Impairments in foot skin microcirculation are thought to contribute to sensory and motor dysfunction and to the development of plantar ulcerations in individuals with type 2 diabetes (T2D) and lower extremity peripheral artery disease (PAD). Although foot microvascular abnormalities have been examined previously, most work has focused on the dorsal surface rather than the plantar, load-bearing regions where ulceration risk is greatest. Microvascular function in the plantar hallux, a site highly susceptible to ulceration, remains poorly characterized. Objective: To characterize plantar hallux cutaneous vascular responses to local heating in individuals with T2D, PAD, and non-diabetic controls. Hypothesis: Both T2D and PAD would show reduced cutaneous hyperemia to local heating, with the greatest impairment in PAD. Methods: Participants included non-diabetic controls (n=20, 16 females, 63±8 yr, HbA1c 5.7±0.4%, ankle–brachial index ABI 1.15±0.06), T2D (n=11, 6 females, 65±7 yr, HbA1c 7.2±1.0%, ABI 1.14±0.16), and PAD (n=9, 2 females, 69±9 yr, HbA1c 7.0±1.3%, ABI 0.64±0.15). A local heating apparatus was placed on the skin of the plantar hallux, and laser-Doppler flowmetry probes were inserted into the probe holders of the heaters to continuously measure red blood cell flux. After a 10-minute baseline at 33°C, the temperature was increased to 42°C for 50 minutes. At minute 40, ankle cuffs were inflated to 220 mmHg for 5 minutes and then released to elicit reactive hyperemia. Local heating evokes a biphasic vasodilatory response: an initial neurally mediated peak followed by an endothelial-mediated plateau. The initial peak was defined as the highest 30-second segment within the first 5 minutes; the plateau as the highest stable 5-minute segment before cuff inflation. Mean arterial pressure (MAP) was recorded every 5 minutes. Cutaneous vascular conductance (CVC = flux/MAP) was expressed as % maximal CVC and averaged between toes. Group differences were assessed using ANOVA with Tukey post hoc tests. Results: Baseline %CVC was significantly higher in T2D (23.3±11.1%, p=0.04) and PAD (29.0±15.9%, p=0.02) compared to controls (13.3±7.6%). PAD demonstrated a markedly blunted neurally mediated response (ΔCVC% baseline-to-initial peak: 22.8±9.8% vs. 53.6±22.7% in controls, p=0.001), whereas responses in T2D were preserved (53.5±19.8%, p=0.9 vs. controls). Sustained plateau responses did not differ among groups (ΔCVC% baseline-to-plateau: controls 47.9±15.9%; T2D 46.9±12.9%; PAD 46.7±16.7%; p >0.05). Conclusions: Individuals with T2D and PAD exhibit altered resting vasomotor regulation at the plantar hallux, and PAD is characterized by impaired neurally mediated vasodilation during local heating. These abnormalities may contribute to plantar tissue vulnerability and elevated ulceration risk in PAD. Funding: Supported by The John Martinson Honors College’s Research Breakthrough Award from Purdue University. This abstract was presented at the American Physiology Summit 2026 and is only available in HTML format. There is no downloadable file or PDF version. The Physiology editorial board was not involved in the peer review process.
Gallo et al. (Fri,) studied this question.