Carbohydrate ingestion exerts its benefit by increasing cerebral glucose uptake and maintaining central neural drive NH 3 can cross the blood—brain barrier and has the potential to affect central neurotransmitter levels and central neural fatigue. Of note, carbohydrate ingestion attenuates muscle and plasma NH 3 accumulation during exercise , another potential mechanism through which carbohydrate ingestion exerts its ergogenic effect.
Enhanced exercise performance has also been observed from simply having carbohydrate in the mouth, an effect that has been linked to activation of brain centres involved in motor control Increased plasma fatty acid availability decreases muscle glycogen utilization and carbohydrate oxidation during exercise , , High-fat diets have also been proposed as a strategy to decrease reliance on carbohydrate and improve endurance performance.
Other studies have demonstrated increased fat oxidation and lower rates of muscle glycogen use and carbohydrate oxidation after adaptation to a short-term high-fat diet, even with restoration of muscle glycogen levels, but no effect on endurance exercise performance , If anything, high-intensity exercise performance is impaired on the high-fat diet , apparently as a result of an inability to fully activate glycogenolysis and PDH during intense exercise Furthermore, a high-fat diet has been shown to impair exercise economy and performance in elite race walkers A related issue with high-fat, low carbohydrate diets is the induction of nutritional ketosis after 2—3 weeks.
However, when this diet is adhered to for 3 weeks, and the concentrations of ketone bodies are elevated, a decrease in performance has been observed in elite race walkers The rationale for following this dietary approach to optimize performance has been called into question Although training on a high-fat diet appears to result in suboptimal adaptations in previously untrained participants , some studies have reported enhanced responses to training with low carbohydrate availability in well-trained participants , Over the years, endurance athletes have commonly undertaken some of their training in a relatively low-carbohydrate state.
However, maintaining an intense training program is difficult without adequate dietary carbohydrate intake Furthermore, given the heavy dependence on carbohydrate during many of the events at the Olympics 9 , the most effective strategy for competition would appear to be one that maximizes carbohydrate availability and utilization.
Nutritional ketosis can also be induced by the acute ingestion of ketone esters, which has been suggested to alter fuel preference and enhance performance The metabolic state induced is different from diet-induced ketosis and has the potential to alter the use of fat and carbohydrate as fuels during exercise. However, published studies on trained male athletes from at least four independent laboratories to date do not support an increase in performance. Acute ingestion of ketone esters has been found to have no effect on 5-km and km trial performance , , or performance during an incremental cycling ergometer test A further study has reported that ketone ester ingestion decreases performance during a The rate of ketone provision and metabolism in skeletal muscle during high-intensity exercise appears likely to be insufficient to substitute for the rate at which carbohydrate can provide energy.
Early work on the ingestion of high doses of caffeine 6—9 mg caffeine per kg body mass 60 min before exercise has indicated enhanced lipolysis and fat oxidation during exercise, decreased muscle glycogen use and increased endurance performance in some individuals , , These effects appear to be a result of caffeine-induced increases in catecholamines, which increase lipolysis and consequently fatty acid concentrations during the rest period before exercise.
After exercise onset, these circulating fatty acids are quickly taken up by the tissues of the body 10—15 min , fatty acid concentrations return to normal, and no increases in fat oxidation are apparent.
This observation suggests that the ergogenic effects are mediated not through metabolic events but through binding to adenosine receptors in the central and peripheral nervous systems.
Caffeine has been proposed to increase self-sustained firing, as well as voluntary activation and maximal force in the central nervous system, and to decrease the sensations associated with force, pain and perceived exertion or effort during exercise in the peripheral nervous system , The ingestion of low doses of caffeine is also associated with fewer or none of the adverse effects reported with high caffeine doses anxiety, jitters, insomnia, inability to focus, gastrointestinal unrest or irritability.
The potential of supplementation with l -carnitine has received much interest, because this compound has a major role in moving fatty acids across the mitochondrial membrane and regulating the amount of acetyl-CoA in the mitochondria.
The need for supplemental carnitine assumes that a shortage occurs during exercise, during which fat is used as a fuel. Although this outcome does not appear to occur during low-intensity and moderate-intensity exercise, free carnitine levels are low in high-intensity exercise and may contribute to the downregulation of fat oxidation at these intensities.
However, oral supplementation with carnitine alone leads to only small increases in plasma carnitine levels and does not increase the muscle carnitine content However, to date, there is no evidence that carnitine supplementation can improve performance during the higher exercise intensities common to endurance sports.
NO is an important bioactive molecule with multiple physiological roles within the body. It is produced from l -arginine via the action of nitric oxide synthase and can also be formed by the nonenzymatic reduction of nitrate and nitrite. The observation that dietary nitrate decreases the oxygen cost of exercise has stimulated interest in the potential of nitrate, often ingested in the form of beetroot juice, as an ergogenic aid during exercise.
Indeed, several studies have observed enhanced exercise performance associated with lower oxygen cost and increased muscle efficiency after beetroot-juice ingestion , , The effect of nitrate supplementation appears to be less apparent in well-trained athletes , , although results in the literature are varied Dietary nitrate supplementation may have beneficial effects through an improvement in excitation—contraction coupling , , because supplementation with beetroot juice does not alter mitochondrial efficiency in human skeletal muscle , and the results with inorganic nitrate supplementation have been equivocal , Lactate is not thought to have a major negative effect on force and power generation and, as mentioned earlier, is an important metabolic intermediate and signalling molecule.
Of greater importance is the acidosis arising from increased muscle metabolism and strong ion fluxes. In humans, acidosis does not appear to impair maximal isometric-force production, but it does limit the ability to maintain submaximal force output , thus suggesting an effect on energy metabolism and ATP generation Ingestion of oral alkalizers, such as bicarbonate, is often associated with increased high-intensity exercise performance , , partly because of improved energy metabolism and ionic regulation , As previously mentioned, high-intensity exercise training increases muscle buffer capacity 74 , A major determinant of the muscle buffering capacity is carnosine content, which is higher in sprinters and rowers than in marathon runners or untrained individuals During exercise, ROS, such as superoxide anions, hydrogen peroxide and hydroxyl radicals, are produced and have important roles as signalling molecules mediating the acute and chronic responses to exercise However, ROS accumulation at higher levels can negatively affect muscle force and power production and induce fatigue 68 , Whether dietary antioxidant supplementation can improve exercise performance is equivocal , although ingestion of N -acetylcysteine enhances muscle oxidant capacity and attenuates muscle fatigue during prolonged exercise Some reports have suggested that antioxidant supplementation may potentially attenuate skeletal muscle adaptation to regular exercise , , Overall, ROS may have a key role in mediating adaptations to acute and chronic exercise but, when they accumulate during strenuous exercise, may exert fatigue effects that limit exercise performance.
The negative effects of hyperthermia are potentiated by sweating-induced fluid losses and dehydration , particularly decreased skeletal muscle blood flow and increased muscle glycogen utilization during exercise in heat Increased plasma catecholamines and elevated muscle temperatures also accelerate muscle glycogenolysis during exercise in heat , , Strategies to minimize the negative effects of hyperthermia on muscle metabolism and performance include acclimation, pre-exercise cooling and fluid ingestion , , , To meet the increased energy needs of exercise, skeletal muscle has a variety of metabolic pathways that produce ATP both anaerobically requiring no oxygen and aerobically.
These pathways are activated simultaneously from the onset of exercise to precisely meet the demands of a given exercise situation. Although the aerobic pathways are the default, dominant energy-producing pathways during endurance exercise, they require time seconds to minutes to fully activate, and the anaerobic systems rapidly in milliseconds to seconds provide energy to cover what the aerobic system cannot provide.
Anaerobic energy provision is also important in situations of high-intensity exercise, such as sprinting, in which the requirement for energy far exceeds the rate that the aerobic systems can provide. This situation is common in stop-and-go sports, in which transitions from lower-energy to higher-energy needs are numerous, and provision of both aerobic and anaerobic energy contributes energy for athletic success. Together, the aerobic energy production using fat and carbohydrate as fuels and the anaerobic energy provision from PCr breakdown and carbohydrate use in the glycolytic pathway permit Olympic athletes to meet the high energy needs of particular events or sports.
The various metabolic pathways are regulated by a range of intramuscular and hormonal signals that influence enzyme activation and substrate availability, thus ensuring that the rate of ATP resynthesis is closely matched to the ATP demands of exercise.
Regular training and various nutritional interventions have been used to enhance fatigue resistance via modulation of substrate availability and the effects of metabolic end products. The understanding of exercise energy provision, the regulation of metabolism and the use of fat and carbohydrate fuels during exercise has increased over more than years, on the basis of studies using various methods including indirect calorimetry, tissue samples from contracting skeletal muscle, metabolic-tracer sampling, isolated skeletal muscle preparations, and analysis of whole-body and regional arteriovenous blood samples.
However, in virtually all areas of the regulation of fat and carbohydrate metabolism, much remains unknown. The introduction of molecular biology techniques has provided opportunities for further insights into the acute and chronic responses to exercise and their regulation, but even those studies are limited by the ability to repeatedly sample muscle in human participants to fully examine the varied time courses of key events. The ability to fully translate findings from in vitro experiments and animal studies to exercising humans in competitive settings remains limited.
The field also continues to struggle with measures specific to the various compartments that exist in the cell, and knowledge remains lacking regarding the physical structures and scaffolding inside these compartments, and the communication between proteins and metabolic pathways within compartments.
A clear example of these issues is in studying the events that occur in the mitochondria during exercise. One area that has not advanced as rapidly as needed is the ability to non-invasively measure the fuels, metabolites and proteins in the various important muscle cell compartments that are involved in regulating metabolism during exercise.
Although magnetic resonance spectroscopy has been able to measure certain compounds non-invasively, measuring changes that occur with exercise at the molecular and cellular levels is generally not possible.
Some researchers are investigating exercise metabolism at the whole-body level through a physiological approach, and others are examining the intricacies of cell signalling and molecular changes through a reductionist approach.
New opportunities exist for the integrated use of genomics, proteomics, metabolomics and systems biology approaches in data analyses, which should provide new insights into the molecular regulation of exercise metabolism. Many questions remain in every area of energy metabolism, the regulation of fat and carbohydrate metabolism during exercise, optimal training interventions and the potential for manipulation of metabolic responses for ergogenic benefits. Exercise biology will thus continue to be a fruitful research area for many years as researchers seek a greater understanding of the metabolic bases for the athletic successes that will be enjoyed and celebrated during the quadrennial Olympic festival of sport.
Hawley, J. Integrative biology of exercise. Cell , — Sahlin, K. Energy supply and muscle fatigue in humans. Acta Physiol. Anaerobic energy release in working muscle during 30 s to 3 min of exhausting bicycling. Parolin, M. Regulation of skeletal muscle glycogen phosphorylase and PDH during maximal intermittent exercise. Greenhaff, P. The metabolic responses of human type I and II muscle fibres during maximal treadmill sprinting.
Article Google Scholar. Relative importance of aerobic and anaerobic energy release during short-lasting exhausting bicycle exercise. Tesch, P. Muscle metabolism during intense, heavy-resistance exercise.
Koopman, R. Intramyocellular lipid and glycogen content are reduced following resistance exercise in untrained healthy males. Carbohydrate dependence during prolonged, intense endurance exercise. Sports Med. Carbohydrate dependence during marathon running. Sports Exerc. Romijn, J. Regulation of endogenous fat and carbohydrate metabolism in relation to exercise intensity and duration. The effects of increasing exercise intensity on muscle fuel utilisation in humans. A study of the glycogen metabolism during exercise in man.
Wahren, J. Glucose metabolism during leg exercise in man. Ahlborg, G. Substrate turnover during prolonged exercise in man. Watt, M. Intramuscular triacylglycerol, glycogen and acetyl group metabolism during 4 h of moderate exercise in man. Inhibition of adipose tissue lipolysis increases intramuscular lipid and glycogen use in vivo in humans. Wasserman, D. Four grams of glucose. Coggan, A. Effect of endurance training on hepatic glycogenolysis and gluconeogenesis during prolonged exercise in men.
Coyle, E. Carbohydrate feeding during prolonged strenuous exercise can delay fatigue. Horowitz, J. Lipid metabolism during endurance exercise. Kiens, B. Skeletal muscle lipid metabolism in exercise and insulin resistance. Stellingwerff, T. Significant intramyocellular lipid use during prolonged cycling in endurance-trained males as assessed by three different methodologies.
Spriet, L. An enzymatic approach to lactate production in human skeletal muscle during exercise. Brooks, G. The lactate shuttle during exercise and recovery. Miller, B. Lactate and glucose interactions during rest and exercise in men: effect of exogenous lactate infusion. Lactate elimination and glycogen resynthesis after intense bicycling. Hashimoto, T. Lactate sensitive transcription factor network in L6 cells: activation of MCT1 and mitochondrial biogenesis.
Takahashi, H. Metab 1 , — Scheiman, J. Meta-omics analysis of elite athletes identifies a performance-enhancing microbe that functions via lactate metabolism. Rennie, M. Effect of exercise on protein turnover in man. Wagenmakers, A. Carbohydrate supplementation, glycogen depletion, and amino acid metabolism during exercise. Howarth, K. Effect of glycogen availability on human skeletal muscle protein turnover during exercise and recovery.
McKenzie, S. Endurance exercise training attenuates leucine oxidation and BCOAD activation during exercise in humans. Wilkinson, S. Differential effects of resistance and endurance exercise in the fed state on signalling molecule phosphorylation and protein synthesis in human muscle.
Egan, B. Exercise metabolism and the molecular regulation of skeletal muscle adaptation. Cell Metab. New insights into the interaction of carbohydrate and fat metabolism during exercise. Hargreaves, M. Exercise metabolism: fuels for the fire. Cold Spring Harb. Richter, E. Muscle glycogenolysis during exercise: dual control by epinephrine and contractions.
Gaitanos, G. Human muscle metabolism during intermittent maximal exercise. Kowalchuk, J. In presynaptic terminals and postsynaptic dendritic compartments, more evidence is needed to understand the relative importance of neuronal and astrocytic glycolysis.
We now turn to the question of what cellular mechanisms may allow the transient excess of glycolysis over oxphos when neurons are stimulated. Neuronal activity requires the expenditure and resupply of metabolic energy. Rapid electrical signaling involves ion movement on the order of thousands of ions per millisecond per open channel, and the steady-state ion concentrations must be restored and maintained by ATP-dependent active transport.
Recycling and repackaging of neurotransmitters like glutamate and GABA into synaptic vesicles requires active transport, and the synaptic vesicles themselves must be retrieved, requiring additional energy. What signals coordinate the metabolic response to this energy demand? Both of these agents can regulate glycolysis and oxphos rates via multiple mechanisms. Also, for glycolysis and oxphos to run at different rates, there must be slippage or uncoupling at the interface between them: lactate-pyruvate partitioning controlled by the NADH CYT ratio.
ADP 3- enters the mitochondrial matrix through the adenine nucleotide translocase in exchange for ATP 4- , equivalent to one positive charge entering the mitochondrion; once inside, it interacts with the ATP synthase also known as complex V and is converted to ATP coordinately with the downhill transport of three protons from cytosol to matrix; an additional proton is transported to bring inorganic phosphate into the matrix.
The consumption of O 2 and matrix NADH correspond with two of the readily measured metabolic responses to neuronal stimulation. Oxygen consumption is monitored with a Clark-style electrochemical sensor of O 2 concentration; in brain slices, [O 2 ] shows a pronounced dip with stimulation, corresponding with increased O 2 consumption Hall et al. Upon stimulation of neurons in a brain slice Kann et al. Kann et al. An early study using two-photon microscopy of the NAD P H signal had claimed that although the dip occurred in neuronal mitochondria, the overshoot was evidence of glycolytic metabolism in astrocytic cytosol Kasischke et al.
Despite the ability, in principle, to segregate signals based on the actual spatial locations of astrocytes, they performed a pixel-by-pixel analysis with a low signal-to-noise ratio to argue that pixels showing a dip were likely to have a smaller overshoot. A study that instead used pharmacological inhibition of glycolysis but in the presence of 1 mM pyruvate as a mitochondrial fuel, which will incidentally suppress cytosolic NADH transients showed that much of the overshoot signal could not arise from glycolysis and instead must be mitochondrial in origin Brennan et al.
Extended intense stimulation may increase demand to the point that some glycolytic NADH also contributes to the autofluorescence signal; in addition, the quantitative contributions of glycolysis and oxphos can vary with oxygenation Ivanov et al.
If both components of the NAD P H signal are substantially mitochondrial in origin, then what accounts for the overshoot? This agrees with the results of Duchen and with the experimental and modeling studies in slice by Kann et al.
However, it is hard to reconcile this with the clear finding by Shuttleworth et al. Other possible sources of the NAD P H overshoot in the mitochondrial compartment would be an increased supply of pyruvate to mitochondria or increased NADH shuttling from the cytosol. An increased supply of pyruvate could occur with up-regulation of glycolysis though the increased production of pyruvate would be somewhat offset by conversion to lactate because of elevated NADH CYT. Clearly, we do not have a complete understanding of the oxphos-related mitochondrial signals that result from neuronal excitation.
The mechanisms that are engaged by neuronal excitation can vary with the degree of stimulation and with the environmental conditions of [glucose] and [O 2 ] during experiments, which usually vary from the in vivo condition, and the mechanisms may also vary with cell type. Uncoupling between glycolysis and oxphos involves the partitioning between pyruvate the primary substrate for glucose-driven oxphos and lactate.
Lactate is generally thought to be a terminal metabolite for glycolysis that must be converted back to pyruvate in the cytosol to serve as a substrate for oxphos Nelson and Cox, , though this is debated by some Schurr, For instance, it has been argued that pyruvate is limiting i.
Both of these effects suggest that elevated NADH CYT by itself can both affect glucose flux through glycolysis and shunt pyruvate toward lactate and away from utilization for oxphos. As discussed, there are three main influences corresponding with the dominant cytosolic NADH dehydrogenases in neurons Fig. This NADH will accumulate in the cell and ultimately inhibit continued glycolysis unless it is recycled by one of two recycling routes. The second recycling route is through malate dehydrogenase, usually as the first step in the MAS.
The shuttle is the primary route for moving reducing equivalents across the mitochondrial inner membrane because NADH itself does not cross. One key unsolved question is how neuronal glycolysis is triggered by neuronal activity. One additional possibility is that like cancer cells, astrocytes perform glycolysis not primarily for energy but rather for anabolic biosynthesis: For instance, astrocytes and not neurons express the phosphoglycerate dehydrogenase involved in serine biosynthesis Ehmsen et al.
This conversion of glucose to serine produces twice as much NADH as conversion of glucose to pyruvate although flux through the first pathway may be smaller.
Another likely contributor to elevated cytosolic NADH redox in astrocytes is diminished shuttling of redox equivalents to mitochondria via the MAS. What are the implications of higher cytosolic NADH redox in astrocytes? The clearest case for glial supply of energy to neurons is in ischemic situations, as shown best for white matter axons that can be supported by glial glycogen in the absence of an external supply of glucose Brown et al.
Shuttling of lactate from astrocytes to neurons may be physiologically important as a chronic resting process, but the most direct evidence argues that upon neuronal stimulation, the classical ANLS hypothesis does not apply and that instead, there is an increase in neuronal glycolysis accompanied by a smaller increase in neuronal oxphos.
The best direct evidence on this point is for neuronal cell bodies in both hippocampus and cerebral cortex, and it remains possible that an activity-dependent ANLS could function in specific subcellular compartments during activation; however, at this time, there is more evidence for direct glucose utilization in presynaptic terminals than evidence for lactate uptake.
This question about the geography of fuel utilization by neurons is a valuable target for future research. Finally, why might neurons temporarily allow glycolysis to exceed oxphos in the face of acute energy demand? One speculation is that glycolysis, although it produces a lower yield of ATP than oxphos, provides a faster resupply of energy.
Some evolutionary support for this speculation comes from muscle: fast-twitch muscle, requiring the greatest acute supply of energy, tends to be far more glycolytic and to have fewer mitochondria than the slow-twitch muscle used for postural control Crow and Kushmerick, ; Spriet, Neurons possess many mitochondria and rely chronically on them as a major source of ATP Hall et al.
There is also evidence that the glycolytic enzymes may be localized right where the neuron most requires acute resupply of ATP: at the plasma membrane and on the synaptic vesicles where major ion pumping is performed by transport ATPases Ikemoto et al. Certainly glycolysis alone is insufficient to power neuronal ion pumping Hall et al.
Further work is needed to test the idea that glycolysis is critical for fast energy resupply. Expression of ample levels of glycolytic and related enzymes in both astrocytes and neurons of the central nervous system.
Left: Transcriptional expression from quantitative RNA sequencing of the glycolytic enzymes and the cytosolic dehydrogenases associated with the NADH shuttles.
Data from Zhang et al. Right: Proteomics data Sharma et al. The data plotted are for cultured astrocytes and for cultured neurons at day-in-vitro Common names are given at the left, and gene names are shown between the two graphs. Note that in neurons, the expression level differences for LDH isoforms and for MCT isoforms are actually quite small using either measure of expression. The expression level for the cytosolic malate dehydrogenase MDH1 is substantially higher than for cytosolic glycerol-P-dehydrogenase GPD1 , consistent with the dominance of the MAS over the glycerol—phosphate shuttle.
Relationships of some major bioenergetic pools in the neuronal cytosol and mitochondria and their regulation. B The impact of neuronal stimulation on these pathways as measured experimentally by monitoring NAD P H autofluorescence is diagrammed.
Sign In or Create an Account. Advanced Search. User Tools. Sign In. Skip Nav Destination Article Navigation. Perspective May 11 Fueling thought: Management of glycolysis and oxidative phosphorylation in neuronal metabolism In Special Collection:. Gary Yellen Gary Yellen. This Site. Google Scholar. It is also important to evaluate the combination effects of glycolytic inhibitors and other therapeutic modalities such as chemotherapeutic agents and radiation, and develop optimal combination regimens for effective treatment of cancer.
J Biol Chem : — Lancet : — Baumann M, Brand K. Cancer Res 48 : — Cancer Investig 8 : — BMC Med Genet 6 : 39— Blood Cells Mol Dis 23 : — Biochem Biophys Res Commun : — Cancer Res 65 : — Cancer Res 55 : — Vet Hum Toxicol 38 : 85— Prot Sci 2 : 31— Pancreas 22 : 1—7. Int Rev Cytol : — Eur J Cancer 39 : — Brown J. Metabolism 11 : — Clin Cancer Res 4 : — Nature : — Bustamante E, Pedersen PL.
Biochim Biophys Acta : — Carew JS, Huang P. Mol Cancer 1 : 9— Leukemia 17 : — Exp Cell Res : — Annu Rev Pharmacol Toxicol 45 : — Eur J Biochem : — Clin Lab 51 : — Dastoor Z, Dreyer JL.
J Cell Sci : — Eur J Cancer 37 : — Drugs Today Barc 39 : — Anticancer Res 24 : — Cancer Res 64 : — Cancer Lett : — FEBS Lett : 47— Tumour Biol 12 : — Science : — Biochem Pharmacol 56 : — J Natl Cancer Inst 66 : — Ford WC.
Hum Reprod Update 12 : — Int J Cancer : — Antioxid Redox Signal 7 : — Nat Rev Cancer 4 : — Expert Rev Anticancer Ther 4 : — Cancer Res 62 : — Eur J Cancer 40 : — J Bioenerg Biomembr 29 : — Genes Dev 15 : — Clin Cancer Res 10 : — Harrison RA. Anal Biochem 61 : — Yeast 11 : — Br J Cancer 74 : — Ishitani R, Chuang DM. Toxicol Sci 62 : — Xenobiotica 27 : — Life Sci 78 : — Oncogene 22 : — Acta Neuropathol Berl 26 : — Cancer Lett : 83— Cancer Res 53 : — Cancer Res 63 : — Proteomics 6 : — Nutr Cancer 31 : — Crit Rev Eukaryotic Gene Expression 4 : 1— Biochemistry 40 : — Biochem Pharmacol 64 : — J Cell Biol : — Cancer Chemother Pharmacol 53 : — Mol Cell Biol 24 : — J Neurochem 31 : — Apoptosis 6 : — Anticancer Drugs 7 : — Cancer Invest 12 : — Cancer Res 64 : 31— Semin Cancer Biol 15 : — Cancer Res 50 : — Oncology 41 : 7— J Am Med Assoc : — Niederacher D, Entian KD.
Cancer Res 58 : — Br J Cancer 86 : — J Neurooncol 63 : 81— J Clin Oncol 21 : — Curr Med Chem 10 : — Familial Cancer 4 : 49— Drug Resist Update 7 : 97— J Neurosci Res 77 : 35— Ann Med 35 : — FEBS Lett : — Mol Cell Biol 23 : — Cancer Res 56 : — Biochem J : — Cancer Chemother Pharmacol 25 : 32— Br J Cancer 82 : — Cancer Cell 7 : 77— Novartis Found Symp : Serkova N, Boros LG. Am J Pharmacogenomics 5 : — NeuroReport 10 : — Strahlenther Onkol : — Singh KK. This would be why, with relative improvements in efficiency, the energy cost of an exercise can be reduced Figure 3 Table 2.
Table 2 Four energy system model and their percentage contribution to total energy output during all-out exercise of different durations [33]. Figure 3 Schematic of the proposed 4 pathway energy time line. Much research is based on sub maximal intensity and submaximal effort but these results are then used to extrapolate what is expected at higher intensity levels.
Actual measurement of world class performance is scant as it is usually deemed to be too difficult to achieve accurate results. We collected data on national and international level swimming performances immediately following completion of race events and used this to model the responses seen in this paper.
A model of three energy pathways, CP, Anaerobic and Aerobic has been used for a number of years. It has given overall definition to the use of energy systems but has not allowed many of the distinguishing points of exercise limitations to be explained.
A new model has been proposed based upon the recruitment of muscle fibre type and the difference in glycolysis and glycogenolysis. This adds a 4 th element to the pathway model.
By doing this we are able to accurately predict timelines to exhaustion in performance level sporting activities. This new model of explaining the time line of pathways at maximal effort, over both short time periods 20 sec and long time periods up to 60 minutes , has proved to be accurate in identifying what has taken place within the race performance.
Using data from this study, it has been possible to create a predictive tool that allows us to observe the individual response to high demand sporting events that matches the observations within the race.
This provides an accurate tool for assessing training outcome and suitability to ensure that the athlete is correctly prepared for their target events at target competitions. This is an open access article distributed under the terms of the, which permits unrestricted use, distribution, and build upon your work non-commercially.
Withdrawal Guidlines. Publication Ethics. Withdrawal Policies Publication Ethics. Research Article Volume 2 Issue 1. Keywords : Energy systems; Sports; Lactate system. Sec 5 24 48 CP 80 20 11 7 4 2 1.
Exercise Physiology: Exercise, performance and clinical applications. Mosby, USA; Gastin PB. Sports Med. Energy system contribution to m and m track running events. J Sci Med Sport. Energy system contribution to metre and metre track running.
J Sports Sci. Biochemical and ultrastructural changes of skeletal muscle mitochondria after chronic electrical stimulation in rabbits. Pedersen PK, Juel C. Gladden LB. Lactate metabolism during exercise. Principles of Exercise Biochemistry. Rushall B. Anaerobic capacity determined by max accumulated Oxygen deficit. J Appl Physiol. Astrand PO, Saltin B. Oxygen uptake during the first minutes of heavy muscular exercise. Variable resistance all-out test to generate accumulated oxygen deficit and predict anaerobic capacity.
Katch V. Kinetics of oxygen uptake and recovery for supramaximal work of short duration. Int Z Angew Physiol. Kavanagh MF, Jacobs I. Breath-by-breath oxygen consumption during performance of the Wingate test. Can J Sport Sci. Exercise Physiology, Theory and application to physical performance, 7th edn. Essentials of Exercise Physiology. Physiology of soccer: an update. Strong correlation of maximal squat strength with sprint performance and vertical jump height in elite soccer players.
Br J Sports Med. Exercise Physiology for Health. Fitness and Performance, 2nd ed. Benjamin Cummings, USA; Relationship among different performance tests to estimate maximal aerobic swimming speed.
Medicine and Science in Sports and Exercise. Sahlin K. Muscle glucose metabolism during exercise. Ann Med. Brooks GA. Importance of the crossover concept in exercise metabolism. Clin Exp Pharmacol Physiol. Wahren J, Ekberg K. Splanchnic regulation of glucose production.
Annu Rev Nutr. Richter EA, Hargreaves M. Exercise, GLUT4 and skeletal muscle glucose uptake. Physiol Rev. Blood glucose turnover during high and low intensity exercise. Am J Physiol. Interaction between aerobic and anaerobic metabolism during intense muscle contraction.
0コメント