Exercise physiology is an old profession that dates back to 1500 B.C.E., having rises and falls in intervening years. The author provides comments from firsthand observations he has experienced in the past six decades. Events in the 1950s and 1960s caused a rise in exercise physiology in the next decades, with a decline being initiated in the late 1990s by the Center for Scientific Review's decision to treat exercise by individual organs or individual diseases rather than as a preexisting vibrant translational science for human health. In the opinion of this author and of some National Institutes of Health (NIH) program officials, the decline of qualified individuals to wisely spend taxpayer's monies on exercise research has resulted in the December 13, 2013 publication of the NIH's “Request for Information (RFI): Identifying Gaps in Understanding the Mechanisms of Physical Activity-Induced Health Benefits.”
Frank W. Booth
Manu V. Chakravarthy, Frank W. Booth, and Espen E. Spangenburg
Approximately 50% of humans older than 85 years have physical frailty due to weak skeletal muscles. This indicates a need for determining mechanisms to combat this problem. A critical cellular factor for postnatal muscle growth is a population of myogenic precursor cells called satellite cells. Given the complex process of sarcopenia, it has been postulated that, at some point in this process, a limited satellite cell proliferation potential could become rate-limiting to the regrowth of old muscles. It is conceivable that if satellite cell proliferative capacity can be maintained or enhanced with advanced age, sarcopenia could potentially be delayed or prevented. Therefore, the purposes of this paper are to describe whether IGF-I can prevent muscular atrophy induced by repeated cycles of hindlimb immobilization, increase the in vitro proliferation in satellite cells from these muscles and, if so, the molecular mechanisms by which IGF-1 mediates this increased proliferation. Our results provide evidence that IGFI can enhance aged muscle regrowth possibly through increased satellite cell proliferation. The results also suggest that IGF-I enhances satellite cell proliferation by decreasing the cell cycle inhibitor, p27 Kip1 , through the PI3’-K/Akt pathway. These data provide molecular evidence for IGF-I’s rescue effect upon aging-associated skeletal muscle atrophy.