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Letters |
Exercise and Sports Science Laboratories and School of Human Movement Studies Charles Sturt University, Bathurst NSW 2795, Australia
Email: fmarino{at}csu.edu.au
The study by Ross et al. (2007) represents a significant advancement in the understanding of muscular fatigue following long duration exercise and perhaps finally establishes that the brain ‘decides’ how much drive to the muscle is directed in the postexercise period. Ross et al. (2007) established that, following a marathon, the voluntary activation and force output of the tibialis anterior immediately postexercise was significantly reduced. The authors also reported that the maximal voluntary contraction (MVC) of the wrist flexors was not reduced following the marathon. This protocol where the subsequent force output and voluntary activation of the ‘used’ muscles (in this case the tibialis anterior) are compared with that of the ‘unused’ muscles (wrist flexors) in the preceding exercise has been used previously to extrapolate whether or not the fatigue induced by the exercise is indeed generalized. By using this protocol, Ross et al. (2007) confirm that the decrease in MVC in the tibialis anterior was not the result of reduced motivation or general whole-body fatigue. Figure 1 shows data redrawn from Ross et al. (2007). The change in the MVC for the tibialis anterior from baseline to postexercise is equivalent to 16.7% reduction and, in terms of voluntary activation, is 13.6% reduction. Interestingly, the MVC remains depressed up to 4 h post marathon but the voluntary activation is restored by this time. Contrast this to the wrist flexors, which do not reach statistical significance at any point following the marathon. The finding that the wrist flexor MVC was maintained is a crucial result, which supports the proposition that the CNS is able to discriminate and attenuate motor unit recruitment according to which muscles are most likely to experience high metabolic demands and increase the likelihood of catastrophe.
Although Ross et al. (2007) did not measure the voluntary activation of the wrist flexors through either cortical or electrical stimulation and therefore could not definitively conclude that prolonged exercise does not induce generalized fatigue, the authors did provide an enticing hypothesis. That is, in contrast to other studies, including our own (Saboisky et al. 2003; Martin et al. 2005), which show that the CNS can recover quickly following endurance exercise, cortical drive to the tibialis anterior, or rather the skeletal muscles ‘used’ during the previous exercise bout, continues to be depressed for at least 20 min following the marathon. These findings lend support to the theory that generalized CNS fatigue is not a common phenomenon as hypothesized by others (Nybo & Nielsen, 2001) but rather there is a selective attenuation in the CNS motor drive even during exercise-induced hyperthermia and regardless of contraction type (Martin et al. 2005). It is also worth noting that the CNS does not only discriminate between ‘used’ and ‘unused’ muscle groups, but it also most probably provides a priming of contralateral fatigue for the upper limbs (Todd et al. 2003) and for the lower limbs (Rattey et al. 2006), with possible differences between sexes (Rattey & Martin, 2007). Although the editorial by Rasmussen et al. (2007) in this same issue of the journal contends that the paper by Ross et al. (2007) does not advance our understanding of the mechanisms responsible for the development of central fatigue, even though these authors speculate that brain metabolism is a major determinant, from a neurological point of view, consideration should be given to a reduced motor drive to the skeletal muscles as a means of protecting the organism from physiological catastrophe.
Therefore, the conclusion that is most important in relation to the findings of Ross et al. (2007) and those studies which show a selective attenuation in motor drive is that generalized muscular fatigue as a consequence of endurance exercise is not easily identified, at least with the studies and methodologies currently employed, and that the avoidance of physiological catastrophe is possibly the main purpose for attenuated central drive to skeletal muscle.
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Martin PG, Marino FE, Rattey J, Kay D & Cannon J (2005). Reduced voluntary activation of human skeletal muscle during shortening and lengthening contractions in whole body hyperthermia. Exp Physiol 90, 225–236.
Nybo L & Nielsen B (2001). Hyperthermia and central fatigue during prolonged exercise in humans. J Appl Physiol 91, 1055–1060.
Rasmussen P, Secher N & Petersen NT (2007). Viewpoints: Understanding central fatigue: where to go? Exp Physiol 92, 369–370.
Rattey J & Martin PG (2007). Central fatigue explains sex differences in muscle fatigue and contralateral cross-over effects of maximal contractions. Pflugers Arch DOI 10.1007/s00424-007-0243-1.[CrossRef][Medline]
Rattey J, Martin PG, Kay D, Cannon J & Marino FE (2006). Contralateral muscle fatigue in human quadriceps muscle: evidence for a centrally mediated fatigue response and cross-over effect. Pflugers Arch 452, 199–207.[CrossRef][Medline]
Ross EZ, Middleton N, Shave R, George K & Nowicky A (2007). Corticomotor excitability contributes to neuromuscular fatigue following marathon running in man. Exp Physiol 92, 417–426.
Saboisky J, Marino FE, Kay D & Cannon J (2003). Exercise heat stress does not reduce central activation to non-exercised human skeletal muscle. Exp Physiol 88, 783–790.[Abstract]
Todd G, Petersen NT, Taylor JL & Gandevia SC (2003). The effect of a contralateral contraction on maximal voluntary activation and central fatigue in elbow flexor muscles. Exp Brain Res 103, 308–313.
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