High-intensity interval exercise (HIIE) is associated with increased fatty acid oxidation, and the majority of fatty acids in skeletal muscle is stored in a form of intramuscular triglycerides (IMTG). The common ACE I/D gene polymorphism has been associated with exercise performance, with the I allele more prevalent in endurance-type athletes, who often have more IMTG and more fatty acid oxidation during exercise. We therefore hypothesise that the ACE I/D variant is associated with key genes controlling IMTG oxidation.
We analysed sixteen moderately-trained Caucasian males (age=30.2±7.9) from the Gene Smart cohort (Yan et al 2017), ten homozygous for the D allele (ACE DD), and six homozygous for the I allele (ACE II). A graded exercise test (GXT) was used to assess peak power (Wpeak) and lactate threshold (LT), both key endurance exercise phenotypes. A single session of HIIE (8 2-min intervals with 1 min rest between intervals) was completed by each participant. A muscle biopsy was taken before, immediately after, and 3 hours post HIIE from the vastus lateralis muscle and analysed for the expression of PGC1α, PPARα and PPARδ.
The expression of PGC1α was not different between the DD and II individuals at baseline (0.91±0.25 vs 0.71±0.09, p=0.08). There was no difference in PPARα (1.40±0.55 vs 1.90± 0.48, p=0.09) or PPARδ (0.82±0.35 vs 0.60±0.11, p=0.17). Three hours post HIIE, the expression of PGC1α, PPARα, PPARδ all increased (by 4.63±2.30, 5.61±3.40, 1.95±1.18 fold, respectively, p<0.05). However, the increase did not depend on ACE I/D gene polymorphism (4.11±2.57 vs 5.49±1.57, 5.67±4.22 vs 5.49±1.66, 1.92±1.42 vs 1.99±0.74 between DD and II individuals).
These preliminary results indicate a single session of HIIE significantly increased the expression of PGC1α, PPARα and PPARδ. However, this increase was not associated with the ACE I/D genotype. We are currently increasing the sample size to confirm these preliminary findings.