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BioMed Central, Cardiovascular Diabetology, 1(14), 2015

DOI: 10.1186/s12933-015-0235-y

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The inflammation, vascular repair and injury responses to exercise in fit males with and without Type 1 diabetes: an observational study

This paper is made freely available by the publisher.
This paper is made freely available by the publisher.

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Data provided by SHERPA/RoMEO

Abstract

Abstract Background Type 1 diabetes is associated with raised inflammation, impaired endothelial progenitor cell mobilisation and increased markers of vascular injury. Both acute and chronic exercise is known to influence these markers in non-diabetic controls, but limited data exists in Type 1 diabetes. We assessed inflammation, vascular repair and injury at rest and after exercise in physically-fit males with and without Type 1 diabetes. Methods Ten well-controlled type 1 diabetes (27 ± 2 years; BMI 24 ± 0.7 kg.m 2 ; HbA 1c 53.3 ± 2.4 mmol/mol) and nine non-diabetic control males (27 ± 1 years; BMI 23 ± 0.8 kg.m 2 ) matched for age, BMI and fitness completed 45-min of running. Venous blood samples were collected 60-min before and 60-min after exercise, and again on the following morning. Blood samples were processed for TNF-α using ELISA, and circulating endothelial progenitor cells (cEPCs; CD45 dim CD34 + VEGFR2 + ) and endothelial cells (cECs; CD45 dim CD133 - CD34 + CD144 + ) counts using flow-cytometry. Results TNF-α concentrations were 4-fold higher at all-time points in Type 1 diabetes, when compared with control ( P   0.05). Within the Type 1 diabetes group, the delta change in cEPCS from rest to the following morning was related to HbA 1c ( r  = -0.65, P  = 0.021) and TNF-α ( r  = -0.766, P  = 0.005). Conclusions Resting cEPCs and cECs in Type 1 diabetes patients with excellent HbA 1c and high physical-fitness are comparable to healthy controls, despite eliciting 4-fold greater TNF-α. Furthermore, Type 1 diabetes patients appear to have a blunted post-exercise cEPCs response (vascular repair), whilst a biomarker of vascular injury (cECs) remained comparable to healthy controls.