Felix Morales-Palomo 1 , Miguel Ramirez-Jimenez 1 , Juan F Ortega 1 , Alfonso Moreno-Cabañas 1 , Ricardo Mora-Rodriguez 1 Show Affiliations »
Abstract
BACKGROUND: Statins reduce atherogenic dyslipidemia and cardiovascular disease (CVD) risk in metabolic syndrome (MetS) individuals. Exercise training could also contribute to reduce CVD by improving cardiorespiratory fitness and fat oxidation. However, statin use could interfere with training adaptations. METHODS: A total of 106 MetS individuals were divided into statin users (statin group, n = 46) and statin-naïve (control group, n = 60). Groups were matched by age, weight, and MetS components. Subjects completed 16 weeks of high intensity interval training (HIIT). Before and after HIIT, muscle biopsies were collected to assess mitochondrial content (citrate synthase [CS] activity) and the activity of the rate limiting β-oxidation enzyme (3-hydroxyacyl-CoA-dehydrogenase [HAD]). Fasting plasma glucose, insulin, TG, HDL-c, and LDL-c concentrations were measured. Exercise maximal fat oxidation (FOMAX) and oxygen uptake (VO2PEAK) were determined. RESULTS: Training improved MetS similarly in both groups (MetS z-score -0.26 ± 0.38 vs. -0.22 ± 0.31; P < 0.001 for time and P = 0.60 for time x group). Before training, the statin group had reduced muscle HAD activity and whole body FOMAX compared to the control group. However, 16 weeks of HIIT increased HAD and FOMAX in both groups (P < 0.03, time-effect). The statin group did not prevent the increases in CS with HIIT observed in the control group (38% vs 64%, respectively; P < 0.001, time-effect). Conversely, with training VO2PEAK improved less in the statin than in the control group (12% vs. 19%, respectively; P = 0.013, time × group effect). CONCLUSION: Chronic statin use in MetS does not interfere with exercise training improvements in MetS components, FOMAX, or mitochondrial muscle enzymes (ie, CS and HAD). However, the statin group attenuated the improvements in VO2PEAK with training. CLINICAL TRIAL INFORMATION: ClinicalTrials.gov identifier no. NCT03019796, January 13, 2017. © Endocrine Society 2019. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com.
BACKGROUND: Statins reduce atherogenic dyslipidemia and cardiovascular disease (CVD ) risk in metabolic syndrome (MetS) individuals. Exercise training could also contribute to reduce CVD by improving cardiorespiratory fitness and fat oxidation. However, statin use could interfere with training adaptations. METHODS: A total of 106 MetS individuals were divided into statin users (statin group, n = 46) and statin-naïve (control group, n = 60). Groups were matched by age, weight, and MetS components. Subjects completed 16 weeks of high intensity interval training (HIIT). Before and after HIIT, muscle biopsies were collected to assess mitochondrial content (citrate synthase [CS ] activity) and the activity of the rate limiting β-oxidation enzyme (3-hydroxyacyl-CoA -dehydrogenase [HAD ]). Fasting plasma glucose , insulin , TG , HDL-c, and LDL-c concentrations were measured. Exercise maximal fat oxidation (FOMAX ) and oxygen uptake (VO2PEAK) were determined. RESULTS: Training improved MetS similarly in both groups (MetS z-score -0.26 ± 0.38 vs. -0.22 ± 0.31; P < 0.001 for time and P = 0.60 for time x group). Before training, the statin group had reduced muscle HAD activity and whole body FOMAX compared to the control group. However, 16 weeks of HIIT increased HAD and FOMAX in both groups (P < 0.03, time-effect). The statin group did not prevent the increases in CS with HIIT observed in the control group (38% vs 64%, respectively; P < 0.001, time-effect). Conversely, with training VO2PEAK improved less in the statin than in the control group (12% vs. 19%, respectively; P = 0.013, time × group effect). CONCLUSION: Chronic statin use in MetS does not interfere with exercise training improvements in MetS components, FOMAX , or mitochondrial muscle enzymes (ie, CS and HAD ). However, the statin group attenuated the improvements in VO2PEAK with training. CLINICAL TRIAL INFORMATION: ClinicalTrials.gov identifier no. NCT03019796, January 13, 2017. © Endocrine Society 2019. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com.
Entities: Chemical
Disease
Gene
Keywords:
maximal fat oxidation; 3-hydroxyacyl-CoA-dehydrogenase; atherogenic dyslipidemia; cardiorespiratory fitness; high-intensity interval training; syndrome X
Year: 2020
PMID： 31875915 DOI： 10.1210/clinem/dgz304
Source DB: PubMed Journal: J Clin Endocrinol Metab ISSN： 0021-972X Impact factor: 5.958