Androgen cytosol binding in exercise-induced sparing of muscle atrophy

1984 ◽  
Vol 247 (5) ◽  
pp. E597-E603
Author(s):  
R. C. Hickson ◽  
T. T. Kurowski ◽  
J. A. Capaccio ◽  
R. T. Chatterton
Keyword(s):  
Muscle Atrophy ◽  
Specific Binding ◽  
Exercise Group ◽  
Treadmill Running ◽  
Female Rats ◽  
Binding Model ◽  
Subcutaneous Injections ◽  
Treatment Groups ◽  
Exercise Induced ◽  
Gastrocnemius Muscles

This study was undertaken to determine whether the exercise-induced sparing of glucocorticoid-induced muscle atrophy is related to increased androgen cytosol binding. Female rats were divided into a sedentary or an exercise group that was trained by treadmill running 100 min/day for 13-15 wk. During the last 12 days of training, each of these groups was further subdivided into groups that received daily subcutaneous injections of cortisone acetate (CA) (100 mg/kg body wt) or the vehicle 1% carboxymethyl cellulose. Exercise prevented 30-40% of the weight loss due to CA treatment in gastrocnemius and plantaris muscles. Scatchard analyses of specific binding of [3H]methyltrienolone (R1881), a synthetic androgen that binds to androgen receptors, were nonlinear in muscles from vehicle-treated sedentary and trained rats and were resolved by a two-component binding model. The lower affinity component, which was attributed to a glucocorticoid receptor, disappeared in muscles of glucocorticoid-treated animals as evidenced by linear Scatchard plots. Receptor concentrations of the androgenic component of [3H]methyltrienolone binding were similar in gastrocnemius and plantaris muscles in all treatment groups. In binding specificity studies of gastrocnemius muscles, the relatively high competition by various glucocorticoids and progesterone for [3H]methyltrienolone binding in the vehicle-treated groups was reduced by CA treatment. The lack of change in androgen cytosol receptor levels suggests that this is not a mechanism by which exercise protects against glucocorticoid-induced muscle atrophy.

Glucocorticoid-induced cardiac hypertrophy: additive effects of exercise

1984 ◽  
Vol 57 (2) ◽  
pp. 514-519 ◽  
Author(s):  
T. T. Kurowski ◽  
R. T. Chatterton ◽  
R. C. Hickson
Keyword(s):  
Specific Binding ◽  
Exercise Program ◽  
Exercise Group ◽  
Treadmill Running ◽  
Female Rats ◽  
Additive Effects ◽  
Glucocorticoid Treatment ◽  
Subcutaneous Injections ◽  
Body Weights ◽  
Cardiac Enlargement

Female rats were divided into a sedentary control and an exercise group that was trained by treadmill running 100 min/day for 13–15 wk. During the last 12 days of training, they were further subdivided into trained and sedentary groups that received either daily subcutaneous injections of cortisone acetate (CA) (100 mg/kg body wt) or the vehicle, 1% (wt/vol) carboxymethylcellulose. As a result of the exercise program, ventricular weights were 15% (P less than 0.01) heavier in the vehicle-treated runners than in the vehicle-treated controls, but there were no changes in cardiac androgen (methyltrienolone, R1881) or glucocorticoid (dexamethasone, DEX) cytosol-specific binding concentrations. Body weights were decreased by 11–12% in both CA-treated groups. Ventricular weights of the CA-treated controls were 11% (P less than 0.01) heavier than the weights of the vehicle-treated controls. The combination of exercise and glucocorticoid treatments resulted in ventricular weights that were 21% heavier than those in the vehicle-treated controls and 8 and 5% (P less than 0.05) greater than those resulting from CA and endurance training individually. Both R1881 and DEX binding were decreased in hearts of CA-treated animals from those of vehicle-treated animals, and exercise did not modify this response. These results show that glucocorticoid treatment can induce cardiac enlargement, and the combination of glucocorticoids and exercise can have additive effects on the growth, yet their mechanisms appear different.

Exercise interrupts ongoing glucocorticoid-induced muscle atrophy and glutamine synthetase induction

1992 ◽  
Vol 263 (6) ◽  
pp. E1157-E1163 ◽  
Author(s):  
M. T. Falduto ◽  
A. P. Young ◽  
R. C. Hickson
Keyword(s):  
Enzyme Activity ◽  
Glutamine Synthetase ◽  
Muscle Atrophy ◽  
Contractile Activity ◽  
Hormone Treatment ◽  
Quadriceps Muscle ◽  
Treadmill Running ◽  
Female Rats ◽  
Glucocorticoid Treatment ◽  
Fast Twitch

This study was undertaken to determine whether regular endurance exercise is a deterrent to a developing state of muscle atrophy from glucocorticoids and to evaluate whether the contractile activity antagonizes the hormonal actions on glutamine synthetase, alanine aminotransferase, and cytosolic aspartate aminotransferase (cAspAT). Adult female rats were administered cortisol acetate (CA, 100 mg/kg body wt) or an equal volume of the vehicle solution for up to 15 days. Exercise (treadmill running at 31 m/min, 10% grade, 90 min/day) was introduced after 4 days of CA treatment, at which time plantaris and quadriceps muscle mass had been reduced to 90% of control levels. Running for 11 consecutive days prevented 40 mg of the 90-mg loss and 227 mg of the 808-mg loss that were subsequently observed in plantaris and quadriceps muscles, respectively, in the sedentary animals. Glutamine synthetase mRNA and enzyme activity were elevated threefold by glucocorticoid treatment in the deep quadriceps (fast-twitch red) muscles after 4 days. Initiating exercise completely interfered with the further hormonal induction (to approximately 5-fold) of this enzyme and, after 11 consecutive days of the exercise regimen, glutamine synthetase mRNA and enzyme activity were 58 and 68% of values from CA-treated sedentary animals. In vehicle-treated groups, basal levels of glutamine synthetase expression were also diminished by exercise to approximately 40% of the values in sedentary controls. Hormone treatment did not alter either aminotransferase enzyme activity but reduced cAspAT mRNA in fast-twitch red muscles by 50%. Exercise abolished the glucocorticoid effect on cAspAT mRNA.(ABSTRACT TRUNCATED AT 250 WORDS)

Testosterone fails to prevent skeletal muscle atrophy from glucocorticoids

1987 ◽  
Vol 63 (1) ◽  
pp. 328-334 ◽  
Author(s):  
J. A. Capaccio ◽  
T. T. Kurowski ◽  
S. M. Czerwinski ◽  
R. T. Chatterton ◽  
R. C. Hickson
Keyword(s):  
Triamcinolone Acetonide ◽  
Muscle Atrophy ◽  
Specific Binding ◽  
Muscle Growth ◽  
Deae Cellulose ◽  
Treated Group ◽  
Female Rats ◽  
Skeletal Muscle Atrophy ◽  
Glucocorticoid Treatment ◽  
Group A

This study was undertaken to determine whether testosterone can stimulate muscle growth as well as counteract the muscle wasting caused by excess glucocorticoids. Female rats were divided into four groups: a vehicle (1% carboxymethycellulose)-treated group, a testosterone acetate (Te)-treated group, a cortisol acetate (Co)-treated group, and a Te + Co group. Animals were injected with the steroids (Te, 40 mg/kg body wt; Co, 20 mg/kg body wt) subcutaneously for 12 consecutive days. Absolute gastrocnemius muscle weights were 8% heavier after testosterone treatment, (P less than 0.05), 20% lighter after glucocorticoid treatment, and 18% lighter after both treatments than those of vehicle-treated animals. However, total body weight loss was less in the Te + Co group than in the group receiving just Co. Specific binding of [3H]triamcinolone acetonide, a synthetic glucocorticoid, in femtomoles per milligram gastrocnemius cytosol protein, was similar between the vehicle-treated (52.9 +/- 4.7) and Te-treated (48.9 +/- 3.6) groups. Specific cytosol binding was also depleted to the same extent (to 11–12 fmol/mg protein) by either the Co or Te + Co injections. There was minimal competition by testosterone for glucocorticoid binding; however, most of the displacement was observed in the corticosteroid binder IB form of the activated triamcinolone acetonide-receptor complex on DEAE-cellulose chromatography. We conclude that Te was ineffective in preventing muscle atrophy caused by Co treatment despite its ability to induce muscle growth. The binding specificity studies lead to the conclusion that most of the testosterone and cortisol functioning were occurring primarily through separate receptor systems.

Partial prevention of glucocorticoid-induced muscle atrophy by endurance training

1981 ◽  
Vol 241 (3) ◽  
pp. E226-E232 ◽  
Author(s):  
R. C. Hickson ◽  
J. R. Davis
Keyword(s):  
Muscle Atrophy ◽  
Protein Concentration ◽  
Gastrocnemius Muscle ◽  
Citrate Synthase ◽  
Treadmill Running ◽  
Male Rats ◽  
Total Protein Concentration ◽  
Muscle Weight ◽  
Subcutaneous Injections ◽  
Fast Twitch

Male rats were either sham-operated (N) or castrated (C) at 65 days of age. They were further subdivided into sedentary or exercise groups that were trained by treadmill running 5 days/wk for 12 wk. During the last 10 days of training, the animals received daily subcutaneous injections of cortisone acetate (CA) (100 mg/kg) or 1% carboxymethylcellulose. Body weight decreased approximately 25% in all groups that received CA. The fast-twitch plantaris and gastrocnemius muscle weights were approximately 35% lower in CA-treated versus cortisone-free N and C sedentary animals. Exercise prevented from one-fourth to one-half of the muscle weight loss in N and C runners when compared to their respective pair weight controls. Muscle weights of the CA-treated freely eating N controls were significantly less than that of N runners that received CA. In plantaris muscles of both N and C animals that received CA, total protein concentration and citrate synthase activity, a mitochondrial marker, remained constant, but their amounts per muscle decreased in proportion to the atrophy. However, myoglobin concentration increased in plantaris muscles of CA-treated animals, although total myoglobin per muscle was reduced slightly. Myoglobin levels were increased in plantaris muscles both as a result of training and CA, but citrate synthase activity was increased only as a result of the exercise. These results show that exercise can retard the glucocorticoid-induced muscle atrophy.

Glucocorticoid cytosol binding in exercise-induced sparing of muscle atrophy

1986 ◽  
Vol 60 (4) ◽  
pp. 1413-1419 ◽  
Author(s):  
R. C. Hickson ◽  
T. T. Kurowski ◽  
G. H. Andrews ◽  
J. A. Capaccio ◽  
R. T. Chatterton
Keyword(s):  
Receptor Binding ◽  
Single Injection ◽  
Serum Cortisol ◽  
Exercise Group ◽  
Treadmill Running ◽  
Female Rats ◽  
Base Line ◽  
Fiber Types ◽  
Muscle Weight ◽  
Muscle Types

Female rats were initially divided into a sedentary or an exercise group that was trained by treadmill running to a final work rate of 31 m/min, 100 min/day, for 13–18 wk. During the last 12 days of training each of these groups were further subdivided into groups that received daily subcutaneous injections of cortisol acetate (CA) (100 mg/kg body wt) or the vehicle (1% carboxymethyl cellulose). Exercise prevented approximately 40% of the gastrocnemius muscle weight loss due to CA treatment. Training did not influence glucocorticoid cytosol-receptor binding concentrations, using [3H]triamcinolone acetonide (TA) as the labeled glucocorticoid in any of the skeletal muscle types investigated. TA-receptor binding capacities were depleted by the multiple injections but were higher in the red fiber types of the CA-treated trained than those in the CA-treated sedentary animals. In a second series of experiments in which receptor depletion and repletion rates were studied using a single injection of cortisol, TA binding capacities 2 h after the cortisol injection were higher in slow-twitch red soleus muscles of trained as compared with sedentary rats (36.4 +/- 2.0 vs. 26.8 +/- 2.5 fmol/mg protein). Similar patterns of TA binding were also observed at 2 h between trained and sedentary animals in the fast-twitch red muscle types, whereas no training related differences were observed in white muscle types. Total and free serum cortisol concentrations also returned to base-line values faster in the trained animals following the single injection protocol.(ABSTRACT TRUNCATED AT 250 WORDS)

Exercise interrupts ongoing glucocorticoid-induced muscle atrophy and glutamine synthetase induction

2006 ◽  
Vol 263 (6) ◽  
pp. E1157-E1163
Author(s):  
M. T. Falduto ◽  
A. P. Young ◽  
R. C. Hickson
Keyword(s):  
Enzyme Activity ◽  
Glutamine Synthetase ◽  
Muscle Atrophy ◽  
Contractile Activity ◽  
Hormone Treatment ◽  
Quadriceps Muscle ◽  
Treadmill Running ◽  
Female Rats ◽  
Glucocorticoid Treatment ◽  
Fast Twitch

This study was undertaken to determine whether regular endurance exercise is a deterrent to a developing state of muscle atrophy from glucocorticoids and to evaluate whether the contractile activity antagonizes the hormonal actions on glutamine synthetase, alanine aminotransferase, and cytosolic aspartate aminotransferase (cAspAT). Adult female rats were administered cortisol acetate (CA, 100 mg/kg body wt) or an equal volume of the vehicle solution for up to 15 days. Exercise (treadmill running at 31 m/min, 10% grade, 90 min/day) was introduced after 4 days of CA treatment, at which time plantaris and quadriceps muscle mass had been reduced to 90% of control levels. Running for 11 consecutive days prevented 40 mg of the 90-mg loss and 227 mg of the 808-mg loss that were subsequently observed in plantaris and quadriceps muscles, respectively, in the sedentary animals. Glutamine synthetase mRNA and enzyme activity were elevated threefold by glucocorticoid treatment in the deep quadriceps (fast-twitch red) muscles after 4 days. Initiating exercise completely interfered with the further hormonal induction (to approximately 5-fold) of this enzyme and, after 11 consecutive days of the exercise regimen, glutamine synthetase mRNA and enzyme activity were 58 and 68% of values from CA-treated sedentary animals. In vehicle-treated groups, basal levels of glutamine synthetase expression were also diminished by exercise to approximately 40% of the values in sedentary controls. Hormone treatment did not alter either aminotransferase enzyme activity but reduced cAspAT mRNA in fast-twitch red muscles by 50%. Exercise abolished the glucocorticoid effect on cAspAT mRNA.(ABSTRACT TRUNCATED AT 250 WORDS)

Initiating regular exercise protects against muscle atrophy from glucocorticoids

1987 ◽  
Vol 63 (4) ◽  
pp. 1504-1510 ◽  
Author(s):  
S. M. Czerwinski ◽  
T. G. Kurowski ◽  
T. M. O'Neill ◽  
R. C. Hickson
Keyword(s):  
Muscle Atrophy ◽  
Citrate Synthase ◽  
Exercise Program ◽  
Exercise Group ◽  
Female Rats ◽  
Exercise Session ◽  
Hormone Administration ◽  
Sedentary Group ◽  
Muscle Sparing ◽  
Muscle Mass Loss

This study was undertaken to examine whether exercise can prevent glucocorticoid-induced muscle atrophy in previously untrained individuals and to evaluate whether the time of hormone administration is a determinant in the muscle's response to glucocorticoids. Female rats were divided into five groups: 1) a sedentary group that received cortisol acetate (CA, 100 mg/kg body wt); 2) a sedentary group that received the dosing vehicle (1% aqueous carboxymethyl cellulose); 3) an exercise group that received CA immediately after each exercise session; 4) an exercise group that received CA 90 min after each exercise session; and 5) an exercise group that received the vehicle. Steroid treatment and exercise (28.7 m/min for 90 min/day) were performed for 11 consecutive days. Initiation of training prevented muscle mass loss by 60% in plantaris (P) muscles and by 25% in gastrocnemius (G) muscles. Time of steroid injection was not related to the muscle sparing response. In the glucocorticoid-treated exercised rats, the activities of citrate synthase, a training marker, increased 60% in P and 37% in G. Thus the exercise appeared to cause a greater recruitment of P muscles. These data support the hypothesis that entering into an exercise program can be effective in retarding glucocorticoid-induced muscle atrophy. The degree of atrophy prevention, however, may be related to the extent that specific muscles are recruited during exercise.

Effects of tissue fractionation on exercise-induced alterations in SR function in rat gastrocnemius muscle

1996 ◽  
Vol 80 (3) ◽  
pp. 940-948 ◽  
Author(s):  
E. R. Chin ◽  
H. J. Green
Keyword(s):  
Atpase Activity ◽  
Treadmill Running ◽  
Sr Protein ◽  
Isolation Techniques ◽  
Exercise Induced ◽  
Gastrocnemius Muscles ◽  
Whole Muscle ◽  
Tissue Fractionation ◽  
Muscle Homogenate

Because studies into exercise-induced alterations in sarcoplasmic reticulum (SR) Ca2+ sequestration have produced conflicting reports, we have hypothesized that the differences in SR Ca(2+)-adenosinetriphosphatase (ATPase) activity and Ca2+ uptake in SR fractions observed in different studies are due to different SR isolation techniques. To investigate this possibility, rat white and red gastrocnemius muscles from control and run animals were studied by using two conventional isolation techniques to obtain a crude microsomal fraction and an isolated SR vesicle (SRV) fraction. Indexes of CM and SRV function were compared with measurements from whole muscle homogenate. Treadmill running to exhaustion did not alter SR protein yields, percent SR extraction, or basal or Ca(2+)-ATPase purification in either fraction. Ca(2+)-activated ATPase activity was not altered by exercise in any of the fractions examined, but Ca2+ uptake was reduced in the homogenates (9.48 +/- 1.4 to 6.90 +/- 0.8 nmol . mg-1.min-1) and SRV fractions (84.0 +/- 11.5 to 50.7 +/- 14.0 nmol . mg-1.min-1) from the red gastrocnemius at free Ca2+ concentrations of 600-700 nM. These data indicate that reductions in SR Ca2+ uptake are dissociated from changes in Ca(2+)-ATPase in vitro and occur only in a specific population of vesicles. The mechanisms underlying these alterations are not known but may involve a reduction in the number of Ca(2+)-ATPase enzymes or a selective sedimentation of damaged vesicles in the SRV fraction.

Skeletal muscle respiratory capacity, endurance, and glycogen utilization

1975 ◽  
Vol 228 (4) ◽  
pp. 1029-1033 ◽  
Author(s):  
RH Fitts ◽  
FW Booth ◽  
WW Winder ◽  
JO Holloszy
Keyword(s):  
Skeletal Muscle ◽  
Citrate Synthase ◽  
Treadmill Running ◽  
Mitochondrial Content ◽  
Respiratory Capacity ◽  
Leg Muscles ◽  
Glycogen Utilization ◽  
Exercise Induced ◽  
Gastrocnemius Muscles ◽  
The Relationship

This study was undertaken to evaluate the relationship between physical performance capacity and the mitochondrial content of skeletal muscle. Four groups of rats were trained by means of treadmill running 5 days/wk for 13 wk. One group ran 10 min/day, a second group ran 30 min/day, a third group ran 60 min/day, and a fourth group ran 120 min/day. The magnitude of the exercise-induced adaptive increase in gastrocnemius muscle respiratory capacity varied over a twofold range in the four groups. There were significant correlations between the levels of three mitochondrial markers (cytochrome c, citrate synthase, respiratory capacity) in the animals' gastrocnemius muscles and the duration of a run to exhaustion. There was also a significant correlation between the amounts of glycogen remaining in liver and skeletal muscle after a 30-min-long exercise test and the respiratory capacity of the animal's leg muscles. These findings are compatible with the interpretation that a close relationshiop exists between skeletal muscle mitochondrial content and the capacity to perform endurance exercise.

scholarly journals The Acute Effects of Swimming Exercise on PGC-1α-FNDC5/Irisin-UCP1 Expression in Male C57BL/6J Mice

Metabolites ◽  
2021 ◽  
Vol 11 (2) ◽  
pp. 111
Author(s):  
Eunhee Cho ◽  
Da Yeon Jeong ◽  
Jae Geun Kim ◽  
Sewon Lee
Keyword(s):  
Adipose Tissue ◽  
Protein Expression ◽  
Swimming Exercise ◽  
Enzyme Linked Immunosorbent Assay ◽  
Control Group ◽  
Brown Adipose ◽  
Mrna And Protein Expression ◽  
Ucp1 Expression ◽  
Exercise Induced ◽  
Gastrocnemius Muscles

Irisin is a myokine primarily secreted by skeletal muscles and is known as an exercise-induced hormone. The purpose of this study was to determine whether the PGC-1α -FNDC5 /Irisin-UCP1 expression which is an irisin-related signaling pathway, is activated by an acute swimming exercise. Fourteen to sixteen weeks old male C57BL/6J mice (n = 20) were divided into control (CON, n = 10) and swimming exercise groups (SEG, n = 10). The SEG mice performed 90 min of acute swimming exercise, while control (non-exercised) mice were exposed to shallow water (2 cm of depth) for 90 min. The mRNA and protein expression of PGC-1α, FNDC5 and browning markers including UCP1 were evaluated by quantitative real-time PCR and western blotting. Serum irisin concentration was measured by enzyme-linked immunosorbent assay. An acute swimming exercise did not lead to alterations in the mRNA and protein expression of PGC-1α in both soleus and gastrocnemius muscles, the mRNA and protein expression of UCP1 in brown adipose tissue, mRNA browning markers in visceral adipose tissue and circulating irisin when compared with the control group. On the other hand, an acute swimming exercise led to increases in the mRNA and protein expressions of FNDC5 in the soleus muscle, the protein expression of FNDC5 in the gastrocnemius muscles and the protein expression of UCP1 in subcutaneous adipose tissue.

Sign in / Sign up

Export Citation Format

Share Document