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POINT:COUNTERPOINT COMMENTS
1Institute of Physiology and Biophysics
2Department of Sport Science
University of Aarhus
Århus, Denmark
e-mail: obn{at}fi.au.dk
The following letters are in response to the Point:Counterpoint "Lactic acid accumulation is an advantage/disadvantage during muscle activity" that appeared in the April issue (http://jap.physiology.org/content/vol100/
To the Editor: The arguments brought forward in this Point:Counterpoint debate (2) mostly relate to the hypothesis that elevated [K+]o contributes to fatigue by lowering muscle excitability. However, the exact role of elevated [K+]o and excitability in the etiology of fatigue is presently unclear. In many kinds of exercise, reduced excitability may never contribute to fatigue because endogenous protection via activation of the Na+-K+ pumps and/or development of acidosis is sufficient to maintain excitability. If so, acidosis may be important in preventing loss of excitability during work but, at the same time, addition of exogenous lactate or lactic acid to muscles may be without effect on endurance because sufficient protective effects are established via endogenous mechanisms. Despite this, Karelis et al. (1) showed that lactate infusion in rats improved contractile endurance and the maintenance of excitability in plantaris muscle stimulated intermittently in situ. In addition, studies on humans have shown that when the lowering of muscle pH during contractions is blunted, muscle fatigue occurs at a lower [K+]o than in control subjects (3). Likewise, fatigue occurs at a higher [K+]o if the reduction in pH is increased by prior arm exercise (4). Bangsbo and Juel interpreted these findings as indications of increased K+ loss from muscles induced by lowered pH. These observations also suggest, however, that muscles are able to work at higher [K+]o when pH is reduced. Together with the work of Karelis et al. (1), this supports the notion that the protective effect of lactic acid on muscle excitability (5) is operating in animals and humans.
REFERENCES
GIH
Stockholm, Sweden
To the Editor: One of the current trends in muscle and exercise physiology is to dismiss lactic acid (HLa) as a fatiguing agent. The conclusion is to a major extent based on experiments with contracting single fibers or isolated muscles. Although these techniques are necessary tools in revealing the mechanisms of fatigue, one should be aware of the limitations when extrapolating to in vivo conditions. In their Point:Counterpoint (1) contribution, both groups reference the work of Pedersen et al. (2), where the major finding was that acidosis protects from K+-induced activation failure. Although activation failure can easily be demonstrated during electrical-induced contractions, it has rarely been demonstrated during voluntary exercise. The focus on muscle activation as an important site in fatigue may therefore not be relevant for in vivo conditions.
There is much evidence that accumulation of HLa causes a slowing of force relaxation. Although Lamb and Stephenson recognize the effect of acidosis on the SR Ca2+ pump function, they consider it to be an advantage that [can help increase cytoplasmic [Ca2+]. However, whole body exercise often involves rapid movements where well timing of contraction and relaxation is important. Slowing of relaxation will interfere with this coordinated muscle function and will thus impair exercise performance.
I would agree with Lamb and Stephenson that there is limited evidence that HLa is of importance in fatigue when studied as maximal isometric force in single fibers. However, there is convincing evidence that HLa generation is involved in fatigue during whole body exercise.
REFERENCES
1University of Ottawa
Cellular Molecular Medicine Department
e-mail: jmrenaud{at}uottawa.ca
To the Editor: Bangsbo and Juel (2) argue that lactic acid is a factor contributing to muscle fatigue using evidence from human studies and in vitro studies in which lactic acid depresses muscle performance. Human studies are difficult to interpret because changes in lactic acid (or pH) affect other physiological parameters, such as O2 binding to hemoglobin or K+ fluxes; so the question arises as to which, lactic acid, O2 binding, or K+, directly affects muscle performance. Although most in vitro studies do not give evidence for a role of lactic acid, Bangsbo and Juel cite some studies supporting the contrary. In one study (4), however, the hyperosmolarity created by the addition of 20–50 mM lactic acid undoubtedly contributed to the decrease in force, especially at 37°C, because the stimulation frequency, which was 100 Hz, was essentially submaximal. In another study (1), forces, as absolute values, were significantly lower in the presence than in the absence of lactic acid, but the decreases in force during fatigue were all faster in the absence than in the presence of lactic acid. Finally, one cannot ignore the fact that after fatigue 1) pHi recovers within 10 min (6) compared with 60 min for force in single muscle fibers (5) and 2) reducing or preventing pHi recovery by exposing muscles to lactic acid immediately after fatigue has no effect on force recovery (3). Thus, overall, there is overwhelming evidence for the point that lactic acid and perhaps the concomitant change in pHi contribute little to the etiology of muscle fatigue.
REFERENCES
This article has been cited by other articles:
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  M. I. Lindinger Combating muscle fatigue: extracellular lactic acidosis and catecholamines J. Physiol., June 1, 2007; 581(2): 419 - 419. [Full Text] [PDF]
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