Skeletal muscle fatigue and physical endurance of young and old mice

Pagala, Murali; Ravindran, K.; Namba, Tatsuji; Grob, David

doi:10.1002/(sici)1097-4598(199812)21:12<1729::aid-mus16>3.0.co;2-v

Cited by 35 publications

(38 citation statements)

References 41 publications

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“…To measure endurance in fish, critical swimming speed (U crit ) was determined by monitoring the ability to swim against an increasing current over time (Pagala et al, 1998;Plaut, 2000). Fish were placed in a swimming tunnel and a water current was applied.…”

Section: G93r Adult Fish Develop Progressive Motor Abnormalitiesmentioning

confidence: 93%

A genetic model of amyotrophic lateral sclerosis in zebrafish displays phenotypic hallmarks of motoneuron disease

Ramesh

Lyon²,

Pineda³

et al. 2010

Disease Models &Amp; Mechanisms

135

128

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SUMMARYAmyotrophic lateral sclerosis (ALS) is a progressive neurodegenerative disorder that, for ~80% of patients, is fatal within five years of diagnosis. To better understand ALS, animal models have been essential; however, only rodent models of ALS exhibit the major hallmarks of the disease. Here, we report the generation of transgenic zebrafish overexpressing mutant Sod1. The construct used to generate these lines contained the zebrafish sod1 gene and ~16 kb of flanking sequences. We generated lines expressing the G93R mutation, as well as lines expressing wild-type Sod1. Focusing on two G93R lines, we found that they displayed the major phenotypes of ALS. Changes at the neuromuscular junction were observed at larval and adult stages. In adulthood the G93R mutants exhibited decreased endurance in a swim tunnel test. An analysis of muscle revealed normal muscle force, however, at the end stage the fish exhibited motoneuron loss, muscle atrophy, paralysis and premature death. These phenotypes were more severe in lines expressing higher levels of mutant Sod1 and were absent in lines overexpressing wild-type Sod1. Thus, we have generated a vertebrate model of ALS to complement existing mammal models.

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Section: G93r Adult Fish Develop Progressive Motor Abnormalitiesmentioning

confidence: 93%

A genetic model of amyotrophic lateral sclerosis in zebrafish displays phenotypic hallmarks of motoneuron disease

Ramesh

Lyon²,

Pineda³

et al. 2010

Disease Models &Amp; Mechanisms

135

128

View full text Add to dashboard Cite

show abstract

“…There is general agreement that in really old skeletal muscles, myofiber size is decreased (atrophy), numbers of myofibers remain similar (although some reports dispute this), there are changes in myofiber types, wider seams of interstitial connective tissue (endomysium and perimysium) as well as degeneration of nerves and blood vessels (reviewed in (Desaki 2008)), also reduced movement/mobility indicating impaired muscle function (Pagala et al 1998;Carlson et al 2001;Edstrom and Ulfhake 2005). Many of these changes are widely reported for geriatric rats (e.g.…”

Section: Features Of Geriatric Muscles and Micementioning

confidence: 99%

“…Genetics influence aging and there are striking differences in the longevity of mice strains with the mean survival age in days being 576 ± 152 for SJL/J mice (that have a myopathy) and much longer at 793 ± 160 and 767 ± 147 for BALB/c and C57Bl/6J strains, respectively. An age related decline in general function is evident by 18 months, mice aged 18-24 months are considered 'old' and roughly correspond to 56-69 years in humans, 50% of mice die after this time with very few surviving beyond 30 months (corresponding to *80 years in humans) and the maximum life-span is 36 months for C57Bl/6J mice (http://research.jax.org/faculty/harrison/ger1v Lifespan1.html): unusually old C57Bl mice aged 34-37 months were used in one study of muscle fatigue and endurance (Pagala et al 1998). To rigorously test whether the capacity of myogenic cells to form new muscle is compromised in really old (geriatric) muscles, our cross-transplantation whole muscle graft experiments (Smythe et al 2008) were repeated using very old C57Bl/6J mice aged between 27 and 29 months.…”

Section: Introductionmentioning

confidence: 99%

Delayed but excellent myogenic stem cell response of regenerating geriatric skeletal muscles in mice

2009

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The ability of very old animals to make new muscle after injury remains controversial. This issue has major implications for the regenerative potential of damaged geriatric human muscle, to age-related loss of muscle mass (sarcopenia) and to the proposed need for muscle stem cell therapy for the aged. To further address issues of inherent myogenic capacity and the role of host systemic factors in new muscle formation, whole muscle grafts were transplanted between geriatric (aged 27-29 months) and young (3 months) C57Bl/6J mice and compared with autografts in geriatric and young mice. Grafts were sampled at 5 and 10 days for histological analysis. Inflammation and formation of new myotubes was strikingly impaired at 5 days in the geriatric muscle autografts. However, there was a strong inflammatory response by the geriatric hosts to young muscle grafts and geriatric muscles provoked an inflammatory response by young hosts at 5 days. At 10 days, extensive myotube formation in geriatric muscle autografts (equivalent to that seen in young autografts and both other groups) confirmed excellent intrinsic capacity of myogenic (stem) cells to proliferate and fuse. The key conclusion is that a weaker chemotactic stimulus by damaged geriatric muscle, combined with a reduced inflammatory response of old hosts, results in delayed inflammation in geriatric muscle autografts. This delay is transient. Once inflammation occurs, myogenesis can proceed. The presence of well developed myotubes in old muscle autografts at 10 days confirms a very good inherent myogenic response of geriatric skeletal muscle.

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“…Foot shock at the rear of the belt (1.2 mA, 2 Hz) were automatically delivered to keep mice running and prevent them from freezing (Pagala et al, 1998). While mice were acclimated to the apparatus during the first 2 min, the velocity was accelerated from 21 m/min to 30 m/min.…”

Section: Treadmill Testsmentioning

confidence: 99%

Whole-scale neurobehavioral assessments of photothrombotic ischemia in freely moving mice

Zhou

Chai

et al. 2015

Journal of Neuroscience Methods

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Skeletal muscle fatigue and physical endurance of young and old mice

Cited by 35 publications

References 41 publications

A genetic model of amyotrophic lateral sclerosis in zebrafish displays phenotypic hallmarks of motoneuron disease

A genetic model of amyotrophic lateral sclerosis in zebrafish displays phenotypic hallmarks of motoneuron disease

Delayed but excellent myogenic stem cell response of regenerating geriatric skeletal muscles in mice

Whole-scale neurobehavioral assessments of photothrombotic ischemia in freely moving mice

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