Abstract

Individuals with type 2 diabetes mellitus (T2DM) have a greater blood pressure (BP) response to acute maximal exercise compared to those without T2DM; however, whether they exhibit a different arterial stiffness response to maximal exercise has yet to be explored. Adults with (n=66) and without T2DM (n=61) underwent an arterial stress test: at rest and immediately postexercise, carotid-femoral pulse wave velocity, the gold standard measure of arterial stiffness, brachial BP, heart rate, and other hemodynamic measurements were assessed. Linear regression models were used to evaluate between-group differences at rest, and the response to exercise (postexercise value), adjusting for covariates including BP and heart rate when relevant, and the corresponding baseline value of each parameter. All participants (mean±SD: age 59.3±10.6 years; body mass index 31.2±3.9 kg/m2) had hypertension (mean BP 130±14/80±9 mm Hg). At rest, participants with T2DM had significantly higher carotid-femoral pulse wave velocity (10.3±2.7 versus 9.1±1.9 m/s), heart rate (69±11 versus 66±10 beats/min), and lower diastolic BP (79±9 versus 83±9 mm Hg), but systolic BP (129±15 versus 131±13 mm Hg) was similar. In response to exercise, participants with T2DM showed greater increases in carotid-femoral pulse wave velocity (1.6 [95% CI, 0.4-2.9 m/s]) and systolic BP (9 [95% CI, 1-17 mm Hg]) than participants without T2DM. A greater proportion of participants with T2DM had a hypertensive response to exercise compared to participants without T2DM (n=23, 35% versus n=11, 18%; P=0.033). By incorporating exercise as a vascular stressor, we provide evidence of a greater increase in arterial stiffness in individuals with T2DM, independently of resting arterial stiffness, and the BP postexercise.

Highlights

  • Abstract —Individuals with type 2 diabetes mellitus (T2DM) have a greater blood pressure (BP) response to acute maximal exercise compared to those without T2DM; whether they exhibit a different arterial stiffness response to maximal exercise has yet to be explored

  • During maximal exercise, individuals with T2DM are more likely to experience an exaggerated blood pressure (BP) response[3]; this is defined as a rise in systolic BP (SBP) exceeding 210 mm Hg in men and 190 mm Hg in women and is associated with higher cardiovascular disease (CVD) risk and mortality.[4]

  • We evaluated the BP-independent changes in arterial stiffness (AS) by calculating an index of stiffness that is considered equivalent to the intrinsic stiffness index β0, where β0 is the exponent of the pressure (P)-diameter (D) relationship within the vessel[22]: P = P e . β

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Summary

Introduction

Abstract —Individuals with type 2 diabetes mellitus (T2DM) have a greater blood pressure (BP) response to acute maximal exercise compared to those without T2DM; whether they exhibit a different arterial stiffness response to maximal exercise has yet to be explored. Type 2 diabetes mellitus (T2DM) increases arterial stiffness (AS) through pathological changes in the vasculature, including reduced nitric oxide bioavailability, increased oxidative stress, and inflammation, as well as structural changes within the arterial wall.[1] As a result, for many individuals with T2DM, their vascular age surpasses their chronological age.[2] during maximal exercise, individuals with T2DM are more likely to experience an exaggerated blood pressure (BP) response[3]; this is defined as a rise in systolic BP (SBP) exceeding 210 mm Hg in men and 190 mm Hg in women and is associated with higher cardiovascular disease (CVD) risk and mortality.[4] The physiological changes underlying this altered response have not been fully elucidated but underlying vascular abnormalities are thought to play a pivotal role.[5] whether individuals with T2DM have a different AS response to exercise, independent of the resting value, has yet to be explored In this context, increased demands associated with acute exercise might exaggerate vascular abnormalities present in these individuals. We aimed to examine the acute response of AS and hemodynamic parameters to maximal

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