lactic acid is the deviant that impairs exercise performance. Experiments on isolated muscle suggest that acidosis has little detrimental effect or may even improve muscle performance during high-intensity exercise. In contrast, induced acidosis can exacerbate fatigue during whole-body dynamic exercise and alkalosis can improve exercise performance in events lasting 1-10 minutes. To reconcile the findings from isolated muscle fibres through to whole-body exercise, it is hypothesised that a severe plasma acidosis in humans might impair exercise performance by causing a reduced CNS drive to muscle.
PMID: 16573355 [PubMed - in process]
Cerebral changes during exercise in the heat.
Institute of Exercise and Sport Sciences, University of Copenhagen, Copenhagen, Denmark.
This review focuses on cerebral changes during combined exercise and heat stress, and their relation to fatigue. Dynamic exercise can elevate the core temperature rapidly and high internal body temperatures seem to be an independent cause of fatigue during exercise in hot environments. Thus, in laboratory settings, trained participants become exhausted when they reach a core temperature of approximately 40 degrees C. The observation that exercise-induced hyperthermia reduces the central activation percentage during maximal isometric muscle contractions supports the idea that central fatigue is involved in the aetiology of hyperthermia-induced fatigue. Thus, hyperthermia does not impair the ability of the muscles to generate force, but sustained force production is lowered as a consequence of a reduced neural drive from the CNS. During ongoing dynamic exercise in hot environments, there is a gradual slowing of the electroencephalogram (EEG) whereas hyperthermia does not affect the electromyogram. The frequency shift of the EEG is highly correlated with the participants' perception of exertion, which furthermore may indicate that alterations in cerebral activity, rather than peripheral fatigue, are associated with the hyperthermia-induced development of fatigue. Cerebral blood flow is reduced by approximately 20% during exercise with hyperthermia due to hyperventilation, which causes a lowering of the arterial CO(2) pressure. However, in spite of the reduced blood flow, cerebral glucose and oxygen uptake does not seem to be impaired. Removal of heat from the brain is also an important function of the cerebral blood flow and the lowered perfusion of the brain during exercise and heat stress appears to reduce heat removal by the venous blood. Heat is consequently stored in the brain. The causal relationship between the circulatory changes, the EEG changes and the hyperthermia-induced central fatigue is at the present not well understood and future studies should focus on this aspect.
PMID: 12477374 [PubMed - indexed for MEDLINE]
CNS fatigue and prolonged exercise: effect of glucose supplementation.
Department of Human Physiology, Institute of Exercise and Sport Sciences, University of Copenhagen, Copenhagen, Denmark. lnnielsen@aki.ku.dk
INTRODUCTION: Ingestion of carbohydrates during prolonged exercise may improve endurance, whereas an insufficient supply of glucose results in hypoglycemia and fatigue. Fatigue, defined as a loss of force-generating capacity, may develop for a variety of reasons and involve both central and peripheral factors. This study investigated whether CNS activation of the skeletal muscles was affected by prolonged exercise with or without glucose supplementation. METHODS: Voluntary force production and central activation ratios, assessed by the twitch interpolation technique, were determined during a 2-min sustained maximal knee extension in eight endurance-trained males in a baseline condition and immediately after 3 h of cycling randomized to be with or without glucose supplementation. RESULTS: The exercise bout without glucose supplementation (placebo trial) reduced the blood glucose concentration from 4.5 +/- 0.2 to 3.0 +/- 0.2 mM, whereas blood glucose homeostasis was maintained during the glucose trial. The average force during the sustained maximal voluntary muscle contraction was 248 +/- 23 N at baseline, 222 +/- 20 N in the glucose trial, and 197 +/- 21 N in the placebo trial (P < 0.05 between conditions). In the placebo trial, the lowered force production was accompanied by a reduced level of CNS activation compared with the other two conditions (P < 0.05), whereas the central activation ratios were similar in the glucose trial as compared with baseline. CONCLUSION: Exercise-induced hypoglycemia attenuates CNS activation during a sustained maximal muscle contraction, whereas central activation appears to be unaffected by 3 h of moderately intense exercise in endurance-trained athletes when euglycemia is maintained by carbohydrate ingestion
Possible mechanisms of central nervous system fatigue during exercise.
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.
Pyruvate carboxylase: an astrocyte-specific enzyme implicated in the replenishment of amino acid neurotransmitter pools.
Pyruvate carboxylase is the predominant anaplerotic enzyme in CNS tissues, and thus provides for net utilization of glucose to generate citric acid cycle intermediates such as alpha-ketoglutarate and malate for replenishment of the neurotransmitter pools of glutamate, GABA and aspartate. Studies reported in this paper involving immunocytochemical and biochemical techniques demonstrate: (1) the enzyme is localized in astrocytes as visualized by immunofluorescence in sections of cerebellum and (2) the enzyme activity in astrocyte-enriched populations is 3 X higher than in granule cell-enriched populations isolated from the cerebellum; similarly activity in different synaptosomal preparations parallels that for glutamine synthetase. We conclude from these results that the enzyme pyruvate carboxylase is an astrocyte-specific marker. This localization substantiates some recent hypotheses for astrocyte functions, including CO2 fixation in the CNS and the replenishment of citric acid cycle intermediates by astrocytes as precursors for amino acid neurotransmitter pools.
Heat and cold : what does the environment do to the marathon runner?
School of Sport and Exercise Sciences, Loughborough University, Leicestershire, UK.
The marathon poses a considerable physical challenge for athletes of all levels. When combined with high heat and humidity, not only is performance potentially compromised, but health and well-being are also at risk. There are well recognised effects of heat and hydration status on the cardiovascular and thermoregulatory systems that can account for the decreased performance and increased sensation of effort that are experienced when competing in the heat. Elevated exercise heart rate and core temperature at the same absolute exercise intensity are commonly reported. Dehydration occurring during exercise in the heat and results in reductions in stroke volume, cardiac output and blood pressure, as well as a marked decline in blood flow to the working muscles. Recent work suggests that hyperthermia may have a direct affect on the CNS and the brain may contribute to fatigue during prolonged exercise in a warm environment. At present, evidence supports a significant role of catecholaminergic neurotransmission, but there are a number of metabolic and circulatory perturbations occurring within the brain that may also be important in the fatigue process.
Possible mechanisms of central nervous system fatigue during exercise.
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.
Amino acid metabolism, branched-chain amino acid feeding and brain monoamine function.
Department of Physical Education and Sport Sciences, University of Limerick, Republic of Ireland.
Although fatigue during prolonged exercise has traditionally been associated with peripheral factors relating to muscle metabolism, such as the depletion of muscle glycogen, more recent research has generated a renewed interest in amino acid metabolism per se and in the role of amino acids as precursors of brain neurotransmitter function. The concept of a 'central fatigue hypothesis' has done much to stimulate scientists to explore the functional role of the brain and CNS in the aetiology of the fatigue process. The concept has also generated a number of testable hypotheses by which it is possible to examine how the 'central' component of fatigue may act. The present review has attempted to bring together the current research in this area. There is good reason to believe that nutritional intervention may play an important role in relation to fatigue residing within the brain and CNS. Although an exciting possibility exists that nutritional manipulation may affect brain neurochemistry and ultimately sports performance, the experimental evidence to support this claim is, as yet, equivocal. A greater understanding of amino acid metabolism and, in particular, amino acid transport, will greatly improve future experimental designs used to test the efficacy of nutritional manipulation of amino acids and their effect on the central component of the fatigue process.PMID: 9571706 [PubMed - indexed for MEDLINE]
Regeneration of central nervous system: its concept and strategy
Department of Physiology, Keio University School of Medicine.
It had been long believed that our adult mammalian central nervous system (CNS) does not regenerate after damage due to injuries or degenerative diseases, as Santiago Ramony Cajal had indicated long time ago. Today, however, CNS came to be recognized as an important target of so called "regenerative medicine". We have been proposing that regeneration of CNS does include the following three concepts: i) re-growth of the damaged neuronal axons, ii) replenishment of lost neural (or neuronal) cells and iii) recovery of lost neural functions. Here, we would like to emphasize that to recapitulate normal neural development is an essential strategy for CNS-regeneration. In this review, we would like to take Parkinson's disease and spinal cord injury as examples to discuss actual strategy aiming for CNS-regeneration.
Neurogenesis in the adult central nervous system.
National Neuroscience Institute, Singapore, 11 Jalan Tan Tock Seng, Singapore 308433.
Contrary to the long-held dogma, neurogenesis occurs throughout adulthood, and neural stem cells reside in the adult central nervous system (CNS) in mammals. The developmental process of the brain may thus never end, and the brain may be amenable to repair. Neurogenesis is modulated in a wide variety of physiological and pathological conditions, and is involved in processes such as learning and memory and depression. However, the relative contribution of newly generated neuronal cells to these processes, as well as to CNS plasticity, remains to be determined. Thus, not only neurogenesis contributes to reshaping the adult brain, it will ultimately lead us to redefine our knowledge and understanding of the nervous system.
Serotonin and brain development.
Department of Pharmacology, Vanderbilt University, Nashville, Tennessee 37232, USA.
The role of the serotonergic system in the neuroplastic events that create, repair, and degenerate the brain has been explored. Synaptic plasticity occurs throughout life and is critical during brain development. Evidence from biochemical, pharmacological, and clinical studies demonstrates the huge importance of an intact serotonergic system for normal central nervous system (CNS)function. Serotonin acts as a growth factor during embryogenesis, and serotonin receptor activity forms a crucial part of the cascade of events leading to changes in brain structure. The serotonergic system interacts with brain-derived neurotrophic factor (BDNF), S100beta, and other chemical messengers, in addition to ts cross talk with the GABAergic, glutamatergic, and dopaminergic neurotransmitter systems. Disruption of these processes may contribute to CNS disorders that have been associated with impaired development. Furthermore, many psychiatric drugs alter serotonergic activity and have been shown to create changes in brain structure with long-term treatment. However, the mechanisms for their therapeutic efficacy are still unclear. Treatments for psychiatric illness are usually chronic and alleviate psychiatric symptoms, rather than cure these diseases. Therefore, greater exploration of the serotonin system during brain development and growth could lead to real progress in the discovery of treatments for mental disorders.PMID: 15006487 [PubMed - indexed for MEDLINE]
Nerve injury induces a rapid efflux of nitric oxide (NO) detected with a novel NO microsensor.
of Biological Sciences, Purdue University, West Lafayette, Indiana 47907, USA.
An early step in repair of the leech CNS is the appearance of endothelial nitric oxide synthase (eNOS) immunoreactivity and NOS activity, but coincident generation of NO at the lesion after injury has not been shown. This is important because NO can regulate microglial cell motility and axon growth. Indirect measurement of NO with the standard citrulline assay demonstrated that NO was generated within 30 min after nerve cord injury. A polarographic NO-selective self-referencing microelectrode that measures NO flux noninvasively was developed to obtain higher spatial and temporal resolution. With this probe, it was possible to demonstrate that immediately after the leech CNS was injured, NO left the lesion with a mean peak efflux of 803 +/- 99 fmol NO cm(-2) sec(-1). NO efflux exponentially declined to a constant value, as described through the equation f(t) = y(o) + ae(-t/tau), with tau = 117 +/- 30 sec. The constant y(o) = 15.8 +/- 4.5 fmol cm(-2) represents a sustained efflux of NO. Approximately 200 pmol NO cm(-2) is produced at the lesion (n = 8). Thus, injury activates eNOS already present in the CNS and precedes the accumulation of microglia at the lesion, consistent with the hypothesis that NO acts to stop the migrating microglia at the lesion site.PMID: 11150338 [PubMed - indexed for MEDLINE] [Neuro spheres as a source of cells for repair of the central nervous system][Article in Spanish] Departamento de Biologia Molecular, Facultad de Medicina, Universidad de Cantabria, Santander, Espana. fanarrag@galeno.medi.unican.esINTRODUCTION: Neurons and oligodendrocytes are terminally differentiated cells. This means that once they have differentiated from their precursor cells, they cannot proliferate. A direct consequence of this type of differentiation is that cell repair is impossible in areas where neurodegenerative disease have caused the death of neurons and oligodendroglia. Recently multipotential neuroepithelial precursors of the central nervous system (CNS) have been isolated and characterized in vitro. DEVELOPMENT: In this study we review the capacity for nervous repair of these neuroepithelial precursors from the neurobiological point of view. These cells, known as neuro-spheres can be cultivated, amplified and cryopreserved for subsequent transplanting. Already there are many studies showing how neuro-spheres maintain their capacity for differentiation in vivo and that they can reach certain localized areas of the CNS. CONCLUSIONS: From this review we conclude that through the study and manipulation of these neuro-spheres, new goals in CNS repair may be achieved.
Immunoregulators in the nervous system.
School of Life and Health Sciences, University of Delaware, Newark 19716.
The nervous system, through the production of neuroregulators (neurotransmitters, neuromodulators and neuropeptides) can regulate specific immune system functions, while the immune system, through the production of immunoregulators (immunomodulators and immunopeptides) can regulate specific nervous system functions. This indicates a reciprocal communication between the nervous and immune systems. The presence of immunoregulators in the brain and cerebrospinal fluid is the result of local synthesis--by intrinsic and blood-derived macrophages, activated T-lymphocytes that cross the blood-brain barrier, endothelial cells of the cerebrovasculature, microglia, astrocytes, and neuronal components--and/or uptake from the peripheral blood through the blood-brain barrier (in specific cases) and circumventricular organs. Acute and chronic pathological processes (infection, inflammation, immunological reactions, malignancy, necrosis) stimulate the synthesis and release of immunoregulators in various cell systems. These immunoregulators have pivotal roles in the coordination of the host defense mechanisms and repair, and induce a series of immunological, endocrinological, metabolical and neurological responses. This review summarizes studies concerning immunoregulators--such as interleukins, tumor necrosis factor, interferons, transforming growth factors, thymic peptides, tuftsin, platelet activating factor, neuro-immunoregulators--in the nervous system. It also describes the monitoring of immunoregulators by the central nervous system (CNS) as part of the regulatory factors that induce neurological manifestations (e.g., fever, somnolence, appetite suppression, neuroendocrine alterations) frequently accompanying acute and chronic pathological processes.
Be the first to rate this post - Currently 0/5 Stars.
- 1
- 2
- 3
- 4
- 5
Related posts
|
|