Vitamin C supplementation does not alter high-intensity endurance training-induced mitochondrial biogenesis in rat epitrochlearis muscle
Autor: | Koichi Yada, Hideki Matoba |
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Rok vydání: | 2013 |
Předmět: |
Male
medicine.medical_specialty Antioxidant Physiology medicine.medical_treatment education Ascorbic Acid Citrate (si)-Synthase Mitochondrion Antioxidants Endurance training Internal medicine medicine Animals Citrate synthase Lactic Acid Rats Wistar Muscle Skeletal Swimming Dose-Response Relationship Drug biology Vitamin C Skeletal muscle Mitochondrial Turnover Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha Mitochondria Muscle Rats Dose–response relationship Endocrinology medicine.anatomical_structure Mitochondrial biogenesis Dietary Supplements Physical Endurance biology.protein Transcription Factors |
Zdroj: | The Journal of Physiological Sciences. 64:113-118 |
ISSN: | 1880-6562 1880-6546 |
DOI: | 10.1007/s12576-013-0300-9 |
Popis: | The purpose of this study was to investigate whether vitamin C supplementation prevents high-intensity intermittent endurance training-induced mitochondrial biogenesis in the skeletal muscle. Male Wistar-strain rats were assigned to one of five groups: a control group, training group, small dose vitamin C supplemented training group, middle dose vitamin C supplemented training group, and large dose vitamin C supplemented training group. The rats of the trained groups were subjected to intense intermittent swimming training. The vitamin C supplemented groups were administrated vitamin C for the pretraining and training periods. High-intensity intermittent swimming training without vitamin C supplementation significantly increased peroxisome proliferator-activated receptor-γ coactivator-1α protein content and citrate synthase activity in the epitrochlearis muscle. The vitamin C supplementation did not alter the training-induced increase of these regardless of the dose of vitamin C supplementation. The results demonstrate that vitamin C supplementation does not prevent high-intensity intermittent training-induced mitochondrial biogenesis in the skeletal muscle. |
Databáze: | OpenAIRE |
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