TY - JOUR
T1 - Central and peripheral arterial stiffness responses to uninterrupted prolonged sitting combined with a high-fat meal
T2 - a randomized controlled crossover trial
AU - Fryer, Simon
AU - Stone, Keeron
AU - Paterson, Craig
AU - Brown, Meghan
AU - Faulkner, James
AU - Lambrick, Danielle
AU - Credeur, Daniel
AU - Zieff, Gabriel
AU - Martínez Aguirre-Betolaza, Aitor
AU - Stoner, Lee
N1 - Publisher Copyright:
© 2021, The Author(s).
PY - 2021/8/2
Y1 - 2021/8/2
N2 - Independently, prolonged uninterrupted sitting and the consumption of a meal high in saturated fats acutely disrupt normal cardiovascular function. Currently, the acute effects of these behaviors performed in combination on arterial stiffness, a marker of cardiovascular health, are unknown. This study sought to determine the effect of consuming a high-fat meal (Δ = 51 g fat) in conjunction with prolonged uninterrupted sitting (180 min) on measures of central and peripheral arterial stiffness. Using a randomized crossover design, 13 young healthy males consumed a high-fat (61 g) or low-fat (10 g) meal before 180 min of uninterrupted sitting. Carotid-femoral (cf) and femoral-ankle (fa) pulse wave velocity (PWV), aortic-femoral stiffness gradient (af-SG), superficial femoral PWV beta (β), and oscillometric pulse wave analysis outcomes were assessed pre and post sitting. cfPWV increased significantly more following the high-fat (mean difference [MD] = 0.59 m·s−1) meal than following the low-fat (MD = 0.2 m·s−1) meal, with no change in faPWV in either condition. The af-SG significantly decreased (worsened) (ηp2 = 0.569) over time in the high- and low-fat conditions (ratio = 0.1 and 0.1, respectively). Superficial femoral PWVβ significantly increased over time in the high- and low-fat conditions (ηp2 = 0.321; 0.8 and 0.4 m·s−1, respectively). Triglycerides increased over time in the high-fat trial only (ηp2 = 0.761). There were no significant changes in blood pressure. Consuming a high-fat meal prior to 180 min of uninterrupted sitting augments markers of cardiovascular disease risk more than consuming a low-fat meal prior to sitting.
AB - Independently, prolonged uninterrupted sitting and the consumption of a meal high in saturated fats acutely disrupt normal cardiovascular function. Currently, the acute effects of these behaviors performed in combination on arterial stiffness, a marker of cardiovascular health, are unknown. This study sought to determine the effect of consuming a high-fat meal (Δ = 51 g fat) in conjunction with prolonged uninterrupted sitting (180 min) on measures of central and peripheral arterial stiffness. Using a randomized crossover design, 13 young healthy males consumed a high-fat (61 g) or low-fat (10 g) meal before 180 min of uninterrupted sitting. Carotid-femoral (cf) and femoral-ankle (fa) pulse wave velocity (PWV), aortic-femoral stiffness gradient (af-SG), superficial femoral PWV beta (β), and oscillometric pulse wave analysis outcomes were assessed pre and post sitting. cfPWV increased significantly more following the high-fat (mean difference [MD] = 0.59 m·s−1) meal than following the low-fat (MD = 0.2 m·s−1) meal, with no change in faPWV in either condition. The af-SG significantly decreased (worsened) (ηp2 = 0.569) over time in the high- and low-fat conditions (ratio = 0.1 and 0.1, respectively). Superficial femoral PWVβ significantly increased over time in the high- and low-fat conditions (ηp2 = 0.321; 0.8 and 0.4 m·s−1, respectively). Triglycerides increased over time in the high-fat trial only (ηp2 = 0.761). There were no significant changes in blood pressure. Consuming a high-fat meal prior to 180 min of uninterrupted sitting augments markers of cardiovascular disease risk more than consuming a low-fat meal prior to sitting.
KW - Dietary behavior
KW - Hypertension
KW - Sedentary behavior
KW - Vascular function
UR - http://www.scopus.com/inward/record.url?scp=85111799857&partnerID=8YFLogxK
U2 - 10.1038/s41440-021-00708-z
DO - 10.1038/s41440-021-00708-z
M3 - Article
C2 - 34334790
AN - SCOPUS:85111799857
SN - 0916-9636
VL - 44
SP - 1332
EP - 1340
JO - Hypertension Research
JF - Hypertension Research
IS - 10
ER -