Disproportionate loss of thin filaments in human soleus muscle after 17-day bed rest

Riley, Denise; Bain, James L. W.; Thompson, Joyce L.; Fitts, Robert H.; Widrick, Jeffrey J.; Trappe, Scott; Trappe, Todd A.; Costill, David L.

doi:10.1002/(sici)1097-4598(199810)21:10<1280::aid-mus6>3.0.co;2-7

Cited by 83 publications

(61 citation statements)

References 32 publications

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“…1 D, top), to a magnitude similar to that detected by electron microscopy. Earlier electron microscopy studies revealed, on the other hand, that disuse decreases thin fi lament density and length in human soleus muscle after spacefl ight and after bed rest (Riley et al, 1998). The present study quantifi ed the change in the average thin fi lament length, in that it was shorter by ‫1.0ف‬ μm after disuse (1.07 ± 0.02 vs. 1.18 ± 0.01 μm; P < 0.05) (expressed as I-Z-I Muscle bundles ‫03ف(‬ mg) were solubilized and run for gel electrophoresis.…”

Section: R E S U Lt S a N D Discussionmentioning

confidence: 72%

“…Considering a possible role of nebulin as a ruler for thin fi lament formation (Littlefi eld and Fowler, 1998), a slight reduction in its protein level may in part be responsible for the shortening of thin fi laments (Fig. 1 D) (Riley et al, 1998. We also observed isoform switching of myosin-binding protein C (MyBP-C), from the slow type (Cs) to the fast type (Cf) as well as to the intermediate type (Ci) (Fig.…”

Section: R E S U Lt S a N D Discussionmentioning

confidence: 99%

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Disuse-induced Preferential Loss of the Giant Protein Titin Depresses Muscle Performance via Abnormal Sarcomeric Organization

Udaka¹,

Ohmori²,

Terui³

et al. 2008

J Cell Biol

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Persistent muscle weakness due to disuse-associated skeletal muscle atrophy limits the quality of life for patients with various diseases and individuals who are confi ned to bed. Fibers from disused muscle exhibit a marked reduction in active force production, which can exacerbate motor function, coupled with the well-known loss of muscle quantity. Despite recent understanding of the signaling pathways leading to the quantity loss, the molecular mechanisms of the depressed qualitative performance still remain elusive. Here we show that long-term disuse causes preferential loss of the giant sarcomere protein titin, associated with changes in physiologic muscle function. Ca 2+ sensitivity of active force decreased following 6 wk of hindlimb immobilization in the soleus muscle of the rat, accompanied by a shift in the length-active force relationship to the shorter length side. Our analyses revealed marked changes in the disused sarcomere, with shortening of thick and thin fi laments responsible for altered length dependence and expansion of interfi lament lattice spacing leading to a reduction in Ca 2+ sensitivity. These results provide a novel view that disuse-induced preferential titin loss results in altered muscle function via abnormal sarcomeric organization.

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Section: R E S U Lt S a N D Discussionmentioning

confidence: 72%

Section: R E S U Lt S a N D Discussionmentioning

confidence: 99%

Disuse-induced Preferential Loss of the Giant Protein Titin Depresses Muscle Performance via Abnormal Sarcomeric Organization

Udaka¹,

Ohmori²,

Terui³

et al. 2008

J Cell Biol

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show abstract

“…Later, the related literature provided reports of distinct response to atrophic stimuli between different muscles, suggesting that oxidative muscles (e.g., soleus) are more susceptible to damage due to inactivity or unloading, whereas glycolytic muscles (e.g., plantaris or extensor digitorum longus) tend to be more affected in diseased conditions (42,47,51,58,59). Considering that HF is a degenerative and rather complex disease, there is no absolute agreement on which muscle will present the most pronounced damage after MI; therefore, we decided to evaluate both soleus and plantaris muscle due to their contrasting metabolic properties.…”

Section: Discussionmentioning

confidence: 99%

High- versus moderate-intensity aerobic exercise training effects on skeletal muscle of infarcted rats

Moreira

Bechara

Bozi

et al. 2013

Journal of Applied Physiology

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Moreira JB, Bechara LR, Bozi LH, Jannig PR, Monteiro AW, Dourado PM, Wisløff U, Brum PC. High-versus moderate-intensity aerobic exercise training effects on skeletal muscle of infarcted rats. J Appl Physiol 114: 1029 -1041, 2013. First published February 21, 2013 doi:10.1152/japplphysiol.00760.2012.-Poor skeletal muscle performance was shown to strongly predict mortality and long-term prognosis in a variety of diseases, including heart failure (HF). Despite the known benefits of aerobic exercise training (AET) in improving the skeletal muscle phenotype in HF, the optimal exercise intensity to elicit maximal outcomes is still under debate. Therefore, the aim of the present study was to compare the effects of highintensity AET with those of a moderate-intensity protocol on skeletal muscle of infarcted rats. Wistar rats underwent myocardial infarction (MI) or sham surgery. MI groups were submitted either to an untrained (MI-UNT); moderate-intensity (MI-CMT, 60% V O2 max); or matched volume, high-intensity AET (MI-HIT, intervals at 85% V O2 max) protocol. High-intensity AET (HIT) was superior to moderate-intensity AET (CMT) in improving aerobic capacity, assessed by treadmill running tests. Cardiac contractile function, measured by echocardiography, was equally improved by both AET protocols. CMT and HIT prevented the MI-induced decay of skeletal muscle citrate synthase and hexokinase maximal activities, and increased glycogen content, without significant differences between protocols. Similar improvements in skeletal muscle redox balance and deactivation of the ubiquitin-proteasome system were also observed after CMT and HIT. Such intracellular findings were accompanied by prevented skeletal muscle atrophy in both MI-CMT and MI-HIT groups, whereas no major differences were observed between protocols. Taken together, our data suggest that despite superior effects of HIT in improving functional capacity, skeletal muscle adaptations were remarkably similar among protocols, leading to the conclusion that skeletal myopathy in infarcted rats was equally prevented by either moderate-intensity or high-intensity AET. atrophy; heart failure; proteasome; oxidative stress SKELETAL MUSCLE ABNORMALITIES in systemic diseases have been described for decades (9, 14, 29, 52), including in heart failure (HF). Capillary rarefaction, switch from type I (oxidative) to type II (glycolytic) fibers, impaired metabolism, and skeletal muscle atrophy have been shown in human and experimental models of HF (14,21,29,43,49,52). This maladaptation seems to impair skeletal muscle performance, which was proposed as the main determinant of exercise capacity in patients with HF (21,32,40). Additionally, skeletal muscle loss was shown to be an independent predictor of mortality in HF (3).Recent efforts by researchers have identified possible intracellular mechanisms underlying the skeletal muscle abnormalities in cardiovascular diseases, and promising targets such as metabolic enzymes, calcium handling-related proteins, antioxidant scavengers, and in...

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“…Bed rest-and spaceflight-induced changes in muscle fiber function are related to alterations in cell ultrastructure (18,19). Preliminary observations reveal that more severe cellular degradation, distinct from bed rest and spaceflight, occurs in fibers exposed to the ULLS procedure (D. A. Riley and R. H. Fitts, unpublished observations).…”

Section: Discussionmentioning

confidence: 99%

“…Post-ULLS fibers obtained from the present subjects displayed areas of central corelike degeneration that were devoid of myosin immunostaining, particularly in slow fibers. In contrast, central corelike lesions were not observed in fibers obtained after bed rest or spaceflight (18,19). Thus the greater myofibrillar disorganization after ULLS may be responsible for the greater reductions in force and shortening velocity noted for this model.…”

Section: Discussionmentioning

confidence: 99%

Unilateral lower limb suspension does not mimic bed rest or spaceflight effects on human muscle fiber function

Widrick

Trappe

Romatowski

et al. 2002

Journal of Applied Physiology

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. Unilateral lower limb suspension does not mimic bed rest or spaceflight effects on human muscle fiber function. J Appl Physiol 93: 354-360, 2002. First published April 5, 2002 10.1152/japplphysiol.01245. 2001.-We used Ca 2ϩ -activated skinned muscle fibers to test the hypothesis that unilateral lower leg suspension (ULLS) alters cross-bridge mechanisms of muscle contraction. Soleus and gastrocnemius biopsies were obtained from eight subjects before ULLS, immediately after 12 days of ULLS (post-0 h), and after 6 h of reambulation (post-6 h). Post-0 h soleus fibers expressing type I myosin heavy chain (MHC) showed significant reductions in diameter, absolute and specific peak Ca 2ϩ -activated force, unloaded shortening velocity, and absolute and normalized peak power. Fibers obtained from the gastrocnemius were less affected by ULLS, particularly fibers expressing fast MHC isoforms. Post-6 h soleus fibers produced less absolute and specific peak force than did post-0 h fibers, suggesting that reambulation after ULLS induced cell damage. Like bed rest and spaceflight, ULLS primarily affects soleus over gastrocnemius fibers. However, in contrast to these other models, slow soleus fibers obtained after ULLS showed a decrease in unloaded shortening velocity and a greater reduction in specific force. muscle atrophy; muscle disuse; muscle damage; weightlessness HUMANS EXPOSED TO SPACEFLIGHT experience skeletal muscle atrophy, particularly of the antigravity, postural muscles of the lower limbs and back (8). Efforts to understand the mechanisms underlying the adaptations of skeletal muscle to microgravity have been hindered by the limited number of human spaceflights and by the expense and logistical problems associated with studying humans in space. An alternative approach has been to use ground-based models of nonweight bearing that mimic the effects of spaceflight. The most commonly used ground-based model of spaceflight has been bed rest. This model appears to induce adaptations in muscle cells that are similar to those experienced during spaceflight (25-27). However, although ground-based bed rest eliminates or reduces many of the problems associated with human spaceflight, the procedure is still relatively expensive and logistically complex.An alternative ground-based model of non-weight bearing is unilateral lower limb suspension (ULLS). In this model, as originally described by Berg et al. (2), the treatment limb is flexed and suspended above the ground by the use of a shoulder harness. Subjects ambulate using crutches and are thus able to participate in most of their routine daily activities. The procedure reduces many of the expenses and logistical issues associated with bed rest studies, induces atrophy of the extensor muscles that comprise the treatment limb, and results in a decline in the voluntary neuromuscular strength of these muscle groups (1-3, 5, 11). Consequently, the procedure has been proposed as an alternative ground-based model of spaceflight (2, 5).In previous work, our laboratory reported t...

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Disproportionate loss of thin filaments in human soleus muscle after 17-day bed rest

Cited by 83 publications

References 32 publications

Disuse-induced Preferential Loss of the Giant Protein Titin Depresses Muscle Performance via Abnormal Sarcomeric Organization

Disuse-induced Preferential Loss of the Giant Protein Titin Depresses Muscle Performance via Abnormal Sarcomeric Organization

High- versus moderate-intensity aerobic exercise training effects on skeletal muscle of infarcted rats

Unilateral lower limb suspension does not mimic bed rest or spaceflight effects on human muscle fiber function

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