Independent effect of type 2 diabetes beyond characteristic comorbidities and medications on immediate but not continued knee extensor exercise hyperemia.

We tested the hypothesis that type 2 diabetes (T2D), when present in the characteristic constellation of comorbidities (obesity, hypertension, dyslipidemia) and medications, slows the dynamic adjustment of exercising muscle perfusion and blunts the steady state relative to that of controls matched for age, body mass index, fitness, comorbidities, and non-T2D medications. Thirteen persons with T2D and 11 who served as controls performed rhythmic single-leg isometric quadriceps exercise (rest-to-6 kg and 6-to-12 kg transitions, 5 min at each intensity). Measurements included leg blood flow (LBF, femoral artery ultrasound), mean arterial pressure (MAP, finger photoplethysmography), and leg vascular conductance (LVK, calculated). Dynamics were quantified using mean response time (MRT). Measures of amplitude were also used to compare response adjustment: the change from baseline to 1) the peak initial response (greatest 1-s average in the first 10 s; ΔLBFPIR, ΔLVKPIR) and 2) the on-transient (average from curve fit at 15, 45, and 75 s; ΔLBFON, ΔLVKON). ΔLBFPIR was significantly blunted in T2D vs. control individuals (P = 0.037); this was due to a tendency for reduced ΔLVKPIR (P = 0.063). In contrast, the overall response speed was not different between groups (MRT P = 0.856, ΔLBFON P = 0.150) nor was the change from baseline to steady state (P = 0.204). ΔLBFPIR, ΔLBFON, and LBF MRT did not differ between rest-to-6 kg and 6-to-12 kg workload transitions (all P > 0.05). Despite a transient amplitude impairment at the onset of exercise, there is no robust or consistent effect of T2D on top of the comorbidities and medications typical of this population on the overall dynamic adjustment of LBF, or the steady-state levels achieved during low- or moderate-intensity exercise.