Comparison of the effects of inorganic phosphate on caffeine-induced Ca<sup>2+</sup> release in fast- and slow-twitch mammalian skeletal muscle

Posterino, Giuseppe Saverio; Dunn, Stacey Leanne

doi:10.1152/ajpcell.00155.2007

Cited by 9 publications

(5 citation statements)

References 39 publications

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“…Because mM concentrations of caffeine stimulate Ca 2 + release from the SR Ca 2 + release channel (RyR1), and thereby by-pass upstream components of excitation-contraction coupling, force production during caffeine contracture testing can be inferred as an index of contractile protein content and, when compared to voltage-induced force production, as an index of excitation contraction coupling failure. [32][33][34][35][36]39,[47][48][49][50] The caffeine contracture forces observed in this study (Fig. 3F) are consistent with the supposition that repair of VML injury with the TE-MR construct, is due, at least in part, to the presence of more contractile machinery; when compared to no repair or scaffold-only repair.…”

Section: Discussionsupporting

confidence: 86%

A Tissue-Engineered Muscle Repair Construct for Functional Restoration of an Irrecoverable Muscle Injury in a Murine Model

Machingal

Corona

Walters

et al. 2011

Tissue Engineering Part A

162

207

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There are no effective clinical treatments for volumetric muscle loss (VML) resulting from traumatic injury, tumor excision, or other degenerative diseases of skeletal muscle. The goal of this study was to develop and characterize a more clinically relevant tissue-engineered muscle repair (TE-MR) construct for functional restoration of a VML injury in the mouse lattissimus dorsi (LD) muscle. To this end, TE-MR constructs developed by seeding rat myoblasts on porcine bladder acellular matrix were preconditioned in a bioreactor for 1 week and implanted in nude mice at the site of a VML injury created by excising 50% of the native LD. Two months postinjury and implantation of TE-MR, maximal tetanic force was ∼72% of that observed in native LD muscle. In contrast, injured LD muscles that were not repaired, or were repaired with scaffold alone, produced only ∼50% of native LD muscle force after 2 months. Histological analyses of LD tissue retrieved 2 months after implantation demonstrated remodeling of the TE-MR construct as well as the presence of desmin-positive myofibers, blood vessels, and neurovascular bundles within the TE-MR construct. Overall, these encouraging initial observations document significant functional recovery within 2 months of implantation of TE-MR constructs and provide clear proof of concept for the applicability of this technology in a murine VML injury model.

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Section: Discussionsupporting

confidence: 86%

A Tissue-Engineered Muscle Repair Construct for Functional Restoration of an Irrecoverable Muscle Injury in a Murine Model

Machingal

Corona

Walters

et al. 2011

Tissue Engineering Part A

162

207

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“…Thus our data, which show that neither H 2 O 2 (nor subsequent glutathionylation with GSH) nor GSNO alters the Ca 2ϩ sensitivity of the contractile apparatus of slow-twitch fibers, may represent one mechanism for fatigue resistance. The relative insensitivity of slow-twitch fibers to these effects is similar to recent data that show that slow-twitch fibers are largely insensitive to a number of compounds thought to be involved in fatigue (16,24,30). However, again it is possible that under extreme conditions, slow-twitch muscle may still succumb to elevated levels of ROS, where more potent molecular species may be generated (such as hydroxyl radical, OH ⅐ ; 20), particularly at elevated temperatures (such as superoxide; 8).…”

Section: Effects Of Gsno and H 2 O 2 On Slow-twitch Skeletal Muscle Asupporting

confidence: 82%

“…Fast-twitch fibers also fatigue rapidly with repeated activity whilst slow-twitch fibers appear largely fatigue resistant. We and others have recently shown that, unlike fast-twitch fibers, the fatigue resistance of slow-twitch fibers appears to arise in part due to a lack of sensitivity to various metabolites involved in fatigue in fasttwitch fibers (such as inorganic phosphate and ADP; 16,24). To date, there has been no systematic comparison of the effects of both ROS and NO on the Ca 2ϩ sensitivity of both fiber types, with nothing known about the effects of NO on slowtwitch fiber Ca 2ϩ sensitivity.…”

mentioning

confidence: 99%

Sequential effects of GSNO and H₂O₂ on the Ca²⁺ sensitivity of the contractile apparatus of fast- and slow-twitch skeletal muscle fibers from the rat

Spencer

Posterino²

2009

American Journal of Physiology-Cell Physiology

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Spencer T, Posterino GS. Sequential effects of GSNO and H2O2 on the Ca 2ϩ sensitivity of the contractile apparatus of fast-and slow-twitch skeletal muscle fibers from the rat. Am J Physiol Cell Physiol 296: C1015-C1023, 2009. First published February 18, 2009 doi:10.1152/ajpcell.00251.2008.-Reactive oxygen species (ROS), such as hydrogen peroxide (H2O2) and nitric oxide (NO), have been shown to differentially alter the Ca 2ϩ sensitivity of the contractile apparatus of fast-twitch skeletal muscle, leading to the proposal that normal muscle function is controlled by perturbations in the amounts of these two groups of molecules (28). However, no previous studies have examined whether these opposing actions are retained when the contractile apparatus is subjected to both molecule types. Using mechanically skinned fast-and slow-twitch skeletal muscle fibers of the rat, we compared the effects of sequential addition of nitrosoglutathione (GSNO), a NO donor, and H2O2 on the Ca 2ϩ sensitivity of the contractile apparatus. As expected from previous reports in fast-twitch fibers, when added separately, GSNO (1 mM) reduced the Ca 2ϩ sensitivity of the contractile apparatus, whereas H2O2 (10 mM; added during contractions) increased the Ca 2ϩ sensitivity of the contractile apparatus. When added sequentially to the same fiber, such that the oxidation by one molecule (e.g., GSNO) preceded the oxidation by the other (e.g., H2O2), and vice versa, the individual effects of both molecules on the Ca 2ϩ sensitivity were retained. Interestingly, neither molecule had any effect on the Ca 2ϩ sensitivity of slow-twitch skeletal muscle. The data show that H 2O2 and GSNO retain the capacity to independently affect the contractile apparatus to modulate force. Furthermore, the absence of effects in slow-twitch muscle may further explain why this fiber type is relatively insensitive to fatigue. nitric oxide; reactive oxygen species; nitrosoglutathione; hydrogen peroxide THE REDOX STATE OF A SKELETAL muscle cell has been hypothesized to affect the force output in a similar fashion to other homeostatic variables such as pH and temperature (28). Skeletal muscle is known to produce a number of reactive oxygen species (termed ROS) as well as a variety of nitrogen-based compounds that include nitric oxide (NO) (see review in Ref. 29) that contribute to the redox state of the cell. The production of both ROS and NO occurs at varying rates during both rest and activity (29) as a by-product of oxidative metabolism (5). Reid et al. (28) had proposed a model depicting a biphasic effect of changes in cellular redox state on isometric force. The model predicted that basal (resting) levels of ROS (and/or NO) in muscle normally maintain a suboptimal performance level that can be modified by activity that results in deviations in contractile force output both potentially increasing and decreasing force. To date, there have been a number of studies in both intact muscle and skinned muscle fibers examining the effects of both ROS and NO on contractile a...

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“…In their experiments a 2 min exposure to 30 mM P i was sufficient to reduce Ca 2+ release to a steady level suggesting that this mechanism would have time to operate during a fatigue protocol of this or greater length. This mechanism appears to be substantially smaller in slow fibers compared to fast, which may contribute to the fatigue-resistance of slow fibers (Posterino and Dunn, 2008). …”

Section: The Effect Of Pi On Ca2+ Releasementioning

confidence: 99%

The multiple roles of phosphate in muscle fatigue

Allen¹,

Trajanovska²

2012

Front. Physio.

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Muscle fatigue is the decline in performance of muscles observed during periods of intense activity. ATP consumption exceeds production during intense activity and there are multiple changes in intracellular metabolites which may contribute to the changes in crossbridge activity. It is also well-established that a reduction in activation, either through action potential changes or reduction in Ca2+ release from the sarcoplasmic reticulum (SR), makes an additional contribution to fatigue. In this review we focus on the role of intracellular inorganic phosphate (Pi) whose concentration can increase rapidly from around 5–30 mM during intense fatigue. Studies from skinned muscle fibers show that these changes substantially impair myofibrillar performance although the effects are strongly temperature dependent. Increased Pi can also cause reduced Ca2+ release from the SR and may therefore contribute to the reduced activation. In a recent study, we have measured both Pi and Ca2+ release in a blood-perfused mammalian preparation and the results from this preparation allows us to test the extent to which the combined effects of Pi and Ca2+ changes may contribute to fatigue.

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Comparison of the effects of inorganic phosphate on caffeine-induced Ca²⁺ release in fast- and slow-twitch mammalian skeletal muscle

Cited by 9 publications

References 39 publications

A Tissue-Engineered Muscle Repair Construct for Functional Restoration of an Irrecoverable Muscle Injury in a Murine Model

A Tissue-Engineered Muscle Repair Construct for Functional Restoration of an Irrecoverable Muscle Injury in a Murine Model

Sequential effects of GSNO and H₂O₂ on the Ca²⁺ sensitivity of the contractile apparatus of fast- and slow-twitch skeletal muscle fibers from the rat

The multiple roles of phosphate in muscle fatigue

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Comparison of the effects of inorganic phosphate on caffeine-induced Ca2+ release in fast- and slow-twitch mammalian skeletal muscle

Cited by 9 publications

References 39 publications

A Tissue-Engineered Muscle Repair Construct for Functional Restoration of an Irrecoverable Muscle Injury in a Murine Model

A Tissue-Engineered Muscle Repair Construct for Functional Restoration of an Irrecoverable Muscle Injury in a Murine Model

Sequential effects of GSNO and H2O2 on the Ca2+ sensitivity of the contractile apparatus of fast- and slow-twitch skeletal muscle fibers from the rat

The multiple roles of phosphate in muscle fatigue

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Comparison of the effects of inorganic phosphate on caffeine-induced Ca²⁺ release in fast- and slow-twitch mammalian skeletal muscle

Sequential effects of GSNO and H₂O₂ on the Ca²⁺ sensitivity of the contractile apparatus of fast- and slow-twitch skeletal muscle fibers from the rat