Abbi D Lane-Cordova1, Shane A Phillips2, Tracy Baynard3, Jeffrey A Woods4, Robert W Motl4, Bo Fernhall3. 1. Department of Preventive Medicine, Feinberg School of Medicine, Northwestern University, Chicago, IL, USA. 2. Department of Physical Therapy, University of Illinois at Chicago, Chicago, IL, USA. 3. Department of Kinesiology, Nutrition, and Rehabilitation, University of Illinois at Chicago, Chicago, IL, USA. 4. Department of Kinesiology and Community Health, University of Illinois at Urbana-Champaign, Urbana, IL, USA.
Abstract
NEW FINDINGS: What is the central question of this study? Do older and younger adults have similar vascular endothelial and blood pressure responses to acute inflammation? Does physical activity affect these responses? What is the main finding and its importance? Older adults reduce blood pressure whereas younger adults reduce endothelial function during acute inflammation. Physical activity does not provide protection against these inflammation-induced changes. This is important because older adults regularly experience acute increases in systemic inflammation that may predispose older adults to cardiovascular events through dysregulation of blood pressure. Ageing is characterized by chronic, low-grade inflammation that is related to endothelial dysfunction and arterial stiffness. Physical activity can protect older adults (OAs) from cardiovascular dysfunction and increased inflammation. Acute inflammation causes transient endothelial dysfunction and arterial stiffening in younger adults (YAs), but may not have the same effect in OAs. We hypothesized that acute inflammation would increase blood pressure (BP) and endothelial impairment to a greater extent in OAs versus YAs, but that physical activity would be protective. We induced inflammation with an influenza vaccine in 22 OAs (55-75 years old) and 31 YAs (18-35 years old) and measured brachial flow-mediated dilatation (FMD), BP and serum inflammatory markers before vaccination and at 24 and 48 h afterwards. Physical activity data were collected using accelerometry. During inflammation, only OAs reduced systolic BP (from 120 ± 3 to 115 ± 2 to 115 ± 3 mmHg, P < 0.05), but only YAs reduced FMD (from 11.3 ± 0.7 to 8.5 ± 0.6 to 8.9 ± 0.6% in YAs and from 6.7 ± 0.6 to 5.3 ± 0.7 to 6.0 ± 0.6% in OAs, P < 0.05 for time and interaction effects). The entire cohort increased C-reactive protein (P < 0.05), but only YAs increased interleukin-6 (P < 0.05 for time × age group interaction). Physical activity was related to the percentage change in inflammation in OAs (r = -0.50, P < 0.05) but not to the change in arterial function in either group (P > 0.05 for all). We conclude that acute inflammation reduced FMD only in YAs and reduced BP only in OAs. Physical activity did not affect arterial function during acute inflammation. Clinicians should be aware that all OAs are vulnerable to inflammation-mediated reductions in BP and cardiovascular complications.
NEW FINDINGS: What is the central question of this study? Do older and younger adults have similar vascular endothelial and blood pressure responses to acute inflammation? Does physical activity affect these responses? What is the main finding and its importance? Older adults reduce blood pressure whereas younger adults reduce endothelial function during acute inflammation. Physical activity does not provide protection against these inflammation-induced changes. This is important because older adults regularly experience acute increases in systemic inflammation that may predispose older adults to cardiovascular events through dysregulation of blood pressure. Ageing is characterized by chronic, low-grade inflammation that is related to endothelial dysfunction and arterial stiffness. Physical activity can protect older adults (OAs) from cardiovascular dysfunction and increased inflammation. Acute inflammation causes transient endothelial dysfunction and arterial stiffening in younger adults (YAs), but may not have the same effect in OAs. We hypothesized that acute inflammation would increase blood pressure (BP) and endothelial impairment to a greater extent in OAs versus YAs, but that physical activity would be protective. We induced inflammation with an influenza vaccine in 22 OAs (55-75 years old) and 31 YAs (18-35 years old) and measured brachial flow-mediated dilatation (FMD), BP and serum inflammatory markers before vaccination and at 24 and 48 h afterwards. Physical activity data were collected using accelerometry. During inflammation, only OAs reduced systolic BP (from 120 ± 3 to 115 ± 2 to 115 ± 3 mmHg, P < 0.05), but only YAs reduced FMD (from 11.3 ± 0.7 to 8.5 ± 0.6 to 8.9 ± 0.6% in YAs and from 6.7 ± 0.6 to 5.3 ± 0.7 to 6.0 ± 0.6% in OAs, P < 0.05 for time and interaction effects). The entire cohort increased C-reactive protein (P < 0.05), but only YAs increased interleukin-6 (P < 0.05 for time × age group interaction). Physical activity was related to the percentage change in inflammation in OAs (r = -0.50, P < 0.05) but not to the change in arterial function in either group (P > 0.05 for all). We conclude that acute inflammation reduced FMD only in YAs and reduced BP only in OAs. Physical activity did not affect arterial function during acute inflammation. Clinicians should be aware that all OAs are vulnerable to inflammation-mediated reductions in BP and cardiovascular complications.
Authors: Elizabeth C Lefferts; Brooks A Hibner; Wesley K Lefferts; Natalia S Lima; Tracy Baynard; Jacob M Haus; Abbi D Lane-Cordova; Shane A Phillips; Bo Fernhall Journal: Physiol Rep Date: 2021-11
Authors: Luca Zanoli; Marie Briet; Jean P Empana; Pedro G Cunha; Kaisa M Mäki-Petäjä; Athanase D Protogerou; Alain Tedgui; Rhian M Touyz; Ernesto L Schiffrin; Bart Spronck; Philippe Bouchard; Charalambos Vlachopoulos; Rosa M Bruno; Pierre Boutouyrie Journal: J Hypertens Date: 2020-09 Impact factor: 4.776