• Muscle strength produced during physical activity depends to a large extent by the formation of chemical energy (ATP) by the anaerobic and aerobic metabolism. • The Fatigue develops when you run out the elements that are used to produce ATP, or when there is an accumulation of metabolic byproducts. • These metabolic changes can cause fatigue by acting on the nerve processes that activate muscles. Both the central and peripheral nervous system may be compromised. • The reduction in muscle levels of ATP, phosphocreatine, and glycogen, and low availability of glucose in the blood can affect the performance of skeletal muscle. A low concentration of glucose in the blood can have a negative effect on the function of the central nervous system. • An increase in the levels of intramuscular magnesium, ADP, inorganic phosphate, hydrogen ions and free radicals impair muscle function. Other factors that contribute to fatigue, probably by acting on the central nervous system, have a greater presence of ammonia and hyperthermia. • Appropriate training programs and nutritional interventions improve physical endurance and athletic performance by improving the ability of muscles to extend the production of ATP. INTRODUCTION Adenosine triphosphate (ATP) is the main source of chemical energy for muscle contraction. Given the scarcity of intramuscular stores of ATP, the continuous regeneration is critical for the maintenance of muscle power needed during intense physical activity. The high-intensity exercise (for example as when shooting) is made possible thanks to the production of ATP by anaerobic process, following the breakdown of phosphocreatine (PCr) or degradation of muscle glycogen to lactate. In contrast, when the lower power outputs, such as during prolonged exercise (endurance), the aerobic glycolysis of carbohydrates (muscle glycogen and glucose that is formed in the blood) and lipids (fatty acids derived from triglyceride present in the muscles and adipose tissue) provides virtually all the ATP required for cellular processes. These metabolic processes and their importance during exercise have long been studied (Coyle, 2000; Sahlin et al., 1998). Much attention has been paid to the potential mechanisms of fatigue during exercise and metabolic factors that affect those changes. These factors can be defined as depletion of energy sources (ATP and other biochemical compounds used in the production of ATP) and accumulation of metabolic byproducts (Table 1). TABLE 1 Metabolic factors in fatigue Depletion of energy sources ATP Phosphocreatine (Pcr) muscle glycogen Glucose that is created in the blood metabolic by-products Magnesium ions (Mg2) Adenosine phosphate (ADP) Inorganic phosphate (Pi) Lithium lactate Hydrogen ions (H) ammonia free Radicals heat RESEARCH REVIEW Potential sites of fatigue Fatigue is a multifactorial process that reduces the exercise and athletic performance. It can be generally defined as the inability or reduced effectiveness in maintaining the strength and power required or expected. Although fatigue may involve different organs, the more attention is paid to the skeletal muscles and their ability to generate force. Therefore, when assessing potential areas of fatigue, one must take into account all the stages involved in the activation of the muscles. All this is well summarized in Figure 1, which shows the locations of fatigue ie those processes that can be affected by the lack of energy sources and / or accumulation of metabolic byproducts. For the experts in the industry it is common to consider in addition to the main mechanisms including those related to the peripheral etiology of fatigue because, of course, both levels help to reduce muscle performance during exercise. For more detailed information can be found in two comprehensive Fitts, 1994; Gandevia, (2001). Exhaustion of sources Reduced availability of basic biochemical substrates involved in energy production limits the supply of ATP during exercise and compromise the function of the muscles and the central nervous system. These include PCr, muscle glycogen and glucose in the blood. ATP. Many research studies have shown that the concentration of ATP in samples of muscle fibers is mixed well protected during intense exercise, although drops of 30-40% approximately. However, in analyzes of single muscle fibers, ATP levels can fall to a greater extent in type II fast after intense physical activity and limit the ability of these fibers to contribute to the production of power (Casey et al., 1996). In addition, there may be small, for times and districts in the availability of ATP for micro-local modifications of certain key enzymes related to ATP (myosin ATPase, Na + / K + ATPase, sarcoplasmic reticulum Ca2 + ATPase), and within the channels of Ca2 + release of the sarcoplasmic reticulum. That the decrease in ATP can contribute to fatigue has been demonstrated by Dutka and Lamb (2004) on mice. In their experiments, a decrease in ATP concentration impaired the excitation-contraction coupling and force production in muscle fibers of the skin. In men, during intense physical activity and short-term and in the latter stages of prolonged strenuous exercise, a certain increase in breakdown of ATP, implies that the level of utilization of ATP exceeds resynthesis of the same (Sahlin et al. , 1998). PCr. Another high-energy phosphate, PCr plays an important role in the supply of ATP during muscle activity (PCr + ADP Cr + ATP). The levels of PCr can be almost depleted after maximal exercise (Bogdanis et al., 1995, Casey et al., 1996), and this lack of PCr to the rapid decline in power output that occurs after this kind of physical activity (Sahlin et al., 1998). The recovery of the ability to generate power at maximum power after activity is closely linked to the resynthesis of PCr (Bogdanis et al., 1995). Increased muscle PCr availability is a possible explanation for the enhanced performance very intense, on a par with what is observed with creatine supplementation in the diet (Greenhaff & Casey, 2000). PCr levels can be reduced in many muscle fibers during fatigue during prolonged and almost maximum, which coincides with the depletion of muscle glycogen as a reflection - probably - an inability to maintain a sufficient degree of resynthesis of ATP (Sahlin et al., 1998). However, not all studies have observed such changes in phosphates during prolonged physical activity (Baldwin et al., 2003). Muscle glycogen. The association between fatigue and decreased muscle glycogen stores during prolonged, strenuous exercise has been studied regularly for almost 40 years (Hermansen et al., 1967). Early studies from Scandinavia the use of glycogen loading which can improve performance in events lasting longer than 90 minutes (Hawley et al., 1997). The availability of muscle glycogen is also important for the maintenance phase in the high-intensity intermittent activity (Balsom et al., 1999). The relationship between glycogen depletion and muscle fatigue has been proposed as an inability to maintain a sufficient level of ATP resynthesis secondary to reduced availability of pyruvate and other key metabolic intermediates (Sahlin et al., 1990). By contrast, another study had shown little disruption to the muscle levels of ATP, PCr and other metabolic intermediates after physical activity to fatigue if you had availability in pre-exercise muscle glycogen (Baldwin et al. , 2003). It can not, however, exclude the possibility of depletion of glycogen in key areas within the muscle, which can not be determined with certainty from a biopsy sample. Or, it is possible that the consumption of glycogen causes fatigue of other mechanisms. For example, it has been observed that muscle glycogen depletion impairs the excitation-contraction coupling (Chin & Allen, 1997; Stephenson et al., 1999). Regardless of the underlying mechanisms, there is a strong relationship between muscle glycogen depletion and fatigue during prolonged, strenuous exercise. Blood glucose. When you are not of glucose supplementation (eg carbohydrate intake), the levels of glucose in the blood decline progressively during prolonged exercise, as glycogen in the liver runs out. The availability of smaller quantities of glucose is in connection with a worst oxidation of carbohydrates and with fatigue, while increasing glucose levels, as a consequence of carbohydrate intake increase the oxidation of carbohydrates and improve endurance performance (Coyle et al., 1983, 1986). This is in part due to enhanced glucose uptake in muscle (McConell et al., 1994) and a positivization energy balance muscle (Spencer et al., 1991), but apparently not to a reduction in the use of muscle glycogen (Coyle et al., 1986). Because glucose is the key substrate for the brain, low blood glucose (hypoglycemia) help to reduce the absorption of glucose in the brain and thereby a central fatigue (Nybo & Secher, 2004). Therefore, the ergogenic benefi t of carbohydrate ingestion during prolonged strenuous exercise can be caused by a cerebral energy balance and the conservation of central neural drive (Nybo & Secher, 2004). Recent studies have shown a development of physical and mental functions with carbohydrate intake during intermittent exercise that kind of team sports. (Welsh et al., 2002; Winnick et al., 2005). Accumulation of metabolic byproducts The activation of the metabolic pathway that produces ATP also results in increased levels of several metabolic byproducts that potentially contribute to fatigue. These include magnesium (Mg2 +), ADP, inorganic phosphate (Pi), lactate ion and hydrogen ion (H +), ammonia (NH3), free radicals and heat. Mg2 +, ADP, Pi. If you experience a rapid breakdown of ATP and PCr, increase the levels of Mg2 +, ADP and Pi in skeletal muscle. An increase in the Mg2 + inhibits the release of Ca2 + from the sarcoplasmic reticulum and damages the production of power, especially when combined with the decreased levels of ATP in the muscle (Dutka & Lamb, 2004). High concentrations of ADP can reduce power and slow muscle relaxation of the muscles by impairing the contractile fibers and absorption of Ca2 + in the lattice scarcoplasmatico (MacDonald & Stephenson, 2004). An increase of Pi also reduces, the contractile force and the release of Ca2 + from the sarcoplasmic reticulum. The latter effect appears to be due to the degradation of calcium phosphate within the sarcoplasmic reticulum (Allen & Westerblad, 2001). Finally, increases in ADP and Pi reduce the release of energy during the collapse of ATP (Sahlin et al., 1998). Lactate, H +. The rapid depletion of glycogen and glucose in the muscles during intense exercise causes a large increase in the production of lactic acid. Generally, the lactate ion does not seem to have an adverse effect on the ability of skeletal muscle to generate force, although the literature is full of conflicting information. Of greater consequence, however, the increase in the intramuscular concentration of H + (lower pH and acidosis) connected to a high rate of depletion of ATP, the oxidative ATP production and movement of strong ions such as K +, the membrane the muscle cell. Many scientists are of the opinion that the increase in H + can interfere with the excitation-contraction coupling and force production in the myofilaments. However, in many studies of isolated muscle at physiological temperatures, acidosis did not appear to exert major negative effects. Consistent with these findings, some observations that maximal isometric force (Sahlin & Ren, 1989) and the dynamic power (Bogdanis et al., 1995) recover fairly quickly after intense exercise, despite the fact that a persistently low muscle pH. In contrast, the ability to maintain isometric force and power production in humans is compromised by acidosis, with a possible explanation is the reduced ATP turnover (Sahlin & Ren, 1989). Note that in human skeletal muscle, acidosis may inhibit the breakdown of glycogen (Spriet et al., 1989) and aerobic ATP production (Jubrias et al., 2003). In addition, intake of sodium bicarbonate, an alkalizing agent, enhances time to fatigue during high-intensity exercise followed by a series of repeated sprints (Costill et al., 1984); However, it is difficult to separate the various mechanisms that cause fatigue in such conditions. It important to know that a major adaptation to fast (sprints and sprint) (Sharp et al., 1986) and, interval high intensity (Weston et al., 1997) is an aid to the buffering capacity of skeletal muscles . Ammonia (NH3). Ammonia is produced by skeletal muscle as a byproduct of the breakdown of ATP or amino acids. During exercise, increases the release of NH3 from contracting skeletal muscle in the blood and as a result you will have an increase in plasma ammonia levels. Given that this substance can cross the blood-brain barrier, an increase in plasma NH3 increases their absorption in the brain that can affect neurotransmitters and cause general fatigue (Nybo & Secher, 2004). Are needed, however, more detailed studies to be able to fully examine the role of ammonia in the etiology of fatigue. We know that carbohydrate intake reduces the accumulation of NH3 in the plasma (Snow et al., 2000) and the uptake in the brain (Nybo & Secher, 2004) during prolonged exercise, and what makes it even more secure l importance and ergogenic effects of carbohydrate intake. Another aspect of central fatigue during prolonged exercise involves the possible interactions between the branched chain amino acids (BCAA, leucine, isoleucine and valine), the absorption of tryptophan and brain serotonin levels. Tryptophan is a precursor of serotonin and tryptophan uptake by the brain is connected both to its concentration in plasma, which in its report in the plasma concentration compared to that of amino acids. During exercise, the degradation in plasma BCAA levels and the increase in tryptophan may result in increased levels of serotonin in the brain and therefore the sense of general fatigue (Nybo & Secher, 2004). E was proposed taking of BCAA as a strategy to maintain plasma levels and reduce the absorption of tryptophan by the brain, but does not seem to be effective (Van Hall et al., 1995). A better strategy might be the intake of carbohydrates, which absorb the increase in free fatty acids as a result of physical activity. (Since free fatty acids and tryptophan compete for binding sites on albumin in plasma, the lower level of fatty acids during exercise is achieved by the intake of carbohydrates, reduces the growth of the ratio free tryptophan / BCAA (Davis et al., 1992).) Free radicals. During exercise, aerobic metabolism and other cellular reactions can give rise to free radicals such as the anions (negative ions) of hydrogen peroxide and superoxide (Reid, 2001). In small quantities, these metabolites play an important role in the regulation of skeletal muscle function, but their accumulation causes fatigue (Barclay & Hansel, 1991; Moopanar & Allen, 2005). There are many enzymatic antioxidants (superoxide dismutase, catalase, glutathione peroxidase) within skeletal muscle that cause the degradation of free radicals, and there are also non-enzymatic antioxidants such as reduced glutathione, beta-carotene and vitamins C and E that act against free radicals (Reid, 2001). The administration of compound N-acetylcysteine (mucolytics) may increase the non-enzymatic antioxidant activity in the muscle. This effect is linked to a reduced fatigue during muscle stimulation (Reid et al., 1994) and an improvement in the performance of life for well-trained cyclists (Medved et al., 2004). Studies with supplements of vitamin E and C are equivocal, but the antioxidant levels of endogenous enzymes increased by training. Heat. Approximately 20% of the oxygen consumed during exercise is converted into mechanical work, the rest is converted into heat, the major metabolic byproduct of strenuous exercise. Although much of this heat is dissipated, a particularly high levels of intensity and outdoor temperatures and humidity, you can generate a significant increase in body temperature (hyperthermia), which causes fatigue and, in extreme cases, even death. Hyperthermia can affect both central and peripheral processes involved in the production of muscle strength and power (Nybo & Secher, 2004; Todd et al., 2005) and impairs the performance of sprinters and distance runners (Gonzalez-Alonso et al., 1999 ). Among the strategies designed to minimize the negative impact from the high temperature at a general level and at the level of the muscle on the athletic performance, there are heat acclimatization, cooling the pre-race (Gonzalez-Alonso et al. 1999) and fluid intake (Hamilton et al., 1991). CONCLUSIONS The production of ATP with anaerobic and aerobic process in skeletal muscle is crucial for the maintenance of strength and for the production of power during exercise. However, the depletion of sources and the accumulation of metabolic by-products are possible causes of fatigue. Reduced availability of PCr limits the power output during sprint exercise, where the lack of carbohydrates is a major limitation for cross-country skiers. During sprint exercise, the increase in Pi and H + may contribute to the onset of fatigue during prolonged strenuous exercise, the accumulation of NH3, free radicals and heat can limit performance. Appropriate training programs and a proper education food are potential strategies to improve the fatigue resistance and, consequently, athletic performance.
Posted on: Sun, 24 Aug 2014 16:49:45 +0000
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