Circulating Soluble-Klotho and IGF-I Responses to Different Exercise Modalities in Young, Elderly and CAD Patients
Saghiv M*
Exercise Physiology Department, University of Mary, USA
2Professor of Clinical Medicine, Drexel University College of Medicine, USA
Submission: March 08, 2017; Published: April 06, 2017
*Corresponding author: Moran S Saghiv, Associate Professor, Exercise Physiology Department, Casey Center, Room 141B, University of Mary, 7500 University Drive, Bismarck, ND 58504, USA, Fax: 701-255-7687; Tel:702-908-2390; Email:mssaghiv@umary.edu
How to cite this article: Saghiv M. Circulating Soluble-Klotho and IGF-I Responses to Different Exercise Modalities in Young, Elderly and CAD Patients. J Cardiol & Cardiovasc Ther 2017; 4(3): 555637. DOI:10.19080/JOCCT.2017.04.555637
Keywords: Aerobic exercise; Epigenetic; Aging; Anaerobic exercise; Coronary artery disease; Master athletes; Elite athletes
Introduction
Klotho gene expression in positively influenced by different exercise modalities acting as an epigenetic influencer [1], resulting in increased work capacity, performance, and lifespan, and decreased aging in healthy and diseased populations [2-4]. As is the case with exercise, positive adaptations decrease and diminish with time if exercise training is not maintained.
S-Klotho
Klotho is a transmembrane protein that provides some control over the sensitivity of the organism to Insulin and appears to be involved in aging [5]. Age-related declines are manifest by a decreased ability for aged skeletal muscle to respond to physiological stimuli such as muscle loading or acute injury, and disease related effects [6-10].
IGF-I
IGF-I is critical for normal body growth, development and maintenance, and has important roles in multiple biological systems [11,12]. A variety of cellular responses are induced by IGF-I, including cell proliferation, differentiation, migration and survival [13,14]. These cellular responses have implicated IGF-I in several conditions such as the pathophysiology of several cancers [15], or the mitogenic and myogenic processes during muscle development, regeneration or hypertrophy, since, unlike other growth factors, IGF-I acts as both a mitogen and a differentiation factor [16].
Deficiency of IGF-I in skeletal muscle may contribute to Sarcopenia by severely impacting protein synthesis. IGF-I has anabolic effects on muscle protein content by inhibiting protein degradation and promoting Myogenesis. Indirect data have supported the concept that IGF-I may be atherogenetic because it can induce vascular smooth muscle cell proliferation in vitro [17]. Thus, IGF-I has been considered a promoter of arterial obstructive lesions [18].
The Influence of Exercise Modalities on S-Klotho and IGF-I
Regular aerobic exercise participation promotes health and disease prevention [19]. Endurance exercise like biking, walking, swimming and running, appear to benefit longer life expectancy than anaerobic exercise like power lifting [20]. It has been suggested that circulating Klotho levels are up regulated in response to an acute exercise bout, but that the response may be dependent on fitness level [21-24].
Compared to sedentary young and old subjects, in the elite well aerobic trained young runners and master athletes s-Klotho levels are markedly elevated while, IGF-I levels were decreased [25]. IGF-I is generally thought to be associated with anabolism and wellbeing [26], yet, signaling through IGF-I and Insulin receptors is negatively related to adults [27]. A meta-analysis study indicated that increased circulating concentrations of IGF-I are associated with increased risks for colorectal, prostate, and premenopausal breast cancers [28].
Several clinical studies have suggested that Klotho gene exerts strong cardio-protective effects. S-Klotho has been proposed as a key regulator of the development of cardiovascular disease. Associations between low levels ofs-Klotho and the occurrence and severity of cardiovascular disease have been reported, as well as a reduction of cardiovascular risk when levels were high [28]. This protein is related to the attenuation of vascular calcification as well as prevention of cardiac hypertrophy.
Conclusion
IGF-I is critical for normal body growth, development and maintenance, and has important roles in multiple biological systems [11,12]. A variety of cellular responses are induced by IGF-I, including cell proliferation, differentiation, migration and survival [13,14]. These cellular responses have implicated IGF-I in several conditions such as the pathophysiology of several cancers [15], or the mitogenic and myogenic processes during muscle development, regeneration or hypertrophy, since, unlike other growth factors, IGF-I acts as both a mitogen and a differentiation factor [16].
Deficiency of IGF-I in skeletal muscle may contribute to Sarcopenia by severely impacting protein synthesis. IGF-I has anabolic effects on muscle protein content by inhibiting protein degradation and promoting Myogenesis. Indirect data have supported the concept that IGF-I may be atherogenetic because it can induce vascular smooth muscle cell proliferation in vitro [17]. Thus, IGF-I has been considered a promoter of arterial obstructive lesions [18].
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