Pressor Response During Exercise and Muscle Metaboreflex Activation in Patients with Type 1 Diabetes Mellitus

Individuals with Type 1 diabetes (T1D) are 2–4 times more likely to develop cardiovascular diseases (CVD), which account for approximately 50% of diabetes-related deaths. Regular physical activity is strongly recommended for T1D management, as it helps reduce the risk of CVD. However, some human studies report that T1D patients exhibit a heightened blood pressure response to exercise, which increases the risk of acute, life-threatening cardiovascular events. Research in an animal model of T1D suggests that an exaggerated muscle metaboreflex may contribute to this heightened pressor response during an acute bout of exercise. Whether this phenomenon occurs in humans with T1D remains unclear. Herein, we tested the hypothesis that T1D patients exhibit an exaggerated pressor response during muscle metaboreflex activation compared to age-matched healthy adults. We studied 14 T1D patients and 14 healthy controls [mean ± SEM; Age (T1D: 28 ± 3 yr; Healthy: 27 ± 3 yr; p = 0.93); BMI (T1D: 25.8 ± 1.3 kg/m 2 ; Healthy: 23.7 ± 0.9 kg/m 2 ; p = 0.18); HbA1c (T1D: 7.4 ± 0.6%; Healthy: 5.2 ± 0.1%; p = 0.002); MVC (T1D: 60.1 ± 4.1 kg; Healthy: 61.1 ± 4.7 kg; p = 0.87)]. T1D duration was 13 ± 3 yr. Heart rate (HR; ECG) and beat-to-beat blood pressure (BP; finger plethysmography) were measured during 2 minutes of static handgrip exercise at 30% and 40% MVC, followed by muscle metaboreflex activation via post-exercise ischemia (PEI; suprasystolic cuff inflation) on the exercising arm for 2 minutes and 15 seconds. Stroke volume (SV) was computed using the modelflow method. The cold pressor test (CPT) was used to assess pressor response to a generalized sympatho-excitatory stimulus. Resting mean arterial pressure (MAP) (T1D = 84 ± 2 mmHg; Healthy = 83 ± 2 mmHg; p = 0.53) and SV (T1D = 101.6 ± 7.7 mL; Healthy = 89.4 ± 3.7 mL; p = 0.15) were not significantly different between groups. However, resting HR (T1D = 65 ± 3 bpm; Healthy = 57 ± 2 bpm; p = 0.02) and cardiac output (T1D = 6.5 ± 0.5 L; Healthy = 5.1 ± 0.2 L; p = 0.01) were higher in T1D. The groups had similar pressor responses during the last 30 seconds of exercise [30% MVC (T1D = 25 ± 3 mmHg; Healthy = 22 ± 2 mmHg; p = 0.49); 40% MVC (T1D = 35 ± 4 mmHg; Healthy = 38 ± 3 mmHg; p = 0.47)]. Also, there were no significant differences in the pressor responses when muscle metaboreflex was isolated during PEI [30% MVC (T1D = 20 ± 4 mmHg; healthy = 18 ± 2 mmHg; p = 0.55); 40% MVC (T1D = 29 ± 3 mmHg; healthy = 32 ± 3 mmHg; p = 0.37)] or during CPT (T1D = 27 ± 2 mmHg; Healthy = 26 ± 3 mmHg; p = 0.90). These findings suggest that T1D patients do not exhibit exaggerated pressor responses during isometric exercise or muscle metaboreflex activation compared to matched healthy controls. Department of Kinesiology and Health Education, UT Austin This abstract was presented at the American Physiology Summit 2025 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.