Dissociation of local and global skeletal muscle oxygen transport metrics in type 2 diabetes
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 bloo...
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| Veröffentlicht in: | Journal of diabetes and its complications Jg. 31; H. 8; S. 1311 - 1317 |
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01.08.2017
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| Abstract | 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.
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.
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.
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.
•Muscle oxygenation is impaired in type 2 diabetes despite normal limb blood flow and local microvascular recruitment.•Correlations between local oxygen transport metrics and VO2peak are abolished in type 2 diabetes.•The correlation between blood flow and VO2peak is abolished in type 2 diabetes.•The correlation between blood flow and local microvascular recruitment is abolished in type 2 diabetes. |
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| AbstractList | 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.AIMSExercise 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.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.METHODSIn 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.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.RESULTSWe 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.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.CONCLUSIONSThese 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 VO2peakare 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. 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. 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 (VO ), and near-infrared spectroscopy-derived measures of exercise-induced changes in skeletal muscle oxygenation and blood volume/hematocrit. 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 VO are all mutually correlated. None of these correlations were preserved in type 2 diabetes. 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. 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. 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. 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. 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. 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. •Muscle oxygenation is impaired in type 2 diabetes despite normal limb blood flow and local microvascular recruitment.•Correlations between local oxygen transport metrics and VO2peak are abolished in type 2 diabetes.•The correlation between blood flow and VO2peak is abolished in type 2 diabetes.•The correlation between blood flow and local microvascular recruitment is abolished in type 2 diabetes. |
| Author | Huebschmann, Amy G. Reusch, Jane E.B. Mason McClatchey, P. Schauer, Irene E. Regensteiner, Judith G. Bauer, Timothy A. |
| AuthorAffiliation | a Division of Endocrinology, University of Colorado Anschutz Medical Campus, Aurora, CO, United States e Center for Women’s Health Research, University of Colorado Anschutz Medical Campus, Aurora, CO, United States c Department of Medicine, Denver Veterans Affairs Medical Center, Denver, CO, United States b Department of Bioengineering, University of Colorado Anschutz Medical Campus, Aurora, CO, United States d Division of General Internal Medicine, University of Colorado Anschutz Medical Campus, Aurora, CO, United States |
| AuthorAffiliation_xml | – name: b Department of Bioengineering, University of Colorado Anschutz Medical Campus, Aurora, CO, United States – name: e Center for Women’s Health Research, University of Colorado Anschutz Medical Campus, Aurora, CO, United States – name: d Division of General Internal Medicine, University of Colorado Anschutz Medical Campus, Aurora, CO, United States – name: c Department of Medicine, Denver Veterans Affairs Medical Center, Denver, CO, United States – name: a Division of Endocrinology, University of Colorado Anschutz Medical Campus, Aurora, CO, United States |
| Author_xml | – sequence: 1 givenname: P. surname: Mason McClatchey fullname: Mason McClatchey, P. organization: Division of Endocrinology, University of Colorado Anschutz Medical Campus, Aurora, CO, United States – sequence: 2 givenname: Timothy A. surname: Bauer fullname: Bauer, Timothy A. organization: Division of General Internal Medicine, University of Colorado Anschutz Medical Campus, Aurora, CO, United States – sequence: 3 givenname: Judith G. surname: Regensteiner fullname: Regensteiner, Judith G. organization: Division of General Internal Medicine, University of Colorado Anschutz Medical Campus, Aurora, CO, United States – sequence: 4 givenname: Irene E. surname: Schauer fullname: Schauer, Irene E. organization: Division of Endocrinology, University of Colorado Anschutz Medical Campus, Aurora, CO, United States – sequence: 5 givenname: Amy G. surname: Huebschmann fullname: Huebschmann, Amy G. organization: Division of General Internal Medicine, University of Colorado Anschutz Medical Campus, Aurora, CO, United States – sequence: 6 givenname: Jane E.B. surname: Reusch fullname: Reusch, Jane E.B. email: jane.reusch@ucdenver.edu organization: Division of Endocrinology, University of Colorado Anschutz Medical Campus, Aurora, CO, United States |
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| Keywords | Type 2 diabetes Perfusion heterogeneity Oxygen delivery Exercise capacity Oxygen transport Near-infrared spectroscopy exercise capacity oxygen transport oxygen delivery near-infrared spectroscopy type 2 diabetes perfusion heterogeneity |
| Language | English |
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| Snippet | Exercise capacity is impaired in type 2 diabetes, and this impairment predicts excess morbidity and mortality. This defect appears to involve excess skeletal... Abstract Aims Exercise capacity is impaired in type 2 diabetes, and this impairment predicts excess morbidity and mortality. This defect appears to involve... Aims Exercise capacity is impaired in type 2 diabetes, and this impairment predicts excess morbidity and mortality. This defect appears to involve excess... |
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| StartPage | 1311 |
| SubjectTerms | Adult Aerobics Aging Bicycling Blood Blood Vessels - physiopathology Capillary Resistance Diabetes Diabetes Mellitus, Type 2 - complications Diabetic Angiopathies - blood Diabetic Angiopathies - metabolism Diabetic Angiopathies - physiopathology Diabetic retinopathy Endocrinology & Metabolism Exercise Exercise capacity Exercise Tolerance Female Hemoglobins - analysis Humans Leg Male Metabolic syndrome Microcirculation Microvessels - physiopathology Middle Aged Muscle, Skeletal - blood supply Muscle, Skeletal - metabolism Musculoskeletal system Near-infrared spectroscopy Oxygen Oxygen - blood Oxygen - metabolism Oxygen Consumption Oxygen delivery Oxygen transport Oxyhemoglobins - metabolism Perfusion heterogeneity Physical fitness Regional Blood Flow Spectroscopy, Near-Infrared Spectrum analysis Type 2 diabetes Vascular Resistance |
| Title | Dissociation of local and global skeletal muscle oxygen transport metrics in type 2 diabetes |
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