Effects of exercise of varying duration on sarcoplasmic reticulum function

Byrd, S. K.; Bode, Allison; Klug, G. A.

doi:10.1152/jappl.1989.66.3.1383

Cited by 90 publications

(102 citation statements)

References 18 publications

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“…Luminal Ca 2ϩ content is dependent on several factors including, but not limited to, function of the SR Ca 2ϩ ATPase, leakiness of the SR membrane and/or RYR channel, and the total amount of Ca 2ϩ released that is a function of duration and frequency of the contractile protocol. Inhibition of the SR ATPase (22,91) and reductions in Ca 2ϩ accumulation by SR have been demonstrated after exhaustive running in rats (22,78), in single-fiber experiments (135,141), and in exercising humans (17). Evidence suggests that with prolonged stimulation resting intracellular Ca 2ϩ concentrations are significantly elevated (89).…”

Section: Sr Ca 2ϩ Release From An Experimental Perspectivementioning

confidence: 99%

“…It is possible that SR Ca 2ϩ content becomes diminished, considering that the catalytic activity of the SR Ca 2ϩ -ATPase is inhibited by a single bout of muscle activity (22,78,135) or that ''releasable'' Ca 2ϩ may be buffered by luminal phosphate that becomes elevated in skeletal muscle undergoing activity (55,103,132). This area will be addressed in BIOPHYSICAL REGULATION OF SR Ca 2ϩ RELEASE.…”

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confidence: 99%

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Sarcoplasmic reticulum Ca²⁺release and muscle fatigue

Favero

1999

Journal of Applied Physiology

111

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Efforts to examine the relevant mechanisms involved in skeletal muscle fatigue are focusing on Ca2+ handling within the active muscle cell. It has been demonstrated time and again that reductions in sarcoplasmic reticulum (SR) Ca2+release resulting from increased or intense muscle contraction will compromise tension development. This review seeks to accomplish two related goals: 1) to provide an up-to-date molecular understanding of the Ca2+-release process, with considerable attention devoted to the SR Ca2+ channel, including its associated proteins and their regulation by endogenous compounds; and 2) to examine several putative mechanisms by which cellular alterations resulting from intense and/or prolonged contractile activity will modify SR Ca2+ release. The mechanisms that are likely candidates to explain the reductions in SR Ca2+ channel function following contractile activity include elevated Ca2+ concentrations, alterations in metabolic homeostasis within the “microcompartmentalized” triadic space, and modification by reactive oxygen species.

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Section: Sr Ca 2ϩ Release From An Experimental Perspectivementioning

confidence: 99%

mentioning

confidence: 99%

Sarcoplasmic reticulum Ca²⁺release and muscle fatigue

Favero

1999

Journal of Applied Physiology

111

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“…A23187), and once without an ionophore in the measuring medium. The ratio of these two activities is a measure for the integrity of the membrane (BYRD et al, 1989 …”

Section: Investigations Of Muscle Camentioning

confidence: 99%

Regulation of intracellular Ca<sup>2+</sup> concentration and meat quality in pigs

Küchenmeister

Kuhn

2003

Arch. Anim. Breed.

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The meat quality of pigs is essentially dependent on the rate and intensity of energy metabolism after slaughter. The major cellular processes in muscle cells are regulated by the Ca 2+ concentration in the cytoplasm, stimulating different energy consuming ATPases. The most essential regulator of the Ca 2+ concentration is the sarcoplasmic reticulum (SR) with its membranes, the SR Ca 2+ ATPase (Ca 2+ pump), and the calcium release channel (CRC). Defects of one or more of these elements will be of influence on the metabolism and ultimately on the meat quality. This is widely investigated in pigs with a mutated CRC. However, pigs without a mutation in the CRC also show a wide variability in their meat quality, dependent on other factors e.g. stress or season of the year. The variability in meat quality in these "normal" pigs is at least partly a result of differences in SR Ca 2+ transport and the resulting metabolism. IntroductionThe pig breeding systems aiming for an increase of the lean meat percentage have been very successful in the preceding decades. However, parallel with an increased meat content there was an increasing part of carcasses showing inferior meat quality and also an increase in losses by death during transportation or other kinds of stresses. A major reason for this relationship has been shown to be a mutated calcium release channel (CRC) of the sarcoplasmic reticulum (SR) (MCLENNAN and PHILLIPS, 1992). It turned out, that this mutation causes an insufficient regulation of the intracellular Ca 2+ concentration, activating metabolic processes not only in the live pig muscle, but also after slaughtering the animals. Currently all major pig producing

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“…It has been previously suggested that glycogen may be required for contractile processes independent of energy metabolism (21). Studies in both animals (6,8,36) and humans (4) have suggested a link between sarcoplasmic reticulum Ca 2ϩ uptake and release and glycogen availability. In addition, topographical localization of glycogen within human skeletal muscle has been observed (19).…”

Section: Muscle Metabolism During Exercisementioning

confidence: 99%

Skeletal muscle energy metabolism during prolonged, fatiguing exercise

Febbraio

Dancey

1999

Journal of Applied Physiology

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Febbraio, Mark A., and Jane Dancey. Skeletal muscle energy metabolism during prolonged, fatiguing exercise. J. Appl. Physiol. 87(6): 2341-2347.-A depletion of phosphocreatine (PCr), fall in the total adenine nucleotide pool (TAN ϭ ATP ϩ ADP ϩ AMP), and increase in TAN degradation products inosine 5Ј-monophosphate (IMP) and hypoxanthine are observed at fatigue during prolonged exercise at 70% maximal O 2 uptake in untrained subjects [J. Baldwin, R. J. Snow, M. F. Carey, and M. A. Febbraio. Am. J. Physiol. 277 (Regulatory Integrative Comp. Physiol. 46): R295-R300, 1999]. The present study aimed to examine whether these metabolic changes are also prevalent when exercise is performed below the blood lactate threshold (LT). Six healthy, untrained humans exercised on a cycle ergometer to voluntary exhaustion at an intensity equivalent to 93 Ϯ 3% of LT (ϳ65% peak O 2 uptake). Muscle biopsy samples were obtained at rest, at 10 min of exercise, ϳ40 min before fatigue (FϪ40 ϭ143 Ϯ 13 min), and at fatigue (F ϭ 186 Ϯ 31 min). Glycogen concentration progressively declined (P Ͻ 0.01) to very low levels at fatigue (28 Ϯ 6 mmol glucosyl U/kg dry wt). Despite this, PCr content was not different when FϪ40 was compared with F and was only reduced by 40% when F was compared with rest (52.8 Ϯ 3.7 vs. 87.8 Ϯ 2.0 mmol/kg dry wt; P Ͻ 0.01). In addition, TAN concentration was not reduced, IMP did not increase significantly throughout exercise, and hypoxanthine was not detected in any muscle samples. A significant correlation (r ϭ 0.95; P Ͻ 0.05) was observed between exercise time and glycogen use, indicating that glycogen availability is a limiting factor during prolonged exercise below LT. However, because TAN was not reduced, PCr was not depleted, and no correlation was observed between glycogen content and IMP when glycogen stores were compromised, fatigue may be related to processes other than those involved in muscle high-energy phosphagen metabolism.total adenine nucleotides; phosphocreatine; lactate threshold; glycogen IT IS WELL ESTABLISHED that fatigue during prolonged exercise coincides with low intramuscular glycogen stores (2,3,9,12,13,25,32,34,38). Although there are several possible reasons as to the requirement for carbohydrate in the maintenance of contractile force (for review, see Ref. 18), it is widely accepted that metabolic processes are limited by carbohydrate availability. It has been suggested that as muscle glycogen stores are progressively compromised during exercise, flux through glycolysis is reduced, leading to a fall in pyruvate formation and a reduction in tricarboxylic acid cycle intermediates, in turn resulting in an impairment in ATP provision via oxidative phosphorylation (32,34). Because ATP demand during prolonged exercise is maintained, such a decrease in ATP provision leads to transient ADP formation and ATP generation from alternative pathways, including creatine phosphokinase (CPK) and adenylate kinase (AK) (32). Because CPK has a much higher activity in skeletal muscle compared with AK (7), ph...

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Effects of exercise of varying duration on sarcoplasmic reticulum function

Cited by 90 publications

References 18 publications

Sarcoplasmic reticulum Ca²⁺release and muscle fatigue

Sarcoplasmic reticulum Ca²⁺release and muscle fatigue

Regulation of intracellular Ca<sup>2+</sup> concentration and meat quality in pigs

Skeletal muscle energy metabolism during prolonged, fatiguing exercise

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Effects of exercise of varying duration on sarcoplasmic reticulum function

Cited by 90 publications

References 18 publications

Sarcoplasmic reticulum Ca2+release and muscle fatigue

Sarcoplasmic reticulum Ca2+release and muscle fatigue

Regulation of intracellular Ca&lt;sup&gt;2+&lt;/sup&gt; concentration and meat quality in pigs

Skeletal muscle energy metabolism during prolonged, fatiguing exercise

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Sarcoplasmic reticulum Ca²⁺release and muscle fatigue

Sarcoplasmic reticulum Ca²⁺release and muscle fatigue

Regulation of intracellular Ca<sup>2+</sup> concentration and meat quality in pigs