Muscular fatigue investigated by phosphorus nuclear magnetic resonance

Dawson, M. Joan; Gadian, David G.; Wilkie, D.

doi:10.1038/274861a0

Cited by 438 publications

(338 citation statements)

References 27 publications

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“…In resting myofiber cells, intracellular phosphate ion concentrations are 1-6 mm and can accumulate in muscle contraction to levels approaching 30 mm, which inhibits force production and slows muscle relaxation in skeletal muscle fatigue. [27][28][29][30][31] Phosphate ion applied intracellularly or extracellularly to myofiber cells enters the sarcoplasmic reticulum and precipitates calcium, which in turn decreases muscle contraction. 32,33 Thus, sodium phosphate injections into muscle could somehow aid the entry of plasmid DNA into muscle cells.…”

Section: Discussionmentioning

confidence: 99%

Sodium phosphate enhances plasmid DNA expression in vivo

et al. 2000

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Section: Discussionmentioning

confidence: 99%

Sodium phosphate enhances plasmid DNA expression in vivo

et al. 2000

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“…For this reason, a high rate of ATP use cannot be sustained in muscle and ATP use must thus be regulated (Hochachka, 1994;Hochachka and Matheson, 1992;Myburgh, 2004). We know that muscle fibers can preserve ATP because the ATP level usually decreases by only 20-25% during exercise (Argov et al, 2000;Dawson et al, 1978) and rarely falls below 50% of its initial value (Karatzaferi et al, 2001;Spriet et al, 1987).…”

Section: Introductionmentioning

confidence: 99%

Skeletal muscle fatigue – regulation of excitation–contraction coupling to avoid metabolic catastrophe

MacIntosh¹,

Holash²,

Renaud³

2012

Journal of Cell Science

101

119

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Summary ATP provides the energy in our muscles to generate force, through its use by myosin ATPases, and helps to terminate contraction by pumping Ca 2+ back into the sarcoplasmic reticulum, achieved by Ca 2+ ATPase. The capacity to use ATP through these mechanisms is sufficiently high enough so that muscles could quickly deplete ATP. However, this potentially catastrophic depletion is avoided. It has been proposed that ATP is preserved not only by the control of metabolic pathways providing ATP but also by the regulation of the processes that use ATP. Considering that contraction (i.e. myosin ATPase activity) is triggered by release of Ca 2+ , the use of ATP can be attenuated by decreasing Ca 2+ release within each cell. A lower level of Ca 2+ release can be accomplished by control of membrane potential and by direct regulation of the ryanodine receptor (RyR, the Ca 2+ release channel in the terminal cisternae). These highly redundant control mechanisms provide an effective means by which ATP can be preserved at the cellular level, avoiding metabolic catastrophe. This Commentary will review some of the known mechanisms by which this regulation of Ca 2+ release and contractile response is achieved, demonstrating that skeletal muscle fatigue is a consequence of attenuation of contractile activation; a process that allows avoidance of metabolic catastrophe.Key words: Endurance, Membrane excitability, Skeletal muscle contraction Introduction Typically, when exercise scientists think of control of skeletal muscle contraction, they consider motor unit recruitment and rate coding, the primary means by which the brain regulates the magnitude of muscle contraction. However, the magnitude of skeletal muscle contraction can also be regulated at the cellular level. This level of control is necessary to avoid cellular metabolic catastrophe, i.e. the situation in which ATP depletion reaches a level that is damaging to the fiber.ATP is the common final source for energy in the cell, and its concentration [along with the concentrations of ADP and inorganic phosphate (Pi)] affects the magnitude of energy that is made available from its hydrolysis. At rest, skeletal muscle has a low metabolic rate, not unlike many other passive tissues, and the intracellular concentration of ATP is in the 5-7 mM range (Hochachka and Matheson, 1992). However, during muscle activity, there are three major ATPases that require ATP for their function (Box 1); during exercise, skeletal muscle can increase its rate of ATP use by more than 100 times (Hochachka and McClelland, 1997), a rate that is much faster than can be replenished by aerobic metabolism. This latter point is clear from the fact that the muscle power output can greatly exceed the level that can be supported by aerobic metabolism (MacIntosh et al., 2000). To accommodate this additional energy requirement, ATP is provided by non-aerobic means (through phosphocreatine hydrolysis and glycolysis resulting in lactate formation), but this alternative source of ATP has limited capacity (Monod ...

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“…There is a straight relation between muscular acidosis and fatigue, due to the following effects of the H + i ons: 1) inhibition of the maximal velocity of muscular shortening (4) ; 2) inhibition of the miofibrilar ATPase and the enzymes important for the regulation of the glycolytic anaerobic process of energy obtaining (4,6) ; 3) reduction of the crossed bridges formation through inhibition of the Ca ++ to the TNC site of the troponin (4)(5)(6) ; and 4) reduction of the Ca ++ return by the inhibition of the sarcoplasmatic ATPase, which leads to reduction in the Ca ++ release (4) . Therefore, as previously mentioned, a reduction in the H + concentration in the muscular cell promotes delay in fatigue besides allowing that the glycolytic way is used for a longer period.…”

Section: Discussionmentioning

confidence: 99%

“…The decrease of the intramuscular pH is related with a series of events which harm the muscular contraction-relaxation and energy obtaining processes (4)(5)(6) . In this context, several studies have researched the ergogenic action of alkaline substances in activities of high intensity and short duration.…”

Section: Introductionmentioning

confidence: 99%

A ingestão de bicarbonato de sódio pode contribuir para o desempenho em lutas de judô?

Artioli

Coelho

Benatti

et al. 2006

Rev Bras Med Esporte

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The objective of this study was to investigate the effect of the NaHCO 3 ingestion on the judo performance. Six male athletes ingested 0.3 g • kg -1 body weight of NaHCO 3 or CaCO 3 (placebo) 2 h before 3 fights of 5 min, with 15 min recovery. Immediately afterwards, and 15 min after each fight, the athletes related their perceived exertion. The blood lactate concentration was verified in rest, after warming up, 0, 3, 5, 7, 10 and 15 min after each fight. The same experimental protocol was repeated twice by each athlete, except for the ingested substance. The study adopted the counterbalanced double-blind model. There was no significant difference for the performance variables. The perceived exertion did not differ among the treatments, and the blood lactate concentration was significantly greater (p < 0.05) after NaHCO 3 ingestion in the first moments of the protocol. In conclusion, the ergogenic effects of NaH-CO 3 are not enough to contribute to the improvement of the performance in judo fights. However, the model limitations must be considered when generalizing these results. Future studies should use other tools to evaluate the performance in judo.

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Muscular fatigue investigated by phosphorus nuclear magnetic resonance

Abstract: Muscular fatigue has been studied using 31PNMR to measure the levels and rates of utilisation of several key metabolites and the free-energy change for ATP hydrolysis. Force development is closely correlated with metabolite levels and is proportional to the rate at which ATP is hydrolysed.

Cited by 438 publications

References 27 publications

Sodium phosphate enhances plasmid DNA expression in vivo

Sodium phosphate enhances plasmid DNA expression in vivo

Skeletal muscle fatigue – regulation of excitation–contraction coupling to avoid metabolic catastrophe

A ingestão de bicarbonato de sódio pode contribuir para o desempenho em lutas de judô?

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