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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Vydáno v:Journal of diabetes and its complications Ročník 31; číslo 8; s. 1311 - 1317
Hlavní autoři: Mason McClatchey, P., Bauer, Timothy A., Regensteiner, Judith G., Schauer, Irene E., Huebschmann, Amy G., Reusch, Jane E.B.
Médium: Journal Article
Jazyk:angličtina
Vydáno: United States Elsevier Inc 01.08.2017
Elsevier Limited
Témata:
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
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
ISSN:1056-8727, 1873-460X, 1873-460X
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Shrnutí: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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ISSN:1056-8727
1873-460X
1873-460X
DOI:10.1016/j.jdiacomp.2017.05.004