Lactate and force production in skeletal muscle

Kristensen, Michael; Albertsen, Janni; Rentsch, M; Juel, Carsten

doi:10.1113/jphysiol.2004.078014

Cited by 75 publications

(74 citation statements)

References 23 publications

(30 reference statements)

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“…During the subsequent fatiguing stimulation period, the added lactic acid would hinder the export of lactate and hydrogen ions produced by glycogenolysis and in this way exaggerate the fatigue-induced acidification. Nevertheless, the addition of lactic acid did not have any marked effect on fatigue development in either soleus or EDL muscles, which agrees with recent results on rat soleus muscles (Kristensen et al 2005). Thus, these results support the conclusion that accumulation of lactate and hydrogen ions is not a major cause of fatigue (Pate et al 1995;Bangsbo et al 1996;Bruton et al 1998;Posterino et al 2001;Lamb, 2002;Westerblad et al 2002).…”

Section: Discussionsupporting

confidence: 82%

Limited oxygen diffusion accelerates fatigue development in mouse skeletal muscle

Zhang

Bruton

Katz

et al. 2006

The Journal of Physiology

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Isolated whole skeletal muscles fatigue more rapidly than isolated single muscle fibres. We have now employed this difference to study mechanisms of skeletal muscle fatigue. Isolated whole soleus and extensor digitorum longus (EDL) muscles were fatigued by repeated tetanic stimulation while measuring force production. Neither application of 10 mM lactic acid nor increasing the [K + ] of the bath solution from 5 to 10 mM had any significant effect on the rate of force decline during fatigue induced by repeated brief tetani. Soleus muscles fatigued slightly faster during continuous tetanic stimulation in 10 mM [K + ]. Inhibition of mitochondrial respiration with cyanide resulted in a faster fatigue development in both soleus and EDL muscles. Single soleus muscle fibres were fatigued by repeated tetani while measuring force and myoplasmic free [Ca 2+ ] ([Ca 2+ ] i ). Under control conditions, the single fibres were substantially more fatigue resistant than the whole soleus muscles; tetanic force at the end of a series of 100 tetani was reduced by about 10% and 50%, respectively. However, in the presence of cyanide, fatigue developed at a similar rate in whole muscles and single fibres, and tetanic force at the end of fatiguing stimulation was reduced by ∼80%. The force decrease in the presence of cyanide was associated with a ∼50% decrease in tetanic [Ca 2+ ] i , compared with an increase of ∼20% without cyanide. In conclusion, lactic acid or [K + ] has little impact on fatigue induced by repeated tetani, whereas hypoxia speeds up fatigue development and this is mainly due to an impaired Ca 2+release from the sarcoplasmic reticulum.

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Section: Discussionsupporting

confidence: 82%

Limited oxygen diffusion accelerates fatigue development in mouse skeletal muscle

Zhang

Bruton

Katz

et al. 2006

The Journal of Physiology

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“…Previous studies (10,15,31,36,38) on K ϩ -induced inhibition of contractile force and the protective effects of Na ϩ -K ϩ pump stimulation and acidosis, have focused on slow-twitch muscles. Because a large fraction of skeletal muscles are composed of fast-twitch fibers, it was of interest to characterize the response of these fibers to high [K ϩ ] o , Na ϩ -K ϩ pump stimulation, and acidosis, in particular because in these fibers, excitation induces a much more pronounced loss of K ϩ than in slow-twitch fibers (14).…”

Section: Discussionmentioning

confidence: 99%

“…Recent in vitro studies (30,31,36) on slow-twitch muscles have shown that in these muscles, the depressing effect of high [K ϩ ] o on excitability and contractility can also be counteracted by lactic acid. The effect on excitability is secondary to the ensuing reduction in muscle pH and might be related to an inhibitory effect of acidosis on the chloride conductance (38,39).…”

mentioning

confidence: 99%

Effects of lactic acid and catecholamines on contractility in fast-twitch muscles exposed to hyperkalemia

Hansen¹,

Clausen²,

Nielsen³

2005

American Journal of Physiology-Cell Physiology

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Intensive exercise is associated with a pronounced increase in extracellular K+ ([K+]o). Because of the ensuing depolarization and loss of excitability, this contributes to muscle fatigue. Intensive exercise also increases the level of circulating catecholamines and lactic acid, which both have been shown to alleviate the depressing effect of hyperkalemia in slow-twitch muscles. Because of their larger exercise-induced loss of K+, fast-twitch muscles are more prone to fatigue caused by increased [K+]o than slow-twitch muscles. Fast-twitch muscles also produce more lactic acid. We therefore compared the effects of catecholamines and lactic acid on the maintenance of contractility in rat fast-twitch [extensor digitorum longus (EDL)] and slow-twitch (soleus) muscles. Intact muscles were mounted on force transducers and stimulated electrically to evoke short isometric tetani. Elevated [K+]o (11 and 13 mM) was used to reduce force to ∼20% of control force at 4 mM K+. In EDL, the β2-agonist salbutamol (10−5 M) restored tetanic force to 83 ± 2% of control force, whereas in soleus salbutamol restored tetanic force to 93 ± 1%. In both muscles, salbutamol induced hyperpolarization (5–8 mV), reduced intracellular Na+ content and increased Na+-K+ pump activity, leading to an increased K+ tolerance. Lactic acid (24 mM) restored force from 22 ± 4% to 58 ± 2% of control force in EDL, an effect that was significantly lower than in soleus muscle. These results amplify and generalize the concept that the exercise-induced acidification and increase in plasma catecholamines counterbalance fatigue arising from rundown of Na+ and K+ gradients.

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“…This view is not recognised by all. By contrast, Kristensen et al (2005) questioned whether this phenomenon can be extended to a whole-system model during exercise. These authors reported that muscle preparations in vitro were unable to produce a similar amount of force compared with controls when incubated in a 20·mmol·l -1 Na-lactate, 12·mmol·l -1 Na-lactate + 8·mmol·l -1 lactic acid or a 20·mmol·l -1 lactic acid solution and stimulated to fatigue.…”

Section: Lactate As the Cause Or Consequence Of Fatigue?mentioning

confidence: 99%

Lactate – a signal coordinating cell and systemic function

Philp¹,

Macdonald

Watt³

2005

Journal of Experimental Biology

262

177

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SUMMARY Since its first documented observation in exhausted animal muscle in the early 19th century, the role of lactate (lactic acid) has fascinated muscle physiologists and biochemists. Initial interpretation was that lactate appeared as a waste product and was responsible in some way for exhaustion during exercise. Recent evidence, and new lines of investigation, now place lactate as an active metabolite, capable of moving between cells, tissues and organs, where it may be oxidised as a fuel or reconverted to form pyruvate or glucose. The questions now to be asked concern the effects of lactate at the systemic and cellular level on metabolic processes. Does lactate act as a metabolic signal to specific tissues, becoming a metabolite pseudo-hormone?Does lactate have a role in whole-body coordination of sympathetic/parasympathetic nerve system control? And, finally, does lactate play a role in maintaining muscle excitability during intense muscle contraction? The concept of lactate acting as a signalling compound is a relatively new hypothesis stemming from a combination of comparative, cell and whole-organism investigations. It has been clearly demonstrated that lactate is capable of entering cells via the monocarboxylate transporter (MCT) protein shuttle system and that conversion of lactate to and from pyruvate is governed by specific lactate dehydrogenase isoforms, thereby forming a highly adaptable metabolic intermediate system. This review is structured in three sections,the first covering pertinent topics in lactate's history that led to the model of lactate as a waste product. The second section will discuss the potential of lactate as a signalling compound, and the third section will identify ways in which such a hypothesis might be investigated. In examining the history of lactate research, it appears that periods have occurred when advances in scientific techniques allowed investigation of this metabolite to expand. Similar to developments made first in the 1920s and then in the 1980s, contemporary advances in stable isotope, gene microarray and RNA interference technologies may allow the next stage of understanding of the role of this compound, so that, finally, the fundamental questions of lactate's role in whole-body and localised muscle function may be answered.

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Lactate and force production in skeletal muscle

Cited by 75 publications

References 23 publications

Limited oxygen diffusion accelerates fatigue development in mouse skeletal muscle

Limited oxygen diffusion accelerates fatigue development in mouse skeletal muscle

Effects of lactic acid and catecholamines on contractility in fast-twitch muscles exposed to hyperkalemia

Lactate – a signal coordinating cell and systemic function

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