- 著者
- Tetsuya Izawa Jun-etsu Ogasawara Takuya Sakurai Sachiko Nomura Takako Kizaki Hideki Ohno
- 出版者
- 一般社団法人日本体力医学会
- 雑誌
- The Journal of Physical Fitness and Sports Medicine (ISSN:21868131)
- 巻号頁・発行日
- vol.1, no.3, pp.381-387, 2012-09-25 (Released:2012-10-23)
- 参考文献数
- 64
- 被引用文献数
- 2
White adipose tissue (WAT) is located beneath the skin as subcutaneous adipose tissue (SAT), around internal organs as visceral adipose tissue (VAT), pericardial and epicardial adipose tissue, and inside muscles in human beings. Recent studies indicate that developmental and patterning genes are differentially expressed in SAT and VAT, and some of these genes exhibit changes in expression that closely correlate with the extent of obesity and pattern of fat distribution. Furthermore, the development of adipocytes from mesenchymal stem/progenitor cells is thought to be mediated by developmental signaling molecules including nodal, Wnt/wingless (Wg), bone morphogenetic proteins (BMPs), fibroblast growth factors (FGF), and others. Of these, BMPs and the FGF family have been suggested to play a role in maintaining energy homeostasis. However, it remains unclear whether these developmental and patterning genes are associated with morphological changes in WAT in response to exercise training (TR). On the other hand, when TR reduces the number of adipocytes in WAT, it increases preadipocyte factor 1 mRNA expression but down-regulates peroxisome proliferator-activated receptor-γ mRNA expression in stromal-vascular fraction cells, including adipose tissue-derived stromal cells, via the up-regulation of hypoxia-inducible factor-1α, which may also up-regulate the mRNA expression of vascular endothelial growth factor-A and its receptor. The purpose of this review is to summarize the research to date on the morphology of WAT and adipose tissue cellularity in exercise adaptation.
- 著者
- Shinya Masuda Hisashi Takakura Hisashi Kato Tetsuya Izawa
- 出版者
- 一般社団法人日本体力医学会
- 雑誌
- The Journal of Physical Fitness and Sports Medicine (ISSN:21868131)
- 巻号頁・発行日
- vol.3, no.4, pp.435-439, 2014-09-25 (Released:2014-10-02)
- 参考文献数
- 57
A number of changes occur with aging in skeletal muscles including a reduction in muscle fiber size and fiber number. However, recent studies have indicated that the elderly tend to be more resistant to fatigue than the young, particularly during prolonged isometric muscle contraction. In this review, we explore the molecular mechanisms in muscle cells that are involved in this phenomenon. Aging has been thought to induce preferential loss of fast-type fibers. However, previous studies have shown that a fiber-type shift with aging is specific to the region, type and/or function of the muscles. Aging promotes the production of reactive oxygen species (ROS) in skeletal muscle, and ROS is suggested to activate AMP-activated protein kinase (AMPK). AMPK signaling is involved in muscle atrophy, and it activates peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC-1α). PGC-1α is considered a key regulator of mitochondrial biogenesis, and furthermore, it could be involved in the reinnervation of muscle fibers that have been denervated due to aging. Thus, the balance between AMPK and PGC-1α could play an important role in increasing fatigue resistance in aged skeletal muscle.