Publication

Beneficial Molecular Adaptations In -Mutation Carriers By Combined HIT/HIRT Intervention: Results From A Pilot Study

Journal Paper/Review - Jun 10, 2020

Units
PubMed
Doi

Citation
Bizjak D, Janni W, Huober J, Leinert E, Ebner F, Kirsten J, Otto S, Schumann U, Schulz S, Steinacker J. Beneficial Molecular Adaptations In -Mutation Carriers By Combined HIT/HIRT Intervention: Results From A Pilot Study. Cancers (Basel) 2020; 12
Type
Journal Paper/Review (English)
Journal
Cancers (Basel) 2020; 12
Publication Date
Jun 10, 2020
Issn Print
2072-6694
Brief description/objective

Based on growing evidence that breast cancer (BRCA) also plays a pivotal role in the regulation of skeletal muscle metabolism and the response to anti-oxidative stress, we examined the influence of regular exercise in human mutation carriers on their BRCA1 gene/protein expression and inflammatory/oxidative response. Sixteen -mutation carriers were assigned to an intervention (IG) or control group (CG). IG received a combination of high-intensity interval endurance (HIT) and strength training (HIRT) for six weeks, whereas CG received a low-intensity activity program. Before (T0) and at the end of the intervention (T1), muscle biopsy, physiological performance, blood withdrawal and anthropometry were obtained. Parameters included: Muscle BRCA1 gene/protein expression, inflammatory/oxidative stress, anti-oxidative capacity, peak oxygen capacity (VOpeak) and 1-repetition maximum (1-RM) at six different training machines. VOpeak and 1-RM of IG were increased at T1 compared to T0, whereas CG performance, physiological and molecular parameters remained unchanged. IG showed increased BRCA1 protein concentration as well as anti-oxidative capacity, whereas gene expression was unaltered. IG inflammatory and oxidative damage did not differ between time points. Combined HIT/HIRT increases aerobic and strength performance of -mutation carriers with up regulated BRCA1 protein expression and improved anti-oxidative status without showing an increased inflammatory response.