Effects of ovariectomy and hindlimb unloading on skeletal muscle

1998 ◽  
Vol 85 (4) ◽  
pp. 1316-1321 ◽  
Author(s):  
Jonathan S. Fisher ◽  
Eileen M. Hasser ◽  
Marybeth Brown

Female rats (7–8 mo old, n = 40) were randomly placed into the intact control (Int) and ovariectomized control (Ovx) groups. Two weeks after ovariectomy, animals were further divided into intact 2-wk hindlimb unloaded (Int-HU) and ovariectomized hindlimb unloaded (Ovx-HU). We hypothesized that there would be greater hindlimb unloading-related atrophy in Ovx than in Int rats. In situ contractile tests were performed on soleus (Sol), plantaris (Plan), peroneus longus (Per), and extensor digitorum longus (EDL) muscles. Body weight and Sol mass were ∼22% larger in Ovx than in Int group and ∼18% smaller in both HU groups than in Int rats (Ovx × HU interaction, P < 0.05), and there was a similar trend in Plan muscle ( P< 0.07). There were main effects ( P< 0.05) for both ovariectomy (growth) and hindlimb unloading (atrophy) on gastrocnemius mass. Mass of the Per and EDL muscles was unaffected by either ovariectomy or hindlimb unloading. Time to peak twitch tension for EDL and one-half relaxation times for Sol, Plan, Per, and EDL muscles were faster ( P< 0.05) in Ovx than in Int animals. The results suggest that 1) ovariectomy led to similar increases of ∼20% in body weight and plantar flexor mass; 2) hindlimb unloading may have prevented ovariectomy-related muscle growth; 3) greater atrophy may have occurred in Sol and Plan of Ovx animals compared with controls; and 4) removal of ovarian hormonal influence decreased skeletal muscle contraction times.

1994 ◽  
Vol 58 (3) ◽  
pp. 357-364 ◽  
Author(s):  
H. Gallbraith ◽  
A. D. Berry

AbstractTwenty-five Border Leicester ♂ × Blackface ♀ wether lambs aged about 4 months and weighing on average 28·5 kg were allocated to be treated with the naturally occurring steroid testosterone or trenbolone acetate or nandrolone phenylpropionate which are steroids synthetically produced. Treatment groups were as follows: untreated controls (C); 50 mg testosterone (T); 50 mg trenbolone acetate (TA); 50 mg testosterone + 50 mg trenbolone acetate (TTA) or 50 mg nandrolone phenylpropionate (N). Implants were given at 100 and again at 63 days before slaughter. The lambs were offered to appetite a good quality diet containing, per kg dry matter, an estimated 11·0 MJ metabolizable energy and 185 g crude protein. Comparisons were made for the main effects of T and TA and also interactions between T and TA. Effects due to N were assessed statistically against untreated controls. Treatment with T, on average, increased live-weight gain (LWG), empty body weight (EBW) and reduced backfat thickness and the weight (g/kg EBW) of perirenal and retroperitoneal fat. Main effects due to TA were increases in killing-out ratio and depth of the gigot joint and reductions in backfat thickness. Treatment with N increased the empty body weight and (g/kg) carcass ash. Non-significant (P > 0·05) trends were suggested for increases in carcass crude protein due to T and TA treatments. T and TA but not N treatments exhibited marked androgenic activity in increasing the weight (mg/kg EBW) of the accessary vesicular gland. TA and N, but not T, reduced the weight (g/kg EBW) of the thymus gland.The maximum binding capacity of post-morte m skeletal muscle (m. gluteus) for (3H)-dexamethasone was reduced by TA but increased by T and N. These results suggest differences in the binding capacity of corticosteroid receptors which may be related to differences in the effects of T and TA on protein metabolism in skeletal muscle.


1978 ◽  
Vol 44 (2) ◽  
pp. 225-230 ◽  
Author(s):  
F. W. Booth

The recovery time course of muscle atrophied by immobilization was followed after removal of hindlimb casts from adult female rats. Increases of only 9% in body weight, 4% in gastrocnemius weight, and 10% in soleus weight occurred in controls during the 78-day duration of the experiment. There were no increases in the amounts of total protein or of citrate synthase activities in gastrocnemius or soleus during the first 3 days after removal of hindlimb casts; thereafter, there were increases in these paramters. Citrate synthase activities per mg of gastrocnemius protein were significantly higher at the 16th and 50th day of recovery. No significant differences for citrate synthase activity per mg of soleus occurred during recovery. Until the 50th day of recovery, no significant differences for total protein in soleus and for total protein and wet weight of gastrocnemius were observed between control and recovery values. However, the wet weight of the soleus returned rapidly during recovery and was not significantly different from control during recovery.


Animals ◽  
2019 ◽  
Vol 10 (1) ◽  
pp. 10
Author(s):  
Grzegorz Smołucha ◽  
Anna Kozubska-Sobocińska ◽  
Anna Koseniuk ◽  
Kacper Żukowski ◽  
Mirosław Lisowski ◽  
...  

Myostatin, also known as growth differentiation factor 8 (GDF8), belongs to the TGF- β superfamily of proteins. MSTN is a highly conserved protein that acts as a negative regulator of skeletal muscle growth. Loss of myostatin functionality causes the phenotype to appear in the form of ‘double musculature’, among others in cattle, sheep, and house mice. The presented results of the research were carried out on two geese breeds—Landes and Kielecka. The aim of the study was to identify mutations in the MSTN gene and study their impact on body weight in both geese breeds in different periods of life. Analysis of the obtained results showed the existence of polymorphism in exon 3 (c.1231C>T) and suggested a possible association (p < 0.05) between BW and genotype in 12 weeks of life in male Kielecka geese breed. The identified polymorphism may be one of the factors important for improving body weight in the studied Kielecka breed, therefore, it is necessary to conduct further research on a larger population of geese breeds in order to more accurately estimate the effect of the identified SNP c.1231C>T on BW in geese.


1996 ◽  
Vol 149 (1) ◽  
pp. 81-91 ◽  
Author(s):  
S P Kirk ◽  
M A Whittle ◽  
J M Oldham ◽  
P M Dobbie ◽  
J J Bass

Abstract GH enhances skeletal muscle growth, and IGF-II peptide is highly expressed during regeneration. We have therefore investigated the effect of GH administration on IGF-II binding and expression in regenerating rat skeletal muscle using the techniques of receptor autoradiography and in situ hybridisation. Notexin, a myotoxin, was injected into the right M. biceps femoris (day 0), causing affected fibres to undergo necrosis followed by rapid regeneration. Animals were administered either GH (200 μg/100 g body weight) or saline vehicle daily. Contralateral muscles were used as regeneration controls. GH administration during regeneration resulted in significant increases in body weight, and damaged and undamaged muscle weights (P<0·001). IGF-II expression, which was examined in regenerating fibres, survivor fibres and undamaged fibres, varied according to tissue type (P< 0·001). Specifically, IGF-II expression in regenerating fibres was elevated relative to control and survivor fibres after day 3 (P<0·05), with a peak on day 9 (P<0·001). GH did not affect IGF-II message levels. 125I-IGF-II binding in regenerating muscle was examined in the same fibre types as well as in connective tissue. 125I-IGF-II binding in regenerating fibres was higher (P<0·001) than in other tissue types on day 5. GH administration increased 125I-IGF-II binding in all damaged muscle tissues on day 5 (P<0·001, regenerating fibres; P<0·01, others). We believe that this shows for the first time an effect of GH on the Type 2 IGF receptor in regenerating skeletal muscle. Journal of Endocrinology (1996) 149, 81–91


2012 ◽  
Vol 113 (5) ◽  
pp. 719-726 ◽  
Author(s):  
Satoshi Koba ◽  
Kenshi Yoshinaga ◽  
Sayaka Fujita ◽  
Michio Miyoshi ◽  
Tatsuo Watanabe

In women, sympathoexcitation during static handgrip exercise is reduced during the follicular phase of the ovarian cycle compared with the menstrual phase. Previous animal studies have demonstrated that estrogen modulates the exercise pressor reflex, a sympathoexcitatory mechanism originating in contracting skeletal muscle. The present study was conducted in female rats to determine whether skeletal muscle contraction-evoked reflex sympathoexcitation fluctuates with the estrous cycle. The estrous cycle was judged by vaginal smear. Plasma concentrations of estrogen were significantly ( P < 0.05) higher in rats during the proestrus phase of the estrus cycle than those during the diestrus phase. In decerebrate rats, either electrically induced 30-s continuous static contraction of the hindlimb muscle or 30-s passive stretch of Achilles tendon (a maneuver that selectively stimulates mechanically sensitive muscle afferents) evoked less renal sympathoexcitatory and pressor responses in the proestrus animals than in the diestrus animals. Renal sympathoexcitatory response to 1-min intermittent (1- to 4-s stimulation to relaxation) bouts of static contraction was also significantly less in the proestrus rats than that in the diestrus rats. In ovariectomized female rats, 17β-estradiol applied into a well covering the dorsal surface of the lumbar spinal cord significantly reduced skeletal muscle contraction-evoked responses. These observations demonstrate that the exercise pressor reflex function and its mechanical component fluctuate with the estrous cycle in rats. Estrogen may cause these fluctuations through its attenuating effects on the spinal component of the reflex arc.


2012 ◽  
Vol 302 (5) ◽  
pp. R643-R654 ◽  
Author(s):  
Thomas Chaillou ◽  
Nathalie Koulmann ◽  
Nadine Simler ◽  
Adélie Meunier ◽  
Bernard Serrurier ◽  
...  

Hypoxia induces a loss of skeletal muscle mass, but the signaling pathways and molecular mechanisms involved remain poorly understood. We hypothesized that hypoxia could impair skeletal muscle hypertrophy induced by functional overload (Ov). To test this hypothesis, plantaris muscles were overloaded during 5, 12, and 56 days in female rats exposed to hypobaric hypoxia (5,500 m), and then, we examined the responses of specific signaling pathways involved in protein synthesis (Akt/mTOR) and breakdown (atrogenes). Hypoxia minimized the Ov-induced hypertrophy at days 5 and 12 but did not affect the hypertrophic response measured at day 56. Hypoxia early reduced the phosphorylation levels of mTOR and its downstream targets P70S6K and rpS6, but it did not affect the phosphorylation levels of Akt and 4E-BP1, in Ov muscles. The role played by specific inhibitors of mTOR, such as AMPK and hypoxia-induced factors (i.e., REDD1 and BNIP-3) was studied. REDD1 protein levels were reduced by overload and were not affected by hypoxia in Ov muscles, whereas AMPK was not activated by hypoxia. Although hypoxia significantly increased BNIP-3 mRNA levels at day 5, protein levels remained unaffected. The mRNA levels of the two atrogenes MURF1 and MAFbx were early increased by hypoxia in Ov muscles. In conclusion, hypoxia induced a transient alteration of muscle growth in this hypertrophic model, at least partly due to a specific impairment of the mTOR/P70S6K pathway, independently of Akt, by an undefined mechanism, and increased transcript levels for MURF1 and MAFbx that could contribute to stimulate the proteasomal proteolysis.


2004 ◽  
Vol 16 (2) ◽  
pp. 275-283 ◽  
Author(s):  
Tara G. McDaneld ◽  
Deana L. Hancock ◽  
Diane E. Moody

β-Adrenergic receptor agonists (BA) stimulate skeletal muscle growth. However, downstream signaling pathways that facilitate this effect remain poorly defined. Objectives of this study were to identify genes differentially expressed after administration of a novel BA and to evaluate the expression of one of those genes in additional models of skeletal muscle growth. Differentially expressed gene fragments were identified through differential display of skeletal muscle biopsies from five steers 24 h after administration of the BA. Five gene fragments designated DD53, DD143, DD163, DD209, and DD214 were identified. Tissue distribution of these genes was evaluated by RT-PCR. While DD53, DD163, DD209, and DD214 were expressed across tissues, DD143 mRNA expression was most abundant in skeletal muscle. DD143, later identified as bovine ASB15, was evaluated in rats following administration of anabolic compounds. Thirteen 7-wk-old female rats were randomly assigned to each of four treatment groups including: control, clenbuterol, trenbolone acetate (TBA), and growth hormone (GH). Changes in rat Asb-15 mRNA were measured at 30 min, 12 h, and 24 h following intraperitoneal injections of each compound. Clenbuterol treatment decreased Asb-15 mRNA in skeletal muscle at 12 and 24 h ( P < 0.01) and also decreased mRNA in lung at 12 h ( P < 0.05). TBA and GH treatments did not alter Asb-15 mRNA in any of the tissues evaluated ( P > 0.10). These results are the first to associate an Asb gene family member with muscle growth or BA administration and suggest a potential role for ASB15 in β-agonist-induced skeletal muscle hypertrophy.


1996 ◽  
Vol 271 (5) ◽  
pp. R1422-R1428 ◽  
Author(s):  
D. Martin ◽  
E. Merkel ◽  
K. K. Tucker ◽  
J. L. McManaman ◽  
D. Albert ◽  
...  

Recombinant human ciliary neurotrophic factor (rh-CNTF) was reported to attenuate skeletal muscle wasting in rats after unilateral transection of the sciatic nerve (M. E. Helgren, S. P. Squinto, H. L. Davis, D. J. Parry, T. G. Bolton, C. S. Heck, Y. Zhu, G. D. Yancopoulos, R. M. Lindsay, and P. S. DiStefano. Cell 76: 493-504, 1994). Under the experimental conditions reported herein, the absolute masses of the denervated gastrocnemius and soleus muscles were not increased in mature or immature rats of either sex by treatment with rhCNTF. At the highest doses of rhCNTF (1 and 0.1 mg/kg), increases in the ratio of the masses of the denervated to the contralateral innervated gastrocnemius and soleus muscles could be attributed entirely to a muscle-wasting effect on the contralateral innervated muscle rather than any muscle-sparing effect on the denervated muscle. The muscle-wasting effects of rhCNTF were associated with reductions in body weight gain and reduced food intake. Pair-fed rats lost less body weight and skeletal muscle mass than rhCNTF-injected freely fed rats but experienced significantly greater loss of visceral mass. Male rats displayed greater loss of body weight and skeletal muscle mass than female rats. Recombinant inhibitors of the cachectic cytokines, tumor necrosis factor and interleukin-1, did not significantly alter the wasting effects of rhCNTF. These findings demonstrate that, in contrast to its well-characterized trophic effects on cells of the nervous system, rhCNTF causes atrophy of skeletal muscle by mechanisms involving both anorexia and cachexia based on the results of pair-feeding experiments.


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