Megan E Osler1, Tomas Fritz2, Kenneth Caidahl3, Anna Krook4, Juleen R Zierath5, Harriet Wallberg-Henriksson6. 1. Department of Molecular Medicine and Surgery, Integrative Physiology, Karolinska Institutet, Stockholm, Sweden. 2. Center for Family and Community Medicine, Karolinska Institutet, Huddinge, Sweden. 3. Department of Molecular Medicine and Surgery, Clinical Physiology, Karolinska Institutet, Stockholm, Sweden. 4. Department of Physiology and Pharmacology, Integrative Physiology, Karolinska Institutet, Stockholm, Sweden. 5. Department of Molecular Medicine and Surgery, Integrative Physiology, Karolinska Institutet, Stockholm, Sweden Department of Physiology and Pharmacology, Integrative Physiology, Karolinska Institutet, Stockholm, Sweden juleen.zierath@ki.se. 6. Department of Molecular Medicine and Surgery, Integrative Physiology, Karolinska Institutet, Stockholm, Sweden Department of Physiology and Pharmacology, Integrative Physiology, Karolinska Institutet, Stockholm, Sweden.
Abstract
OBJECTIVE: Daily physical activity remains an effective strategy to prevent obesity and type 2 diabetes. However, the metabolic response to exercise training is variable, and the precise clinical and molecular determinants that mark the metabolic improvements remain unknown. We tested the hypothesis that clinical improvements in glucose control after low-intensity exercise in individuals with impaired glucose tolerance (IGT) are coupled to alterations in skeletal muscle gene expression. RESEARCH DESIGN AND METHODS: We investigated 14 overweight individuals with IGT before and after a 4-monthlow-intensity unsupervised walking exercise intervention. Clinical and anthropometric measurements and glucose tolerance were determined before and after the intervention. Skeletal muscle biopsy specimens were obtained for mRNA expression analysis. RESULTS:Waist circumference and work capacity during cycle ergometry were improved in individuals who achieved normal glucose tolerance (NGT) after exercise training (IGT-NGT; n = 9) but in not individuals who remained IGT (IGT-IGT; n = 5). Pretraining glycemic control was better in IGT-NGT compared with IGT-IGT. mRNAexpression of mitochondrial markers and transcription factors was increased in IGT-NGT after exercise intervention and normalized to levels measured in a separate cohort of nonexercised individuals with NGT. Conversely, these markers were unaltered after exercise intervention in IGT-IGT. CONCLUSIONS: Normalization of metabolic control can be achieved after low-intensity exercise in individuals with IGT. This can be tracked with increased mRNA expression of mitochondrial and metabolic genes in skeletal muscle. However, for individuals presenting with a greater derangement in glycemia, the potential for clinical and metabolic improvements after this low-intensity unsupervised exercise protocol appears to be limited.
RCT Entities:
OBJECTIVE: Daily physical activity remains an effective strategy to prevent obesity and type 2 diabetes. However, the metabolic response to exercise training is variable, and the precise clinical and molecular determinants that mark the metabolic improvements remain unknown. We tested the hypothesis that clinical improvements in glucose control after low-intensity exercise in individuals with impaired glucose tolerance (IGT) are coupled to alterations in skeletal muscle gene expression. RESEARCH DESIGN AND METHODS: We investigated 14 overweight individuals with IGT before and after a 4-month low-intensity unsupervised walking exercise intervention. Clinical and anthropometric measurements and glucose tolerance were determined before and after the intervention. Skeletal muscle biopsy specimens were obtained for mRNA expression analysis. RESULTS: Waist circumference and work capacity during cycle ergometry were improved in individuals who achieved normal glucose tolerance (NGT) after exercise training (IGT-NGT; n = 9) but in not individuals who remained IGT (IGT-IGT; n = 5). Pretraining glycemic control was better in IGT-NGT compared with IGT-IGT. mRNA expression of mitochondrial markers and transcription factors was increased in IGT-NGT after exercise intervention and normalized to levels measured in a separate cohort of nonexercised individuals with NGT. Conversely, these markers were unaltered after exercise intervention in IGT-IGT. CONCLUSIONS: Normalization of metabolic control can be achieved after low-intensity exercise in individuals with IGT. This can be tracked with increased mRNA expression of mitochondrial and metabolic genes in skeletal muscle. However, for individuals presenting with a greater derangement in glycemia, the potential for clinical and metabolic improvements after this low-intensity unsupervised exercise protocol appears to be limited.
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