Skeletal Muscle Size (skeletal + muscle_size)

Distribution by Scientific Domains


Selected Abstracts


Changes in skeletal muscle size, fibre-type composition and capillary supply after chronic venous occlusion in rats

ACTA PHYSIOLOGICA, Issue 4 2008
S. Kawada
Abstract Aim:, We have previously shown that surgical occlusion of some veins from skeletal muscle results in muscle hypertrophy without mechanical overloading in the rat. The present study investigated the changes in muscle-fibre composition and capillary supply in hypertrophied muscles after venous occlusion in the rat hindlimb. Methods:, Sixteen male Wistar rats were randomly assigned into two groups: (i) sham operated (sham-operated group; n = 7); (ii) venous occluded for 2 weeks (2-week-occluded group; n = 9). At the end of the experimental period, specimens of the plantaris muscle were dissected from the hindlimbs and subjected to biochemical and histochemical analyses. Results:, Two weeks after the occlusion, both the wet weight of plantaris muscle relative to body weight and absolute muscle weight showed significant increases in the 2-week-occluded group (,15%) when compared with those in the sham-operated group. The concentrations of muscle glycogen and lactate were higher in the 2-week-occluded group, whereas staining intensity of muscle lipid droplets was lower in the 2-week-occluded group than those in the sham-operated group. The percentage of type I muscle fibre decreased, whereas that of type IIb fibre increased in the 2-week-occluded group when compared with the sham-operated group. Although the expression of vascular endothelial growth factor-188 mRNA increased, the number of capillaries around the muscle fibres tended to decrease (P = 0.07). Conclusion:, Chronic venous occlusion causes skeletal muscle hypertrophy with fibre-type transition towards faster types and changes in contents of muscle metabolites. [source]


Myotendinous plasticity to ageing and resistance exercise in humans

EXPERIMENTAL PHYSIOLOGY, Issue 3 2006
N. D. Reeves
The age-related loss of muscle mass known as senile sarcopenia is one of the main determinants of frailty in old age. Molecular, cellular, nutritional and hormonal mechanisms are at the basis of sarcopenia and are responsible for a progressive deterioration in skeletal muscle size and function. Both at single-fibre and at whole-muscle level, the loss of force exceeds that predicted by the decrease in muscle size. For single fibres, the loss of intrinsic force is mostly due to a loss in myofibrillar protein content. For whole muscle, in addition to changes in neural drive, alterations in muscle architecture and in tendon mechanical properties, exemplified by a reduction in tendon stiffness, have recently been shown to contribute to this phenomenon. Resistance training can, however, cause substantial gains in muscle mass and strength and provides a protective effect against several of the cellular and molecular changes associated with muscle wasting and weakness. In old age, not only muscles but also tendons are highly responsive to training, since an increase in tendon stiffness has been observed after a period of increased loading. Many of the myotendinous factors characterizing ageing can be at least partly reversed by resistance training. [source]


Human skeletal muscle size and architecture: Variability and interdependence

AMERICAN JOURNAL OF HUMAN BIOLOGY, Issue 6 2006
Y. Kawakami
Seven hundred and eleven women and men (aged 3,94 years, including normal individuals and highly trained bodybuilders) were tested for the thickness and pennation angles of their triceps brachii (TB), vastus lateralis (VL), and gastrocnemius medialis (GM) muscles. The variations of muscle thickness and pennation angles were largest in TB (6,66 mm and 5,55°), followed by VL (8,45 mm and 7,33°) and GM (11,36mm and 12,33°), and women showed smaller variations than men. These results suggest the existence of muscle- and gender-specificity in the variability of muscle dimensions. Significant positive correlations were observed between muscle thickness and pennation angles (r = 0.81, 0.61, and 0.56, for TB, VL, and GM, respectively), indicating that the size-dependence of the pennation angle is a general feature of pennate muscles. Am. J. Hum. Biol. 18:845,848, 2006. © 2006 Wiley-Liss, Inc. [source]


Regulation of STARS and its downstream targets suggest a novel pathway involved in human skeletal muscle hypertrophy and atrophy

THE JOURNAL OF PHYSIOLOGY, Issue 8 2009
Séverine Lamon
Skeletal muscle atrophy is a severe consequence of ageing, neurological disorders and chronic disease. Identifying the intracellular signalling pathways controlling changes in skeletal muscle size and function is vital for the future development of potential therapeutic interventions. Striated activator of Rho signalling (STARS), an actin-binding protein, has been implicated in rodent cardiac hypertrophy; however its role in human skeletal muscle has not been determined. This study aimed to establish if STARS, as well as its downstream signalling targets, RhoA, myocardin-related transcription factors A and B (MRTF-A/B) and serum response factor (SRF), were increased and decreased respectively, in human quadriceps muscle biopsies taken after 8 weeks of both hypertrophy-stimulating resistance training and atrophy-stimulating de-training. The mRNA levels of the SRF target genes involved in muscle structure, function and growth, such as ,-actin, myosin heavy chain IIa (MHCIIa) and insulin-like growth factor-1 (IGF-1), were also measured. Following resistance training, STARS, MRTF-A, MRTF-B, SRF, ,-actin, MHCIIa and IGF-1 mRNA, as well as RhoA and nuclear SRF protein levels were all significantly increased by between 1.25- and 3.6-fold. Following the de-training period all measured targets, except for RhoA, which remained elevated, returned to base-line. Our results show that the STARS signalling pathway is responsive to changes in skeletal muscle loading and appears to play a role in both human skeletal muscle hypertrophy and atrophy. [source]