Low-intensity exercise induces acute shifts in liver and skeletal muscle substrate metabolism but not chronic adaptations in tissue oxidative capacity
| Autor: | Scott Fuller, Tai-Yu Huang, J. Jason Collier, Jacob Simon, John M. Brown, Susan J. Burke, Callie M. Waskom, Heidi M. Batdorf, Matthew C. Scott, Robert C. Noland, Nabil M. Essajee |
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| Rok vydání: | 2019 |
| Předmět: |
Male
0301 basic medicine Physiology Acclimatization Musculoskeletal Physiological Phenomena 030209 endocrinology & metabolism Mitochondrion Mice 03 medical and health sciences 0302 clinical medicine Physical Conditioning Animal Physiology (medical) medicine Animals Muscle Skeletal Chemistry Substrate (chemistry) Skeletal muscle Metabolism Peroxisome Lipid Metabolism Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha Mitochondria Mitochondria Muscle Cell biology Mice Inbred C57BL Oxidative Stress 030104 developmental biology medicine.anatomical_structure Liver Low intensity exercise Exercise Test Oxidative capacity Oxidation-Reduction Glycogen Transcription Factors Research Article |
| Zdroj: | J Appl Physiol (1985) |
| ISSN: | 1522-1601 8750-7587 |
| Popis: | Adaptations in hepatic and skeletal muscle substrate metabolism following acute and chronic (6 wk; 5 days/wk; 1 h/day) low-intensity treadmill exercise were tested in healthy male C57BL/6J mice. Low-intensity exercise maximizes lipid utilization; therefore, we hypothesized pathways involved in lipid metabolism would be most robustly affected. Acute exercise nearly depleted liver glycogen immediately postexercise (0 h), whereas hepatic triglyceride (TAG) stores increased in the early stages after exercise (0–3 h). Also, hepatic peroxisome proliferator-activated receptor-γ coactivator-1α ( PGC-1α) gene expression and fat oxidation (mitochondrial and peroxisomal) increased immediately postexercise (0 h), whereas carbohydrate and amino acid oxidation in liver peaked 24–48 h later. Alternatively, skeletal muscle exhibited a less robust response to acute exercise as stored substrates (glycogen and TAG) remained unchanged, induction of PGC-1α gene expression was delayed (up at 3 h), and mitochondrial substrate oxidation pathways (carbohydrate, amino acid, and lipid) were largely unaltered. Peroxisomal lipid oxidation exhibited the most dynamic changes in skeletal muscle substrate metabolism after acute exercise; however, this response was also delayed (peaked 3–24 h postexercise), and expression of peroxisomal genes remained unaffected. Interestingly, 6 wk of training at a similar intensity limited weight gain, increased muscle glycogen, and reduced TAG accrual in liver and muscle; however, substrate oxidation pathways remained unaltered in both tissues. Collectively, these results suggest changes in substrate metabolism induced by an acute low-intensity exercise bout in healthy mice are more rapid and robust in liver than in skeletal muscle; however, training at a similar intensity for 6 wk is insufficient to induce remodeling of substrate metabolism pathways in either tissue. NEW & NOTEWORTHY Effects of low-intensity exercise on substrate metabolism pathways were tested in liver and skeletal muscle of healthy mice. This is the first study to describe exercise-induced adaptations in peroxisomal lipid metabolism and also reports comprehensive adaptations in mitochondrial substrate metabolism pathways (carbohydrate, lipid, and amino acid). Acute low-intensity exercise induced shifts in mitochondrial and peroxisomal metabolism in both tissues, but training at this intensity did not induce adaptive remodeling of metabolic pathways in healthy mice. |
| Databáze: | OpenAIRE |
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