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Results for “Muscle atrophy”

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PubMed1991

Glucocorticoid-mediated muscle atrophy: alterations in transcriptional activity of skeletal muscle nuclei.

Glucocorticoid-induced muscle atrophy is associated with a decrease in the level of protein synthesis and a loss of RNA. This paper reports the behaviour of RNA polymerase I- and RNA polymerase II-directed transcription (EC 2.7.7.6) in nuclei isolated from skeletal muscles of rats given a catabolic dose of dexamethasone acetate (5 mg per Kg body weight) over a period of 4 days. Both activities were altered by the dexamethasone treatment. In the case of RNA polymerase I-mediated transcription there was a loss of template-engaged enzymes indicating the existence of an inhibition of initiation of transcription while the rate of elongation of bound enzymes was unaltered. The number of RNA polymerase II-chromatin bound enzymes was increased, but the mean polynucleotide elongation rate was reduced. The possibility that glucocorticoids may impair the elongation stage of transcription in skeletal muscle by increasing the frequency of premature termination of transcripts is discussed. No evidence was obtained for any increase in ribonuclease activity in muscle nuclei of dexamethasone-treated animals.

Animals↗

PubMed1989

[Anesthetic management of spinal progressive muscle atrophy (SPMA)].

The patient with spinal progressive muscle atrophy (SPMA) has many anesthetic problems; muscle atrophy, respiratory complications, hypersensitivity to non-depolarizing muscle relaxants and succinylcholine-induced hyperkalemia. Although neurological complications following spinal and epidural anesthesia have been reported in various neurologic diseases, we chose epidural anesthesia for the patient with SPMA and experienced no problems during and after the operation. We conclude that epidural anesthesia is a useful technique for the patient with SPMA.

Adult↗

PubMed1987

Muscle atrophy in rheumatoid arthritis.

The purpose of this paper is to describe some research opportunities in the area of muscle atrophy secondary to arthritis. Future research should utilize quantitative methods of evaluating muscle atrophy such as computerized tomography or ultrasonography. The gross muscle atrophy should be further characterized by muscle fiber type measurements. These techniques as well as biochemical determinations should be utilized to identify mechanisms of muscle atrophy as well as determine ideal methods for reversing muscle atrophy and weakness.

Arthritis, Rheumatoid↗

PubMed1992

Immobilization-induced muscle atrophy is not reversed by lengthening the muscle.

In clinical practice, repaired tendocalcaneus (Achilles tendon) ruptures are often protected in immobilization casts for 4 weeks in the fully plantar flexed position and for up to another 4 weeks after returning the ankle to joint neutral. Moderate to severe muscle atrophy occurs within 4 weeks of immobilization in plantar flexion, but it is not known if this atrophy is minimized or reversed following restoration of joint neutral position. We tested the hypothesis that the extent of atrophy could be reduced by returning the ankle to joint neutral after 4 weeks of immobilization. Eighteen rabbits were anesthetized, and their right hind-limbs were casted with the knee flexed 90 degrees and the ankle fully plantar flexed. Three animals each were studied after 3, 4, 6, or 8 weeks of immobilization. After 4 weeks of immobilization, the immobilization casts of the remaining six rabbits were modified to return the ankle to joint neutral for another 2 or 4 weeks. For muscle studies, the animals were anesthetized, and the soleus (SOL), plantaris (PLN), and gastrocnemius (GST) muscles were removed and weighed; the SOL and PLN were quick frozen and processed for histochemical fiber typing and fiber cross-sectional area measurement. All three muscles showed significantly reduced muscle weight to body weight ratios after 3 weeks of immobilization. SOL was the most affected, and GST was least affected. There was no significant further atrophy through 8 weeks of immobilization. The atrophy correlated with a significant reduction of mean fiber area (MFA) for Types I, IIo, and IIc fibers in SOL and PLN. In PLN, Type IIg fiber area was not significantly reduced.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed2006

Human skeletal muscle atrophy in amyotrophic lateral sclerosis reveals a reduction in Akt and an increase in atrogin-1.

The molecular mechanisms influencing muscle atrophy in humans are poorly understood. Atrogin-1 and MuRF1, two ubiquitin E3-ligases, mediate rodent and cell muscle atrophy and are suggested to be regulated by an Akt/Forkhead (FKHR) signaling pathway. Here we investigated the expression of atrogin-1, MuRF1, and the activity of Akt and its catabolic (FKHR and FKHRL1) and anabolic (p70(s6k) and GSK-3beta) targets in human skeletal muscle atrophy. The muscle atrophy model used was amyotrophic lateral sclerosis (ALS). All measurements were performed in biopsies from 22 ALS patients and 16 healthy controls as well as in G93A ALS mice. ALS patients had a significant increase in atrogin-1 mRNA and protein content, which was associated with a decrease in Akt activity. There was no difference in the mRNA and protein content of FKHR, FKHRL1, p70(s6k), and GSK-3beta. Similar observations were made in the G93A ALS mice. Human skeletal muscle atrophy, as seen in the ALS model, is associated with an increase in atrogin-1 and a decrease in Akt. The transcriptional regulation of human atrogin-1 may be controlled by an Akt-mediated transcription factor other than FKHR or via another signaling pathway.

Adult↗

PubMed2005

Insulin-like growth factor-I gene transfer by electroporation prevents skeletal muscle atrophy in glucocorticoid-treated rats.

Catabolic states caused by injury are characterized by a loss of skeletal muscle. The anabolic action of IGF-I on muscle and the reduction of its muscle content in response to injury suggest that restoration of muscle IGF-I content might prevent skeletal muscle loss caused by injury. We investigated whether local overexpression of IGF-I protein by gene transfer could prevent skeletal muscle atrophy induced by glucocorticoids, a crucial mediator of muscle atrophy in catabolic states. Localized overexpression of IGF-I in tibialis anterior (TA) muscle was performed by injection of IGF-I cDNA followed by electroporation 3 d before starting dexamethasone injections (0.1 mg/kg.d sc). A control plasmid was electroporated in the contralateral TA muscle. Dexamethasone induced atrophy of the TA muscle as illustrated by reduction in muscle mass (403 +/- 11 vs. 461 +/- 19 mg, P < 0.05) and fiber cross-sectional area (1759 +/- 131 vs. 2517 +/- 93 mum(2), P < 0.05). This muscle atrophy was paralleled by a decrease in the IGF-I muscle content (7.2 +/- 0.9 vs. 15.7 +/- 1.4 ng/g of muscle, P < 0.001). As the result of IGF-I gene transfer, the IGF-I muscle content increased 2-fold (15.8 +/- 1.2 vs. 7.2 +/- 0.9 ng/g of muscle, P < 0.001). In addition, the muscle mass (437 +/- 8 vs. 403 +/- 11 mg, P < 0.01) and the fiber cross-sectional area (2269 +/- 129 vs. 1759 +/- 131 mum(2), P < 0.05) were increased in the TA muscle electroporated with IGF-I DNA, compared with the contralateral muscle electroporated with a control plasmid. Our results show therefore that IGF-I gene transfer by electroporation prevents muscle atrophy in glucocorticoid-treated rats. Our observation supports the important role of decreased muscle IGF-I in the muscle atrophy caused by glucocorticoids.

Animals↗

PubMed1988

Thigh muscle atrophy and postoperative osteoarthrosis after knee ligament tears.

The aim of the study was to clarify if atrophy of the thigh muscles was related to the radiological and clinical long-term healing results of primary knee ligament surgery. At the Tampere University Central Hospital a radiological and clinical reexamination was performed in 61 patients on an average 40 months after primary operation of acute knee ligament injury. The study group consisted of 26 patients having clear quadriceps muscle atrophy in the injured knee at the follow-up. Thirty-four patients with equal circumference of the thighs, served as controls. One patient was excluded. The groups did not differ significantly from each other in respect to age, sex, physical activity, type of ligament injury, meniscectomy, and follow-up time. In radiological evaluation the previously developed knee scoring scale was used taking into account only changes caused by the studied injury. The mean score of the study group was 93.7 +/- 6.2 (range 73-100) and the controls 96.2 +/- 4.0 (87-100); p less than 0.05. In both the most common changes of post-traumatic osteoarthrosis were osteophytes, ligament calcification and joint space narrowing. In clinical examination the patients of the study group were placed significantly more often in the groups of fair or poor healing in subjective, objective, overall (in each p less than 0.001) and functional (p less than 0.05) evaluation. According to this study, it seems that thigh muscle atrophy plays an important role as a poor prognostic factor of knee ligament injuries being thus a good target for efforts to stop the continuous deterioration of the injured knee. Obviously the post-traumatic osteoarthrotic process is a vicious circle: thigh atrophy increases dynamic knee instability, which in turn not only starts or accelerates the arthrotic process but also increases--by discomfort and disuse of the knee--the atrophy itself.

Adolescent↗

PubMed2006

Nuclear translocation of EndoG at the initiation of disuse muscle atrophy and apoptosis is specific to myonuclei.

Skeletal muscle atrophy is associated with an increase in apoptosis, and we showed previously that endonuclease G (EndoG) is localized to nuclei following unloading. The goal of this study was to determine whether the onset of apoptosis in response to disuse was consistent with the hypothesis that EndoG is involved in myofiber nuclear loss. Atrophy was induced by hindlimb suspension for 12 h or 1, 2, 4 and 7 days in 6-mo-old rats. Soleus myofiber cross-sectional area decreased significantly by 2 days, whereas muscle mass and muscle-to-body mass ratio decreased by 4 and 7 days, respectively. By contrast, a significant increase in apoptosis, evidenced by terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling (TUNEL)-positive nuclei, occurred as early as 12 h after suspension, preceding the elevation in muscle atrophy F-box gene expression. The early increase in apoptosis appeared to be specific to myofiber nuclei, whereas TUNEL-positive interstitial cells did not become significantly elevated until 2 days after suspension. Furthermore, TUNEL-positive myofiber nuclei colocalized with EndoG as early as 12 h after suspension, and no such localization was observed in interstitial cells. Although no significant change in total activated caspase-3, -7, or -12 protein abundance was apparent, activated caspase-3 was expressed in interstitial cells undergoing apoptosis, some of which were endothelial cells. These data indicate that apoptosis is an early, and therefore possibly causative, event in the process of muscle atrophy, and that EndoG nuclear translocation is specific for myofiber nuclear apoptosis, whereas interstitial cells may undergo apoptosis via a more classical, caspase-dependent pathway.

Active Transport, Cell Nucleus↗

PubMed2006

FBXO25, an F-box protein homologue of atrogin-1, is not induced in atrophying muscle.

Atrogin-1/MAFbx/FBXO32 is a muscle-specific ubiquitin-ligase (E3) that is dramatically increased in atrophying muscle. Here, we have investigated the functional relationship between atrogin-1 and FBXO25 which shares 65% amino acid identity. Using a RT-PCR, we demonstrated that FBXO25 is highly expressed in brain, kidney, and intestine, whereas atrogin-1 expression is largely restricted to striate muscle. FBXO25 was shown here to contain a functional F-box domain that binds to Skp1 and thereby to Roc1 and Cul1, the major components of SCF-type E3s. In addition, the productive SCF complex containing FBXO25 showed ubiquitin ligase activity. We investigated the differential expression of atrogin-1 and FBXO25 in fasted and dexamethasone-treated mice and also in rats with streptozotocin-induced diabetes. Although the atrogin-1 was strongly induced in muscle in all three models, no changes were observed in the expression of FBXO25. Therefore, here we have shown that FBXO25 is a novel F-box protein analogous to atrogin-1, which is not involved in muscle atrophy. Further functional studies should elucidate the exact role of FBXO25 in the ubiquitin-proteasome pathway.

Amino Acid Sequence↗

PubMed2004

Severe obstructive sleep apnea in a patient with spinal muscle atrophy.

Patients with spinal muscle atrophy (SMA) who survive to adulthood experience a slow, continuous loss of motor function but typically have a normal life expectancy. These patients, however, require vigilance on the part of their health-care providers to reverse treatable disorders to maintain a satisfactory quality of life. We report on a patient with obstructive sleep apnea and type 3 SMA. The treatment of his sleep-disordered breathing resulted in the resolution of symptoms that were initially attributed to his neuromuscular disease.

Humans↗

PubMed2004

Detection of muscle atrophy on routine sonography of the shoulder.

OBJECTIVE: To describe the utility of sonography in visualizing muscle atrophy during routine sonographic examination of the shoulder for evaluation of the rotator cuff tendons. METHODS: A retrospective review of 199 shoulder sonographic examinations performed by 2 musculoskeletal radiologists trained in musculoskeletal sonography with knowledge of the typical sonographic findings of muscle atrophy was performed. Reports were reviewed for the presence of muscle atrophy. If atrophy was present, the reports from those examinations were rereviewed for concomitant rotator cuff abnormalities. RESULTS: Forty-five examinations (23%) showed atrophy in at least 1 muscle on the basis of the criteria of increased echogenicity and decreased bulk. There were a total of 81 individual muscles that showed atrophy, with the following distribution: 16% supraspinatus (n = 13), 31% infraspinatus (n = 25), 36% teres minor (n = 29), 2% subscapularis (n = 2), and 6% biceps brachii (n = 5). In 34 of the 45 examinations with muscle atrophy, there were 57 concomitant full-thickness tendon tears: 64% supraspinatus (n = 29), 38% infraspinatus (n = 17), 7% subscapularis (n = 3), 0% teres minor (n = 0), 16% long head of biceps (n = 7), and 2% deltoid (n = 1). CONCLUSIONS: Although primary sonographic evaluation of the painful shoulder concentrates on the tendons of the rotator cuff, we suggest that examination of the muscles should become a standard component of the comprehensive shoulder sonographic examination, particularly given the potential clinical implications of muscle atrophy on the outcome of rotator cuff surgery.

Adult↗

PubMed1999

Reduced glycogen phosphorylase activity in denervated hindlimb muscles of rat is related to muscle atrophy and fibre type.

Changes in the activity of muscle glycogen synthase or phosphorylase (GP) may be responsible for the deregulation of glycogen synthesis and storage which occurs in diabetes mellitus. To clarify the relationship between muscle atrophy, fibre type, insulin-stimulated glucose uptake and GP activity during insulin resistance, we used sciatic nerve severance to induce insulin resistance in rat hindlimb muscles and compared the above parameters in muscles with a range of fibre types. Changes were analysed by comparison with the contralateral hindlimb, which bears more weight due to denervation of the opposing limb, as well as the sham-operated and contralateral limb of a separate rat. Denervation caused a decrease in insulin-stimulated glucose uptake by 1 day after denervation and a decline of GP activity after 7 days in all muscles investigated. GP activity decreased by 73% in soleus, 36% in red gastrocnemius, 35% in tibialis and 13% in white gastrocnemius, which was related to the degree of muscle atrophy and inversely related to the overall GP activity in non-denervated muscles. GP activity in muscles of the contralateral limb from the denervated rat did not differ from either hindlimb of the sham-operated rat. We conclude that the fibre-type related reduction in insulin-stimulated glucose uptake of denervated muscle determines the change in its metabolism and it is this metabolic change which determines the mechanism, rate and degree of muscle atrophy, which is directly related to the decline in GP activity.

Animals↗

PubMed1998

Muscle atrophy is prevented in patients with acute spinal cord injury using functional electrical stimulation.

Severe muscle atrophy occurs rapidly following traumatic spinal cord injury (SCI). Previous research shows that neuromuscular or 'functional' electrical stimulation (FES), particularly FES-cycle ergometry (FES-CE) can cause muscle hypertrophy in individuals with chronic SCI (> 1 year post-injury). However, the modest degree of hypertrophy in these already atrophied muscles has lessened earlier hopes that FES therapy would reduce secondary impairments of SCI. It is not known whether FES treatments are effective when used to prevent, rather than reverse, muscle atrophy in individuals with acute SCI. This study explored whether unloaded isometric FES contractions (FES-IC) or FES-CE decreased subsequent muscle atrophy in individual with acute SCI (< 3 months post-injury). Twenty-six subjects, 14-15 weeks post-traumatic SCI, were assigned to control, FES-IC, or FES-CE against progessively increasing resistance. Subjects were involved in the study for 3 or 6 months. Total body lean body mass (TB-LBM), lower limb lean body mass (LL-LBM), and gluteal lean body mass (G-LBM) were determined before the study, and at 3 and 6 months using dual energy X-ray absorptiometry (DEXA). Controls lost an average of 6.1%, 10.1%, 12.4%, after 3 months and 9.5%, 21.4%, 26.8% after 6 months in TB-LBM, LL-LBM and G-LBM respectively. Subjects in the FES-IC group consistently lost less lean body mass than controls, however, only 6 month G-LBM loss was significantly attenuated in this group relative to the controls. In the FES-CE group, LL-LBM and G-LBM loss were prevented at both 3 and 6 months, and TB-LBM loss was prevented at 6 months. In addition, FES-CE significantly increased G-LBM and LL-LBM after 6 months of training relative to pre-training levels. Within the control group, there was no significant relationship between LL-LBM loss (3 and 6 months) and the number of days between injury and baseline measurement. In summary, this study shows that FES-CE, but not FES-IC, training prevents muscle atrophy in acute SCI after 3 months of training, and causes significant hypertrophy after 6 months. The magnitude of differences in regionalized LBM between controls and FES-CE subject raises hopes that such treatment may indeed be beneficial in preventing secondary impairments of SCI if employed before extensive post-injury atrophy occurs.

Adult↗

PubMed2006

Estrogen administration attenuates immobilization-induced skeletal muscle atrophy in male rats.

We tested the hypothesis that estrogen administration would retard immobilization-induced muscle atrophy in adult male rats. The rats were injected for 24 days with either estrogen (40 microg/kg(-1), beta-estradiol 3-benzoate in olive oil vehicle), or vehicle alone. At day 14 of estrogen treatment, the hindlimb muscles of one leg were immobilized in plantar flexion position by the use of a plaster cast. Following 10 days of immobilzation, the atrophic and the contralateral soleus muscles were both removed and analyzed to determine the level of muscle atrophy along with the measurement of the protein levels of Cu-Zn-superoxide dismutase (Cu-Zn-SOD), heat shock protein 72 (HSP72), and selected proteases. Compared to placebo animals, estrogen treatment significantly reduced (-35%) muscle atrophy. Further, estrogen significantly abridged the expression of the calcium-activated protease, calpain, in the atrophied hindlimb muscle. In contrast, estrogen treatment did not alter the protein levels of HSP72 in the immobilized soleus muscle. These results support the postulate that estrogen attenuates the rate of disuse muscle atrophy, partly because of reductions in immobilization-induced calcium-activated protease levels.

Animals↗

PubMed2005

Matrix metalloproteinase imbalance in muscle disuse atrophy.

Muscle atrophy commonly occurs as a consequence of prolonged muscle inactivity, as observed after cast immobilization, bed rest or space flights. The molecular mechanisms responsible for muscle atrophy are still unknown, but a role has been proposed for altered permeability of the sarcolemma and of the surrounding connective tissue. Matrix metallo-proteinases (MMPs) are a family of enzymes with proteolytic activity toward a number of extracellular matrix (ECM) components; they are inhibited by tissue inhibitors of MMPs (TIMPs). In a rat tail-suspension experimental model, we show that after fourteen days of non-weight bearing there is increased expression of MMP-2 in the atrophic soleus and gastrocnemius and decreased expression of TIMP-2. In the same experimental model the expression of Collagen I and Collagen IV, two main ECM components present in the muscles, was reduced and unevenly distributed in unloaded animals. The difference was more evident in the soleus than in the gastrocnemius muscle. This suggests that muscle disuse induces a proteolytic imbalance, which could be responsible for the breakdown of basal lamina structures such as Collagen I and Collagen IV, and that this leads to an altered permeability with consequent atrophy. In conclusion, an MMP-2/TIMP-2 imbalance could have a role in the mechanism underlying muscle disuse atrophy; more studies are needed to expand our molecular knowledge on this issue and to explore the possibility of targeting the proteolytic imbalance with MMP inhibitors.

Animals↗

PubMed1994

Resistance exercise and growth hormone as countermeasures for skeletal muscle atrophy in hindlimb-suspended rats.

Unweighting of rat hindlimb muscles results in skeletal muscle atrophy, decreased protein synthesis, and reduced growth hormone (GH) secretion. Resistance exercise (ladder climbing) and GH treatment partially attenuate skeletal muscle atrophy in hypophysectomized hindlimb-suspended rats. It was hypothesized that a combination of multiple bouts of daily resistance exercise and GH (1 mg.kg-1.day-1) would prevent skeletal muscle atrophy in growing nonhypophysectomized hindlimb-suspended rats. Hindlimb suspension decreased the absolute (mg/pair) and relative (mg/100 g body wt) weights of the soleus, a slow-twitch plantar flexor, by 30 and 21%, respectively, and the absolute and relative weights of the gastrocnemius, a predominantly fast-twitch plantar flexor, by 20 and 11%, respectively (P < 0.05). Exercise did not increase soleus mass but attenuated loss of relative wet weight in the gastrocnemius muscles of hindlimb-suspended rats (P < 0.05). Hindlimb suspension decreased gastrocnemius myofibrillar protein content and synthesis (mg/day) by 26 and 64%, respectively (P < 0.05). The combination of exercise and GH attenuated loss of gastrocnemius myofibrillar protein content and synthesis by 70 and 23%, respectively (P < 0.05). Results of the present investigation indicate that a combination of GH and resistance exercise attenuates atrophy of unweighted fast-twitch skeletal muscles.

Animals↗

PubMed2003

Beneficial effects of GH/IGF-1 on skeletal muscle atrophy and function in experimental heart failure.

Muscle atrophy is a determinant of exercise capacity in heart failure (CHF). Myocyte apoptosis, triggered by tumor necrosis factor-alpha (TNF-alpha) or its second messenger sphingosine (SPH), is one of the causes of atrophy. Growth hormone (GH) improves hemodynamic and cardiac trophism in several experimental models of CHF, but its effect on skeletal muscle in CHF is not yet clear. We tested the hypothesis that GH can prevent skeletal muscle apoptosis in rats with CHF. CHF was induced by injecting monocrotaline. After 2 wk, 2 groups of rats were treated with GH (0.2 mg.kg(-1).day(-1) and 1.0 mg.kg(-1).day(-1)) subcutaneously. A third group of controls had saline. After 2 additional weeks, rats were killed. Tibialis anterior cross-sectional area, myosin heavy chain (MHC) composition, and a study on myocyte apoptosis and serum levels of TNF-alpha and SPH were carried out. The number of apoptotic nuclei, muscle atrophy, and serum levels of TNF-alpha and SPH were decreased with GH at high but not at low doses compared with CHF rats. Bcl-2 was increased, whereas activated caspases and bax were decreased. The MHC pattern in GH-treated animals was similar to that of controls. Monocrotaline slowed down both contraction and relaxation but did not affect specific tetanic force, whereas absolute force was decreased. GH treatment restored contraction and relaxation to control values and brought muscle mass and absolute twitch and tetanic tension to normal levels. These findings may provide an insight into the therapeutic strategy of GH given to patients with CHF to improve exercise capacity.

Angiotensin II↗

PubMed2006

Effect of flywheel-based resistance exercise on processes contributing to muscle atrophy during unloading in adult rats.

Flywheel-based resistance exercise (RE) attenuates muscle atrophy during hindlimb suspension. We have previously shown that protein synthesis is elevated in response to RE, but the effect on protein degradation, cell proliferation, or apoptosis was not investigated. We hypothesized that, in addition to affecting protein synthesis, RE inhibits processes that actively contribute to muscle atrophy during hindlimb suspension. Male rats were housed in regular cages (control), tail suspended for 2 wk (HS), or HS with RE every other day for 2 wk (HSRE). Although RE attenuated soleus muscle atrophy during HS, the observed fivefold elevation in apoptosis and the 53% decrease in cell proliferation observed with HS were unaffected by RE. Expression of genes encoding components of the ubiquitin-proteasome pathway of protein degradation were elevated with HS, including ubiquitin, MAFbx, Murf-1, Nedd4, and XIAP, and proteasome subunits C2 and C9. Total ubiquitinated protein was increased with HS, but proteasome activity was not different from control. RE selectively altered the expression of different components of this pathway: MAFbx, Murf-1, and ubiquitin mRNA abundance were downregulated, whereas C2 and C9 subunits remained elevated. Similarly, Nedd4 and XIAP continued to be upregulated, potentially accounting for the observed augmentation in total ubiquitinated protein with RE. Thus a different constellation of proteins is likely ubiquitinated with RE due to altered ubiquitin ligase composition. In summary, the flywheel-based resistance exercise paradigm used in this study is associated with the inhibition of some mechanisms associated with muscle atrophy, such as the increase in MAFbx and Murf-1, but not with others, such as proteasome subunit remodeling, apoptosis, and decreased proliferation, potentially accounting for the inability to completely restore muscle mass. Identifying specific exercise parameters that affect these latter processes may be useful in designing effective exercise strategies in the elderly or during spaceflight.

Animals↗