Abstract:The aims of the present study were to show the distribution of individual myosin light chain (MyLC) isoforms in fast-twitch (FT) and slowtwitch (ST) muscles and between FT muscles in order to find differences between MyLC isoforms in these muscles, to identify similarities with the distribution of myosin heavy chain (MyHC) isoforms and to investigate changes in these relations during adaptation to endurance and resistance training. Male Wistar strain rats were used in this study. One-dimensional electrophoresis was used for separation of MyHC and MyLC isoforms and two-dimensional electrophoresis was used for identification of MyLC different isoforms. A difference in the relative content of MyLC isoforms between FT muscles exists only in the case of MyLC 1 slow and 2 slow isoforms. Differences in the relative content of MyHC between FT muscles are considerably larger than differences in the MyLC isoforms. MyHC and MyLC isoforms both participate in the remodelling of contractile proteins during exercise training. In conclusion: The present study shows some discrepancy between the modulation of MyHC and MyLC isoforms in muscles with different oxidative potential during adaptation to endurance and resistance training. In ST muscles, there is full agreement between the increase in the relative content of MyHC IIa isoform and MyLC 2 fast and 3 fast isoforms during resistance training without significant changes during endurance training. The ratio of MyLC 3 and MyLC 2 isoforms increases during both types of exercise training, but it is two times higher during resistance training.(Biol.Sport 26:215-234, 2009)
Background:
Aging leads to changes in skeletal muscle quantity and quality and is
accompanied with increase in body mass and fat mass, whereas fat-free mass either decreases or
remains unchanged. The body composition of rodents has been an important factor for clinical trials
in the laboratory. Glucocorticoids such as dexamethasone are widely used in clinical medicine, but
may induce myopathy, characterized by muscle weakness, atrophy, and fatigue. In animals treated
with glucocorticoids, a dose-dependent reduction of body weight has been observed. This weight
loss is usually followed by muscle atrophy and a reduction of several muscle proteins, contributing
to impaired muscle function. This study was designed to describe changes in body composition and
BMC of 22-month-old rats during 10- and 20-day recovery period after 10-day dexamethasone
administration.
Method:
Data on body mass, lean body mass, fat mass and bone mineral content of the rats were
obtained with dual energy X-ray absorptiometry scan.
Result:
Significant reduction in body mass, lean body mass, fat mass and fast-twitch muscle mass
was observed after dexamethasone treatment. Body mass, fat mass and fast-twitch muscle mass
stayed decreased during 20 days after terminating the hormone administration; lean body mass
reached the preadministration level after 20-day recovery period. There were no significant changes
in bone mineral density during the recovery period. Dexamethasone treatment gradually reduced
hindlimb grip strength that also stayed decreased during the 20-day recovery period.
Conclusion:
his study demonstrated that a 10-day period of overexprosure to glycocorticoids
induced longlasting changes in old rats’ body composition and these values did not attain the
baseline level even after 20-day recovery period.
The objective of the study was to examine skeletal muscle regeneration capacity of young and very old rats during autotransplantation. In 3.5 and 30 month-old Wistar rats, gastrocnemius muscle was removed and grafted back to its original bed. Incorporation of 3H leucine into myofibrillar and sarcoplasmic protein fractions, their relative contents in autografts and synthesis rate of MyHC and actin were recorded. The relative muscle mass of old rats was about 67% of that of young rats; the absolute mass of autografted muscle was 61% intact in the young rat group and 51% in the old rat group. Content of myofibrillar protein in the autografts of young rats was 46% of the intact muscle content, and 39% in the old rat group. In conclusion, the difference in skeletal muscle regeneration capacity of young and very old rats is about ten percent. In the autografts of both young and old rats, the regeneration of the contractile apparatus is less effective in comparison with the sarcoplasmic compartment.
Viscoelastic properties of skeletal muscle are associated with a complex network of cytoskeletal proteins where titin and nebulin play a substantial role. The need for evaluation of muscle viscoelastic properties is widely accepted in clinical use to evaluate the effect of treatment or progression of muscle pathology (atrophy). We tested the hypothesis that the viscoelastic properties (elasticity, tone and stiffness) change in atrophied muscles with concomitant changes in cytoskeletal proteins (titin, nebulin) and contractile protein (myosin heavy chain) proportion. Sixteen 24-week-old male rats of the Wistar strain were randomly allocated to two groups: dexamethasone group treated each day for 10 consecutive days with dexamethasone in order to induce atrophy and control group. Skeletal muscle viscoelastic properties (elasticity, tone and stiffness) were determined using a myotonometer. Titin, nebulin and myosin heavy chain content were quantified using SDS-PAGE electrophoresis. We found that glucocorticoid-induced muscle atrophy is accompanied by reduced elasticity and increased tone and stiffness, with concomitant changes in titin, nebulin and myosin heavy chain content. The elasticity decreased by 10.9% (P < 0.05), tone increased from 26.69 Hz to 37.73 Hz (P < 0.05), and stiffness was significantly lower in dexamethasone group (627.3 N/m vs 758.6 N/m); (P < 0.05). Compared with the control group, the content of titin, nebulin and myosin heavy chain in atrophied muscle was 76.4%, 70.6% and 82.3%, respectively. Our results may lead to a better understanding of the mechanism of muscle atrophy and provide better guidance for rehabilitation practices and help to find rational therapeutic intervention in the future.
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