Hypercapnic acidosis and increased H2PO4- concentration do not decrease force in cat skeletal muscle

Adams, Gregory R.; Fisher, M. J.; Meyer, Ronald A.

doi:10.1152/ajpcell.1991.260.4.c805

Cited by 69 publications

(39 citation statements)

References 31 publications

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“…Ranatunga (365) found that twitch and tetanic force in rat EDL bundles at 30 -35°C were not decreased at acid pH i (likely ϳ6.5), but actually potentiated. In cat muscle in vivo at 37°C, decreasing muscle pH i to 6.3 by hypercapnia reduced maximum tetanic force by only ϳ5-10% in soleus and biceps brachii muscles (2). In intact single fibers from mouse at 32°C, decreasing pH i from 7.17 to 6.67 caused only ϳ10% reduction in maximum tetanic force and no significant slowing of the maximum velocity of shortening (472).…”

Section: Ph I and Muscle Fatiguementioning

confidence: 93%

Skeletal Muscle Fatigue: Cellular Mechanisms

Allen¹,

Lamb²,

Westerblad³

2008

Physiological Reviews

1,895

1,876

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Repeated, intense use of muscles leads to a decline in performance known as muscle fatigue. Many muscle properties change during fatigue including the action potential, extracellular and intracellular ions, and many intracellular metabolites. A range of mechanisms have been identified that contribute to the decline of performance. The traditional explanation, accumulation of intracellular lactate and hydrogen ions causing impaired function of the contractile proteins, is probably of limited importance in mammals. Alternative explanations that will be considered are the effects of ionic changes on the action potential, failure of SR Ca2+ release by various mechanisms, and the effects of reactive oxygen species. Many different activities lead to fatigue, and an important challenge is to identify the various mechanisms that contribute under different circumstances. Most of the mechanistic studies of fatigue are on isolated animal tissues, and another major challenge is to use the knowledge generated in these studies to identify the mechanisms of fatigue in intact animals and particularly in human diseases.

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Section: Ph I and Muscle Fatiguementioning

confidence: 93%

Skeletal Muscle Fatigue: Cellular Mechanisms

Allen¹,

Lamb²,

Westerblad³

2008

Physiological Reviews

1,895

1,876

View full text Add to dashboard Cite

show abstract

“…Vol. 61,2004 Review Article 1003 Figure 1. Typical series of 31 P MR spectra recorded with a time resolution of 2 s at end of exercise (first spectrum, bottom) and during the following recovery period.…”

Section: Contribution Of 31 P Mrs To the Study Of Peripheral Fatiguementioning

confidence: 99%

“…This phenomenon would decrease the proportion of force-producing cross-bridges, leading to a decline in force production. Attempts to show the inhibitory effect of P i on force under physiological conditions have mainly been performed using 31 P MRS [11,61,69,[76][77][78] and focused on P i and H 2 PO 4 -time-dependent changes, one the one hand, and force reduction, on the other hand [75]. A strong correlation has been demonstrated between H 2 PO 4 -accumulation and force reduction in human muscle during different types of experimental protocols including sustained or repeated contractions with maximal or submaximal intensities [69,76,77].…”

Section: P I Accumulation: a Causative Factor Of Fatigue?mentioning

confidence: 99%

Functional investigations of exercising muscle: a noninvasive magnetic resonance spectroscopy-magnetic resonance imaging approach

Bendahan

Giannesini

Cozzone

2004

Cellular and Molecular Life Sciences (CMLS)

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Muscle fatigue, which is defined as the decline in muscle performance during exercise, may occur at different sites along the pathway from the central nervous system through to the intramuscular contractile machinery. Historically, both impairment of neuromuscular transmission and peripheral alterations within the muscle have been proposed as causative factors of fatigue development. However, according to more recent studies, muscle energetics play a key role in this process. Intramyoplasmic accumulation of inorganic phosphate (P(i)) and limitation in ATP availability have been frequently evoked as the main mechanisms leading to fatigue. Although attractive, these hypotheses have been elaborated on the basis of experimental results obtained in vitro, and their physiological relevance has never been clearly demonstrated in vivo. In that context, noninvasive methods such as 31-phosphorus magnetic resonance spectroscopy and surface electromyography have been employed to understand both metabolic and electrical aspects of muscle fatigue under physiological conditions. Mapping of muscles activated during exercise is another interesting issue which can be addressed using magnetic resonance imaging (MRI). Exercise-induced T2 changes have been used in order to locate activated muscles and also as a quantitative index of exercise intensity. The main results related to both issues, i.e. the metabolic and electrical aspects of fatigue and the MRI functional investigation of exercising muscle, are discussed in the present review.

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“…The decline in force has been demonstrated to strongly correlate with an increase in muscle P i concentration (7,44,50). Although the strength of the correlation varies (1), in the later stages of fatigue, when maximal isometric force is depressed by Ͼ70%, the intracellular P i concentration can exceed 30 mM compared with the 1-5 mM level in resting fibers (44). These observations suggest that P i may play a causative role in fatigue.…”

mentioning

confidence: 99%

Fiber type and temperature dependence of inorganic phosphate: implications for fatigue

Debold¹,

Dave²,

Fitts³

2004

American Journal of Physiology-Cell Physiology

114

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Debold, E. P., H. Dave, and R. H. Fitts. Fiber type and temperature dependence of inorganic phosphate: implications for fatigue. Am J Physiol Cell Physiol 287: C673-C681, 2004. First published May 5, 2004; 10.1152/ajpcell.00044.2004.-Elevated levels of P i are thought to cause a substantial proportion of the loss in muscular force and power output during fatigue from intense contractile activity. However, support for this hypothesis is based, in part, on data from skinned single fibers obtained at low temperatures (Յ15°C). The effect of high (30 mM) P i concentration on the contractile function of chemically skinned single fibers was examined at both low (15°C) and high (30°C) temperatures using fibers isolated from rat soleus (type I fibers) and gastrocnemius (type II fibers) muscles. Elevating P i from 0 to 30 mM at saturating free Ca 2ϩ levels depressed maximum isometric force (Po) by 54% at 15°C and by 19% at 30°C (P Ͻ 0.05; significant interaction) in type I fibers. Similarly, the P o of type II fibers was significantly more sensitive to high levels of P i at the lower (50% decrease) vs. higher temperature (5% decrease). The maximal shortening velocity of both type I and type II fibers was not significantly affected by elevated P i at either temperature. However, peak fiber power was depressed by 49% at 15°C but by only 16% at 30°C in type I fibers. Similarly, in type II fibers, peak power was depressed by 40 and 18% at 15 and 30°C, respectively. These data suggest that near physiological temperatures and at saturating levels of intracellular Ca 2ϩ , elevated levels of Pi contribute less to fatigue than might be inferred from data obtained at lower temperatures. skinned single fiber; force; power REPEATED HIGH-FREQUENCY STIMULATION of muscle results in a rapid decline in muscular force and power, with the degree of change dependent on the duration and intensity of activity as well as on the fiber type composition of the muscle (2, 17). The decline in force has been demonstrated to strongly correlate with an increase in muscle P i concentration (7,44,50). Although the strength of the correlation varies (1), in the later stages of fatigue, when maximal isometric force is depressed by Ͼ70%, the intracellular P i concentration can exceed 30 mM compared with the 1-5 mM level in resting fibers (44). These observations suggest that P i may play a causative role in fatigue.Skinned single muscle fiber studies provide convincing evidence that elevations in P i depress maximum isometric force (P o ) in a concentration-dependent manner (9 -11, 18, 28, 30 -32, 38). Notably, Potma et al. (38) observed a 55% decline in P o after increasing P i from 0 to 30 mM at 15°C in chemically skinned rabbit soleus fibers. Even larger P i -induced reductions in P o were observed in psoas myofibrils (43) and in single fibers when the initial P i concentration was reduced to ϳ5 m with the use of a P i mopping enzyme system (36). High levels of P i are thought to reduce force by reversing the P i release/force-generating step by mass act...

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Hypercapnic acidosis and increased H2PO4- concentration do not decrease force in cat skeletal muscle

Cited by 69 publications

References 31 publications

Skeletal Muscle Fatigue: Cellular Mechanisms

Skeletal Muscle Fatigue: Cellular Mechanisms

Functional investigations of exercising muscle: a noninvasive magnetic resonance spectroscopy-magnetic resonance imaging approach

Fiber type and temperature dependence of inorganic phosphate: implications for fatigue

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