Alterations in the contractile properties of motor units within the ageing rat medial gastrocnemius

Einsiedel, L.J.; Luff, A. R.

doi:10.1016/0022-510x(92)90147-d

Cited by 60 publications

(60 citation statements)

References 21 publications

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“…Therefore investigations are important to determine how these changes progress with age to elucidate the underlying mechanisms for sarcopenia and muscle weakness that occurs with age. Mechanical and morphological properties of motor units in the aged rat have been reported previously (Edström and Larsson 1987;Einsiedel and Luff 1992;Kadhiresan et al 1996;Kanda and Hashizume 1989;Kanda et al 1986;Larsson 1995;Larsson andAnsved 1988, 1995;Larsson and Edström 1986;Pettigrew and Noble 1991). These studies have demonstrated that changes in the properties of motor units with advancing age are affected by multiple factors, such as degenerative changes of motoneuron and muscle fiber, the denervation and reinnervation process, transformation of muscle fibers, etc.…”

Section: Introductionsupporting

confidence: 55%

“…In some of these units, this process reduces or even exceeds a decrease in tension due to muscle fiber atrophy and a decrease in the specific tension. Recapturing of denervated muscle fibers and remodeling of motor units in the aged have been reported repeatedly in human subjects (Campbell et al 1973;Stålberg and Thiele 1975) and in experimental animals (Einsiedel and Luff 1992;Kadhiresan et al 1996;Kanda and Hashizume 1989;Larsson 1995). Using the glycogen depletion technique and the computer-assisted method, Ansved et al (1991) found some characteristics in spatial reorganization of motor-unit fibers due to a denervation-reinnervation process.…”

Section: Discussionmentioning

confidence: 79%

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Progress of Age-Related Changes in Properties of Motor Units in the Gastrocnemius Muscle of Rats

Sugiura¹,

Kanda²

2004

Journal of Neurophysiology

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Sugiura, Miho and Kenro Kanada. Progress of age-related changes in properties of motor units in the gastrocnemius muscle of rats. J Neurophysiol 92: 1357-1365, 2004. First published April 14, 2004 10.1152/jn.00947.2003. The mechanical properties of individual motor units in the medial gastrocnemius muscle, as well as the whole muscle properties and innervating motor nucleus, were investigated in dietary-restricted, male Fischer 344/DuCrj rats at ages of 4, 7, 12, 21/22, 27, 31, and 36 mo. The tetanic tension of the type S units continuously increased until the age of 36 mo. Those of type FF and FR units declined from 21/22 to 27 mo of age but did not change further while the whole muscle tension decreased greatly. The atrophy of muscle fibers, the decline in motoneuron number and axonal conduction velocity, and the decrease in the posttetanic potentiation of twitch contraction of motor units seemed to start after 21/22 mo of age and were accelerated with advancing age. Prolongation of twitch contraction time was evident for only type S and FR units in 36-moold rats. The fatigue index was greatly increased for type FF units in 36-mo-old rats. These findings indicated that the progress of changes in various properties occurring in the senescent muscle was different in terms of their time course and degree and also dependent on the types of motor unit. The atrophy and decrease in specific tension of muscle fibers affected the decline in tension output of motor units. This was effectively compensated for by the capture of denervated muscle fibers over time.

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Section: Introductionsupporting

confidence: 55%

Section: Discussionmentioning

confidence: 79%

Progress of Age-Related Changes in Properties of Motor Units in the Gastrocnemius Muscle of Rats

Sugiura¹,

Kanda²

2004

Journal of Neurophysiology

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“…Based on these results, we further hypothesize that the primary cause of the aging-related loss in strength that precedes, and is in excess of, the loss of muscle mass, is a failure to activate satellite cells to repair cumulative injury that results from normal muscle use. The prevention of type IIb fiber loss is intriguing, as it has been proposed that the loss of those fibers during senescence results from the death of the motor neurons that innervate them (24). However, it is unclear if the motor neuron loss is a primary event or a secondary consequence of the inability of fast motor neurons to compete with slow motor neurons for innervation of regenerating fibers (25).…”

Section: Resultsmentioning

confidence: 99%

Viral mediated expression of insulin-like growth factor I blocks the aging-related loss of skeletal muscle function

Barton-Davis

Shoturma

Musarò

et al. 1998

Proc. Natl. Acad. Sci. U.S.A.

632

405

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During the aging process, mammals lose up to a third of their skeletal muscle mass and strength. Although the mechanisms underlying this loss are not entirely understood, we attempted to moderate the loss by increasing the regenerative capacity of muscle. This involved the injection of a recombinant adeno-associated virus directing overexpression of insulin-like growth factor I (IGF-I) in differentiated muscle fibers. We demonstrate that the IGF-I expression promotes an average increase of 15% in muscle mass and a 14% increase in strength in young adult mice, and remarkably, prevents aging-related muscle changes in old adult mice, resulting in a 27% increase in strength as compared with uninjected old muscles. Muscle mass and fiber type distributions were maintained at levels similar to those in young adults. We propose that these effects are primarily due to stimulation of muscle regeneration via the activation of satellite cells by IGF-I. This supports the hypothesis that the primary cause of aging-related impairment of muscle function is a cumulative failure to repair damage sustained during muscle utilization. Our results suggest that gene transfer of IGF-I into muscle could form the basis of a human gene therapy for preventing the loss of muscle function associated with aging and may be of benefit in diseases where the rate of damage to skeletal muscle is accelerated.

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“…These include, but are not limited to, loss of muscle fibres37 and reduced myofibre CSA21, 38, 39 associated with degeneration and structural alterations of the NMJ,40, 41, 42 a decline in functional innervation (partial denervation)41, 43, 44 and loss of motor units 3, 44, 45. Although it is not justified to extrapolate results from transgenic animal models to human muscles (i.e.…”

Section: Introductionmentioning

confidence: 99%

Redox homeostasis and age‐related deficits in neuromuscular integrity and function

Sakellariou

Lightfoot

Earl

et al. 2017

J cachexia sarcopenia muscle

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Skeletal muscle is a major site of metabolic activity and is the most abundant tissue in the human body. Age‐related muscle atrophy (sarcopenia) and weakness, characterized by progressive loss of lean muscle mass and function, is a major contributor to morbidity and has a profound effect on the quality of life of older people. With a continuously growing older population (estimated 2 billion of people aged >60 by 2050), demand for medical and social care due to functional deficits, associated with neuromuscular ageing, will inevitably increase. Despite the importance of this ‘epidemic’ problem, the primary biochemical and molecular mechanisms underlying age‐related deficits in neuromuscular integrity and function have not been fully determined. Skeletal muscle generates reactive oxygen and nitrogen species (RONS) from a variety of subcellular sources, and age‐associated oxidative damage has been suggested to be a major factor contributing to the initiation and progression of muscle atrophy inherent with ageing. RONS can modulate a variety of intracellular signal transduction processes, and disruption of these events over time due to altered redox control has been proposed as an underlying mechanism of ageing. The role of oxidants in ageing has been extensively examined in different model organisms that have undergone genetic manipulations with inconsistent findings. Transgenic and knockout rodent studies have provided insight into the function of RONS regulatory systems in neuromuscular ageing. This review summarizes almost 30 years of research in the field of redox homeostasis and muscle ageing, providing a detailed discussion of the experimental approaches that have been undertaken in murine models to examine the role of redox regulation in age‐related muscle atrophy and weakness.

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Alterations in the contractile properties of motor units within the ageing rat medial gastrocnemius

Cited by 60 publications

References 21 publications

Progress of Age-Related Changes in Properties of Motor Units in the Gastrocnemius Muscle of Rats

Progress of Age-Related Changes in Properties of Motor Units in the Gastrocnemius Muscle of Rats

Viral mediated expression of insulin-like growth factor I blocks the aging-related loss of skeletal muscle function

Redox homeostasis and age‐related deficits in neuromuscular integrity and function

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