Enzyme activities and morphology of Japanese brown frog (Rana japonica) mitochondria in the tibialis anterior muscle during hibernation and active life

2001 ◽  
Vol 79 (7) ◽  
pp. 1316-1321 ◽  
Author(s):  
Iwao Sato ◽  
Kiyoshi Konishi ◽  
Masataka Sunohara ◽  
Akiko Mikami

Enzyme activities in the respiratory chain, as well as the structure and numbers of mitochondria of the tibialis anterior muscle, during hibernation were compared with those of normally active muscle in the Japanese brown frog (Rana japonica). Morphological examination using an electron microscope showed that during hibernation, mitochondria were larger and longer and had clearly distinguishable outer and inner membranes with developed cristae. A significantly greater number of glycogen granules was found in the tibialis anterior muscle of hibernating frogs. The average cross-sectional area (CSA) of muscle fiber was much smaller in the samples from hibernating frogs than those from active frogs. The numbers of mitochondria per CSA were also much higher during hibernation than during active life. Measurements of the enzyme activities of succinate dehydrogenase, NADH-ferricyanide reductase, and succinate-O2 and NADH-O2 oxidoreductases showed different profiles between hibernation and active life. That is, all four activities were significantly higher during hibernation than during active life. Taken together, the results obtained suggest that the seasonal variations in the activities of respiratory-chain systems may be related to the seasonal morphological changes in muscle mitochondria in R. japonica.

2017 ◽  
Vol 77 (1) ◽  
pp. 83-91 ◽  
Author(s):  
A. Pertille ◽  
K. F. Moura ◽  
C. Y. Matsumura ◽  
R. Ferretti ◽  
D. M. Ramos ◽  
...  

Abstract The aim of this study was to analyze muscle regeneration after cryoinjury in the tibialis anterior muscle of young rats that were malnourished and then recovered. Forty Wistar rats were divided into a nourished group that received a normal protein diet (14% casein) for 90 days and a malnourished and recovered rats group (MR) that was submitted to 45 days of malnutrition with a hypoproteic diet (6% casein) followed by 45 days of a normal protein diet (14% casein). After the recovery period, all of the animals underwent cryoinjury in the right tibialis anterior muscle and euthanasia after 7, 14 and 21 days. The amount of connective tissue and the inflammation area was higher in the malnutrition recovered injury MR group (MRI) at 14 days post-injury (p < 0.05). Additionally, the cross-sectional area (CSA) of the regenerated fibers was decreased in the MRI (p < 0.05). The MyoD and myogenin protein levels were higher in the nourished injury group. Similar levels of TGF-β1 were found between groups. The proposed malnutrition protocol was effective in showing delayed changes in the regeneration process of the tibialis anterior muscle of young rats. Furthermore, we observed a delay in muscle repair even after nutritional recovery.


2020 ◽  
Author(s):  
Arik Davidyan ◽  
Keith Baar ◽  
Sue C. Bodine

AbstractTestosterone is considered a potent anabolic agent in skeletal muscle with a well-established role in adolescent growth and development in males. However, alterations in the role of testosterone in the regulation of skeletal muscle mass and function throughout the lifespan has yet to be established. While some studies suggest that testosterone is important for the maintenance of skeletal muscle mass, an understanding of the role this hormone plays in young, adult, and old males with normal and low serum testosterone levels is lacking. We investigated the role testosterone plays in the maintenance of muscle mass by examining the effect of orchiectomy-induced testosterone depletion in C57Bl6 male mice at ages ranging from early postnatal through old age; the age groups we used included 1.5-, 5-, 12-, and 24-month old mice. Following 28 days of testosterone depletion, we assessed mass and fiber cross-sectional-area (CSA) of the tibialis anterior, gastrocnemius, and quadriceps muscles. In addition, we measured global rates of protein synthesis and degradation using the SuNSET method, western blots, and enzyme activity assays. 28 days of testosterone depletion resulted in smaller muscle mass in the two youngest cohorts but had no effect in the two older ones. Mean CSA decreased only in the youngest cohort and only in the tibialis anterior muscle. Testosterone depletion resulted in a general increase in proteasome activity at all ages. We did not detect changes in protein synthesis at the terminal time point. This data suggest that within physiological serum concentrations, testosterone is not important for the maintenance of muscle mass in mature male mice; however, in young mice testosterone is crucial for normal growth.


PLoS ONE ◽  
2021 ◽  
Vol 16 (3) ◽  
pp. e0240278
Author(s):  
Arik Davidyan ◽  
Suraj Pathak ◽  
Keith Baar ◽  
Sue C. Bodine

Testosterone is considered a potent anabolic agent in skeletal muscle with a well-established role in adolescent growth and development in males. However, the role of testosterone in the regulation of skeletal muscle mass and function throughout the lifespan has yet to be fully established. While some studies suggest that testosterone is important for the maintenance of skeletal muscle mass, an understanding of the role this hormone plays in young, adult, and old males with normal and low serum testosterone levels is lacking. We investigated the role testosterone plays in the maintenance of muscle mass by examining the effect of orchiectomy-induced testosterone depletion in C57Bl6 male mice at ages ranging from early postnatal through old age (1.5-, 5-, 12-, and 24-month old mice). Following 28 days of testosterone depletion, we assessed mass and fiber cross-sectional-area (CSA) of the tibialis anterior, gastrocnemius, and quadriceps muscles. In addition, we measured global rates of protein synthesis and degradation using the SuNSET method, western blots, and enzyme activity assays. Twenty-eight days of testosterone depletion resulted in reduced muscle mass in the two youngest cohorts, but had no effect in the two oldest cohorts. Mean CSA decreased only in the youngest cohort and only in the tibialis anterior muscle. Testosterone depletion resulted in a general increase in proteasome activity at all ages. No change in protein synthesis was detected at the terminal time point. These data suggest that within physiological serum concentrations, testosterone may not be critical for the maintenance of muscle mass in mature male mice; however, in young mice testosterone is crucial for normal growth.


2015 ◽  
Vol 309 (2) ◽  
pp. E122-E131 ◽  
Author(s):  
Preeti Chandrashekar ◽  
Ravikumar Manickam ◽  
Xiaojia Ge ◽  
Sabeera Bonala ◽  
Craig McFarlane ◽  
...  

Peroxisome proliferator-activated receptor β/δ ( PPARβ/δ) is a ubiquitously expressed gene with higher levels observed in skeletal muscle. Recently, our laboratory showed (Bonala S, Lokireddy S, Arigela H, Teng S, Wahli W, Sharma M, McFarlane C, Kambadur R. J Biol Chem 287: 12935–12951, 2012) that PPARβ/δ modulates myostatin activity to induce myogenesis in skeletal muscle. In the present study, we show that PPARβ/δ-null mice display reduced body weight, skeletal muscle weight, and myofiber atrophy during postnatal development. In addition, a significant reduction in satellite cell number was observed in PPARβ/δ-null mice, suggesting a role for PPARβ/δ in muscle regeneration. To investigate this, tibialis anterior muscles were injured with notexin, and muscle regeneration was monitored on days 3, 5, 7, and 28 postinjury. Immunohistochemical analysis revealed an increased inflammatory response and reduced myoblast proliferation in regenerating muscle from PPARβ/δ-null mice. Histological analysis confirmed that the regenerated muscle fibers of PPARβ/δ-null mice maintained an atrophy phenotype with reduced numbers of centrally placed nuclei. Even though satellite cell numbers were reduced before injury, satellite cell self-renewal was found to be unaffected in PPARβ/δ-null mice after regeneration. Previously, our laboratory had showed (Bonala S, Lokireddy S, Arigela H, Teng S, Wahli W, Sharma M, McFarlane C, Kambadur R. J Biol Chem 287: 12935–12951, 2012) that inactivation of PPARβ/δ increases myostatin signaling and inhibits myogenesis. Our results here indeed confirm that inactivation of myostatin signaling rescues the atrophy phenotype and improves muscle fiber cross-sectional area in both uninjured and regenerated tibialis anterior muscle from PPARβ/δ-null mice. Taken together, these data suggest that absence of PPARβ/δ leads to loss of satellite cells, impaired skeletal muscle regeneration, and postnatal myogenesis. Furthermore, our results also demonstrate that functional antagonism of myostatin has utility in rescuing these effects.


2001 ◽  
Vol 91 (6) ◽  
pp. 2466-2470 ◽  
Author(s):  
Thomas J. Burkholder

Muscle fiber length adaptation to static stretch or shortening depends on age, with sarcomere addition in young muscle being dependent on mobility. Series sarcomere number can also increase in young animals in response to increased muscle excursion, but it is not clear whether adult muscles respond similarly. The ankle flexor retinaculum was transected in neonatal and adult rats to increase tibialis anterior muscle excursion. Sarcomere number in tibialis anterior was determined after 8 wk of adaptation. Muscle moment arm and excursion were increased 30% ( P < 0.01) in both age groups. Muscle cross-sectional area was reduced by 12% ( P < 0.01) in response to the increased mechanical advantage, and this reduction was unaffected by age. Fiber length change was also unaffected by age, with both groups showing a trend ( P < 0.10) for slightly (6%) increased fiber length. Retinaculum transection results in shorter muscle length in all joint configurations, so this trend opposes the fiber length decrease predicted by an adaptation to muscle length and indicates that fiber length is influenced by dynamic mechanical signals in addition to static length.


1996 ◽  
Vol 81 (2) ◽  
pp. 876-884 ◽  
Author(s):  
K. Nosaka

This study investigated the time course of changes in serum creatine kinase (CK), aspartate aminotransferase (AST), and alanine amino-transferase (ALT) activities after intramuscular injection of bupivacaine into the tibialis anterior (TA) of rats. Morphological changes in muscle cells, relationships between the amount of increase in the enzyme activities and the muscle mass damaged, and responses of serum enzymes to additional injections of bupivacaine hydrochloride (BPVC) were also examined. Adult male Wistar rats (24 wk) were placed into one of four groups. Group A (n = 7) was a control, and no injection was applied. Saline solution (0.5 ml of 0.9%) was injected into the right TA for group B (n = 5). BPVC (0.5 ml of 0.5%) was injected into the right TA for group C (n = 9) and into both the right and left TA for group D (n = 9). No increases in CK, AST, and ALT were observed for groups A and B. After BPVC injection, groups C and D showed significant (P < 0.01) increases in serum enzyme activities. CK peaked 4 h after BPVC injection, and AST and ALT peaked 12 h postinjection, then returned to the baseline by the time infiltration of mononuclear cells into the damaged muscle cells progressed. The amount of enzyme increase was significantly larger (P < 0.01) for group D compared with group C. Injection of BPVC into the right then into the left TA 4 h later displayed a bipolar response, and the second injection into the TA 12 wk after the first injection resulted in smaller increase in serum enzyme activities. It appeared that increases in serum enzyme activities reflected muscle damage; however, changes in enzymes occurred in the early stage of myonecrosis.


1996 ◽  
Vol 74 (3) ◽  
pp. 315-324 ◽  
Author(s):  
A. N. Pernitsky ◽  
L. M. McIntosh ◽  
J. E. Anderson

The effect of hyperthyroidism on muscle repair was examined in mdx and control mice injected with triiodothyronine (T3) for 4 weeks. On day 24 of treatment, the right tibialis anterior (TA) muscle was crush-injured; 3 days later, mice received intraperitoneal [3H]thymidine to label newly synthesized DNA. One day later, muscles from both limbs were removed to study the severity of dystrophy (uncrushed muscle) and the regeneration response (crushed muscle). In uncrushed TA muscle, the area of active dystrophy (fiber damage and infiltration as a proportion of muscle cross-sectional area) was reduced by half after T3 treatment. Uncrushed muscle fiber diameter was lower in T3-treated control muscles. In crushed muscles, the diameter of new myotubes was larger in mdx mice than in controls and was reduced after T3 treatment in control regenerating muscle. In the same muscles, developmental myosin heavy chain was present in new myotubes and in small numbers of mononuclear cells (possibly differentiating myoblasts) near new myotubes and surviving fibers. Myotube density in the regenerating muscles was not changed by T3 treatment, although the number of myotube nuclei per field was decreased in control and increased in mdx T3-treated mice. Results extend previous reports of T3 effects on dystrophy and the strain difference in muscle precursor cell (mpc) proliferation. The results also suggest the hypothesis that excess T3 affects muscle regeneration either by reducing mpc proliferation or by increasing mpc fusion early in regeneration in control and mdx muscle.Key words: hypothyroid, muscle regeneration, crush injury, proliferation, mdx mouse.


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