Chapter I: Introduction
Muscle fatigue has been defined as a failure to maintain force during a sustained or repeated contraction - Muscle Fatigue introduction. Fatigue is an important factor in physical therapy because it may precede injury. Improved performance may decrease or delay the onset of fatigue. Fatigue affects performance in normal individuals and even more in individuals with specific diseases. When fatigue is present the result is usually undesirable; inability to perform an expected work load or the risk of injury. It is a self-protective mechanism against damage of contractile machinery of muscle. A better understanding of the physiological mechanisms behind muscular fatigue will assist the therapist in designing and establishing more scientifically sound treatment protocols for improving a person’s muscle strength and endurance. In addition, designing the most effective methods of recovery from fatigue as they relate to the type, intensity and duration of exercise, will be beneficial for improved performance.
More Essay Examples on Muscle Rubric
Through the years many factors have been studied to find the answer behind muscular fatigue. One of the basic questions facing investigators of muscular fatigue is which factor is causing it or is it a combination of factors under different situations. The events leading to a voluntary muscular contraction involve several links in a controlling chain of command from the brain to actin-myosin cross bridges. Fatigue may be due to impairment at one or more of the links in this chain (Gibson & Edwards, 1985). Indeed some have argued that literally every step in the chain of events for muscle contraction could be a site for fatigue.
A. Central vs. Peripheral Fatigue:
Fatigue can be characterized into two categories: Central and Peripheral. Central fatigue refers to poor motivation, altered central nervous system transmission, or recruitment. Peripheral fatigue refers to impairment of the function of the peripheral nerves, neuromuscular junction transmission, electrical activity of muscle fibers or processes of activation within the fiber.
Bigland-Ritchie and colleagues (1986) have shown that for maximal contractions lasting 45 to 60 seconds, central fatigue does not seem to be a problem despite 50% loss of overall force generating capacity. Thus, they conclude that force generating capacity could result mainly or entirely from failure of the muscle contractile apparatus or peripheral factors. Merton, who maximally stimulated the adductor pollicis muscle (via motor nerves or motor end points ) and compared forces developed to that of maximum voluntary contractions, found no differences between the two forces and concluded that fatigue was peripheral in origin (Asmussen, 1979). According to Edstrom and Grimby, central fatigue presumably has no role in the sports field (Macintosh, 1991).
B. Possible Mechanisms For Muscular Fatigue:
Energy substrate depletion, accumulation of extracellular potassium, excessive lactate buildup and decreased calcium ion release from the sarcoplasmic reticulum have all been studied as important factors contributing to muscular fatigue. During intense exercise lactic acid is formed and accumulates in the muscle. With this increase there is a decrease in the ability to perform work. There is experimental evidence to show that a decrease in intracellular pH related to the increase in hydrogen ions associated with lactate production, could explain the force reduction observed during fatigue (Duchateau et al, 1987). The decrease in pH interferes with the formation of cross bridges between the actin-myosin complex by competing with the calcium ion on its binding site on the protein troponin. The decrease of the number of active actin-myosin interactions results in a decrease contractile force.
Another factor involved in muscle fatigue is depletion of calcium ion in the muscle sarcomere. The biomechanical processes in the sarcomere require high levels of calcium ion secretion from the terminal cistern of the sarcoplasmic reticulum to enable it to bind the molecules covering the binding sites for the cross bridges. Calcium ion is then taken up again by the sarcoplasmic reticulura for reuse. If the firing rates are excessive, there is less time for the reuptake and calcium ion depletion in the reticulum prevents muscle contraction. Vollestad and Sejersted speculate that decreased calcium ion availability for release from the sarcoplasmic reticulum might contribute to a gradual decline in force generating capacity during all types of exercise (Vollestad, & Sejersted, 1988).
Another factor associated with muscle fatigue is the loss of intracellular potassium to the extracellular space during contraction. Potassium is lost from the muscle fibers and is exchanged with sodium which decreases the muscle membrane potential. Sjogaard (1983) suggests that this change in electrolyte concentration may impair muscle contraction and that the lack of potassium in the working muscle is a limiting factor in the contractility of the muscle. In 1986 Sjogaard (1986) concluded that intracellular potassium loss may well impair the excitability of the muscle membrane and thereby the contractility of the muscle fibers.
Muscle glycogen concentration decreases continuously during prolonged intense exercise. Which may suggest that glycogen depletion may contribute to muscle fatigue. It has been known that carbohydrates are one of the primary sources of energy during exercise. Therefore some researchers believe that intramuscular glycogen stores is one of the most important limiting factors of performance capacity during exhaustive exercise.
Chapter II: Muscle Fatigue and Lactic Acid Accumulation
There is strong evidence that during high intensity work, fatigue is associated with the accumulation of lactic acid. A decrease in intracellular pH, related to the increase in hydrogen ion concentration associated with lactate production, could well explain the force reduction observed during fatigue.
A. Aerobic and Anaerobic Glycolysis:
In a muscle cell during exercise there is a rapid breakdown of glycogen to glucose by the enzyme phosphorylase a. Muscle fatigue during brief intense exercise occurs long before the muscle glycogen stores are depleted. Thus, lack of muscle glycogen cannot account for mechanical failure in brief intense exercise. However, it may account for failure in long duration, low intensity exercise.
In the cytoplasm of the muscle cell the glucose that was released from glycogen is converted to pyruvic acid through a series of reactions called glycolysis. Glycolysis liberates some of the energy from glucose for ATP, and it also releases some hydrogens. The hydrogen electrons released in glycolysis bind to the coenzyme NAD+ to form NADH. During moderate levels of energy metabolism when enough oxygen is available to the cells, the hydrogen electrons on NADH are transported into the mitochondria and oxidized to form water and more ATP. A “steady state” exists because hydrogen is oxidized at about the same rate as it is made available. This condition is called aerobic glycolysis and it produces pyruvic acid rather than lactic acid. The pyruvic acid produced by glycolysis also enters the mitochondria to generate still more ATP. The mitochondrial metabolism of both NADH and pyruvic acid, however, requires oxygen.
In strenuous exercise, when energy demands exceed oxygen supply or rate of utilization, all of the hydrogen joined to NADH cannot be processed by the mitochondria. For glycolysis to continue to produce some ATP, the NADH must be converted back to NAD+, otherwise glycolysis would stop. In anaerobic glycolysis, NAD+ is formed when NADH combines with pyruvic acid Once lactic acid is formed, it diffuses into the blood where much of it is carried away for metabolism at the liver. In this way, glycolysis can proceed to give additional anaerobic energy for the resynthesis of ATP.
Although lactic acid formation is an inefficient way of utilizing glycogen for ATP production, it has several advantages over the aerobic ATP forming processes:
1. The maximal rate of ATP production from anaerobic glycolysis is about 2 times higher than from oxidative phosphorylation.
2. ATP production from glycolysis can increase from a low resting
level to the maximal power in less than 5 seconds, which is in contrast to aerobic ATP production which requires a long time to reach the maximal power (2-3 minutes), because it has to adjust the oxygen transport system.
3. Glycolytic ATP production can occur in the absence of oxygen. Anaerobic ATP production would occur when the energy demand is high or when rapid fluctuations occur in the energy demand (Newsholme, 1981).
During exercise lactate may be released into the blood and may accumulate in the muscle cell if exercise is sufficiently intense. This is related to a significant ATP synthesis via glycolysis (anaerobic energy production). Anaerobic exercise implies strenuous, high intensity activities. When this exercise is performed for longer than a few seconds muscular fatigue impairs performance.
B. The Anaerobic Threshold:
The anaerobic threshold denotes an exercise intensity where the metabolism is between aerobic ATP production and anaerobic ATP production through lactic acid formation. The importance of the concept anaerobic threshold is that exercise above this intensity results in a increase in lactic acid. As the level of lactic acid in the blood and muscles increases, it indicates that the formation of ATP cannot keep up with its use and fatigue sets in (Maclaren et al, 1989). This is related to the quality of the muscle fiber composition and the training status of the musculature.
C. Muscle Fiber Types:
In the human being, all muscles have varying percentages of fast twitch and slow twitch muscle fibers. The basic differences between the fast twitch (type 2B) and the slow twitch (type 1) fibers are the following:
1. The enzymes that promote rapid release of energy from the ATP-CP energy systems are two to three times as active in fast twitch as in slow twitch fibers, thus making the maximal
power that can be achieved by fast twitch fibers as great as two times that of slow twitch fibers.
2. Slow twitch fibers are mainly organized for endurance, especially for generation of aerobic energy. They have far more mitochondria than the fast twitch fibers. In addition, the
enzymes of the aerobic metabolic system are more active in slow twitch fibers than in fast twitch fibers.
3. The number of capillaries per mass of fibers is greater in the vicinity of slow twitch fibers than in the vicinity of fast twitch fibers.
In summary, fast twitch fibers can deliver extreme amounts of power for short periods of time. On the other hand slow twitch fibers provide endurance, delivering prolonged strength of contraction over much longer periods of time (Guyton, 1991).
D. Fiber Types, Lactic Acid and Fatigue:
In general it can be concluded that the more fast twitch muscle fibers are recruited, the more lactate is formed and accumulated. As a consequence a subject with a high proportion of fast twitch muscle fibers will form more lactate at the same exercise intensity than one with a lower proportion. It seems reasonable to suggest that these aspects of lactate metabolism are important to muscle power and endurance capacity.
Exercise of short duration and high intensity recruits predominantly fast glycolytic fibers and uses anaerobic glycolysis for the synthesis of the majority of ATP needed for muscle contraction, with accumulation of lactic acid. At a pH of 6.5, 99.8% of lactic acid is ionized and therefore there is also an increase in hydrogen ion concentration (Macintosh, 1991).
Hydrogen ions increase in response to high intensity exercise in response to the use of anaerobic glycolysis, mostly by type 2 fibers. Ions accumulate as nearly all lactic acid is ionized at physiological pH. Most of the hydrogen ions are buffered. pH changes then are the result of the approximately 0.001% of unbuffered hydrogen ions (Katz et al, 1986).
In a study done by Hultman and Spriet this increase in hydrogen ion concentration is expected in the highly glycolytic fast twitch fibers early in stimulation. Progressive failure to activate the fast twitch fibers could account for the decreasing force during the initial 15 minutes and the lower force (25-30% of peak) in the final 30 minutes of stimulation (Hultman et al, 1981).
The results recorded in Duchateau, deMontigny and Hainaut on the human flexor carpi ulnaris indicate that this muscle, which contains proportionally more fast twitch fibers than adductor pollicis, does not resist fatigue as well as the adductor pollicis, which contains proportionally more slow twitch fibers. This is supported by their observation that during fatigue tests the alteration in tetanus time course is larger in flexor carpi ulnaris and is coherent with the finding that lactate production is greater in fast than in slow twitch fibers. In strong sustained contractions the blood circulation is partially occluded and the diffusion of lactate is inhibited. This can explain why lactate concentration increases more after sustained than after intermittent contractions.
This intracellular acidosis will in turn reduce the activity of the glycolytic enzymes. A reduction of the enzyme activity will lead to a reduced rate of glycolysis and, thus, a reduced rate of ATP resynthesis. A reduction in pH limits the conversion of the inactive phophorylase b form to the active a form mostly by inhibition of phosphorylase b kinase (PFK). PFK is commonly thought of as a rate limiting enzyme of glycolysis and has been considered to be inactivated at a pH of 6.5 (Bigland-Ritchie et al, 1986). Control of the regulatory glycolytic enzymes would prevent a high rate of glycogen utilization and accumulation of hydrogen ions, therefore leaving aerobic metabolism as the only major ATP production for muscular contraction (Hultman et al, 1981).
E. An EMG Study:
In a study showing the relationship between muscle lactate accumulation and surface EMG activities during isokinetic contractions, the mean frequency of the surface EMG recorded from the vastas lateralis was decreased while the time lag of torque production after the onset of electrical activity was increased during exercise. These changes corresponded well to muscle lactate accumulation in the same muscle. It was concluded that the changes in the frequency components of the EMG and in the contractile property of the muscle during short term intense exercise correlated with lactate accumulation in the identical muscle, and that the decrease in efficiency of the electrical activity in the muscle suggested peripheral fatigue. They also suggested fatigue might be due to the decrease in propagation velocity of action potentials along the muscle fiber as a result of lactate accumulation within the working muscle (Hogan & Welch, 1986).
The suggestion that hydrogen ion accumulation inhibits the generation of action potentials in excitable membranes by causing physical changes in the arrangement of membrane proteins or as a result of the electric field generated by their charge has been made. Since conduction velocity is directly related to membrane excitability, an increase in acidity in the environment of the membrane would be expected to cause a decrease in membrane conduction velocity. The effects of hydrogen ion accumulation have been outlined above in connection with predominantly anaerobic exercise. In long term, low intensity exercise the lactic acid production and decrease in pH are comparatively small (Macintosh, 1991).
F. Fatigue and Buffer Capacity:
The magnitude of the decrease in muscle pH is determined by the degree of lactic acid accumulation and by the ability of the muscle to buffer hydrogen ions. If the low muscle pH is the limiting factor for high intensity exercise then a higher buffering capacity of the muscle would enable the muscle to accumulate more lactic acid and have a higher anaerobic work capacity. It was reported that 8 weeks of anaerobic training increased the buffer capacity by 37%. The increased buffer capacity in this study also enabled the subjects to accumulate more lactic acid. The amount of energy derived from anaerobic processes was increased and the capacity to perform exercise was also increased accordingly (Newsholme, 1981).
Chapter III. Decreasing Muscle Fatigue during Exercise
A. Importance of Carbohydrates: Muscle Glycogen and Fatigue
The introduction of the muscle biopsy technique to nutritional studies in the 1960s led to the discovery that a high carbohydrate diet undertaken for three days resulted in an elevated muscle glycogen content (Bergstrom et al., 1967). The effect was an increase in time to exhaustion when cycling an ergometer at 75% max compared to a mixed diet, and to a diet high in fat. The same research group also observed that a more pronounced effect could be obtained if the muscle glycogen levels were depleted by exercise before undertaking a high carbohydrate regime for 3 days. Under such circumstances, muscle glycogen concentrations of 4 g per 100 g wet muscle were obtained. This muscle biopsy technique was used to further demonstrate that muscle glycogen concentrations fell during prolonged exercise, and that the very low levels coincided with the development of fatigue. Thus it was concluded that depletion of muscle glycogen caused fatigue.
Since there is much evidence relating muscle glycogen depletion to fatigue during prolonged and possible to high-intensity exercise, there needs to be a consideration as to how much and when to consume carbohydrates in order to replenish the depleted stores. Costill et al. (1981) observed the effects of feeding meals containing 188, 325, 525 or 648 g of carbohydrate in a 24-h period following a 16-km run at approximately 80% max, which was in turn followed by five 1-min sprints corresponding to an exercise intensity of approximately 130% max. The exercise resulted in a 60% decrease in muscle glycogen content, which was only restored when 525-648 g of carbohydrate was consumed; the consumption of 188-325 g of carbohydrate failed to restore muscle glycogen content in a 24-h period. Other studies have reported similar findings insofar as rates of glycogen re-synthesis after depletion were maximal when 0.7-3.0gkg−1 carbohydrate was consumed every 2 h (Blom et al., 1987).
B.Fatigue and Importance of Fluids
Although reductions in muscle and liver glycogen and their consequent restoration are understood to be major factors in the combating fatigue during prolonged exercise, the loss of body fluids leading to dehydration may be another important cause. Mild dehydration will impair performance and reduce the capacity for exercise; a decrease in body weight of 5% due to fluid loss (i.e. 3.5 kg for a 70-kg person) can result in a 30% decrease in physical work capacity (Saltin and Costill, 1988). Fluid loss during exercise is associated with the need to maintain a relatively constant body temperature. Exercise results in an increased production of energy, both metabolic and heat, and it is as a consequence of this that body temperature becomes elevated. Maughan (1991) estimated that the rate of heat production of running a marathon in 2 h 30 min is approximately 80 kJ min−1 (20 kcal min−1). Since the major biological mechanism for losing heat during exercise is by evaporation of sweat, this will result in the loss of 2 l h−1 if all the 4.8 MJ (1200 kcal) of heat is to be removed by this route. This rate is possible, and would lead to a total loss of 3 l during a soccer match, as its intensity is comparable to the energy expenditure of marathon running (Reilly, 1990). A loss of 3 l represents a 4% loss of body weight for a 70-kg person. It has been reported that a 2% body weight decrease due to dehydration results in impaired performance, and as previously stated a 5% decrease in body weight results in a 30% decrease in work capacity (Saltin and Costill, 1988). Clearly there is a need to ensure that dehydration is minimized.
Prolonged exercise in a warm environment results in a significant fluid loss. It would seem quite rational therefore to conclude that the best way of replenishing fluid loss would be to ingest water. Certainly evidence was available from the early 1970s that the rate of gastric emptying from the stomach became compromised if glucose was added to water (Saltin and Costill, 1988), and this led to the widespread favouring of water over carbohydrate drinks. Subsequently the gastric emptying characteristics of many different fluids have been studied, and the results confirm the inhibitory effects of adding calories to water. The rate at which fluids are absorbed by the body is a combination of the rate of gastric emptying and the rate of fluid uptake by the small intestine. It is not advisable therefore to draw conclusions about fluid absorption based solely on gastric emptying rates despite the fact that gastric emptying is slower than fluid uptake by the small intestine. It is conceivable that whilst a dilute glucose drink may reduce the rate of gastric emptying in comparison to water, the glucose stimulation of fluid uptake by the small intestine results in a similar overall rate of fluid absorption. Many studies have been performed to determine the advantages of water or carbohydrate- electrolyte solutions on performance either in the laboratory or in field conditions (Shirreffs and Maughan, 2000). Such studies have invariably concentrated on the enhancement of exercise time to exhaustion rather than on improvements in time to complete a set distance. The advantage of some form of fluid over a no-fluid treatment is well established. What is less clear is whether water had any advantages over a carbohydrate-based fluid or vice versa. When dehydration is believed to be the major factor impairing performance, such as in prolonged exercise in the heat, then ingesting as much water as is deemed necessary to offset dehydration is advisable. The consensus view in the UK is that a sports drink which contains an energy source in the form of carbohydrate together with electrolytes is more effective than plain water in maintaining performance (British Journal of Sports Medicine, 1993).
Many recent studies of the beneficial effects of carbohydrate ingestion on performance have been reported (Coyle, 1991). Factors such as type of carbohydrate, concentration of carbohydrate, and timing of ingestion have been considered. The primary purpose of carbohydrate ingestion during exercise is to maintain blood glucose concentrations, and if the exercise is prolonged, to maintain carbohydrate oxidation rates in the later stages. This would permit continuation of exercise at an adequate intensity. The purpose of carbohydrate ingestion after exercise is to restore the muscle and liver glycogen stores as quickly as possible. When carbohydrate supplementation is provided during prolonged exercise, subjects can exercise for longer, feel less fatigue and produce greater power at the end of such a performance than when given nothing or indeed when provided with water alone (Coggan and Coyle, 1991). So carbohydrate supplementation is recommended whenever the exercise is likely to be severe enough to significantly deplete glycogen stores and so impair performance.
In most of the studies that have been reported where carbohydrate ingestion improved combating of fatigue, subjects were given 30-60gh−1 (Coggan and Coyle, 1991). These authors had previously reported that the glucose infusion rate necessary to restore and maintain blood glucose levels late in exercise and thereby delay fatigue by 45 min was 1 g min−1 or 60 g h−1 (Coggan and Coyle, 1991). It has been shown that glucose infusion can result in a glucose utilization rate of 1.8 g min−1. It appears that the maximum rate at which a carbohydrate can be utilized is approximately 120 g h−1. In order to consume 60 g h−1 of a carbohydrate, it is possible to do so in the following manner: (1) 300 ml of a 20% solution; (2) 600 ml of a 10% solution; (3) 1200 ml of a 5% solution; (4) 2400 ml of a 2% solution. The first drink would appear to be too concentrated and may compromise fluid intake whilst the last drink is too large a volume to ingest in 1 h. The two other drinks would appear to be reasonable; although 600 ml may not be sufficient in fluid intake on a hot and humid day, whilst a 10% concentration of glucose (but not maltodextrin) may inhibit gastric emptying.
C.Fatigue, Caffeine and Creatine
Caffeine is a stimulant in high concentrations, and elicits a number of physiological and psychological responses linked with increasing endurance performance and decreasing of fatigue. The effects are mainly due to an elevation in plasma fatty acids and a consequent sparing of muscle glycogen (Giles and MacLaren, 1984). The International Olympic Committee (IOC) has banned caffeine and set a threshold level of 12 µg ml−1 for urine samples. This may be achieved by ingesting approximately 800 mg of caffeine, comparable to drinking six cups of coffee or 17.5 cans of cola in a short time. In spite of the evidence that caffeine stimulates the release of fatty acids and possibly spare muscle glycogen stores, the research findings are equivocal. Consuming carbohydrate with caffeine negates the fatty acid stimulatory effect of caffeine, and so this combination would have no ergogenic influence. It should also be recognized that caffeine is a diuretic and could lead to dehydration.
Short-duration high-intensity exercise requires the regeneration of ATP primarily from the breakdown of CP and from anaerobic glycolysis. A significant reduction of CP occurs after 6-s of cycle sprinting. A 16% decrease in CP after ten 6-s cycle sprints has been reported and this coincided with a reduction in power output (Gaitanos et al., 1993). Depletion is greater in FG than SO fibres (Greenhaff et al., 1992). It seems that the availability of CP is one of the limiting factors for maintaining the high rates of energy necessary for this type of activity.
Harris et al. (1992) demonstrated that ingestion of 20-30 g of creatine monohydrate per day for more than two days increased the muscle creatine content by up to 50%. Subsequent studies have shown that creatine supplementation resulted in improved performance during repeated 30-s bouts of maximal isokinetic exercise (Greenhaff et al., 1992), during repeated bouts of 6-s sprint cycling, and during 300 and 1000 m running time (Harris et al., 1993). Furthermore, CP re-synthesis during recovery from intense activity was enhanced following supplementation (Greenhaff et al., 1992).
D.Fatigue and Alkalinizers
Sodium bicarbonate and sodium citrate are alkaline salts that possess buffering properties in the human body when ingested. The theory behind their use is relatively simple. If a build-up of lactic acid occurs due to intense exercise, the resultant increase in acidity or reduction in pH is likely to be a contributory factor in the development of fatigue (MacLaren et al., 1989). Alkalinizers increase the normal alkali reserve of the blood and help buffer the acid produced during exercise. Furthermore, the increase in bicarbonate ions in the blood may facilitate the efflux of hydrogen ions from the muscle and thereby maintain a higher pH in the muscle (MacLaren, 1997). Theoretically and practically, alkaline salts enhance performance in events maximising the use of anaerobic glycolysis (i.e. intense exercise lasting between 30 and 120 s), and also intense intermittent exercise where removal of lactic acid from muscle during recovery is required. Maximal exercise tasks of less than 30 s and prolonged endurance tasks such as 5-10 km runs, which rely primarily on oxidative processes, generally do not benefit from the use of alkalinizers (Gledhill, 1984). Sodium bicarbonate ingestion may improve running time to exhaustion at an exercise intensity corresponding to a lactate concentration of 4 mmoll−1; an increase of 17% in time to exhaustion from approximately 26 to 31 min was observed in runners by George and MacLaren (1988). An alternative source of alkalinizer in the form of sodium citrate has been used with limited success. However, Potteiger et al (1996) successfully tested the application of sodium citrate and indicated increase in performance in cycling group at 3% comparing with placebo group.
Asmussen, E. (1979). Muscle fatigue. Medicine and Science in Sports. Vol. 11, No. 4, pp. 313-321.
Bergstrom, J., Hermansen, L., Hultman, E. and Saltin, B. (1967). Diet, muscle glycogen and physical performance. Acta Physiologica Scandinavica, 71: 140-50.
Bigland-Ritchie, F. Furbush and J.J. Woods (1986). Fatigue of intermittent submaximal voluntary contractions: central and peripheral factors. J. Appl. Physiol. 61(2): 421- 429.
Blom, P.C., Hostmark, A.T., Vaage, O. et al. (1987). Effect of different post-exercise sugar
diets on the rate of muscle glycogen synthesis. Medicine and Science in Sports and Exercise, 19: 491-6.
British Journal of Sports Medicine (1993). Consensus statement on fluid replacement in sport and exercise. British Journal of Sports Medicine, 27: 34.
Duchateau, J., L. de Montigny and K. Hainaut. (1987). Electro mechanical failures and lactate production during fatigue. Eur. J. Appl. Physiol. 56: 287-291
Coggan, A.R. and Coyle, E.F. (1991). Carbohydrate ingestion during prolonged exercise.
Effects on metabolism and performance. Exercise and Sports Science Reviews, 19:1-40
Coyle, E.F. (1991). Timing and method of increased carbohydrate intake to cope with heavy
training, competition and recovery. Journal of Sports Sciences, 9: S29-52
Costill, D.L., Sherman, W.M., Fink, W.J. et al. (1981). The role of dietary carbohydrates in
muscle glycogen resynthesis after strenuous running. American Journal of Clinical Nutrition, 34: 1831-6
Gibson, H. and R.H.T. Edwards (1985). Muscular exercise and fatigue. Sports Medicine. 2: 120-132.
Guyton, A.C., Sports Physiology. (1991). Textbook of Medical Physiology. W.B. Saunders Company, Philidelphia, p.945.
Hogan, M.C. and H.G. (1986). Welch. Effect of altered arterial oxygen tensions on muscle metabolism in dog skeletal muscle during fatiguing work. Am. J. Physiol. 251(20):
Hultman, E., H. Sjoholm, K. Sahlin and L. Edstrom. (1981). Glycolytic and oxidative energy metabolism and contraction characteristics of intact human muscle. Human muscle
fatigue: physiological mechanisms. Pitman Medical, London (Ciba Foundation symposium 82) pp 19-40.
Katz, A., Sahlin, K. and J. Henriksson.(1986). Muscle ATP turnover rate during isometric contraction in humans. J. Appl. Physiol. 60(6): 1839-1842.
Maclaren, D.P.M., H. Gibson, M. Parry-Billings and R. H.T. Edwards. (1989) A review of metabolic and physiological factors in fatigue. Exercise and Sport Science Review.
Macintosh, B.R. (1991). Skeletal muscle staircase response with fatigue or dantrolene sodium. Med. Sci. Sports Exerc. Vol. 23, No. 1, pp 56-63.
Maughan, R.J. (1991). Fluid and electrolyte loss and replacement in exercise. Journal of Sports Sciences, 9, 117-42.
Newsholme, E.A. (1981). The glucose/fatty acid cycle and physical exhaustion. Human muscle fatigue: physiological mechanisms. Pitman Medical, London, (Ciba Foundation symposium 82) pp 89-101
Potteiger, J.A., Nickel, G.L., Webster, M.J., Haub, M.D., & Palmer, R.J. (1996). Sodium
citrate ingestion enhances 30-km cycling performance. International Journal of Sports Medicine, 17, 7-11.
Reilly, T. (1990). Football, in Physiology of Sports (eds T. Reilly, N. Secher, P. Snell and C.
Williams), E & FN Spon, London, pp. 371-425.
Saltin, B. and Costill, D.L. (1988). Fluid and electrolyte balance during prolonged exercise,
in Exercise, Nutrition, and Metabolism, (eds E.S. Horton and R.L. Terjung), Macmillan, New York, pp. 150-8
Shirreffs, S.M. and Maughan, R.J. (2000). Rehydration and recovery of fluid balance after
exercise. Exercise and Sports Science Reviews, 28: 27-32.
Sjogaard, G. (1983). Electrolytes in slow and fast muscle fibers of humans at rest and with dynamic exercise. Am. J. Physiol. 245(14): R25-31.
Sjogaard, G. (1986). Water and electrolyte fluxes during exercise and their relation to muscle fatigue. Acta Physiol. Scand. 128(Suppl. 556): 129-136.
Vollestad, N.K. and O.M. Sejersted. (1988) Biochemical correlates of fatigue. Eur. J. Appl. Physiol. 57: 336-347.