Hypertrophy-stimulated myogenic regulatory factor mRNA  increases are attenuated in fast muscle of aged quails

Lowe, Dawn A.; Lund, Troy C.; Alway, Stephen E.

doi:10.1152/ajpcell.1998.275.1.c155

Cited by 105 publications

(79 citation statements)

References 37 publications

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“…In that context, we did not observe changes in VEGF, XRCC1, RANTES, or EGR-1 levels in response to ST. We did observe small increases in IL-1β with ST in young men and women, but not in older men and women, which is consistent with the acute exercise response reported by Jozsi et al (15). In summary, our data compare favorably to existing reports for comparable genes and extend the existing literature by providing the first investigation to examine skeletal muscle gene expression in relation to sex and chronic ST.Several genes that might be hypothesized to be differentially expressed as a result of age (11,16,19,21,25) could not be verified in the present study because they were not represented on the GF211 microarray (e.g., muscle transcription factors). Few of the genes shown in Supplementary Tables S3 and S4, genes differentially expressed in relation to age, are immediately recognizable as previously studied muscle-related genes, with GAPDH, carbonic anhydrase III, and tropomyosin-β being the most studied in skeletal muscle.…”

supporting

confidence: 60%

“…Several genes that might be hypothesized to be differentially expressed as a result of age (11,16,19,21,25) could not be verified in the present study because they were not represented on the GF211 microarray (e.g., muscle transcription factors). Few of the genes shown in Supplementary Tables S3 and S4, genes differentially expressed in relation to age, are immediately recognizable as previously studied muscle-related genes, with GAPDH, carbonic anhydrase III, and tropomyosin-β being the most studied in skeletal muscle.…”

Section: Nih-pa Author Manuscriptmentioning

confidence: 82%

“…Recent evidence has indicated that changes in gene expression with advancing age may contribute to a deterioration in muscle function (11,16,19,21,25). Similarly, limited evidence Address for reprint requests and other correspondence: S. M. Roth, A300 Crabtree Hall-GSPH, Dept.…”

Section: Introductionmentioning

confidence: 99%

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Influence of age, sex, and strength training on human muscle gene expression determined by microarray

Roth

Ferrell

Peters

et al. 2002

Physiological Genomics

117

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The purpose of this study was to determine the influence of age, sex, and strength training (ST) on large-scale gene expression patterns in vastus lateralis muscle biopsies using high-density cDNA microarrays and quantitative PCR. Muscle samples from sedentary young (20-30 yr) and older (65-75 yr) men and women (5 per group) were obtained before and after a 9-wk unilateral heavy resistance ST program. RNA was hybridized to cDNA filter microarrays representing ~4,000 known human genes and comparisons were made among arrays to determine differential gene expression as a result of age and sex differences, and/or response to ST. Sex had the strongest influence on muscle gene expression, with differential expression (>1.7-fold) observed for ~200 genes between men and women (~75% with higher expression in men). Age contributed to differential expression as well, as ~50 genes were identified as differentially expressed (>1.7-fold) in relation to age, representing structural, metabolic, and regulatory gene classes. Sixty-nine genes were identified as being differentially expressed (>1.7-fold) in all groups in response to ST, and the majority of these were downregulated. Quantitative PCR was employed to validate expression levels for caldesmon, SWI/ SNF (BAF60b), and four-and-a-half LIM domains 1. These significant differences suggest that in the analysis of skeletal muscle gene expression issues of sex, age, and habitual physical activity must be addressed, with sex being the most critical variable. Keywordsaging; exercise; gender; transcription; transcriptome THE LOSS OF SKELETAL MUSCLE mass and strength with advancing age is associated with frailty, loss of function, and the deterioration of health status in the elderly (13,33), and these changes may be influenced by sex differences (18,20,28,35). The potential of strength training (ST) to reverse age-associated losses of muscle mass and strength in both men and women is well established (9,17,34); however, little is known about why muscle mass is lost with age or how muscle responds to ST, at the molecular level.Recent evidence has indicated that changes in gene expression with advancing age may contribute to a deterioration in muscle function (11,16,19,21,25). Similarly, limited evidence Address for reprint requests and other correspondence: S. M. Roth, A300 Crabtree Hall-GSPH, Dept. Human Genetics, Univ. of Pittsburgh, Pittsburgh, PA 15261 (sroth@hgen.pitt.edu).. NIH Public Access Author ManuscriptPhysiol Genomics. Author manuscript; available in PMC 2010 January 27. Published in final edited form as:Physiol Genomics. ; 10(3): 181-190. doi:10.1152/physiolgenomics.00028.2002. NIH-PA Author Manuscript NIH-PA Author Manuscript NIH-PA Author Manuscript supports the importance of differences in gene expression in explaining muscle phenotype differences between men and women (7,31,37). Changes in gene expression have been wellcharacterized for a number of muscle-specific genes in response to acute resistance-type exercise (3). A general limitation to previous ...

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supporting

confidence: 60%

Section: Nih-pa Author Manuscriptmentioning

confidence: 82%

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Influence of age, sex, and strength training on human muscle gene expression determined by microarray

Roth

Ferrell

Peters

et al. 2002

Physiological Genomics

117

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“…There are several reports of MRF upregulation in response to various muscle perturbations including stretch overload (11,42), ablation (2, 3), denervation (35), myotoxicity (43), and acute resistance loading (9,22,34,53,61). In a number of these studies, MRF responses and/or muscle repair mechanisms were found to be limited by old age (34,(41)(42)(43)61). This may result from heightened basal levels of MRFs in the aging muscle (7,34,35,49) because MRF expression tends to increase as the degree of sarcopenia advances (17).…”

Section: Effects Of Age On Load-mediated Changes In Regenerative Markersmentioning

confidence: 99%

Efficacy of 3 days/wk resistance training on myofiber hypertrophy and myogenic mechanisms in young vs. older adults

Kosek

Kim

Petrella

et al. 2006

Journal of Applied Physiology

412

336

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. Efficacy of 3 days/wk resistance training on myofiber hypertrophy and myogenic mechanisms in young vs. older adults. J Appl Physiol 101: [531][532][533][534][535][536][537][538][539][540][541][542][543][544] 2006. First published April 13, 2006; doi:10.1152/japplphysiol.01474.2005.-Resistance training (RT) has shown the most promise in reducing/reversing effects of sarcopenia, although the optimum regime specific for older adults remains unclear. We hypothesized myofiber hypertrophy resulting from frequent (3 days/wk, 16 wk) RT would be impaired in older (O; 60 -75 yr; 12 women, 13 men), sarcopenic adults compared with young (Y; 20 -35 yr; 11 women, 13 men) due to slowed repair/regeneration processes. Myofiber-type distribution and crosssectional area (CSA) were determined at 0 and 16 wk. Transcript and protein levels of myogenic regulatory factors (MRFs) were assessed as markers of regeneration at 0 and 24 h postexercise, and after 16 wk. Only Y increased type I CSA 18% (P Ͻ 0.001). O showed smaller type IIa (Ϫ16%) and type IIx (Ϫ24%) myofibers before training (P Ͻ 0.05), with differences most notable in women. Both age groups increased type IIa (O, 16%; Y, 25%) and mean type II (O, 23%; Y, 32%) size (P Ͻ 0.05). Growth was generally most favorable in young men. Percent change scores on fiber size revealed an age ϫ gender interaction for type I fibers (P Ͻ 0.05) as growth among Y (25%) exceeded that of O (4%) men. Myogenin and myogenic differentiation factor D (MyoD) mRNAs increased (P Ͻ 0.05) in Y and O, whereas myogenic factor (myf)-5 mRNA increased in Y only (P Ͻ 0.05). Myf-6 protein increased (P Ͻ 0.05) in both Y and O. The results generally support our hypothesis as 3 days/wk training led to more robust hypertrophy in Y vs. O, particularly among men. However, this differential hypertrophy adaptation was not explained by age variation in MRF expression. sarcopenia; myogenin; MyoD; myosin heavy chain IT IS WELL ESTABLISHED THAT muscle mass declines with age (termed sarcopenia). In the knee extensors (e.g., vastus lateralis), which are important for ambulation and weight-bearing function, a 30% decrease in whole muscle size occurs between the ages of 50 and 80 yr (15,40). This whole muscle atrophy results from atrophy of type II myofibers (34) and apparent loss of both type I and type II motor units as evidence from cadaveric studies of vastus lateralis indicate the number of myofibers, regardless of fiber type, declines substantially between the sixth and eighth decades (39). In the United States, $18.5 billion of total direct health care costs in 2000 were attributable to sarcopenia (31), and this will undoubtedly increase because the percentage of American adults 65 yr and older is expected to increase from one in nine to 20% of the adult population by 2030 (National Institute on Aging statistics). Resistance training has shown the most promise among interventions aimed to decrease the effects of sarcopenia, as it enhances strength, power, and mobility function and induces varying degrees of skeletal musc...

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“…Therefore, events that initiate the hypertrophic response can be studied. 47 Chronic stretch has also been shown to induce hyperplasia (new muscle fiber formation); 5,7,9,16,35 thus the stretch model is valuable for studying mechanisms of new fiber formation. It should be noted that evidence for hyperplasia exists from several other animal hypertrophy models (reviewed by Kelley 41 ) and also after PRE in humans.…”

Section: Chronic Stretch Modelsmentioning

confidence: 99%

Animal Models for Inducing Muscle Hypertrophy: Are They Relevant for Clinical Applications in Humans?

Lowe¹

2002

J Orthop Sports Phys Ther

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Muscle hypertrophy is an adaptive response to overload. Progressive resistance exercise (PRE) is thought to be among the best means to achieve hypertrophy in humans. While functional adaptations to PRE in muscles of humans are made in the clinic, it is difficult to evaluate hypertrophic responses and underlying mechanisms because the adaptations require many weeks or months before they become evident and there is a large variability in response to PRE among humans. In contrast, various animal models have been shown to induce rapid and extensive muscle hypertrophy and some models allow precise control of the exercise parameters. By examining the animal models of muscle hypertrophy and understanding the advantages and disadvantages of each, clinicians may be able to evaluate and use relevant data from these models to design new strategies for modification of PRE in humans. The purpose of this article is to review animal models that are currently used in basic research laboratories, discuss the hypertrophic and functional outcomes, and relate these to PRE used in the clinic. J Orthop Sports Phys Ther 2002;32:36-43. Key Words: muscle growth, muscle strength, overload, resistance training, skeletal muscle A n increase in muscle strength is a desirable outcome of many rehabilitation therapies. Strength gains are often a result of muscle hypertrophy, and progressive resistance exercise (PRE) is the primary mode of producing muscle hypertrophy in the rehabilitation setting. Several recent reviews have detailed the specifics of PRE in terms of modality, specificity of training, and outcomes, 23,43,44,51,61,62,64 and PRE has been shown to be beneficial as a therapeutic intervention in osteoporosis, 46 65 In this commentary, we will focus on the hypertrophic response of skeletal muscle to PRE.Physiological and cellular mechanisms of muscle hypertrophy have been reviewed extensively, 30,39,43,44 and molecular mechanisms that initiate and regulate muscle hypertrophy is a relatively new and rapidly expanding topic in the field of exercise science. 11,15,19,20,30 However, while the functional outcomes of PRE have been identified largely from human studies, much of the data used in deriving cellular and molecular mechanisms of muscle hypertrophy are drawn from studies using laboratory animals. Several different animal models for inducing muscle hypertrophy are used, and some produce outcomes that are similar to those of PRE in humans. By fully understanding the various animal models used, the clinician will be able to interpret muscle hypertrophy research results generated using laboratory animals. This information can be used by the clinician to evaluate current PRE programs and perhaps design new or modified strategies for implementing PRE. The ultimate goal is to optimize PRE in humans to acquire better functional outcomes in the clinic. The purpose of this article is to review animal models that are currently used in basic science laboratories for investigating skeletal muscle hypertrophy. Examples of recent research us...

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Hypertrophy-stimulated myogenic regulatory factor mRNA increases are attenuated in fast muscle of aged quails

Cited by 105 publications

References 37 publications

Influence of age, sex, and strength training on human muscle gene expression determined by microarray

Influence of age, sex, and strength training on human muscle gene expression determined by microarray

Efficacy of 3 days/wk resistance training on myofiber hypertrophy and myogenic mechanisms in young vs. older adults

Animal Models for Inducing Muscle Hypertrophy: Are They Relevant for Clinical Applications in Humans?

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