Bed rest decreases mechanically induced myofiber wounding and consequent wound-mediated FGF release

1998 ◽  
Vol 85 (2) ◽  
pp. 593-600 ◽  
Author(s):  
Mark S. F. Clarke ◽  
Marcas M. Bamman ◽  
Daniel L. Feeback
Keyword(s):  
Skeletal Muscle ◽  
Creatine Kinase ◽  
Exercise Program ◽  
Bed Rest ◽  
Serum Levels ◽  
Skeletal Muscle Atrophy ◽  
Fibroblast Growth ◽  
Resistive Exercise ◽  
Before And After ◽  
Identical Fashion

Using a terrestrial model of spaceflight (i.e., bed rest), we investigated the amount of myofiber wounding and fibroblast growth factor (FGF) release that occurs during unloading. Myofiber wounding was determined by serum levels of the creatine kinase MM (CKMM) isoform before and after bed rest. Serum levels of both acidic FGF (aFGF) and basic FGF were also determined. A second group of subjects was treated in an identical fashion except that they underwent a resistive exercise program during bed rest. Bed rest alone caused significant ( P < 0.05; n = 7) reductions in post-bed-rest serum levels of both CKMM and aFGF, which were paralleled by a significant ( P < 0.05; n = 7) decrease in myofiber size. In contrast, bed rest plus resistive exercise resulted in significant ( P < 0.05; n = 7) increases in post-bed-rest serum levels of both CKMM and aFGF, which were paralleled by inhibition of the atrophic response. These results suggest that mechanically induced, myofiber wound-mediated FGF release may play an important role in the etiology of unloading-induced skeletal muscle atrophy.

scholarly journals Vibration mechanosignals superimposed to resistive exercise result in baseline skeletal muscle transcriptome profiles following chronic disuse in bed rest

2015 ◽  
Vol 5 (1) ◽  
Author(s):  
Michele Salanova ◽  
Guido Gambara ◽  
Manuela Moriggi ◽  
Michele Vasso ◽  
Ute Ungethuem ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Bed Rest ◽  
Resistive Exercise ◽  
Skeletal Muscle Transcriptome

Resistance training affects GLUT-4 content in skeletal muscle of humans after 19 days of head-down bed rest

1999 ◽  
Vol 86 (3) ◽  
pp. 909-914 ◽  
Author(s):  
Izumi Tabata ◽  
Youji Suzuki ◽  
Tetsuo Fukunaga ◽  
Toshiko Yokozeki ◽  
Hiroshi Akima ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Resistance Training ◽  
Membrane Protein ◽  
Vastus Lateralis ◽  
Bed Rest ◽  
Training Group ◽  
Control Group ◽  
Glut 4 ◽  
Before And After ◽  
Voluntary Contractions

This study assessed the effects of inactivity on GLUT-4 content of human skeletal muscle and evaluated resistance training as a countermeasure to inactivity-related changes in GLUT-4 content in skeletal muscle. Nine young men participated in the study. For 19 days, four control subjects remained in a −6° head-down tilt at all times throughout bed rest, except for showering every other day. Five training group subjects also remained at bed rest, except during resistance training once in the morning. The resistance training consisted of 30 isometric maximal voluntary contractions for 3 s each; leg-press exercise was used to recruit the extensor muscles of the ankle, knee, and hip. Pauses (3 s) were allowed between bouts of maximal contraction. Muscle biopsy samples were obtained from the lateral aspect of vastus lateralis (VL) muscle before and after the bed rest. GLUT-4 content in VL muscle of the control group was significantly decreased after bed rest (473 ± 48 vs. 398 ± 66 counts ⋅ min−1 ⋅ μg membrane protein−1, before and after bed rest, respectively), whereas GLUT-4 significantly increased in the training group with bed rest (510 ± 158 vs. 663 ± 189 counts ⋅ min−1 ⋅ μg membrane protein−1, before and after bed rest, respectively). The present study demonstrated that GLUT-4 in VL muscle decreased by ∼16% after 19 days of bed rest, and isometric resistance training during bed rest induced a 30% increase above the value of GLUT-4 before bed rest.

Effects of Rest, Exercise and Warming on Serum Creatine Kinase Levels in Primary Hypothyroidism

1981 ◽  
Vol 60 (5) ◽  
pp. 595-597 ◽  
Author(s):  
B. P. O'Malley ◽  
T. J. Davies ◽  
F. D. Rosenthal
Keyword(s):  
Creatine Kinase ◽  
Body Temperature ◽  
Important Determinant ◽  
Bed Rest ◽  
Primary Hypothyroidism ◽  
Serum Creatine Kinase ◽  
Oral Temperature ◽  
Control Subjects ◽  
Before And After ◽  
Significant Change

1. Serum creatine kinase and oral temperature were measured in 20 patients with primary hypothyroidism before and after 48 h bed rest. Fifteen of these patients were heated during the 48 h period. The remaining five acted as control subjects. In addition, creatine kinase and oral temperature were measured in five control subjects after a 30 min period of exercise and again after a 30 min period of resting. 2. The oral temperature rose and the serum creatine kinase levels fell only in those patients who were actively warmed. In the control subjects the period of exercise followed by resting caused no significant change in creatine kinase levels. 3. A subnormal body temperature appears to be an important determinant of the raised serum creatine kinase levels seen in patients with primary hypothyroidism.

Role of skeletal muscles impairment and brain oxygenation in limiting oxidative metabolism during exercise after bed rest

2010 ◽  
Vol 109 (1) ◽  
pp. 101-111 ◽  
Author(s):  
Simone Porcelli ◽  
Mauro Marzorati ◽  
Francesca Lanfranconi ◽  
Paola Vago ◽  
Rado Pišot ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Gas Exchange ◽  
Oxidative Metabolism ◽  
Skeletal Muscles ◽  
Near Infrared ◽  
Slow Component ◽  
Bed Rest ◽  
Brain Oxygenation ◽  
Before And After

“Central” and “peripheral” limitations to oxidative metabolism during exercise were evaluated in 10 young males following a 35-day horizontal bed rest (BR). Incremental exercise (IE) and moderate- and heavy-intensity constant-load exercises (CLE) were carried out on a cycloergometer before and 1–2 days after BR. Pulmonary gas exchange, cardiac output (Q̇; by impedance cardiography), skeletal muscle (vastus lateralis), and brain (frontal cortex) oxygenation (by near-infrared spectroscopy) were determined. After BR, “peak” (values at exhaustion during IE) workload, peak O2 uptake (V̇o2peak), peak stroke volume, Q̇peak, and peak skeletal muscle O2 extraction were decreased (−18, −18, −22, −19, and −33%, respectively). The gas exchange threshold was ∼60% of V̇o2peak both before and after BR. At the highest workloads, brain oxygenation data suggest an increased O2 extraction, which was unaffected by BR. V̇o2 kinetics during CLE (same percentage of peak workload before and after BR) were slower (time constant of the “fundamental” component: 31.1 ± 2.0 s before vs. 40.0 ± 2.2 s after BR); the amplitude of the “slow component” was unaffected by BR, thus it would be greater, after BR, at the same absolute workload. A more pronounced “overshoot” of skeletal muscle O2 extraction during CLE was observed after BR, suggesting an impaired adjustment of skeletal muscle O2 delivery. The role of skeletal muscles in the impairment of oxidative metabolism during submaximal and maximal exercise after BR was identified. The reduced capacity of peak cardiovascular O2 delivery did not determine a “competition” for the available O2 between skeletal muscles and brain.

scholarly journals A mini review: Proteomics approaches to understand disused vs. exercised human skeletal muscle

2018 ◽  
Vol 50 (9) ◽  
pp. 746-757 ◽  
Author(s):  
Yoshitake Cho ◽  
Robert S. Ross
Keyword(s):  
Skeletal Muscle ◽  
Muscle Mass ◽  
Muscle Atrophy ◽  
Human Skeletal Muscle ◽  
Molecular Mechanisms ◽  
Bed Rest ◽  
Skeletal Muscle Atrophy ◽  
Direct Result ◽  
Muscle Disorders ◽  
Exercise Induced

Immobilization, bed rest, or denervation leads to muscle disuse and subsequent skeletal muscle atrophy. Muscle atrophy can also occur as a component of various chronic diseases such as cancer, AIDS, sepsis, diabetes, and chronic heart failure or as a direct result of genetic muscle disorders. In addition to this atrophic loss of muscle mass, metabolic deregulation of muscle also occurs. In contrast, physical exercise plays a beneficial role in counteracting disuse-induced atrophy by increasing muscle mass and strength. Along with this, exercise can also reduce mitochondrial dysfunction and metabolic deregulation. Still, while exercise causes valuable metabolic and functional adaptations in skeletal muscle, the mechanisms and effectors that lead to these changes such as increased mitochondria content or enhanced protein synthesis are not fully understood. Therefore, mechanistic insights may ultimately provide novel ways to treat disuse induced atrophy and metabolic deregulation. Mass spectrometry (MS)-based proteomics offers enormous promise for investigating the molecular mechanisms underlying disuse and exercise-induced changes in skeletal muscle. This review will focus on initial findings uncovered by using proteomics approaches with human skeletal muscle specimens and discuss their potential for the future study.

Creatine kinase isoenzyme MM variants in skeletal muscle and plasma from marathon runners.

1986 ◽  
Vol 32 (1) ◽  
pp. 41-44 ◽  
Author(s):  
F S Apple ◽  
M A Rogers ◽  
J L Ivy
Keyword(s):  
Skeletal Muscle ◽  
Creatine Kinase ◽  
Strenuous Exercise ◽  
Variant Form ◽  
Distance Runners ◽  
Long Distance ◽  
Marathon Runners ◽  
Creatine Kinase Isoenzyme ◽  
Before And After

Abstract We investigated the patterns of variants of creatine kinase isoenzyme MM (CK-MM) in gastrocnemius muscle and plasma sampled from male and female long-distance runners before and after a marathon race. The proportions of CK-MM variants MM1 (pI 6.90) and MM2 (pI 6.62), identified in the skeletal muscle from both sexes, did not differ significantly from those in skeletal muscle from nonrunning controls or from heart muscle. CK-MM1 was the major (84-85% of total CK-MM) variant form. Patterns of CK-MM in plasma collected from male runners 24, 48, 72, and 96 h after the race were similar to those for female runners, but we detected two new additional variants, which we designate MM1B (pI 6.76) and MM2B (pI 6.49). For both sexes the total CK-MM activities in plasma were significantly (p less than 0.05) greater after the race, but the women's total CK-MM activities were significantly (p less than 0.05) less than the men's. The rates of disappearance of MM1, MM2, and MM3 from plasma after the race differed significantly (p less than 0.05) between men and women, MM1 clearing the fastest. Determination of the CK-MM variants in plasma after strenuous exercise may be of help in assessing CK release from injured skeletal muscle.

Exercise-induced pyruvate dehydrogenase activation is not affected by 7 days of bed rest

2011 ◽  
Vol 111 (3) ◽  
pp. 751-757 ◽  
Author(s):  
Kristian Kiilerich ◽  
Stine Ringholm ◽  
Rasmus S. Biensø ◽  
James P. Fisher ◽  
Ninna Iversen ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Glucose Intolerance ◽  
Muscle Glycogen ◽  
Pyruvate Dehydrogenase ◽  
Active Form ◽  
Bed Rest ◽  
Whole Body ◽  
Oral Glucose ◽  
Before And After ◽  
Exercise Induced

To test the hypothesis that physical inactivity impairs the exercise-induced modulation of pyruvate dehydrogenase (PDH), six healthy normally physically active male subjects completed 7 days of bed rest. Before and immediately after the bed rest, the subjects completed an oral glucose tolerance test (OGTT) and a one-legged knee extensor exercise bout [45 min at 60% maximal load (Wmax)] with muscle biopsies obtained from vastus lateralis before, immediately after exercise, and at 3 h of recovery. Blood samples were taken from the femoral vein and artery before and after 40 min of exercise. Glucose intake elicited a larger ( P ≤ 0.05) insulin response after bed rest than before, indicating glucose intolerance. There were no differences in lactate release/uptake across the exercising muscle before and after bed rest, but glucose uptake after 40 min of exercise was larger ( P ≤ 0.05) before bed rest than after. Muscle glycogen content tended to be higher (0.05< P ≤ 0.10) after bed rest than before, but muscle glycogen breakdown in response to exercise was similar before and after bed rest. PDH-E1α protein content did not change in response to bed rest or in response to the exercise intervention. Exercise increased ( P ≤ 0.05) the activity of PDH in the active form (PDHa) and induced ( P ≤ 0.05) dephosphorylation of PDH-E1α on Ser293, Ser295 and Ser300, with no difference before and after bed rest. In conclusion, although 7 days of bed rest induced whole body glucose intolerance, exercise-induced PDH regulation in skeletal muscle was not changed. This suggests that exercise-induced PDH regulation in skeletal muscle is maintained in glucose-intolerant (e.g., insulin resistant) individuals.

scholarly journals Liver fibrosis-induced muscle atrophy is mediated by elevated levels of circulating TNFα

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Tamaki Kurosawa ◽  
Momo Goto ◽  
Noriyuki Kaji ◽  
Satoshi Aikiyo ◽  
Taiki Mihara ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Liver Cirrhosis ◽  
Liver Fibrosis ◽  
Muscle Atrophy ◽  
Diploid Cell ◽  
Serum Levels ◽  
Skeletal Muscle Atrophy ◽  
Mouse Serum ◽  
Fibrotic Liver ◽  
Duct Ligation

AbstractLiver cirrhosis is a critical health problem associated with several complications, including skeletal muscle atrophy, which adversely affects the clinical outcome of patients independent of their liver functions. However, the precise mechanism underlying liver cirrhosis-induced muscle atrophy has not been elucidated. Here we show that serum factor induced by liver fibrosis leads to skeletal muscle atrophy. Using bile duct ligation (BDL) model of liver injury, we induced liver fibrosis in mice and observed subsequent muscle atrophy and weakness. We developed culture system of human primary myotubes that enables an evaluation of the effects of soluble factors on muscle atrophy and found that serum from BDL mice contains atrophy-inducing factors. This atrophy-inducing effect of BDL mouse serum was mitigated upon inhibition of TNFα signalling but not inhibition of myostatin/activin signalling. The BDL mice exhibited significantly up-regulated serum levels of TNFα when compared with the control mice. Furthermore, the mRNA expression levels of Tnf were markedly up-regulated in the fibrotic liver but not in the skeletal muscles of BDL mice. The gene expression analysis of isolated nuclei revealed that Tnf is exclusively expressed in the non-fibrogenic diploid cell population of the fibrotic liver. These findings reveal the mechanism through which circulating TNFα produced in the damaged liver mediates skeletal muscle atrophy. Additionally, this study demonstrated the importance of inter-organ communication that underlies the pathogenesis of liver cirrhosis.

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