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Does prednisone affect muscle growth. Effect of short-term prednisone use on blood flow, muscle protein metabolism, and function
Does prednisone affect muscle growth
Muscle volume was measured in the psoas muscle and other muscles. The Wilcoxon signed-rank test was used to compare paired data for each patient. The Mann-Whitney U test was used to compare two sets of data sampled from the two groups. The inter-reader agreement showed excellent correlation between the two readers, ranging from 0.
Seven patients with myositis and eight controls were analyzed in this study. The muscle strength, measured using MMT, improved after steroid therapy in all patients with myositis Table 1. Table 1. The most frequent underlying diseases in patients with myositis were chronic obstructive pulmonary disease COPD and interstitial lung disease followed by cancer e. No patients with cancer underwent chemotherapy. All underlying diseases were detected within 2 months of the diagnosis of myositis.
Conversely, chronic kidney disease was the most frequent underlying disease in the control group Table 3. With regard to the rate of muscle volume change between the groups, although the myositis group showed greater muscle volume loss in comparison to the control group, the difference was not statistically significant Fig.
CT computed tomography. Although all patients with myositis showed improvements in muscle strength and serum muscle enzyme levels after steroid therapy, there was a significant loss of muscle volume.
The loss of muscle mass is induced by both extrinsic causes and intrinsic causes. Extrinsic causes of focal muscle atrophy often developed after traumatic injury such as Morel-Lavallee syndrome which is a post-traumatic closed degloving injury [ 16 ].
Our patients did not have a history of trauma. Therefore, we think that extrinsic causes had little involvement in the change of muscle mass in our patients. With regard to intrinsic causes, previous studies have reported that patients with cancer, COPD, and chronic kidney disease exhibited a loss of muscle volume [ 17 , 18 , 19 ].
In the present study, some of the patients had these conditions as underlying diseases. Therefore, the involvement of these underlying diseases may be associated with the observed muscle volume loss in our patients especially in patients with cancer and COPD in the myositis group. However, the patients with myositis who did not develop these underlying diseases also showed a loss of muscle volume. This suggests that steroid therapy itself decreases muscle volume in patients with myositis.
Thus, an improvement in muscle strength in patients with myositis may be attributed to other factors and not to muscle volume change. Some mechanisms have been proposed to explain the etiology of the loss of muscle volume. One of these mechanisms is an imbalance of protein synthesis and catabolism [ 20 ]. Steroid myopathy is induced by the hypercatabolism of skeletal muscle, which might have resulted in the loss of muscle volume in our patients. However, despite the loss of muscle mass, improvement in muscle strength was also observed in patients with myositis who were treated with steroids.
As such, we hypothesize that the improvement in muscle strength is influenced by an improvement in mitochondrial function. Currently, a non-immune cell mediated mechanism in myositis has been proposed [ 21 ]. It was reported that the endoplasmic reticulum ER stress pathways are chronically activated in patients with myositis [ 21 ]. Additionally, the biopsy specimens from patients with myositis and mice models of myositis demonstrated an increase in levels of Grp78 also known as HSPA5 , which is an ER stress-related protein [ 22 ].
The biopsy specimens from patients with myositis also showed co-localization of MHC class I and the ER marker, calnexin [ 22 ]. These results suggest the possibility of the involvement of ER stress in the pathogenesis of myositis. Xiao et al. In contrast, serum HSPA5 levels did not change in non-responders [ 23 ].
The results of the previous study suggest that steroid therapy reduces ER stress in steroid-responsive patients with myositis. ER stress is known to increase reactive oxygen species, which are closely associated with mitochondrial dysfunction, depressed force generation, and activation of muscle catabolic and autophagy pathways [ 21 ]. We speculate that steroid therapy improves muscle strength via the reduction of ER stress and reactive oxygen species followed by an improvement in mitochondrial function.
Our study suggests that the improvement in muscle strength after steroid therapy is not influenced by an improvement in muscle volume, but rather by an improvement in other factors, such as amelioration of mitochondrial dysfunction. Our study has a few limitations.
First, this was a retrospective study and the number of patients was small. The non-significant change in the low muscle attenuation rate after steroid therapy and the non-significant change between the rate of change of muscle volume in patients with myositis associated with COPD and cancer may be partly due to the small sample size.
Second, the regimens for steroid reduction and the timing of implementation of the second CT were different for each of the patients, which makes it difficult to accurately assess the correlations between muscular changes and clinical factors. Third, though patients who experienced disuse syndrome were excluded from the control group, exact scores from the MMT muscular strength of the control group were unknown, which makes it difficult to assess the change of muscle strength in the control group.
However, our study suggests the importance of therapies that not only improve muscle mass but also improve the quality of muscle strength for the treatment of myositis. Hence, this study may provide novel insights into therapies for myositis. Nonetheless, further studies are needed to reveal the mechanism and treatment of muscle weakness in patients with myositis. In patients with myositis treated with steroid therapy, muscle mass decreased after steroid therapy, suggesting that the improvement in muscle strength was due to factors other than changes in muscle volume.
Mechanisms involved in the side effects of glucocorticoids. Pharmacol Ther. Article PubMed Google Scholar. Mechanisms of glucocorticoid-induced myopathy. J Endocrinol. Steroid myopathy in connective tissue disease. Am J Med. Steroid myopathy: incidence and detection in a population with asthma. J Allergy Clin Immunol. Diagnosis and classification of idiopathic inflammatory myopathies.
J Intern Med. Drug therapy of the idiopathic inflammatory myopathies: predictors of response to prednisone, azathioprine, and methotrexate and a comparison of their efficacy. Bioelectrical impedance analysis in clinical practice: a new perspective on its use beyond body composition equations. Regional skeletal muscle measurement: evaluation of new dual-energy X-ray absorptiometry model.
J Appl Physiol Biomarkers of sarcopenia in clinical trials-recommendations from the international working group on sarcopenia. J Cachexia Sarcopenia Muscle. Skeletal muscle area correlates with body surface area in healthy adults. Hepatol Res. MR imaging of skeletal muscle signal alterations: systematic approach to evaluation. Eur J Radiol.
Measurement of skeletal muscle radiation attenuation and basis of its biological variation. Acta Physiol Oxf. Quantitative analysis of skeletal muscle mass in patients with rheumatic diseases under glucocorticoid therapy--comparison among bioelectrical impedance analysis, computed tomography, and magnetic resonance imaging. Mod Rheumatol.
Bohan A, Peter JB. Polymyositis and Dermatomyositis first of two parts. N Engl J Med. Statistical methodology for the concurrent assessment of interrater and intrarater reliability: using goniometric measurements as an example.
Phys Ther. Morel-Lavallee lesions-review of pathophysiology, clinical findings, imaging findings and management. J Clin Diagn Res. Cancer cachexia in the age of obesity: skeletal muscle depletion is a powerful prognostic factor, independent of body mass index.
J Clin Oncol. Peripheral muscle weakness in patients with chronic obstructive pulmonary disease. Fahal IH. Uraemic sarcopenia: aetiology and implications. Nephrol Dial Transplant. Role of glucocorticoids in the molecular regulation of muscle wasting. Crit Care Med. Ann Rheum Dis. Activation of the endoplasmic reticulum stress response in autoimmune myositis: potential role in muscle fiber damage and dysfunction.
Arthritis Rheum. Some of the less common potential side effects of prednisone can make exercise more challenging—or even dangerous—such as irregular heartbeat, dizziness, sweating, or blurred vision. If you have difficulty exercising or experience worsening side effects, reduce the intensity and duration of the exercise and work your way up.
In general, there are no specific exercises that are safer than others while taking prednisone. However, weight-bearing exercises can help prevent osteoporosis—a possible side effect of long-term prednisone use, such as:. Sehgal says. When your healthcare provider prescribes prednisone, make sure to disclose all medications prescription and OTC , vitamins, and supplements you currently are taking—including anything you use to improve workout performance.
Then, your provider can discuss the possible interactions with you. If your healthcare provider has given you the go-ahead, finding a way to exercise while taking prednisone can have several benefits for your health.
One reason people are prescribed prednisone is to reduce inflammation. Exercise can also help minimize inflammation. Katz says. Sehgal explains. Improved circulation further decreases inflammation, a main goal of taking prednisone in the first place.
Often prednisone is prescribed to help relieve symptoms related to asthma. Exercise can also be beneficial for those who have asthma.
All of these can reduce the time it takes for someone with asthma to feel out of breath and may reduce symptoms. Exercise can also improve asthma symptoms because it increases the amount of oxygen you receive. Li says. And as most people know, getting your heart rate up can help you drop pounds—and inflammation. The bottom line? If you feel up to it, and your provider clears you for activity, exercise can aid in your recovery while taking prednisone.
Just start slow and watch out for worsening side effects. Meet your Best of the Best Pharmacy Award winners! Search for a topic or drug. Can I exercise while on prednisone? Just be sure to take note of these considerations. By Cheryl Maguire Mar. Top Reads in Drug Info.
Weekly doses of glucocorticoid steroids, such as prednisone, help speed recovery in muscle injuries, reports a new Northwestern Medicine study published in the Journal of Clinical Investigation. The weekly steroids also repaired muscles damaged by muscular dystrophy.
One of the major problems of using steroids such as prednisone is they cause muscle wasting and weakness when taken long term. This is a significant problem for people who take steroids for many chronic conditions, and can often result in patients having to stop steroid treatments. The study showed prednisone directs the production of annexins, proteins that stimulate muscle healing.
Giving weekly doses of prednisone also stimulated a molecule called KLF15, which is associated with improved muscle performance. Daily doses of prednisone, however, reduced KLF15, leading to muscle wasting.
In the study, normal mice with a muscle injury received steroids just before injury and for two weeks after the injury. Mice receiving two weekly doses of steroids after the injury performed better on treadmill testing and had stronger muscle than mice receiving a placebo. Mice that received daily steroids for two weeks after the muscle injury performed poorly on the treadmill and in muscle strength studies, compared to placebo-treated mice. Scientists also tested the drug in a mouse model of muscular dystrophy, since prednisone is normally given for this disease.
Mice with muscular dystrophy that received weekly prednisone were stronger and performed better on the treadmill than those that received a placebo. When prednisone was given every day, the muscles atrophied and wasted. While years of being on the steroids cause growth suppression, osteoporosis and other bad side effects, boys with Duchenne Muscular Dystrophy walk two to three years longer if they take steroids.
Only boys get Duchenne Muscular Dystrophy because it is on the X chromosome, and males have only one X chromosome. This technique uses a laser to poke a hole in muscle cells. Then the muscle cell is observed in real time as it reseals the hole, a natural repair process.
For the second part of the study, scientists tested steroids in mice. They damaged the leg muscles in mice and noticed the mice receiving the steroids recovered more rapidly from injury.
Her work also implies normal muscle injury would improve more quickly by taking a weekly dose of steroids such as prednisone. In the future, McNally would like to test steroids in humans and is considering studying it in forms of muscular dystrophy in which steroids would not normally be given, like Becker Muscular Dystrophy or Limb Girdle Muscular Dystrophy.
Steroid treatment is not usually offered for these diseases since the side effects are thought to outweigh any potential benefit. Type above and press Enter to search. Press Esc to cancel. News Center. Disease Discoveries. By Marla Paul May 17, Share Facebook Twitter Email. Steroids thought to waste muscles surprisingly turn out to be beneficial in weekly doses Weekly doses of glucocorticoid steroids, such as prednisone, help speed recovery in muscle injuries, reports a new Northwestern Medicine study published in the Journal of Clinical Investigation.
Images of mouse muscle repair with and without prednisone. The red images indicate the area of muscle injury, which is reduced by prednisone. The green images show the repair cap scab forming over the site of injury. The repair complex forms more quickly with prednisone. The studies were conducted in mice, with implications for humans. But the new study showed weekly doses — rather than daily ones — promote muscle repair. Next, the scientists tested to see if steroids could boost the repair process.
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localhost › /05/17 › weekly-steroids-strengthen. The results of the current study demonstrate that postabsorptive whole-body and muscle protein metabolism is not adversely affected by 6 d of oral prednisone. Many patients take prednisone daily for different immune conditions. Known side effects of daily prednisone include weight gain and even muscle. Protein repairs and builds muscle tissue. Extra corticosteroids in the body can break down amino acids. These amino acids then go and make glucose in the liver. Daily prednisone promotes obesity, but weekly prednisone has 'strikingly. Not only is it safe to exercise while taking prednisone, but working out on prednisone can be beneficial. By Cheryl Maguire Mar.Metrics details. Steroid therapy, a key therapy for inflammatory, allergic, and immunological disorders, is often associated with steroid myopathy as one of the side effects. Steroid therapy is considered the first-line therapy for myositis; however, there have been no reports strictly comparing the muscle mass in patients with myositis before and after steroid therapy.
Thus, it is currently unclear whether steroid therapy for such patients affects muscle volume in addition to muscle strength. We aimed to determine the change in muscle mass after steroid therapy via cross-sectional computed tomography CT in patients with myositis.
Data from seven patients with myositis and eight controls, who were all treated with high doses of steroids, were assessed before and after steroid therapy. Clinical factors in patients with myositis included serum muscle enzyme levels and muscular strength.
The cross-sectional area of skeletal muscle and the low muscle attenuation rate at the level of the caudal end of the third lumbar vertebra were obtained using CT and measured using an image analysis program for all patients. Data were subjected to statistical analysis using several well-established statistical tests. The Wilcoxon signed-rank test was used for comparing paired data for each patient.
The Mann-Whitney U test was used to compare sets of data sampled from two groups. Muscular strength and serum muscle enzyme levels improved following steroid therapy in patients with myositis. In patients with myositis treated with steroid therapy, muscle mass decreased after steroid therapy suggesting that the improvement in muscle strength was due to factors other than a change in muscle volume. Our study suggests the importance of therapies that not only improve muscle mass but also improve the quality of muscle strength.
Peer Review reports. Although steroid therapy is useful, there are various side effects, such as an associated increased susceptibility to infection or glucose intolerance [ 1 ]. Steroid myopathy is another side effect of steroid therapy, which is induced by the catabolic action of steroids on skeletal muscles [ 1 , 2 ]. Muscle weakness in steroid myopathy usually begins in the proximal portion of the lower extremities, progresses to the upper proximal extremities, and finally affects the distal extremities [ 3 ].
It is known that steroid myopathy occurs in a dose-related manner. Idiopathic inflammatory myopathies, collectively termed myositis, are autoimmune diseases characterized by skeletal muscle inflammation. Patients with myositis present with muscle weakness and atrophy in the proximal muscles and increases in serum levels of muscular enzymes [ 5 ].
Steroid therapy is considered the first-line therapy for myositis. With steroid therapy, patients with myositis show an improvement in muscle strength [ 6 ]; however, to our knowledge, there have been no reports strictly comparing the muscle mass of patients with myositis before and after steroid therapy.
Therefore, it is unclear whether steroid therapy for patients with myositis improves not only muscle strength but also muscle volume. Recently, several methods for quantifying muscle mass have been proposed. Bioelectrical impedance analysis and dual X-ray absorptiometry estimate the fat-free mass of the whole body or body segments [ 7 , 8 ]. Computed tomography CT and magnetic resonance imaging MRI are also used to measure cross-sectional images that enable the estimation of muscle mass [ 9 , 10 ].
Yoshizumi et al. It has been reported that MRI is a useful tool to diagnose muscle disorders. MRI makes it easy to assess not only muscle mass but also muscle quality, especially chemical shift imaging and Dixon based T2W imaging, which are new useful tools to assess fatty infiltration [ 11 ].
It has also been proposed that CT allows for the assessment of low attenuation of skeletal muscle i. With regard to the muscle volume of patients with rheumatic diseases, Hosono et al. In this study, we retrospectively compared the changes in muscle volume before and after steroid therapy in patients with myositis and in steroid-treated patients without myositis by measuring the skeletal muscle area with CT.
Seven patients with recent-onset myositis diagnosed from to were included in this study five patients had dermatomyositis and two had mixed connective tissue disease. All patients fulfilled the diagnostic criteria proposed by Bohan and Peter [ 14 ]. The mean age was 55 years range, 15—95 years and four patients were female. Eight patients without myositis were also included as a control group. The mean age of the patients in the control group was 70 years range, 46—94 years and six patients were female.
The control group also underwent high-dose steroid therapy at the same maximum corticosteroid dose as the myositis group. Patients who experienced disuse syndrome were excluded prior to the inclusion of the final eight patients in the control group Table 2.
The muscular strength of patients with myositis were measured using a manual muscle test MMT before and after steroid therapy. All patients underwent CT to assess the general involvement before and after steroid therapy, and we retrospectively analyzed the change in muscle mass by comparing the CT findings.
The first CT was performed within 6 weeks before the initiation of high-dose steroid therapy. The second CT was performed during the tapering of steroid therapy. CT data, including images of the caudal end of the third lumbar vertebra, were obtained using standard procedures.
Two radiologists measured the cross-sectional area of the skeletal muscles and the low muscle attenuation rate at the level of caudal end of the third lumbar vertebra. Measurement of the cross-sectional area of skeletal muscle at the level of the caudal end of the third lumbar vertebra. Muscle volume was measured in the psoas muscle and other muscles. The Wilcoxon signed-rank test was used to compare paired data for each patient.
The Mann-Whitney U test was used to compare two sets of data sampled from the two groups. The inter-reader agreement showed excellent correlation between the two readers, ranging from 0. Seven patients with myositis and eight controls were analyzed in this study.
The muscle strength, measured using MMT, improved after steroid therapy in all patients with myositis Table 1. Table 1. The most frequent underlying diseases in patients with myositis were chronic obstructive pulmonary disease COPD and interstitial lung disease followed by cancer e. No patients with cancer underwent chemotherapy. All underlying diseases were detected within 2 months of the diagnosis of myositis.
Conversely, chronic kidney disease was the most frequent underlying disease in the control group Table 3. With regard to the rate of muscle volume change between the groups, although the myositis group showed greater muscle volume loss in comparison to the control group, the difference was not statistically significant Fig.
CT computed tomography. Although all patients with myositis showed improvements in muscle strength and serum muscle enzyme levels after steroid therapy, there was a significant loss of muscle volume.
The loss of muscle mass is induced by both extrinsic causes and intrinsic causes. Extrinsic causes of focal muscle atrophy often developed after traumatic injury such as Morel-Lavallee syndrome which is a post-traumatic closed degloving injury [ 16 ].
Our patients did not have a history of trauma. Therefore, we think that extrinsic causes had little involvement in the change of muscle mass in our patients.
With regard to intrinsic causes, previous studies have reported that patients with cancer, COPD, and chronic kidney disease exhibited a loss of muscle volume [ 17 , 18 , 19 ]. In the present study, some of the patients had these conditions as underlying diseases. Therefore, the involvement of these underlying diseases may be associated with the observed muscle volume loss in our patients especially in patients with cancer and COPD in the myositis group.
However, the patients with myositis who did not develop these underlying diseases also showed a loss of muscle volume. This suggests that steroid therapy itself decreases muscle volume in patients with myositis. Thus, an improvement in muscle strength in patients with myositis may be attributed to other factors and not to muscle volume change.
Some mechanisms have been proposed to explain the etiology of the loss of muscle volume. One of these mechanisms is an imbalance of protein synthesis and catabolism [ 20 ]. Steroid myopathy is induced by the hypercatabolism of skeletal muscle, which might have resulted in the loss of muscle volume in our patients. However, despite the loss of muscle mass, improvement in muscle strength was also observed in patients with myositis who were treated with steroids.
As such, we hypothesize that the improvement in muscle strength is influenced by an improvement in mitochondrial function. Currently, a non-immune cell mediated mechanism in myositis has been proposed [ 21 ]. It was reported that the endoplasmic reticulum ER stress pathways are chronically activated in patients with myositis [ 21 ].
Additionally, the biopsy specimens from patients with myositis and mice models of myositis demonstrated an increase in levels of Grp78 also known as HSPA5 , which is an ER stress-related protein [ 22 ]. The biopsy specimens from patients with myositis also showed co-localization of MHC class I and the ER marker, calnexin [ 22 ].
These results suggest the possibility of the involvement of ER stress in the pathogenesis of myositis. Xiao et al. In contrast, serum HSPA5 levels did not change in non-responders [ 23 ]. The results of the previous study suggest that steroid therapy reduces ER stress in steroid-responsive patients with myositis. ER stress is known to increase reactive oxygen species, which are closely associated with mitochondrial dysfunction, depressed force generation, and activation of muscle catabolic and autophagy pathways [ 21 ].
We speculate that steroid therapy improves muscle strength via the reduction of ER stress and reactive oxygen species followed by an improvement in mitochondrial function. Our study suggests that the improvement in muscle strength after steroid therapy is not influenced by an improvement in muscle volume, but rather by an improvement in other factors, such as amelioration of mitochondrial dysfunction.
Our study has a few limitations. First, this was a retrospective study and the number of patients was small. The non-significant change in the low muscle attenuation rate after steroid therapy and the non-significant change between the rate of change of muscle volume in patients with myositis associated with COPD and cancer may be partly due to the small sample size. Second, the regimens for steroid reduction and the timing of implementation of the second CT were different for each of the patients, which makes it difficult to accurately assess the correlations between muscular changes and clinical factors.
Third, though patients who experienced disuse syndrome were excluded from the control group, exact scores from the MMT muscular strength of the control group were unknown, which makes it difficult to assess the change of muscle strength in the control group.
However, our study suggests the importance of therapies that not only improve muscle mass but also improve the quality of muscle strength for the treatment of myositis.
Hence, this study may provide novel insights into therapies for myositis. Nonetheless, further studies are needed to reveal the mechanism and treatment of muscle weakness in patients with myositis. In patients with myositis treated with steroid therapy, muscle mass decreased after steroid therapy, suggesting that the improvement in muscle strength was due to factors other than changes in muscle volume. Mechanisms involved in the side effects of glucocorticoids.
Pharmacol Ther. Article PubMed Google Scholar.
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