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Published on: May 16, 2021
The Angiotensin Converting Enzyme Insertion/Deletion Polymorphism Modifies Exercise-Induced Muscle Metabolism
David Vaughan1, Michael Brogioli1,2, Thomas Maier1,2
1Institute for Biomedical Research into Human Movement and Health, Manchester Metropolitan University, Manchester, United Kingdom.
The angiotensin-converting enzyme (ACE) DD genotype is linked to reduced aerobic capacity and impaired glucose metabolism in skeletal muscle, potentially leading to a pre-diabetic state during exercise. This is associated with lower muscle capillarisation and altered mitochondrial function.
Area of Science:
- Exercise Physiology
- Human Genetics
- Metabolic Disorders
Background:
- The angiotensin-converting enzyme (ACE) gene I-allele influences aerobic fitness and type II diabetes risk.
- The ACE genotype (DD vs. ID/II) may affect exercise-induced glucose metabolism and muscle capillarisation.
Purpose of the Study:
- To investigate the association between ACE genotype and exercise metabolism in untrained men.
- To determine if ACE genotype influences glucose metabolism and capillarisation in skeletal muscle during exercise.
Main Methods:
- Fifty-three untrained Caucasian men performed one-legged cycling to exhaustion or a marathon.
- Muscle glycogen, serum glucose/lipids, and metabolites were analyzed using UPLC-MS.
- Capillary-to-fibre ratio was assessed in vastus lateralis muscle.
Main Results:
- The ACE-DD genotype exhibited lower maximal respiratory exchange ratio (RER) and a significant increase in serum glucose post-exercise compared to ACE-ID/II genotypes.
- Mitochondrial metabolites in vastus lateralis muscle were altered by exercise in the ACE-DD genotype.
- ACE-DD individuals showed a 24% lower capillary-to-fibre ratio and an abnormal serum glucose increase after marathon running.
Conclusions:
- ACE genotype modulates glucose uptake and oxidation in working skeletal muscle.
- The ACE-DD genotype may predispose individuals to a pre-diabetic state during exhaustive exercise due to reduced muscle capillarisation and impaired mitochondrial metabolism.
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