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The effect of acute maximal exercise on postexercise hemodynamics and central arterial stiffness in obese and normal ‐ weight individuals

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ABSTRACT

Central arterial stiffness is associated with incident hypertension and negative cardiovascular outcomes. Obese individuals have higher central blood pressure (BP) and central arterial stiffness than their normal‐weight counterparts, but it is unclear whether obesity also affects hemodynamics and central arterial stiffness after maximal exercise. We evaluated central hemodynamics and arterial stiffness during recovery from acute maximal aerobic exercise in obese and normal‐weight individuals. Forty‐six normal‐weight and twenty‐one obese individuals underwent measurements of central BP and central arterial stiffness at rest and 15 and 30 min following acute maximal exercise. Central BP and normalized augmentation index (AIx@75) were derived from radial artery applanation tonometry, and central arterial stiffness was obtained via carotid‐femoral pulse wave velocity (cPWV) and corrected for central mean arterial pressure (cPWV/cMAP). Central arterial stiffness increased in obese individuals but decreased in normal‐weight individuals following acute maximal exercise, after adjusting for fitness. Obese individuals also exhibited an overall higher central BP (P < 0.05), with no exercise effect. The increase in heart rate was greater in obese versus normal‐weight individuals following exercise (P < 0.05), but there was no group differences or exercise effect for AIx@75. In conclusion, obese (but not normal‐weight) individuals increased central arterial stiffness following acute maximal exercise. An assessment of arterial stiffness response to acute exercise may serve a useful detection tool for subclinical vascular dysfunction.

No MeSH data available.


Brachial (A–C) and central (D–F) blood pressure (BP) variables at baseline and at 15‐ and 30‐min postmaximal exercise. bSBP, brachial systolic blood pressure (Panel A); bDBP, brachial diastolic blood pressure (Panel B); bMAP, brachial mean arterial pressure (Panel C); cSBP, central systolic blood pressure (Panel D); cDBP, central diastolic blood pressure (Panel E); cMAP, central mean arterial pressure (Panel F). #group difference at baseline (P < 0.05); bmain effect of group (P < 0.05). Values are mean ± SE.
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phy213226-fig-0001: Brachial (A–C) and central (D–F) blood pressure (BP) variables at baseline and at 15‐ and 30‐min postmaximal exercise. bSBP, brachial systolic blood pressure (Panel A); bDBP, brachial diastolic blood pressure (Panel B); bMAP, brachial mean arterial pressure (Panel C); cSBP, central systolic blood pressure (Panel D); cDBP, central diastolic blood pressure (Panel E); cMAP, central mean arterial pressure (Panel F). #group difference at baseline (P < 0.05); bmain effect of group (P < 0.05). Values are mean ± SE.

Mentions: Hemodynamic variables are shown in Figures 1A–F and 2A. At baseline, obese individuals exhibited higher baseline bDBP, bMAP, cSBP, cDBP, and cMAP than normal‐weight individuals (P < 0.05, Fig. 1B–F). Following exercise, HR increased from baseline similarly in both groups, but was overall higher in the obese individuals, even after controlling for the effects of fitness and central BP (VO2peak and cMAP) (P < 0.05, Fig. 2A). No exercise responses were observed bDBP, bMAP, cSBP, cDBP, and cMAP, but these variables were overall higher in obese individuals versus normal‐weight individuals (P < 0.05 for group, Fig. 1B–F). No main effects of group or time were found for bSBP.


The effect of acute maximal exercise on postexercise hemodynamics and central arterial stiffness in obese and normal ‐ weight individuals
Brachial (A–C) and central (D–F) blood pressure (BP) variables at baseline and at 15‐ and 30‐min postmaximal exercise. bSBP, brachial systolic blood pressure (Panel A); bDBP, brachial diastolic blood pressure (Panel B); bMAP, brachial mean arterial pressure (Panel C); cSBP, central systolic blood pressure (Panel D); cDBP, central diastolic blood pressure (Panel E); cMAP, central mean arterial pressure (Panel F). #group difference at baseline (P < 0.05); bmain effect of group (P < 0.05). Values are mean ± SE.
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Show All Figures
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phy213226-fig-0001: Brachial (A–C) and central (D–F) blood pressure (BP) variables at baseline and at 15‐ and 30‐min postmaximal exercise. bSBP, brachial systolic blood pressure (Panel A); bDBP, brachial diastolic blood pressure (Panel B); bMAP, brachial mean arterial pressure (Panel C); cSBP, central systolic blood pressure (Panel D); cDBP, central diastolic blood pressure (Panel E); cMAP, central mean arterial pressure (Panel F). #group difference at baseline (P < 0.05); bmain effect of group (P < 0.05). Values are mean ± SE.
Mentions: Hemodynamic variables are shown in Figures 1A–F and 2A. At baseline, obese individuals exhibited higher baseline bDBP, bMAP, cSBP, cDBP, and cMAP than normal‐weight individuals (P < 0.05, Fig. 1B–F). Following exercise, HR increased from baseline similarly in both groups, but was overall higher in the obese individuals, even after controlling for the effects of fitness and central BP (VO2peak and cMAP) (P < 0.05, Fig. 2A). No exercise responses were observed bDBP, bMAP, cSBP, cDBP, and cMAP, but these variables were overall higher in obese individuals versus normal‐weight individuals (P < 0.05 for group, Fig. 1B–F). No main effects of group or time were found for bSBP.

View Article: PubMed Central - PubMed

ABSTRACT

Central arterial stiffness is associated with incident hypertension and negative cardiovascular outcomes. Obese individuals have higher central blood pressure (BP) and central arterial stiffness than their normal&#8208;weight counterparts, but it is unclear whether obesity also affects hemodynamics and central arterial stiffness after maximal exercise. We evaluated central hemodynamics and arterial stiffness during recovery from acute maximal aerobic exercise in obese and normal&#8208;weight individuals. Forty&#8208;six normal&#8208;weight and twenty&#8208;one obese individuals underwent measurements of central BP and central arterial stiffness at rest and 15 and 30&nbsp;min following acute maximal exercise. Central BP and normalized augmentation index (AIx@75) were derived from radial artery applanation tonometry, and central arterial stiffness was obtained via carotid&#8208;femoral pulse wave velocity (cPWV) and corrected for central mean arterial pressure (cPWV/cMAP). Central arterial stiffness increased in obese individuals but decreased in normal&#8208;weight individuals following acute maximal exercise, after adjusting for fitness. Obese individuals also exhibited an overall higher central BP (P&nbsp;&lt;&nbsp;0.05), with no exercise effect. The increase in heart rate was greater in obese versus normal&#8208;weight individuals following exercise (P&nbsp;&lt;&nbsp;0.05), but there was no group differences or exercise effect for AIx@75. In conclusion, obese (but not normal&#8208;weight) individuals increased central arterial stiffness following acute maximal exercise. An assessment of arterial stiffness response to acute exercise may serve a useful detection tool for subclinical vascular dysfunction.

No MeSH data available.