Morphology and physiology of skeletal muscle in aging rodents

Caccia, M. R.; Harris, John B.; Johnson, Margaret

doi:10.1002/mus.880020308

Cited by 164 publications

(95 citation statements)

References 18 publications

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“…Thirdly, synaptic efficacy began to increase at an age when changes in the major organs were minimal or undetectable, so that the synaptic changes were probably not the sequelae of gross pathophysiologic changes. The mouse may be a particularly suitable experimental animal because in other strains of mouse as well, no major organ pathology was noted at 14-17 months of age (Caccia, Harris & Johnson, 1979), whereas the rat may show nephropathy and other pathology by this age (Caccia et at. 1979;Coleman, Barthold, Osbaldiston, Foster & Jonas, 1977).…”

Section: Discussionmentioning

confidence: 99%

Progression of age changes in synaptic transmission at mouse neuromuscular junctions.

Kelly¹,

Robbins²

1983

The Journal of Physiology

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SUMMARY1. The progression of age-related changes in neuromuscular function was investigated in muscles from CBF-1 mice between 7 and 32 months of age. End-plate potentials (e.p.p.s) were recorded in extensor digitorum longus (e.d.l.), soleus, and diaphragm muscles after neuromuscular transmission was blocked with either (+ )-tubocurarine chloride (curare) or high-Mg/low-Ca Krebs solutions.2. Between 10 and 31 months of age in e.d.l. and soleus but not in diaphragm, there was an increase in e.p.p. amplitude with age. In soleus this increase was approximately two-fold in curare and three-fold in high-Mg solution.3. Increase in e.p.p. amplitude in curarized preparations took place between 20 and 28 months of age in e.d.l. and between 28 and 31 months of age in soleus.4. Indirectly elicited twitch responses were used to determine the time course of age-related changes in sensitivity to Mg block. Increased resistance to block appeared between 15 and 19 months of age in-both e.d.l. and soleus (in which the increase was more gradual).5. E.d.l. muscles from 25-month-old CFW mice also showed an increased resistance to Mg block compared to those from 7-8-month-old animals.6. In Mg-blocked preparations, increased quantum content (measured directly) accounted for the increased e.p.p. amplitude. Spontaneous miniature end-plate potential (m.e.p.p.) frequency in old soleus muscles was not sensitive to low-Ca/highMg solutions although frequency in young soleus and young and old diaphragm was significantly reduced.7. It is concluded that age-related changes in evoked transmitter release begin in mid life and take place more rapidly in e.d.l. than in soleus. This may be due to the difference in muscle type or to the different usage of these muscles. In both muscles, age changes appear before any significant mortality or organ pathology is evident. Decreased sensitivity of transmitter release to low Ca/high Mg is therefore an early sign of altered synaptic transmission in ageing mouse muscle.

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Section: Discussionmentioning

confidence: 99%

Progression of age changes in synaptic transmission at mouse neuromuscular junctions.

Kelly¹,

Robbins²

1983

The Journal of Physiology

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“…The effects of aging on MHC isoform distribution have been studied in humans (Lexell et al, 1983;Lexell, 1995;Lexell et al, 1988;Larsson, 1983) and rodents (Caccia et al, 1979;Kanda and Hashizume, 1989;Kadhiresan et al, 1996). It is understood that aging brings about a loss in fibers (Lexell et al, 1988) and a decrease in type II/type I fiber number (Caccia et al, 1979;Larsson, 1983;Kanda and Hashizume, 1989) and fiber area ratio (Larsson, 1983;Arbanas et al, 2010); this age-related remodeling of motor units appears to involve denervation of fast fibers with reinnervation from nerves that innervate slow fibers (Kadhiresan et al, 1996). We thereby expect the MHC percentages in our study population to be skewed towards higher percentage MHC-1 amounts.…”

Section: Limitationsmentioning

confidence: 99%

Human skeletal muscle biochemical diversity

Tirrell

Cook

Carr

et al. 2012

Journal of Experimental Biology

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SUMMARY The molecular components largely responsible for muscle attributes such as passive tension development (titin and collagen), active tension development (myosin heavy chain, MHC) and mechanosensitive signaling (titin) have been well studied in animals but less is known about their roles in humans. The purpose of this study was to perform a comprehensive analysis of titin, collagen and MHC isoform distributions in a large number of human muscles, to search for common themes and trends in the muscular organization of the human body. In this study, 599 biopsies were obtained from six human cadaveric donors (mean age 83 years). Three assays were performed on each biopsy – titin molecular mass determination, hydroxyproline content (a surrogate for collagen content) and MHC isoform distribution. Titin molecular mass was increased in more distal muscles of the upper and lower limbs. This trend was also observed for collagen. Percentage MHC-1 data followed a pattern similar to collagen in muscles of the upper extremity but this trend was reversed in the lower extremity. Titin molecular mass was the best predictor of anatomical region and muscle functional group. On average, human muscles had more slow myosin than other mammals. Also, larger titins were generally associated with faster muscles. These trends suggest that distal muscles should have higher passive tension than proximal ones, and that titin size variability may potentially act to ‘tune’ the protein's mechanotransduction capability.

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“…Bottai et al, 2003;Cossu and Bianco, 2003;Galli et al, 2005;Vescovi et al, 2002), (3) cell fusion (which may appear similar to a stem cell differentiating into a new lineage when it is transplanted or placed into the niche of a new tissue) (Goodell et al, 2001;Jackson et al, 2002;McKinney-Freeman et al, 2002), (4) adaptation (as in the response to exercise, disuse or aging) (e.g. Allen et al, 2001;Caccia et al, 1979;Harrison et al, 2002;Renault et al, 2002;Thornell et al, 2003), (5) regeneration (as from injury or degenerative neuromuscular and neurological diseases) (e.g. Galli et al.…”

Section: Skeletal Muscle Plasticitymentioning

confidence: 99%

The satellite cell as a companion in skeletal muscle plasticity:currency, conveyance, clue, connector and colander

Anderson

2006

Journal of Experimental Biology

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THE JOURNAL OF EXPERIMENTAL BIOLOGY 2277 Satellite cells in muscle plasticity formed cells fusing to form myoblasts and finally multinucleated muscle fibres.'That conference was a landmark in studies of the satellite cell and muscle regeneration, and was attended by many of the notable and pioneering contributors to the field of muscle development and muscle regeneration. Muir summarized the debate on a working definition of the satellite cell, as follows (Muir, 1970):'The satellite cell of striated muscle can be defined as a mononucleated cell, whose cytoplasm does not contain myofilaments, and which is enclosed by or lies within the basement membrane component of the sarcolemma of the striated muscle fibre. This definition does not exclude cells which are partially or completely separated from the muscle fibre plasma membrane by extensions of the basement membrane, providing that the basement membrane forms a complete investment of their outer surfaces. ' Although there were presentations detailing the observed uptake of 3 H-thymidine into nuclei of satellite cells (Hay, 1970), the role of satellite cells as precursors was not fully established in 1969. In fact there was still very strong debate that a muscle fibre could fragment into blastema cells that led to new formation of muscle. Even at this time, there was more than one paper on the appearance of osteogenic and chondrogenic tissues from minces of muscle replaced under the skin, and a report of muscle fibre nuclei contributed by a labelled connective tissue grafted into a salamander limb during regeneration (Steen, 1970).It wasn't until two seminal reports from the laboratory of Dr Charles Leblond at McGill University (Moss and Leblond, 1970;Moss and Leblond, 1971) that skeletal muscle satellite cells were convincingly identified as the source of precursor cells that proliferate and fuse to form new skeletal muscle fibres. Time-course studies of labelled nuclei in growing muscle showed that satellite cells were the only muscle cells that had incorporated 3 H-thymidine. The report followed work on colchicine-treated rats (MacConnachie et al., 1964) that showed mitotic figures only in the peripheral 'satellite' position on muscle fibres. The idea that muscle fibre nuclei give rise to the increasing number of myonuclei during the growth was convincingly ruled out (Enesco and Puddy, 1964). The notion that satellite cells contribute these domains to a growing or regenerating fibre, one at a time, is daunting in light of the expenditure of proliferative energy and fusion events. However, it speaks strongly to one of the major roles of satellite cells as a currency of muscle (see below). Satellite cells were also observed on intrafusal fibres (Katz, 1961). Two types of satellite cells were identified on these socalled muscle spindle fibres and were distinguished from those on extrafusal fibres (Maynard and Cooper, 1973), although at least one would now be called a myoblast.Although typically quiescent in normal adult muscle, satellite cells are generally con...

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Morphology and physiology of skeletal muscle in aging rodents

Cited by 164 publications

References 18 publications

Progression of age changes in synaptic transmission at mouse neuromuscular junctions.

Progression of age changes in synaptic transmission at mouse neuromuscular junctions.

Human skeletal muscle biochemical diversity

The satellite cell as a companion in skeletal muscle plasticity:currency, conveyance, clue, connector and colander

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