Title: Fatigue and ergogenic aids


Key words: ergogenic aids, sports science, muscle fatigue, high intensity, low intensity, training, endurance, creatine, caffeine, creatine kinase, ATP, adenosine triphosphate, maximal effort, creatine phosphate, hydrolysis, lactate, supplementation, sprinting, cycling, anaerobic glycolysis, creatine loading, muscle creatine, protein synthesis, isometric, ATP flux, adrenaline, noradrenaline, fatty acid, cyclic adenosine monophosphate, cAMP, muscle glycogen, lipolysis, exhaustion, oxidation, catecholamines, glycogen phosphorylase, phosphodiesterase, glycogen breakdown, catabolism, sarcoplasmic reticulum, endoplastic reticulum, calcium, pathways, CNS, central nervous system, adenosine, receptors,  


Date: Oct 2006


Category: Sports


Nutrimed Module:


Type: Article


Author: Morgan, G


Fatigue and ergogenic aids

The increasing competitiveness and commercialisation of sport in recent years has led both to the increasing use of ergogenic aids to promote performance and their scientific and rational use in the field through sports science research. This has added to our knowledge of the physiology of muscle fatigue in both high intensity and endurance sport. The use of creatine and caffeine, which have been shown to be effective in combating these two types of fatigue, will be commented upon here.



Creatine, in the form of creatine phosphate, is essential for the regeneration of ATP during the the initial stages of high intensity anaerobic exercise, a reaction catalysed by creatine kinase. During the first 10 secs of maximal effort a high percentage of ATP is generated by creatine phosphate hydrolysis, but this rapidly declines so that, during the course of a 30 sec sprint for example, only some 25% of ATP is generated by this pathway (Spriet 1995). Creatine phosphate concentration is 5-10% higher in the Type II muscle fibres, functionally most suited to this type of exercise (Greenhaff 1994, Grindstaff 1997). Creatine phosphate hydrolysis also helps to consume hydrogen ions (Terjung et al. 2000), thus minimising lactate accumulation, a major factor in muscle fatigue.


The results of creatine supplementation in sprinting and cycling tasks lasting less than 30 secs appear to be marginal (Terjung et al. 2000). Given the fact that the maximum rate of ATP resynthesis is twice as great from creatine phosphate as it is from anaerobic glycolysis and creatine resynthesis occurs as quickly as 2 minutes (Haseler 1999), it is to be expected that the benefits of creatine loading would be more likely to show up during high intensity/repetitive exercise. Such regimes lead to a 5-10% increase in ATP production from creatine phosphate and significant improvements in repetitive high intensity sprinting or cycling tasks (Balsom 1993, Casey 1996, Maughan 1999, Williams 1999).


Individuals range from 0-40% in their ability to increase their dry muscle creatine content following creatine loading (Greenhaff 1993). Studies such as those of Harris (1992) show that performance gains are directly related to increased muscle creatine levels, those most creatine deficient showing the greatest gains. There is no evidence that creatine stimulates protein synthesis (Terjung et al. 2000) or increases muscular isometric force ((Vandenberghe 1996). Its effects appear to be due solely to increasing the rate of ATP flux during short-term high intensity exercise, allowing a greater work capacity by diminishing muscle fatigue (Casey 1996).



Costill (1978) originally proposed that caffeine, in promoting adrenaline and noradrenaline release, acted as a catalyst for free fatty acid mobilisation and oxidation, thus sparing muscle glycogen and prolonging the time to exhaustion in endurance exercise. Many studies are in support of this model and suggest that lipolysis is indirectly modulated by adrenaline and noradrenaline via cyclic adenosine monophosphate (cAMP) which is increased by caffeine ingestion (Zhang 1977). Other research, however, shows that exercise per se elevates the level of catecholamines and, in fact, caffeine may exert a depressant effect on lipolysis (Chesley 1995), possibly by promoting increased glycogen breakdown and lactate accumulation (Richter 1984,Anselme 1992).


The enzyme phosphodiesterase is inhibited by caffeine, prolonging the half life of cAMP (Beavo 1970, Fredholm 1990), but other enzymes involved in energy modulation such as Na/K ATPase and glycogen phosphorylase are also affected by caffeine (Spriet 1997), so the overall effect on fatty acid and carbohydrate catabolism is uncertain. cAMP also increases calcium release from the sarcoplasmic and endoplasmic reticulum (Weber 1968). This may explain the increased muscle power and diminished fatigueability noted in some research (Williams 1987, Jacobsen 1992).


Given, however, that the phosphodiesterase-dependant cAMP and the calcium pathways operate outside of the physiological range for caffeine (Fredholm 1995), present thinking favours a direct affect on the CNS as an explanation for the prolongation to exhaustion in both high intensity and endurance exercise. It is thought that this is mediated through adenosine receptors in the brain as caffeine has been shown to act as an adenosine antagonist (Graham 1994, Cole 1996, Doherty 2002). Further research needs to be done to clarify these major pathways leading to reduced muscle fatigue.



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