Why the study?
Endothelial dysfunction contributes to atherosclerosis and hypertension, while s-Klotho regulates endothelial nitric oxide production and reflects aerobic fitness levels, prompting review of the relationship between aerobic exercise training and circulating s-Klotho.
Does aerobic exercise training improve endothelial dysfunction by increasing s-Klotho expression?
Does aerobic exercise training improve endothelial dysfunction by increasing s-Klotho expression?
Aerobic exercise may serve as a non-pharmacological intervention to delay endothelial dysfunction and cardiovascular diseases by increasing s-Klotho expression and reducing oxidative stress.
May support exercise for vascular protection; leaves open causal confirmation and outcome trials.
Endothelial dysfunction is characterized by reduced vascular nitric oxide levels, that causes some irregularities in blood artery function. These functional irregularities contribute to atherosclerosis, which promote vasoconstriction of the small arteries, a major factor in hypertension. Secreted klotho (s-klotho) regulates nitric oxide production in the endothelium. It has been suggested that s-Klotho affect nitric oxide thus benefiting endothelial function. S-klotho levels are reflective of aerobic fitness level, s-Klotho is significantly higher in trained individuals compared to untrained. This suggests aerobic training may be an appropriate model for examining the role of physical activity on s-Klotho expression. There is an association with endothelial fusnction improvement with increased s-klotho levels following aerobic exercise training. It is believed that this review will inspire more deliberation on the relationship between aerobic exercise training and circulating s-Klotho, as a possibly effectors on cardiovascular arterial stiffens due to endothelial dysfunction.
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TJ Exford (2020) studied this question.
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