Exaggerated Exercise Pressor Reflex And Mechanical Allodynia Present At Similar Times In Type 2 Diabetes

Previous studies suggest that the presence of pathophysiology of type 2 diabetes (T2D) results in both exaggerated exercise pressor reflex (EPR) and mechanical allodynia (MA). Interestingly, the EPR is evoked by the same type of afferent fibers (i.e., group III and IV) that are involved in MA, leading us to question whether changes to the EPR and MA occur at similar phases during disease progression. PURPOSE: To determine the effect of T2D on the development of MA at disease onset and whether MA occures at similar times as when the EPR is exaggerated. METHODS: Changes in mean arterial pressure (MAP) during 30 s of static contraction, intermittent contraction, and tendon stretch were measured at 7-15 wks after diabetes onset in male University of California Davis-T2D rats (Body weight: 511 ± 13 g, n = 8) and age matched healthy Sprague Dawley (CON) rats (Body weight 689 ± 14 g, n = 7). MA was assessed using the “up-down” method of Von Frey filament application 10 wks and 14 wks after diabetes onset, and is reported as 50% paw withdrawal threshold. The lowest force that elicited a quick paw withdrawal was averaged between the responses of both hind paws. RESULTS: A previous study found that changes in MAP during peak pressor responses during the early onset of the disease were significantly higher in T2D rats compared to CON rats in both static (ΔMAP: 29 ± 4 vs 10 ± 1 mmHg, p = 0.001) and intermittent (ΔMAP: 27 ± 5 vs 9 ± 1 mmHg, p = 0.01) contractions as well as tendon stretch (ΔMAP: 33 ± 7 vs 12 ± 5 mmHg, p = 0.04). Paw withdrawal threshold was significantly lower in T2D rats compared to CON 14 wks (50% paw withdrawal threshold: 35 ± 3 vs 47 ± 4 g, p = 0.02), but not 10 wks (50% paw withdrawal threshold: 45 ± 4 vs 44 ± 5 g, p = 0.93), after onset of the disease. CONCLUSION: Our findings suggesting that T2D may be affecting both MA and the EPR as similar times after the onset the disease. Further studies are needed to identify the contribution of mechanically sensitive group III and IV afferents at this same phase of the disease for both MA and the EPR. Supported by NIH R01 HL144723