Severity of Sarcopenia Correlates with Arterial Stiffness and Hypertension

Many dysfunctions and conditions of aging correlate with one another. For closer correlations, the question is whether this relationship exists because (a) one condition contributes meaningfully to the progression of the other, or (b) both conditions are similar in terms of which forms of underlying age-related cell and tissue damage contribute to their onset and progression. Or both! Here, researchers link the severity of sarcopenia, the age-related loss of muscle mass and strength, with arterial stiffness and hypertension. They review the existing hypotheses for causation in this relationship, noting that mechanisms exist to explain either direction of causation.

This cross-sectional study aimed to determine whether sarcopenia is related to arterial stiffness or hypertension in older adults without underweight and obesity. A total of 2,237 male and female adults in the Korea National Health and Nutritional Examination Survey who were ≥60 years and did not have underweight and obesity (body mass index of 18.5 to 25.0 kg/m2) were involved. Arterial stiffness and systolic and diastolic blood pressure showed an increasing trend from normal to moderate-to-severe sarcopenia. Subjects with moderate or severe sarcopenia were 3.545 or 8.903 times more likely to be in the highest tertile of arterial stiffness, and those with moderate or severe sarcopenia were 2.106 or 11.725 times more likely to be hypertensive.

While the exact mechanisms are not fully understood, several potential explanations for the relationship between sarcopenia, arterial stiffness or hypertension have been proposed. Reduced muscle mass and intramuscular fat infiltration cause a decrease in insulin-responsive target tissue, resulting in insulin resistance; consequently, arterial stiffness increases, which indicates the onset of hypertension. The results of the present study supported this potential mechanism in that insulin resistance, evaluated using the triglyceride-glucose index, showed a significant increasing trend from normal to moderate-to-severe sarcopenia. Additionally, chronic inflammation may be a potential explanation for the relationships of sarcopenia with arterial stiffness and hypertension. This potential mechanism was also supported by the finding in the present study that white blood cell counts showed a significant increasing trend from normal to moderate-to-severe sarcopenia.

Furthermore, individuals with sarcopenia commonly exhibit functional impairment or physical disability, which induces a reduction in muscle contraction-derived anti-inflammatory markers called myokines. Since decreased myokine levels are an independent predictor of increased risk of sarcopenia and arterial issues, myokine deficiency in sarcopenia is more likely to increase the risk of arterial stiffness or hypertension. Unfortunately, the present study does not provide objective data on myokine deficiency in sarcopenia patients. However, given that sarcopenia is a common cause of functional impairment or physical disability, decreased myokine secretion in sarcopenia patients is reasonable.

Finally, increased arterial stiffness may induce pulse pressure amplification in arteries. It may stimulate hypertrophy, remodeling or rarefaction in the microcirculation, which makes blood vessels unresponsive to the demand for changing blood flow, thereby leading to increased oxidative stress in muscles. Oxidative stress damages muscle components, such as reducing the number and function of satellite cells, and may induce muscle mass reduction. Depending on all of these factors, sarcopenia may be a trigger of arterial stiffness or hypertension, and arterial stiffness or hypertension may worsen sarcopenia.

Link: https://doi.org/10.3389/fpubh.2024.1469196

Comment Submission

Post a comment; thoughtful, considered opinions are valued. New comments can be edited for a few minutes following submission. Comments incorporating ad hominem attacks, advertising, and other forms of inappropriate behavior are likely to be deleted.

Note that there is a comment feed for those who like to keep up with conversations.