Physical activity and markers of glycation in older individuals: data from a combined cross-sectional and randomized controlled trial (EXAMIN AGE).


Journal

Clinical science (London, England : 1979)
ISSN: 1470-8736
Titre abrégé: Clin Sci (Lond)
Pays: England
ID NLM: 7905731

Informations de publication

Date de publication:
15 05 2020
Historique:
received: 04 03 2020
revised: 23 04 2020
accepted: 01 05 2020
pubmed: 2 5 2020
medline: 8 10 2020
entrez: 2 5 2020
Statut: ppublish

Résumé

Advanced glycation end products (AGEs) are protein modifications that are predominantly formed from dicarbonyl compounds that arise from glucose and lipid metabolism. AGEs and sedentary behavior have been identified as a driver of accelerated (vascular) aging. The effect of physical activity on AGE accumulation is unknown. Therefore, we investigated whether plasma AGEs and dicarbonyl levels are different across older individuals that were active or sedentary and whether plasma AGEs are affected by high-intensity interval training (HIIT). We included healthy older active (HA, n=38, 44.7% female, 60.1 ± 7.7 years old) and healthy older sedentary (HS, n=36, 72.2% female, 60.0 ± 7.3 years old) individuals as well as older sedentary individuals with increased cardiovascular risk (SR, n=84, 50% female, 58.7 ± 6.6 years old). The SR group was randomized into a 12-week walking-based HIIT program or control group. We measured protein-bound and free plasma AGEs and dicarbonyls by ultra-performance liquid chromatography tandem mass spectrometry (UPLC-MS/MS) at baseline and after the HIIT intervention. Protein-bound AGE Nε-(carboxymethyl)lysine (CML) was lower in SR (2.6 ± 0.5 μmol/l) and HS (3.1 ± 0.5 μmol/l) than in HA (3.6 ± 0.6 μmol/l; P<0.05) and remained significantly lower after adjustment for several potential confounders. None of the other glycation markers were different between HS and HA. HIIT did not change plasma AGEs and dicarbonyls in SR. Although lifestyle interventions may act as important modulators of cardiovascular risk, HIIT is not a potent short-term intervention to reduce glycation in older individuals, underlining the need for other approaches, such as pharmacological agents, to reduce AGEs and lower cardiovascular risk in this population.

Sections du résumé

BACKGROUND
Advanced glycation end products (AGEs) are protein modifications that are predominantly formed from dicarbonyl compounds that arise from glucose and lipid metabolism. AGEs and sedentary behavior have been identified as a driver of accelerated (vascular) aging. The effect of physical activity on AGE accumulation is unknown. Therefore, we investigated whether plasma AGEs and dicarbonyl levels are different across older individuals that were active or sedentary and whether plasma AGEs are affected by high-intensity interval training (HIIT).
METHODS
We included healthy older active (HA, n=38, 44.7% female, 60.1 ± 7.7 years old) and healthy older sedentary (HS, n=36, 72.2% female, 60.0 ± 7.3 years old) individuals as well as older sedentary individuals with increased cardiovascular risk (SR, n=84, 50% female, 58.7 ± 6.6 years old). The SR group was randomized into a 12-week walking-based HIIT program or control group. We measured protein-bound and free plasma AGEs and dicarbonyls by ultra-performance liquid chromatography tandem mass spectrometry (UPLC-MS/MS) at baseline and after the HIIT intervention.
RESULTS
Protein-bound AGE Nε-(carboxymethyl)lysine (CML) was lower in SR (2.6 ± 0.5 μmol/l) and HS (3.1 ± 0.5 μmol/l) than in HA (3.6 ± 0.6 μmol/l; P<0.05) and remained significantly lower after adjustment for several potential confounders. None of the other glycation markers were different between HS and HA. HIIT did not change plasma AGEs and dicarbonyls in SR.
DISCUSSION
Although lifestyle interventions may act as important modulators of cardiovascular risk, HIIT is not a potent short-term intervention to reduce glycation in older individuals, underlining the need for other approaches, such as pharmacological agents, to reduce AGEs and lower cardiovascular risk in this population.

Identifiants

pubmed: 32356559
pii: 223316
doi: 10.1042/CS20200255
doi:

Substances chimiques

Biomarkers 0
Glycation End Products, Advanced 0

Types de publication

Journal Article Randomized Controlled Trial Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

1095-1105

Informations de copyright

© 2020 The Author(s). Published by Portland Press Limited on behalf of the Biochemical Society.

Auteurs

Mathias D G Van den Eynde (MDG)

Department of Internal Medicine, Maastricht University Medical Centre, Maastricht, The Netherlands.
CARIM School for Cardiovascular Diseases, Maastricht, The Netherlands.

Lukas Streese (L)

Division of Sports and Exercise Medicine, Department of Sport, Exercise and Health, University of Basel, Basel, Switzerland.

Alfons J H M Houben (AJHM)

Department of Internal Medicine, Maastricht University Medical Centre, Maastricht, The Netherlands.
CARIM School for Cardiovascular Diseases, Maastricht, The Netherlands.

Coen D A Stehouwer (CDA)

Department of Internal Medicine, Maastricht University Medical Centre, Maastricht, The Netherlands.
CARIM School for Cardiovascular Diseases, Maastricht, The Netherlands.

Jean L J M Scheijen (JLJM)

Department of Internal Medicine, Maastricht University Medical Centre, Maastricht, The Netherlands.
CARIM School for Cardiovascular Diseases, Maastricht, The Netherlands.

Casper G Schalkwijk (CG)

Department of Internal Medicine, Maastricht University Medical Centre, Maastricht, The Netherlands.
CARIM School for Cardiovascular Diseases, Maastricht, The Netherlands.

Nordin M J Hanssen (NMJ)

Department of Internal Medicine, Maastricht University Medical Centre, Maastricht, The Netherlands.
CARIM School for Cardiovascular Diseases, Maastricht, The Netherlands.

Henner Hanssen (H)

Division of Sports and Exercise Medicine, Department of Sport, Exercise and Health, University of Basel, Basel, Switzerland.

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