Effect of acute head-down tilt on skeletal muscle cross-sectional area and proton transverse relaxation time

1996 ◽  
Vol 81 (4) ◽  
pp. 1572-1577 ◽  
Author(s):  
Michael S. Conley ◽  
Jeanne M. Foley ◽  
Lori L. Ploutz-Snyder ◽  
Ronald A. Meyer ◽  
Gary A. Dudley

Conley, Michael S., Jeanne M. Foley, Lori L. Ploutz-Snyder, Ronald A. Meyer, and Gary A. Dudley. Effect of acute head-down tilt on skeletal muscle cross-sectional area and proton transverse relaxation time. J. Appl. Physiol.81(4): 1572–1577, 1996.—This study investigated changes in skeletal muscle cross-sectional area (CSA) evoked by fluid shifts that accompany short-term 6° head-down tilt (HDT) or horizontal bed rest, the time course of the resolution of these changes after resumption of upright posture, and the effect of altered muscle CSA, in the absence of increased contractile activity, on proton transverse relaxation time (T2). Average muscle CSA and T2 were determined by standard spin-echo magnetic resonance imaging. Analyses were performed on contiguous transaxial images of the neck and calf. After a day of normal activity, 24 h of HDT increased neck muscle CSA 19 ± 4 (SE)% ( P < 0.05) while calf muscle CSA decreased 14 ± 3% ( P < 0.05). The horizontal posture (12 h) induced about one-half of these responses: an 11 ± 2% ( P < 0.05) increase in neck muscle CSA and an 8 ± 2% decrease ( P < 0.05) in the calf. Within 2 h after resumption of upright posture, neck and calf muscle CSA returned to within 0.5% ( P > 0.05) of the values assessed after a day of normal activity, with most of the change occurring within the first 30 min. No further change in muscle CSA was observed through 6 h of upright posture. Despite these large alterations in muscle CSA, T2 was not altered by more than 1.1 ± 0.6% ( P > 0.05) and did not relate to muscle size. These results suggest that postural manipulations and subsequent fluid shifts modeling microgravity elicit marked changes in muscle size. Because these responses were not associated with alterations in muscle T2, it does not appear that simple movement of water into muscle can explain the contrast shift observed after exercise.

2007 ◽  
Vol 103 (4) ◽  
pp. 1121-1127 ◽  
Author(s):  
Steven J. Prior ◽  
Stephen M. Roth ◽  
Xiaojing Wang ◽  
Candace Kammerer ◽  
Iva Miljkovic-Gacic ◽  
...  

The aim of this study was to estimate the heritability of and environmental contributions to skeletal muscle phenotypes (appendicular lean mass and calf muscle cross-sectional area) in subjects of African descent and to determine whether heritability estimates are impacted by sex or age. Body composition was measured by dual-energy X-ray absorptiometry and computed tomography in 444 men and women aged 18 yr and older (mean: 43 yr) from eight large, multigenerational Afro-Caribbean families (family size range: 21–112). Using quantitative genetic methods, we estimated heritability and the association of anthropometric, lifestyle, and medical variables with skeletal muscle phenotypes. In the overall group, we estimated the heritability of lean mass and calf muscle cross-sectional area (h2 = 0.18–0.23, P < 0.01) and contribution of environmental factors to these phenotypes ( r2 = 0.27–0.55, P < 0.05). In our age-specific analysis, the heritability of leg lean mass was lower in older vs. younger individuals (h2 = 0.05 vs. 0.23, respectively, P = 0.1). Sex was a significant covariate in our models ( P < 0.001), although sex-specific differences in heritability varied depending on the lean mass phenotype analyzed. High genetic correlations (ρG = 0.69–0.81; P < 0.01) between different lean mass measures suggest these traits share a large proportion of genetic components. Our results demonstrate the heritability of skeletal muscle traits in individuals of African heritage and that heritability may differ as a function of sex and age. As the loss of skeletal muscle mass is related to metabolic abnormalities, disability, and mortality in older individuals, further research is warranted to identify specific genetic loci that contribute to these traits in general and in a sex- and age-specific manner.


2016 ◽  
Vol 48 ◽  
pp. 894
Author(s):  
Rodney C. Wade ◽  
Ashraf S. Gorgey ◽  
Jennifer Hubert ◽  
Ryan Sumrell ◽  
Justin Bengel ◽  
...  

2013 ◽  
Vol 13 (1) ◽  
Author(s):  
Alixe HM Kilgour ◽  
Karen J Ferguson ◽  
Calum D Gray ◽  
Ian J Deary ◽  
Joanna M Wardlaw ◽  
...  

2019 ◽  
Vol 51 (Supplement) ◽  
pp. 945
Author(s):  
Johnathon H. Moore ◽  
Cody T. Haun ◽  
Emily L. Grandprey ◽  
Katelyn P. Joubert ◽  
Christopher G. Vann ◽  
...  

2001 ◽  
Vol 280 (2) ◽  
pp. C288-C295 ◽  
Author(s):  
Robert G. Dennis ◽  
Paul E. Kosnik ◽  
Mark E. Gilbert ◽  
John A. Faulkner

The purpose of this study was to compare the excitability and contractility of three-dimensional skeletal muscle constructs, termed myooids, engineered from C2C12 myoblast and 10T½ fibroblast cell lines, primary muscle cultures from adult C3H mice, and neonatal and adult Sprague-Dawley rats. Myooids were 12 mm long, with diameters of 0.1–1 mm, were excitable by transverse electrical stimulation, and contracted to produce force. After ∼30 days in culture, myooid cross-sectional area, rheobase, chronaxie, resting baseline force, twitch force, time to peak tension, one-half relaxation time, and peak isometric force were measured. Specific force was calculated by dividing peak isometric force by cross-sectional area. The specific force generated by the myooids was 2–8% of that generated by skeletal muscles of control adult rodents. Myooids engineered from C2C12-10T½ cells exhibited greater rheobase, time to peak tension, and one-half relaxation time than myooids engineered from adult rodent cultures, and myooids from C2C12-10T½ and neonatal rat cells had greater resting baseline forces than myooids from adult rodent cultures.


2010 ◽  
Vol 299 (1) ◽  
pp. R268-R276 ◽  
Author(s):  
Anna C. Kayani ◽  
Graeme L. Close ◽  
Wolfgang H. Dillmann ◽  
Ruben Mestril ◽  
Malcolm J. Jackson ◽  
...  

Skeletal muscle atrophy and weakness are major contributors to frailty and impact significantly on quality of life of older people. Muscle aging is characterized by a loss of maximum tetanic force (Po) generation, primarily due to muscle atrophy, to which mitochondrial dysfunction is hypothesized to contribute. We hypothesized that lifelong overexpression of the mitochondrial heat shock protein (HSP) HSP10 in muscle of mice would protect against development of these deficits. Po generation by extensor digitorum longus muscles of adult and old wild-type and HSP10-overexpressing mice was determined in situ. Muscles were subjected to damaging lengthening contractions, and force generation was remeasured at 3 h or 28 days to examine susceptibility to, and recovery from, damage, respectively. Muscles of old wild-type mice had a 23% deficit in Po generation and a 10% deficit in muscle cross-sectional area compared with muscles of adult wild-type mice. Overexpression of HSP10 prevented this age-related fall in Po generation and reduction in cross-sectional area observed in muscles of old wild-type mice. Additionally, overexpression of HSP10 protected against contraction-induced damage independent of age but did not improve recovery if damage occurred. Preservation of muscle force generation and CSA by HSP10 overexpression was associated with protection against the age-related accumulation of protein carbonyls. Data demonstrate that development of age-related muscle weakness may not be inevitable and show, for the first time, that lifelong overexpression of an HSP prevents the age-related loss of Po generation. These findings support the hypothesis that mitochondrial dysfunction is involved in the development of age-related muscle deficits.


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