Circulating Soluble-Klotho and IGF-I Responses to Different Exercise Modalities in Young, Elderly and CAD Patients-Juniper Publishers
JUNIPER PUBLISHERS-OPEN ACCESS JOURNAL OF CARDIOLOGY & CARDIOVASCULAR THERAPY
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.
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 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].
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.
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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