Muscles of mice deficient in α-sarcoglycan maintain large masses and near control force values throughout the life span

Consolino, Christina M.; Duclos, Franck; Lee, Jane; Williamson, Roger A.; Campbell, Kevin P.; Brooks, Susan V.

doi:10.1152/physiolgenomics.00311.2004

Cited by 14 publications

(11 citation statements)

References 51 publications

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“…The mouse skeletal soleus muscle was modeled as a bundle of N = 887 cylindrical fibers of 40 μm diameter and 1 cm length, according to morphometric studies1819. The interstitial space was set to 10 μm2021.…”

Section: Resultsmentioning

confidence: 99%

Local recording of biological magnetic fields using Giant Magneto Resistance-based micro-probes

Barbieri

Trauchessec

Caruso

et al. 2016

Sci Rep

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The electrical activity of brain, heart and skeletal muscles generates magnetic fields but these are recordable only macroscopically, such as in magnetoencephalography, which is used to map neuronal activity at the brain scale. At the local scale, magnetic fields recordings are still pending because of the lack of tools that can come in contact with living tissues. Here we present bio-compatible sensors based on Giant Magneto-Resistance (GMR) spin electronics. We show on a mouse muscle in vitro, using electrophysiology and computational modeling, that this technology permits simultaneous local recordings of the magnetic fields from action potentials. The sensitivity of this type of sensor is almost size independent, allowing the miniaturization and shaping required for in vivo/vitro magnetophysiology. GMR-based technology can constitute the magnetic counterpart of microelectrodes in electrophysiology, and might represent a new fundamental tool to investigate the local sources of neuronal magnetic activity.

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Section: Resultsmentioning

confidence: 99%

Local recording of biological magnetic fields using Giant Magneto Resistance-based micro-probes

Barbieri

Trauchessec

Caruso

et al. 2016

Sci Rep

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“…Interestingly, ␣-sarcoglycan-null mice exhibit larger muscle mass than age-matched wild-type mice, yet the absolute force production was maintained near control levels at all ages (20). However, when eccentric contractions were performed in mice lacking ␥-sarcoglycan, which results in the additional loss of ␤-and ␦-sarcoglycan (35), these (20-wk-old) mice exhibited a significantly greater drop in force (Ϫ30%) than wild-type mice (6).…”

Section: E5 Force Transfer In Skeletal Musclementioning

confidence: 96%

Effects of aging, exercise, and disease on force transfer in skeletal muscle

Hughes

Wallace

Baar

2015

American Journal of Physiology-Endocrinology and Metabolism

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Hughes DC, Wallace MA, Baar K. Effects of aging, exercise, and disease on force transfer in skeletal muscle. Am J Physiol Endocrinol Metab 309: E1-E10, 2015. First published May 12, 2015; doi:10.1152/ajpendo.00095.2015.-The loss of muscle strength and increased injury rate in aging skeletal muscle has previously been attributed to loss of muscle protein (cross-sectional area) and/or decreased neural activation. However, it is becoming clear that force transfer within and between fibers plays a significant role in this process as well. Force transfer involves a secondary matrix of proteins that align and transmit the force produced by the thick and thin filaments along muscle fibers and out to the extracellular matrix. These specialized networks of cytoskeletal proteins aid in passing force through the muscle and also serve to protect individual fibers from injury. This review discusses the cytoskeleton proteins that have been identified as playing a role in muscle force transmission, both longitudinally and laterally, and where possible highlights how disease, aging, and exercise influence the expression and function of these proteins. force transmission; dystrophin-glycoprotein complex; injury; aging ON AVERAGE, HUMANS LOSE AROUND 45% of their muscle mass between their mid-20s and 80s (47,70,71). This loss in muscle mass in the absence of disease is known as sarcopenia (60). The decline in muscle mass is accompanied by, but cannot fully explain, a rapid loss in muscle strength (64). The loss in muscle strength has previously been investigated from the perspectives of loss of muscle protein mass (cross-sectional area) and decreased neural activation. A third possibility, impaired force transfer, has received the least attention in relation to aging, exercise, and disease (66,90,102). However, recent advances in our understanding of this process suggest that force transfer plays an important role in muscle strength and injury prevention, and this fact is the focus of this review. Force TransferOver 60 years ago, Andrew Huxley and his students used electron microscopy to show that during muscle contraction the I-band (containing the thin filament) shortened whereas the A-band (containing the thick filament) remained a constant length (39). Their famous "sliding theory of muscle contraction" provided an image of a muscle shortening end to end as the A-bands drew closer together. Implied in this model is that force is transferred in a longitudinal manner as a result of sarcomere shortening. However, a deeper consideration of this model requires that there be a secondary matrix of proteins that are not visible to the electron microscope, proteins that transmit the force produced by the thick and thin filaments along the muscle fiber to the tendons. These specialized networks of cytoskeletal proteins transmit force through the muscle to the tendon and also serve to protect individual fibers from injury.An important structure in these networks is the "costamere", which connects the sarcolemma with the contractile appar...

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“…1c). Moreover, Sgca -null mice do not develop brain, heart nor vascular pathology6, and have muscle-force values similar to those of control mice7. Therefore, neither cardiac deficiency nor an inability to produce force was the cause of the post-exercise inactivity in the Sgca -null mice.…”

mentioning

confidence: 90%

Sarcolemma-localized nNOS is required to maintain activity after mild exercise

Kobayashi

Rader

Crawford

et al. 2008

Nature

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246

352

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Many neuromuscular conditions are characterized by an exaggerated exercise-induced fatigue response that is disproportionate to activity level. This fatigue does not necessarily correlate with elevated central or peripheral fatigue in patients1, and some patients experience severe fatigue without any demonstrable somatic disease2. Except in myopathies that are due to specific metabolic defects, the mechanism underlying this type of fatigue remains unknown2. With no treatment available, this form of inactivity is a major determinant of disability3. Here we show, using mouse models, that this exaggerated fatigue response is distinct from a loss in specific force production by muscle, and that sarcolemma-localized nNOS signaling in skeletal muscle is required to maintain activity after mild exercise. Of significance, we show that nNOS-null mice do not have muscle pathology and have no loss of muscle specific-force after exercise, but do display this exaggerated fatigue response to mild exercise. In mouse models of nNOS mislocalization from the sarcolemma, prolonged inactivity was only relieved by pharmacologically enhancing the cGMP signal that results from muscle nNOS activation during the nitric oxide signaling response to mild exercise. Our findings suggest that the mechanism underlying the exaggerated fatigue response to mild exercise is a lack of contraction-induced signaling from sarcolemma-localized nNOS, which reduces cGMP-mediated vasomodulation in the vessels that supply active muscle after mild exercise. Notably, sarcolemmal nNOS was reduced in patient biopsies from a large number of distinct myopathies, suggesting a common mechanism of fatigue. Our results suggest that patients with an exaggerated fatigue response to mild exercise would show clinical improvement in response to treatment strategies aimed at improving exercise-induced signaling.

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Muscles of mice deficient in α-sarcoglycan maintain large masses and near control force values throughout the life span

Cited by 14 publications

References 51 publications

Local recording of biological magnetic fields using Giant Magneto Resistance-based micro-probes

Local recording of biological magnetic fields using Giant Magneto Resistance-based micro-probes

Effects of aging, exercise, and disease on force transfer in skeletal muscle

Sarcolemma-localized nNOS is required to maintain activity after mild exercise

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