| 1. |
- Fridén, Cecilia, et al.
(författare)
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Higher pain sensitivity and lower muscle strength in postmenonpausal women with early rheumatoid arthritis compared with age-matched healthy women--a pilot study.
- 2013
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Ingår i: Disability and Rehabilitation. - : Informa UK Limited. - 0963-8288 .- 1464-5165. ; 35:16, s. 1350-6
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Tidskriftsartikel (refereegranskat)abstract
- PURPOSE: The purpose of the study was to examine muscle strength and pain sensitivity in postmenopausal women with and without RA.METHODS: Ten women with and ten without early RA were recruited. All were postmenopausal, and did not use hormone replacement therapy. Measurements of isokinetic muscle strength in knee flexors/extensors, hand grip strength, timed standing, pressure pain thresholds (PPT), suprathreshold pressure pain, and segmental and plurisegmental endogenous pain inhibitory mechanisms during muscle contraction were assessed.RESULTS: Participants with early RA were weaker in knee flexors, in hand grip strength and they needed more time for the timed standing. Women with early RA had higher sensitivity to threshold pain and suprathreshold pressure pain compared to women without RA. PPTs increased in the contracting muscle as well as in a distant resting muscle during static contractions in both groups.CONCLUSIONS: Our results indicate differences in muscular strength between postmenopausal women with and without RA. Furthermore, women with RA had decreased PPT and hyperalgesia, but no dysfunction of segmental or plurisegmental pain inhibitory mechanisms during static exercise compared to healthy controls. The normal function of endogenous pain inhibitory mechanisms despite chronic pain in women with RA might contribute to the good effects of physical activity previously reported.
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| 2. |
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| 3. |
- Yamada, Takashi, et al.
(författare)
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Impaired Myofibrillar Function in the Soleus Muscle of Mice With Collagen-Induced Arthritis
- 2009
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Ingår i: Arthritis and Rheumatism. - : Wiley. - 0004-3591 .- 1529-0131. ; 60:11, s. 3280-3289
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Tidskriftsartikel (refereegranskat)abstract
- Objective. Progressive muscle weakness is a common feature in patients with rheumatoid arthritis (RA). However, little is known about whether the intrinsic contractile properties of muscle fibers are affected in RA. This study was undertaken to investigate muscle contractility and the myoplasmic free Ca2+ concentration ([Ca2+](i)) in the soleus, a major postural muscle, in mice with collagen-induced arthritis (CIA). Methods. Muscle contractility and [Ca2+](i) were assessed in whole muscle and intact single-fiber preparations, respectively. The underlying mechanisms of contractile dysfunction were assessed by investigating redox modifications using Western blotting and antibodies against nitric oxide synthase (NOS), superoxide dismutase (SOD), 3-nitrotyrosine (3-NT), carbonyl, malondialdehyde (MDA), and S-nitrosocysteine (SNO-Cys). Results. The tetanic force per cross-sectional area was markedly decreased in the soleus muscle of mice with CIA, and the change was not due to a decrease in the amplitude of [Ca2+](i) transients. The reduction in force production was accompanied by slowing of the twitch contraction and relaxation and a decrease in the maximum shortening velocity. Immunoblot analyses showed a marked increase in neuronal NOS expression but not in inducible or endothelial NOS expression, which, together with the observed decrease in SOD2 expression, favors peroxynitrite formation. These changes were accompanied by increased 3-NT, carbonyl, and MDA adducts content in myofibrillar proteins from the muscles of mice with CIA. Moreover, there was a significant increase in SNO-Cys content in myosin heavy-chain and troponin I myofibrillar proteins from the soleus muscle of mice with CIA. Conclusion. These findings show impaired contractile function in the soleus muscle of mice with CIA and suggest that this abnormality is due to peroxynitrite-induced modifications in myofibrillar proteins.
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| 4. |
- Yamada, Takashi, et al.
(författare)
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Nitrosative modifications of the Ca2+ release complex and actin underlie arthritis-induced muscle weakness.
- 2015
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Ingår i: Annals of the Rheumatic Diseases. - : BMJ. - 1468-2060 .- 0003-4967. ; 74:10, s. 1907-1914
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Tidskriftsartikel (refereegranskat)abstract
- Skeletal muscle weakness is a prominent clinical feature in patients with rheumatoid arthritis (RA), but the underlying mechanism(s) is unknown. Here we investigate the mechanisms behind arthritis-induced skeletal muscle weakness with special focus on the role of nitrosative stress on intracellular Ca(2+) handling and specific force production.
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