Postprandial hyperglycemia-induced endothelial dysfunction is linked to reduced blood flow during exercise

Background: Postprandial hyperglycemia is defined as blood glucose exceeding 140 mg/dL 1–2 hours after a meal or glucose loading. It attenuates brachial endothelial function (assessed by flow-mediated dilation, FMD) and reduces resting brachial blood flow. Endothelial function is crucial for blood flow regulation both at rest and during exercise. Hyperglycemia-induced endothelial dysfunction may impair vasodilation and decrease vascular conductance (VC) during exercise, potentially reducing exercise-induced BF elevation, although this hypothesis has not been tested. Purpose: This study aimed to investigate the effects of postprandial hyperglycemia on blood flow regulation during exercise. We hypothesized that 1) postprandial hyperglycemia suppresses the increase in brachial BF during exercise, and 2) the hyperglycemia-induced reduction in brachial VC during exercise is associated with the attenuation of brachial FMD after glucose loading. Methods: Thirteen participants (25±5 years; BMI: 21.5 ± 1.4 kg/m 2 ; mean ± SD) with normal fasting glucose levels, who exhibited hyperglycemia after glucose loading, completed two trials: glucose loading trial (glucose trial) and fructose loading trial (sham trial) in random order. Plasma glucose was measured before, 30, 40, 47, and 60 minutes after the loading. FMD was conducted before and 60 minutes after the loading. At 42 minutes post-loading participants performed a dynamic handgrip exercise (30% maximal voluntary contraction) for 3 minutes. During exercise, brachial arterial diameter and mean velocity were measured using a Doppler ultrasound, and BF was calculated as mean velocity times cross-sectional area. VC was calculated by dividing BF by mean arterial pressure. Changes in BF (ΔBF) and VC (ΔVC) were defined as the differences from rest, and the change in FMD (ΔFMD) was defined as the difference from the FMD pre-loading. Results: Blood glucose levels were higher in the glucose trial compared to the sham trial. FMD decreased after loading in the glucose trial (7.5 ± 2.3% to 5.5 ± 1.3%, P = 0.01), but not in the sham trial (7.1 ± 2.3% to 8.1 ± 2.9%, P = 0.23). ΔVC was lower in the glucose trial compared to the sham trial (P < 0.01). Repeated measures correlation revealed a positive relationship between ΔFMD and ΔVC (P = 0.02, r = 0.58). ΔBF during exercise was suppressed in the glucose trial compared to the sham trial (P = 0.01). Conclusion: The current results suggest that the reduction in VC during exercise could be driven by postprandial-induced endothelial dysfunction, which may have contributed to the suppression of the increase in BF during exercise. The findings of this study imply that postprandial hyperglycemia adversely affects blood flow regulation during exercise. This study was supported by JSPS KAKENHI #JP21K11290, #21K11170 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.