Regulation of sarcoplasmic reticulum calcium pump gene expression by hindlimb unweighting

Schulte, Leah M.; Navarro, Javier; Kandarian, Susan C.

doi:10.1152/ajpcell.1993.264.5.c1308

Cited by 87 publications

(76 citation statements)

References 25 publications

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“…These results are in contrast to the previous report of increased Ca-dependent ATPase activity following inactivity in the soleus muscle, which is predominantly composed of the MHC type I and SERCA 2a slow isoforms of myosin and the SR Ca-ATPase, respectively (Peters et al, 1999;Schulte et al, 1993). The increased ATPase activity was attributed to the non-weight bearing-induced increase in the SERCA1 (fast) isoform expression in the soleus (Peters et al, 1999;Schulte et al, 1993).…”

Section: Non-weight Bearing Induced Changescontrasting

confidence: 99%

Age-dependent effects of treadmill exercise during a period of inactivity

Arora

Husom

Ferrington

et al. 2008

Experimental Gerontology

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The objective of this study was to investigate the effect of a treadmill exercise protocol to prevent muscle weakness, atrophy and alterations in calcium regulation in adult, old and very old rats. Adult (7-12 months), old (29-30 months) and very old (34-36 months) F344BNF 1 rats were randomly assigned to weight bearing (WB), weight bearing exercise (WBX), non-weight bearing (NWB) and non-weight bearing exercise (NWBX) groups. The WB group was considered the sedentary-control animals. NWB rats were hindlimb unweighted for 14 days. WBX and NWBX groups were exercised on a treadmill for approximately fifteen minutes four times daily. The contractile properties [diameter, peak active force (P 0 ), specific tension (P 0 /CSA)] of single myosin heavy chain type II fibers and Ca regulation [Ca +2 dependent ATPase activity] were determined. Fiber diameter reduced by 24% in the very old rats with NWB. P 0 and P 0 /CSA declined in the young adult and very old rats with NWB. NWBX attenuated these changes in the young and very old rats. Ca +2 dependent ATPase activity increased with treadmill exercise during non-weight bearing in the young animals. In conclusion, the treadmill exercise is beneficial in attenuating the non-weight bearing induced changes in the individual MHC type II muscle fibers of the gastrocnemius muscle.

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Section: Non-weight Bearing Induced Changescontrasting

confidence: 99%

Age-dependent effects of treadmill exercise during a period of inactivity

Arora

Husom

Ferrington

et al. 2008

Experimental Gerontology

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“…Therefore, activation of calpains, cathepsins, and several other proteases (87) appears to represent an early ratelimiting step in myofibrillar protein degradation during unloading-induced skeletal muscle wasting. Calcium loading rates (91) and mRNA and protein levels of the fast Ca 2ϩ pump (92) and the calcium-binding protein calsequestrin (93) in the sarcoplasmic reticulum increase significantly in soleus muscles during hindlimb suspension, probably in response to oxidative stressinduced excess of intracellular calcium. Atrophying muscles have been found to have markedly increased calcium-dependent thiol protease (calpain) activity both in vivo and in vitro (48, 55, 94) along with enhanced m-calpain mRNA levels (55), suggesting transcriptional regulation of this enzyme.…”

Section: 21) Calcium-dependent Proteolysismentioning

confidence: 99%

Determinants of Disuse-Induced Skeletal Muscle Atrophy: Exercise and Nutrition Countermeasures to Prevent Protein Loss

Bajotto

Shimomura

2006

J Nutr Sci Vitaminol

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Summary Muscle atrophy results from a variety of conditions such as disease states, neuromuscular injuries, disuse, and aging. Absence of gravitational loading during spaceflight or long-term bed rest predisposes humans to undergo substantial loss of muscle mass and, consequently, become unfit and/or unhealthy. Disuse-or inactivity-induced skeletal muscle protein loss takes place by differential modulation of proteolytic and synthetic systems. Transcriptional, translational, and posttranslational events are involved in the regulation of protein synthesis and degradation in myofibers, and these regulatory events are known to be responsive to contractile activity. However, regardless of the numerous studies which have been performed, the intracellular signals that mediate skeletal muscle wasting due to muscular disuse are not completely comprehended. Understanding the triggers of atrophy and the mechanisms that regulate protein loss in unloaded muscles may lead to the development of effective countermeasures such as exercise and dietary intervention. The objective of the present review is to provide a window into the molecular processes that underlie skeletal muscle remodeling and to examine what we know about exercise and nutrition countermeasures designed to minimize muscle atrophy. Key Words Skeletal muscle disuse atrophy, microgravity, hindlimb suspension, protein synthesis and degradation, exercise and nutrition countermeasures Because skeletal muscle is the most abundant tissue of the human body, we may hypothesize that decreases in its mass possibly will profoundly impact the wholebody metabolism and ultimately lead to the development of lifestyle-related diseases. In addition, muscle deconditioning (reduced strength, abnormal reflex patterns, increased fatigability) could limit the ability of astronauts to work in space and/or to rapidly egress the spacecraft in an emergency landing ( 1 ). Even though various functional and morphological alterations are noticeable in inactive muscles, decreased protein content has been regarded as the hallmark of skeletal muscle atrophy. Muscle protein can be either gained or lost by relative changes in protein synthesis and degradation rates, which are known to be modulated by contractile activity. Thus, understanding about the molecular regulators of protein turnover during different mechanical loading conditions and their response to specific treatments leads to the likelihood of developing effective countermeasures for preventing disuseinduced muscle wasting.This article provides a review of muscular adaptations to disuse, with emphasis on protein kinetics. We describe first the general aspects of muscle wasting with regard to exposure to actual or ground-based, simulated microgravity and some of the most significant findings that provide evidence for a close connection between skeletal muscle plasticity and protein metabolism. Next, we present a review of the literature in which results of measurements of protein synthesis/ degradation rates during unloading are avail...

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“…For example, inactivity due to hindlimb unweighting stimulates a general transformation of slow-to fast-twitch protein isoforms in slow-twitch muscle for the Ca-ATPase in young rat muscle. 70 Concomitant with this transformation is the transition from slow-to fast-twitch muscle contractile properties. Thus, the progressive transformation of slow to fast Ca-ATPase is suggested as the mechanism behind faster twitch-time-to-peaktension and half-relaxation, contractile properties that reflect sarcoplasmic reticulum calcium handling, following hindlimb unweighting.…”

Section: Twitch Contractile Propertiesmentioning

confidence: 99%

Skeletal Muscle Adaptations with Age, Inactivity, and Therapeutic Exercise

Thompson¹

2002

J Orthop Sports Phys Ther

104

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One of the remarkable features of skeletal muscle is its adaptability. Skeletal muscle adaptations are characterized by modifications of morphological, biochemical, and molecular variables that alter the functional attributes of specific skeletal muscle fiber types. Skeletal muscle adaptation is diverse and the magnitude of change is dependent on many factors, such as activity pattern, age, and muscle fiber type composition. The adaptation of skeletal muscle in the adult population is well described. In contrast, the adaptation of skeletal muscle in the older population is less documented, especially in the area of inactivity-induced alterations. Age-related changes in skeletal muscle may play a significant role in the magnitude of change with inactivity and influence the rehabilitation process for the older adult.A consistent feature of age and inactivity is limb muscle atrophy and the loss of peak force and power. Differences exist in the rate and mechanisms of muscle wasting and in the susceptibility of a given fiber type to atrophy. Most likely, the rapid muscle wasting might be in part due to a decrease in protein synthesis coupled with an increased degradation. Besides the quantitative change in muscle mass, age and inactivity induce important qualitative changes in the structure of key skeletal muscle proteins that are manifested in alterations in contractile properties.Therefore, the purpose of this clinical commentary is to identify the major effects of age and inactivity on skeletal muscle structure and function, and discuss potential therapeutic interventions. Special emphasis will be placed on how alterations in muscle structure affect function and on the cellular and molecular mechanisms of the age-related and inactivity-induced muscle changes.

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Regulation of sarcoplasmic reticulum calcium pump gene expression by hindlimb unweighting

Cited by 87 publications

References 25 publications

Age-dependent effects of treadmill exercise during a period of inactivity

Age-dependent effects of treadmill exercise during a period of inactivity

Determinants of Disuse-Induced Skeletal Muscle Atrophy: Exercise and Nutrition Countermeasures to Prevent Protein Loss

Skeletal Muscle Adaptations with Age, Inactivity, and Therapeutic Exercise

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