P Mason McClatchey1, Timothy A Bauer2, Judith G Regensteiner3, Irene E Schauer4, Amy G Huebschmann3, Jane E B Reusch5. 1. Division of Endocrinology, University of Colorado Anschutz Medical Campus, Aurora, CO, United States; Department of Bioengineering, University of Colorado Anschutz Medical Campus, Aurora, CO, United States; Department of Medicine, Denver Veterans Affairs Medical Center, Denver, CO, United States. 2. Division of General Internal Medicine, University of Colorado Anschutz Medical Campus, Aurora, CO, United States. 3. Division of General Internal Medicine, University of Colorado Anschutz Medical Campus, Aurora, CO, United States; Center for Women's Health Research, University of Colorado Anschutz Medical Campus, Aurora, CO, United States. 4. Division of Endocrinology, University of Colorado Anschutz Medical Campus, Aurora, CO, United States; Department of Medicine, Denver Veterans Affairs Medical Center, Denver, CO, United States. 5. Division of Endocrinology, University of Colorado Anschutz Medical Campus, Aurora, CO, United States; Department of Medicine, Denver Veterans Affairs Medical Center, Denver, CO, United States; Center for Women's Health Research, University of Colorado Anschutz Medical Campus, Aurora, CO, United States. Electronic address: jane.reusch@ucdenver.edu.
Abstract
AIMS: Exercise capacity is impaired in type 2 diabetes, and this impairment predicts excess morbidity and mortality. This defect appears to involve excess skeletal muscle deoxygenation, but the underlying mechanisms remain unclear. We hypothesized that reduced blood flow, reduced local recruitment of blood volume/hematocrit, or both contribute to excess skeletal muscle deoxygenation in type 2 diabetes. METHODS: In patients with (n=23) and without (n=18) type 2 diabetes, we recorded maximal reactive hyperemic leg blood flow, peak oxygen utilization during cycling ergometer exercise (VO2peak), and near-infrared spectroscopy-derived measures of exercise-induced changes in skeletal muscle oxygenation and blood volume/hematocrit. RESULTS: We observed a significant increase (p<0.05) in skeletal muscle deoxygenation in type 2 diabetes despite similar blood flow and recruitment of local blood volume/hematocrit. Within the control group skeletal muscle deoxygenation, local recruitment of microvascular blood volume/hematocrit, blood flow, and VO2peak are all mutually correlated. None of these correlations were preserved in type 2 diabetes. CONCLUSIONS: These results suggest that in type 2 diabetes 1) skeletal muscle oxygenation is impaired, 2) this impairment may occur independently of bulk blood flow or local recruitment of blood volume/hematocrit, and 3) local and global metrics of oxygen transport are dissociated.
AIMS: Exercise capacity is impaired in type 2 diabetes, and this impairment predicts excess morbidity and mortality. This defect appears to involve excess skeletal muscle deoxygenation, but the underlying mechanisms remain unclear. We hypothesized that reduced blood flow, reduced local recruitment of blood volume/hematocrit, or both contribute to excess skeletal muscle deoxygenation in type 2 diabetes. METHODS: In patients with (n=23) and without (n=18) type 2 diabetes, we recorded maximal reactive hyperemic leg blood flow, peak oxygen utilization during cycling ergometer exercise (VO2peak), and near-infrared spectroscopy-derived measures of exercise-induced changes in skeletal muscle oxygenation and blood volume/hematocrit. RESULTS: We observed a significant increase (p<0.05) in skeletal muscle deoxygenation in type 2 diabetes despite similar blood flow and recruitment of local blood volume/hematocrit. Within the control group skeletal muscle deoxygenation, local recruitment of microvascular blood volume/hematocrit, blood flow, and VO2peak are all mutually correlated. None of these correlations were preserved in type 2 diabetes. CONCLUSIONS: These results suggest that in type 2 diabetes 1) skeletal muscle oxygenation is impaired, 2) this impairment may occur independently of bulk blood flow or local recruitment of blood volume/hematocrit, and 3) local and global metrics of oxygen transport are dissociated.
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