Metabolic factors in fatigue.

The supply of energy is of fundamental importance for the ability to sustain exercise. The maximal duration of exercise is negatively related to the relative intensity both during dynamic and static exercise. Since exercise intensity is linearly related to the rate of energy utilisation this suggests that energetic deficiency plays a major role in the aetiology of muscle fatigue. Characteristic metabolic changes in the muscle are generally observed at fatigue--the pattern being different after short term exercise (lactate accumulation and phosphocreatine depletion) from after prolonged exercise at moderate intensity (glycogen depletion). A common metabolic denominator at fatigue during these and many other conditions is a reduced capacity to generate ATP and is expressed by an increased catabolism of the adenine nucleotide pool in the muscle fibre. Transient increases in ADP are suggested to occur during energetic deficiency and may be the cause of fatigue. Experimental evidence from human studies demonstrate that near maximal power output can be attained during acidotic conditions. Decreases in muscle pH is therefore unlikely to affect the contractile machinery by a direct effect. However, acidosis may interfere with the energy supply possibly by reducing the glycolytic rate, and could by this mechanism be related to muscle fatigue.     

Repeated-sprint ability - part I: factors contributing to fatigue

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

Neural influences on sprint running: training adaptations and acute responses

Performance in sprint exercise is determined by the ability to accelerate, the magnitude of maximal velocity and the ability to maintain velocity against the onset of fatigue. These factors are strongly influenced by metabolic and anthropometric components. Improved temporal sequencing of muscle activation and/or improved fast twitch fibre recruitment may contribute to superior sprint performance. Speed of impulse transmission along the motor axon may also have implications on sprint performance. Nerve conduction velocity (NCV) has been shown to increase in response to a period of sprint training. However, it is difficult to determine if increased NCV is likely to contribute to improved sprint performance. An increase in motoneuron excitability, as measured by the Hoffman reflex (H-reflex), has been reported to produce a more powerful muscular contraction, hence maximising motoneuron excitability would be expected to benefit sprint performance. Motoneuron excitability can be raised acutely by an appropriate stimulus with obvious implications for sprint performance. However, at rest H-reflex has been reported to be lower in athletes trained for explosive events compared with endurance-trained athletes. This may be caused by the relatively high, fast twitch fibre percentage and the consequent high activation thresholds of such motor units in power-trained populations. In contrast, stretch reflexes appear to be enhanced in sprint athletes possibly because of increased muscle spindle sensitivity as a result of sprint training. With muscle in a contracted state, however, there is evidence to suggest greater reflex potentiation among both sprint and resistance-trained populations compared with controls. Again this may be indicative of the predominant types of motor units in these populations, but may also mean an enhanced reflex contribution to force production during running in sprint-trained athletes. Fatigue of neural origin both during and following sprint exercise has implications with respect to optimising training frequency and volume. Research suggests athletes are unable to maintain maximal firing frequencies for the full duration of, for example, a 100m sprint. Fatigue after a single training session may also have a neural manifestation with some athletes unable to voluntarily fully activate muscle or experiencing stretch reflex inhibition after heavy training. This may occur in conjunction with muscle damage. Research investigating the neural influences on sprint performance is limited. Further longitudinal research is necessary to improve our understanding of neural factors that contribute to training-induced improvements in sprint performance.     

Physiological determinants of endurance exercise performance

Performance in endurance events is typically evaluated by the power or velocity that can be maintained for durations of 30 min. to four hours. The two main by-products of intense and prolonged oxidative metabolism that can limit performance are the accumulation of hydrogen ion (i.e. lactic acidosis) and heat (i.e. hyperthermia). A model for endurance performance is presented that revolves around identification of the lactate threshold velocity which is presented as a function of numerous morphological components as well as gross mechanical efficiency. When cycling at 80 RPM, gross mechanical efficiency is positively related to Type I muscle fiber composition, which has great potential to improve endurance performance. Endurance performance can also be influenced by altering the availability of oxygen and blood glucose during exercise. The latter need forms the basis for ingesting carbohydrate at 30-60 grams per hour during exercise. In laboratory simulations of performance, athletes fatigue due to hyperthermia when esophageal is approximately 40 degrees C, in association with near maximal heart rate and perceived exertion. It is likely that the central nervous system is involved in the aetiology of fatigue from hyperthermia. Dehydration during exercise promotes hyperthermia by reducing skin blood flow, sweating rate and thus heat dissipation. The combination of dehydration and hyperthermia during exercise causes large reductions in cardiac output and blood flow to the exercising musculature, and thus has a large potential to impair endurance performance. Endurance performance is optimized when training is aimed specifically at developing individual components of the model presented and nutritional supplementation prevents hypoglycemia and attenuates dehydration and hyperthermia. Indeed, the challenge at the transition to a new millennium is to synergistically integrate these physiological factors in training and competition.     

Physiological models to understand exercise fatigue and the adaptations that predict or enhance athletic performance

A popular concept in the exercise sciences holds that fatigue develops during exercise of moderate to high intensity, when the capacity of the cardiorespiratory system to provide oxygen to the exercising muscles falls behind their demand inducing "anaerobic" metabolism. But this cardiovascular/anaerobic model is unsatisfactory because (i) a more rigorous analysis indicates that the first organ to be affected by anaerobiosis during maximal exercise would likely be the heart, not the skeletal muscles. This probability was fully appreciated by the pioneering exercise physiologists, A. V Hill, A. Bock and D. B. Dill, but has been systematically ignored by modern exercise physiologists; (ii) no study has yet definitely established the presence of either anaerobiosis, hypoxia or ischaemia in skeletal muscle during maximal exercise; (iii) the model is unable to explain why exercise terminates in a variety of conditions including prolonged exercise, exercise in the heat and at altitude, and in those with chronic diseases of the heart and lungs, without any evidence for skeletal muscle anaerobiosis, hypoxia or ischaemia, and before there is full activation of the total skeletal muscle mass, and (iv) cardiovascular and other measures believed to relate to skeletal muscle anaerobiosis, including the maximum oxygen consumption (VO2 max) and the "anaerobic threshold", are indifferent predictors of exercise capacity in athletes with similar abilities. This review considers four additional models that need to be considered when factors limiting either short duration, maximal or prolonged submaximal exercise are evaluated. These additional models are: (i) the energy supply/energy depletion model; (ii) the muscle power/muscle recruitment model; (iii) the biomechanical model and (iv) the psychological model. By reviewing features of these models, this review provides a broad overview of the physiological, metabolic and biomechanical factors that may limit exercise performance under different exercise conditions. A more complete understanding of fatigue during exercise, and the relevance of the adaptations that develop with training, requires that the potential relevance of each model to fatigue under different conditions of exercise must be considered.     

Muscle fatigue during high-intensity exercise in children

Children are able to resist fatigue better than adults during one or several repeated high-intensity exercise bouts. This finding has been reported by measuring mechanical force or power output profiles during sustained isometric maximal contractions or repeated bouts of high-intensity dynamic exercises. The ability of children to better maintain performance during repeated high-intensity exercise bouts could be related to their lower level of fatigue during exercise and/or faster recovery following exercise. This may be explained by muscle characteristics of children, which are quantitatively and qualitatively different to those of adults.Children have less muscle mass than adults and hence, generate lower absolute power during high-intensity exercise. Some researchers also showed that children were equipped better for oxidative than glycolytic pathways during exercise, which would lead to a lower accumulation of muscle by-products. Furthermore, some reports indicated that the lower ability of children to activate their type II muscle fibres would also explain their greater resistance to fatigue during sustained maximal contractions.The lower accumulation of muscle by-products observed in children may be suggestive of a reduced metabolic signal, which induces lower ratings of perceived exertion. Factors such as faster phosphocreatine resynthesis, greater oxidative capacity, better acid-base regulation, faster readjustment of initial cardiorespiratory parameters and higher removal of metabolic by-products in children could also explain their faster recovery following high-intensity exercise.From a clinical point of view, muscle fatigue profiles are different between healthy children and children with muscle and metabolic diseases. Studies of dystrophic muscles in children indicated contradictory findings of changes in contractile properties and the muscle fatigability. Some have found that the muscle of boys with Duchenne muscular dystrophy (DMD) fatigued less than that of healthy boys, but others have reported that the fatigue in DMD and in normal muscle was the same. Children with glycogenosis type V and VII and dermatomyositis, and obese children tolerate exercise weakly and show an early fatigue. Studies that have investigated the fatigability in children with cerebral palsy have indicated that the femoris quadriceps was less fatigable than that of a control group but the fatigability of the triceps surae was the same between the two groups.Further studies are required to elucidate the mechanisms explaining the origins of muscle fatigue in healthy and diseased children. The use of non-invasive measurement tools such as magnetic resonance imaging and magnetic resonance spectroscopy in paediatric exercise science will give researchers more insight in the future.     

Can any metabolites partially alleviate fatigue manifestations at the cross-bridge?

During exercise, intracellular homeostasis depends on the matching of adenosine triphosphate (ATP) supply and ATP demand. Metabolites play a useful role in communicating the extent of ATP demand to the metabolic supply pathways. During fatigue from high-intensity exercise, a major change in the intracellular milieu of skeletal muscle is not ATP depletion but metabolite accumulation that affects the actomyosin cross-bridge interaction. The resulting reduction in myosin ATPase activity, cross-bridge turnover rate, and velocity of contraction can be considered a useful downregulation of ATP demand. Although maximal force is reduced, it is reduced less than myosin ATPase activity. In combination, efficiency of force production at the cross-bridge is thus enhanced. This is a second useful role for metabolites during fatigue because the total ATP cost per unit of force is partially reduced. Theoretical models predict that ADP may alleviate some effects of fatigue by further enhancing cross-bridge efficiency, thus providing a third useful role for metabolite accumulation. Recent experimental evidence reviewed here suggests that this occurs when ATP concentration is dramatically reduced. Single-fiber chemical analyses of fatigued muscle show lower ATP concentrations than other methods, but whether the appropriate microenvironments for effective competition by ADP for the nucleotide binding site occur around some or all of the cross-bridges remains technically difficult to prove at this time. During fatigue, muscle activation is also decreased, a response that potentially has the greatest effect on ATP demand-supply matching. I propose that the mismatch between the expected force production relative to muscle activation and the reduced force production from inorganic phosphate accumulation is the peripheral signal for reduced activation and is therefore the fourth useful role of metabolites in alleviating fatigue.     

Reliability of repeated sprint exercise in non-motorised treadmill ergometry

Although repeated sprint tests are relatively common, there have been few investigations of repeated sprint exercise using non-motorised treadmill ergometry. The purpose of this study was to determine the reliability of a repeated sprint procedure using this apparatus. Ten healthy, active males, performed three repeated sprint tests (six repetitions of 6 s sprints with 30 s recovery) on three separate occasions. Performance as determined by maximal speed, average force production, and fatigue were compared across the three trials. Maximal speed and average force were not significantly different between visits (p < 0.05) and a variety of reliability measures suggested good agreement (e.g., coefficient of variations no more than 5 %). The fatigue indices for maximal speed and for average force were generally less reliable (coefficients of variation around 30 % in both cases). In conclusion, measures of performance (maximal speed and average force) can provide reliable results in a repeated sprint protocol but the reliability of fatigue measures appears to be low.     

Effect of wearing an ice cooling jacket on repeat sprint performance in warm/humid conditions

OBJECTIVE: To examine the effect of cooling the skin with an ice jacket before and between exercise bouts (to simulate quarter and half time breaks) on prolonged repeat sprint exercise performance in warm/humid conditions. METHODS: After an initial familiarisation session, seven trained male hockey players performed two testing sessions (seven days apart), comprising an 80 minute intermittent, repeat sprint cycling exercise protocol inside a climate chamber set at 30 degrees C and 60% relative humidity. On one occasion a skin cooling procedure was implemented (in random counterbalanced order), with subjects wearing an ice cooling jacket both before (for five minutes) and in the recovery periods (2 x 5 min and 1 x 10 min) during the test. Measures of performance (work done and power output on each sprint), heart rates, blood lactate concentrations, core (rectal) and skin temperatures, sweat loss, perceived exertion, and ratings of thirst, thermal discomfort, and fatigue were obtained in both trials. RESULTS: In the cooling condition, chest (torso) skin temperature, thermal discomfort, and rating of thirst were all significantly lower (p<0.05), but no significant difference (p>0.05) was observed between conditions for measures of work done, power output, heart rate, blood lactate concentration, core or mean skin temperature, perceived exertion, sweat loss, or ratings of fatigue. However, high effect sizes indicated trends to lowered lactate concentrations, sweat loss, and mean skin temperatures in the cooling condition. CONCLUSIONS: The intermittent use of an ice cooling jacket, both before and during a repeat sprint cycling protocol in warm/humid conditions, did not improve physical performance, although the perception of thermal load was reduced. Longer periods of cooling both before and during exercise (to lower mean skin temperature by a greater degree than observed here) may be necessary to produce such a change.     

Neural control of force output during maximal and submaximal exercise

A common belief in exercise physiology is that fatigue during exercise is caused by changes in skeletal muscle metabolism. This 'peripheral' fatigue results either from substrate depletion during submaximal exercise or metabolite accumulation during maximal exercise in the exercising muscles. However, if substrate depletion alone caused fatigue, intracellular ATP levels would decrease and lead to rigor and cellular death. Alternatively, metabolite accumulation would prevent any increase in exercise intensity near the end of exercise. At present, neither of these effects has been shown to occur, which suggests that fatigue may be controlled by changes in efferent neural command, generally described as 'central' fatigue. In this review, we examine neural efferent command mechanisms involved in fatigue, including the concepts of muscle wisdom during short term maximal activity, and muscle unit rotation and teleoanticipation during submaximal endurance activity. We propose that neural strategies exist to maintain muscle reserve, and inhibit exercise activity before any irreparable damage to muscles and organs occurs. The finding that symptoms of fatigue occur in the nonexercising state in individuals with chronic fatigue syndrome indicates that fatigue is probably not a physiological entity, but rather a sensory manifestation of these neural regulatory mechanisms.     

Effects of prior warm-up regime on severe-intensity cycling performance

PURPOSE: The purpose of the present study was to determine the effect of three different warm-up regimes on cycling work output during a 7-min performance trial. METHODS: After habituation to the experimental methods, 12 well-trained cyclists completed a series of 7-min performance trials, involving 2 min of constant-work rate exercise at approximately 90% VO2max and a further 5 min during which subjects attempted to maximize power output. This trial was performed without prior intervention and 10 min after bouts of moderate, heavy, or sprint exercise in a random order. Pulmonary gas exchange was measured breath by breath during all performance trials. RESULTS: At the onset of the performance trial, baseline blood [lactate] was significantly elevated after heavy and sprint but not moderate exercise (mean +/- SD: control, 1.0 +/- 0.3 mM; moderate, 1.0 +/- 0.2 mM; heavy, 3.0 +/- 1.1 mM; sprint, 5.9 +/- 1.5 mM). All three interventions significantly increased the amplitude of the primary VO2 response (control, 2.59 +/- 0.28 L x min(-1); moderate, 2.69 +/- 0.27 L x min(-1); heavy, 2.78 +/- 0.26 L x min(-1); sprint, 2.78 +/- 0.30 L x min(-1)). Mean power output was significantly increased by prior moderate and heavy exercise but not significantly reduced after sprint exercise (control, 330 +/- 42 W; moderate, 338 +/- 39 W; heavy, 339 +/- 42 W; sprint, 324 +/- 45 W).Conclusions: These data indicate that priming exercise performed in the moderate- and heavy-intensity domains can improve severe-intensity cycling performance by ~2-3%, the latter condition doing so despite a mild lactacidosis being present at exercise onset.     

Effects of prior exercise on metabolic and gas exchange responses to exercise

'Warm-up' activity is almost universally performed by athletes prior to their participation in training or competition. However, relatively little is known about the optimal intensity and duration for such exercise, or about the potential mechanisms primed by warm-up that might enhance performance. Recent studies demonstrate that vigorous warm-up exercise that normally results in an elevated blood and presumably muscle lactate concentration has the potential to increase the aerobic energy turnover in subsequent high-intensity exercise. The reduced oxygen deficit is associated with a reduction in both the depletion of the intramuscular phosphocreatine stores and the rate at which lactic acid is produced. Furthermore, the oxygen uptake 'slow component' that develops during high-intensity, ostensibly submaximal, exercise is attenuated. These factors would be hypothesised to predispose to increased exercise tolerance. Interestingly, the elevation of muscle temperature by prior exercise does not appear to be implicated in the altered metabolic and gas exchange responses observed during subsequent exercise. The physiological mechanism(s) that limit the rate and the extent to which muscle oxygen uptake increases following the onset of exercise, and which are apparently altered by the performance of prior heavy exercise, are debated. However, these mechanisms could include oxygen availability, enzyme activity and/or availability of metabolic substrate, and motor unit recruitment patterns. Irrespective of the nature of the control mechanisms that are influenced, 'priming' exercise has the potential to significantly enhance exercise tolerance and athletic performance. The optimal combination of the intensity, duration and mode of 'warm-up' exercise, and the recovery period allowed before the criterion exercise challenge, remain to be determined.     

两种恢复方式对士兵冲刺间歇训练效果的影响

 目的 探讨冲刺间歇训练时两种恢复方式(积极性恢复 vs. 消极性恢复)对士兵运动能力和训练效果的影响。方法 选取18名男性武警士兵完成6组冲刺间歇训练(30 s Wingate全力蹬车试验),间歇期(4 min)分别进行消极性恢复(即在功率自行车上休息)和积极性恢复(以1.1 W/kg负荷继续蹬车),每次Wingate试验时(不包括间歇期)记录峰值功率(PP)、平均功率(MP)、疲劳指数(FI)、总做功(TW)和心率(HR)等参数。结果 与消极性恢复比较,积极性恢复PP在第2次Wingate试验时降低(P<0.05),MP和HR在第4~6次Wingate试验时升高,差异均有统计学意义(P<0.05),FI和TW差异无统计学意义(P>0.05)。结论 积极性恢复可提高冲刺间歇训练后期的训练效果, 士兵应根据训练方案选择合理的恢复方式。     

Effect of a previous sprint on the parameters of the work-time to exhaustion relationship in high intensity cycling

The relationships between both metabolic (E) and mechanical (W) energy expended and exhaustion time (t(e)), was determined for 11 well-trained subjects during constant load cycloergometric exercises at 95, 100, 110, 115 % maximal aerobic power performed both from rest and, without interruption, after an all-out sprint of 7 s. These relationships were well described by straight lines: y = a + bt(e), where b was taken as the critical power (metabolic and mechanical) that can be sustained for long periods of time. b was unaffected by the exercise conditions and amounted to 82 - 94 % of maximal aerobic metabolic and mechanical power. The constant a was taken as the anaerobic stores capacity in excess of the O2 deficit. When the test was preceded by the sprint, a (metabolic and mechanical) was reduced to about 60 - 70 % of control values. This reduction was essentially equal to the corresponding E and W output during the sprint. These data support the view that the slope of linear regressions of E and W on t(e) is indeed a measure of the critical power, whereas the y intercept of these same regressions is a measure of the anaerobic capacity.     

Carbohydrate nutrition and fatigue.

Carbohydrates are important substrates for contracting muscle during prolonged, strenuous exercise, and fatigue is often associated with muscle glycogen depletion and/or hypoglycaemia. Thus, the goals of carbohydrate nutritional strategies before, during and after exercise are to optimise the availability of muscle and liver glycogen and blood glucose, with a view to maintaining carbohydrate availability and oxidation during exercise. During heavy training, the carbohydrate requirements of athletes may be as high as 8 to 10 g/kg bodyweight or 60 to 70% of total energy intake. Ingestion of a diet high in carbohydrate should be encouraged in order to maintain carbohydrate reserves and the ability to train intensely. Ingestion of a high carbohydrate meal 3 to 4 hours prior to exercise ensures adequate carbohydrate availability and enhances exercise performance. Although hyperinsulinaemia associated with carbohydrate ingestion in the hour prior to exercise may result in some metabolic alterations during exercise, it may not necessarily impair exercise performance and may, in some cases, enhance performance. Carbohydrate ingestion during prolonged, strenuous exercise, where performance is often limited by carbohydrate availability, delays fatigue. This is due to maintenance of blood glucose levels and a high rate of carbohydrate oxidation, rather than a slowing of muscle glycogen utilisation, although liver glycogen reserves may be spared. During recovery from exercise, muscle glycogen resynthesis is critically dependent upon the ingestion of carbohydrate. Factors influencing the rate of muscle glycogen resynthesis include the timing, amount and type of carbohydrate ingested and muscle damage. Adequate carbohydrate availability before, during and after exercise will maintain carbohydrate oxidation during exercise and is associated with enhanced exercise performance.     

The effects of hockey protective equipment on high-intensity intermittent exercise

PURPOSE: To examine the impact of hockey protective equipment on thermal and fluid homeostasis and power output, during a high-intensity, intermittent, exercise protocol. We hypothesized that protective equipment would increase core temperature and reduce sprint power after a simulated hockey game. METHODS: Eight men (26.8 +/- 1.7 yr) performed a repeated sprint test before and at the completion of a prolonged intermittent exercise protocol (game simulation) on a cycle ergometer under typical hockey ambient conditions. Reduction in exercise performance was calculated by comparing the pre- and postgame repeated sprint power outputs. The protocol was performed twice; once while wearing cotton undergarments only (NOPADS), and once while wearing cotton undergarments and the typical protective equipment worn during a hockey game (PADS). RESULTS: During the simulated game, skin temperatures (34.12 +/- 0.24 degrees C vs 28.85 +/- 0.31 degrees C) and core temperature accumulated area under the curve (70.85 +/- 8.52 vs 48.21 +/- 3.05 degrees C.min) were elevated in PADS versus NOPADS, respectively (P < 0.05). Sweat loss as a percent of body mass was greater in PADS versus NOPAD, as were working and recovery heart rates. Plasma lactate concentration was also higher after the simulated game in PADS versus NOPADS (9.64 vs 5.96 mM, P < 0.05). When comparing post- with pregame sprint power output, both peak and mean power outputs were reduced in PADS (P < 0.05), whereas NOPADS values were unchanged. CONCLUSIONS: Reduced power output at the completion of the simulated game in PADS was attributed to an elevated body temperature, dehydration, and a greater accumulation of blood lactate.     

Interactive processes link the multiple symptoms of fatigue in sport competition

Muscle physiologists often describe fatigue simply as a decline of muscle force and infer this causes an athlete to slow down. In contrast, exercise scientists describe fatigue during sport competition more holistically as an exercise-induced impairment of performance. The aim of this review is to reconcile the different views by evaluating the many performance symptoms/measures and mechanisms of fatigue. We describe how fatigue is assessed with muscle, exercise or competition performance measures. Muscle performance (single muscle test measures) declines due to peripheral fatigue (reduced muscle cell force) and/or central fatigue (reduced motor drive from the CNS). Peak muscle force seldom falls by >30% during sport but is often exacerbated during electrical stimulation and laboratory exercise tasks. Exercise performance (whole-body exercise test measures) reveals impaired physical/technical abilities and subjective fatigue sensations. Exercise intensity is initially sustained by recruitment of new motor units and help from synergistic muscles before it declines. Technique/motor skill execution deviates as exercise proceeds to maintain outcomes before they deteriorate, e.g. reduced accuracy or velocity. The sensation of fatigue incorporates an elevated rating of perceived exertion (RPE) during submaximal tasks, due to a combination of peripheral and higher CNS inputs. Competition performance (sport symptoms) is affected more by decision-making and psychological aspects, since there are opponents and a greater importance on the result. Laboratory based decision making is generally faster or unimpaired. Motivation, self-efficacy and anxiety can change during exercise to modify RPE and, hence, alter physical performance. Symptoms of fatigue during racing, team-game or racquet sports are largely anecdotal, but sometimes assessed with time-motion analysis. Fatigue during brief all-out racing is described biomechanically as a decline of peak velocity, along with altered kinematic components. Longer sport events involve pacing strategies, central and peripheral fatigue contributions and elevated RPE. During match play, the work rate can decline late in a match (or tournament) and/or transiently after intense exercise bursts. Repeated sprint ability, agility and leg strength become slightly impaired. Technique outcomes, such as velocity and accuracy for throwing, passing, hitting and kicking, can deteriorate. Physical and subjective changes are both less severe in real rather than simulated sport activities. Little objective evidence exists to support exercise-induced mental lapses during sport. A model depicting mind-body interactions during sport competition shows that the RPE centre-motor cortex-working muscle sequence drives overall performance levels and, hence, fatigue symptoms. The sporting outputs from this sequence can be modulated by interactions with muscle afferent and circulatory feedback, psychological and decision-making inputs. Importantly, compensatory processes exist at many levels to protect against performance decrements. Small changes of putative fatigue factors can also be protective. We show that individual fatigue factors including diminished carbohydrate availability, elevated serotonin, hypoxia, acidosis, hyperkalaemia, hyperthermia, dehydration and reactive oxygen species, each contribute to several fatigue symptoms. Thus, multiple symptoms of fatigue can occur simultaneously and the underlying mechanisms overlap and interact. Based on this understanding, we reinforce the proposal that fatigue is best described globally as an exercise-induced decline of performance as this is inclusive of all viewpoints.     

Metabolic and performance effects of warm-up intensity on sprint cycling

Warm-up is generally considered beneficial for performance, although the reduction in anaerobic glycolytic metabolism may be detrimental to sprinting. This study examined the effect of warm-up intensity on metabolism and performance in sprint cycling. The mean power was determined during a 1-min sprint on 11 trained males preceded by easy (WE), moderate (WM) or hard (WH) warm-up and a 10-min recovery. Aerobic, anaerobic glycolytic and phosphocreatine energy provision to the sprint was determined from oxygen uptake and lactate production. Blood lactate concentration before the sprint increased with the warm-up intensity (WE: 1.2±0.3; WM: 2.0±0.3; WH: 4.2±0.9 mmol/L, P<0.001), with WH reducing the increase in lactate production during exercise vs WE (WE: 11.6±1.6; WM: 10.9±1.9; WH: 9.2±1.4 mmol/L, P<0.05). Despite the lower relative anaerobic glycolytic energy provision in WH vs WE (WH: 38±5; WM: 36±6; WE: 34±3%, P<0.05), the mean power was unaffected (WE: 516±28; WM: 521±26; WH: 526±34 W, P>0.05) due to increased oxygen uptake in WH during the sprint (WE: 3.2±0.4; WM: 3.3±0.3; WH: 3.4±0.4 liters, P<0.05). This study supports a warm-up-induced reduction in glycolytic rate, although sprint performance, at least of a long duration, may be maintained due to increased oxygen utilization.