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Interaction between the arterial baroreflex and muscle metaboreflex in type 1 diabetes patients
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Individuals with type 1 diabetes (T1D) have an increased risk of cardiovascular morbidity and mortality, and their lifespan is ~12 years shorter than the rest of the population. Previous studies have shown that T1D patients have elevated oxidative stress, which may be a potential underlying mechanism contributing to impaired vascular function and autonomic regulation at rest and during exercise in this group. Autonomic adjustments during exercise result from a complex interplay between the arterial baroreflex, muscle metaboreflex, muscle mechanoreflex and the central command. To date, the interaction between the arterial baroreflex and the muscle metaboreflex in T1D remains unknown. In this study, we tested the hypothesis that cardiac baroreflex sensitivity (cBRS) during muscle metaboreflex activation would be reduced in patients with T1D. In addition, we measured serum levels of oxidized low-density lipoprotein (oxLDL), a marker of oxidative stress, and flow-mediated dilation (FMD) to assess vascular function in these individuals. In thirteen T1D (age = 28 ± 10 yrs, BMI = 25 ± 5 kg/m
2
) and 17 healthy adults (age = 25 ± 10 yrs, p=0.43; BMI = 24 ± 3 kg/m
2
, p = 0.18), the cardiac autonomic function (cBRS) was investigated during 10 minutes of rest and 2 minutes of isolated muscle metaboreflex activation via post exercise ischemia following isometric handgrip (HG) at 30% and 40% of the maximum voluntary contraction (MVC). Lead II ECG (AD Instruments, Sydney, Australia) and finger plethysmography (Finometer; Finapress Medical Systems, Amsterdam, The Netherlands) were used to measure heart rate and blood pressure, respectively, at rest, during HG and PEI. For FMD, a rapidly inflating cuff (Hokanson, Bellevue, WA) was placed on forearm and inflated to 220 mmHg for 5 minutes and the brachial artery blood velocity and diameter were measured (Logiq e, GE Medical Systems) for 3 min at baseline and 3 min after cuff deflation. Fasting blood samples were used to measure oxLDL (human oxLDL ELISA 10-1143-01, Mercodia, Sweden). Overall cBRS during 10-minute baseline was significantly different between T1D and healthy adults (T1D = 16 ± 7 ms/mmHg, healthy = 23 ± 7 ms/mmHg, p = 0.01). During PEI following 30% HG, the cBRS remained unchanged from rest in T1D patients (PEI = 17 ± 8 ms/mmHg, p = 0.79). Similarly, during PEI following 40% HG, cBRS in T1D patients was preserved from baseline (PEI = 16 ± 6 ms/mmHg, p = 0.91). In addition, T1D patients had attenuated FMD% (T1D = 6 ± 3%, healthy = 10 ± 2%, p = 0.002) and elevated oxLDL levels (T1D = 58.9 x 103 ± 12.8 x 103 U/L, healthy = 47.3 x 103 ± 11.2 x 103 U/L, p = 0.04). These preliminary results suggest high oxidative stress in T1D may, in part, contribute to reduced vascular function and resting spontaneous cardiac baroreflex sensitivity, however, the interaction between the muscle metaboreflex and arterial baroreflex remains preserved in T1D.
Funding sources: This research was funded by the 2025 College of Education Smart Research Grant at The University of Texas at Austin.
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.
American Physiological Society
Title: Interaction between the arterial baroreflex and muscle metaboreflex in type 1 diabetes patients
Description:
Individuals with type 1 diabetes (T1D) have an increased risk of cardiovascular morbidity and mortality, and their lifespan is ~12 years shorter than the rest of the population.
Previous studies have shown that T1D patients have elevated oxidative stress, which may be a potential underlying mechanism contributing to impaired vascular function and autonomic regulation at rest and during exercise in this group.
Autonomic adjustments during exercise result from a complex interplay between the arterial baroreflex, muscle metaboreflex, muscle mechanoreflex and the central command.
To date, the interaction between the arterial baroreflex and the muscle metaboreflex in T1D remains unknown.
In this study, we tested the hypothesis that cardiac baroreflex sensitivity (cBRS) during muscle metaboreflex activation would be reduced in patients with T1D.
In addition, we measured serum levels of oxidized low-density lipoprotein (oxLDL), a marker of oxidative stress, and flow-mediated dilation (FMD) to assess vascular function in these individuals.
In thirteen T1D (age = 28 ± 10 yrs, BMI = 25 ± 5 kg/m
2
) and 17 healthy adults (age = 25 ± 10 yrs, p=0.
43; BMI = 24 ± 3 kg/m
2
, p = 0.
18), the cardiac autonomic function (cBRS) was investigated during 10 minutes of rest and 2 minutes of isolated muscle metaboreflex activation via post exercise ischemia following isometric handgrip (HG) at 30% and 40% of the maximum voluntary contraction (MVC).
Lead II ECG (AD Instruments, Sydney, Australia) and finger plethysmography (Finometer; Finapress Medical Systems, Amsterdam, The Netherlands) were used to measure heart rate and blood pressure, respectively, at rest, during HG and PEI.
For FMD, a rapidly inflating cuff (Hokanson, Bellevue, WA) was placed on forearm and inflated to 220 mmHg for 5 minutes and the brachial artery blood velocity and diameter were measured (Logiq e, GE Medical Systems) for 3 min at baseline and 3 min after cuff deflation.
Fasting blood samples were used to measure oxLDL (human oxLDL ELISA 10-1143-01, Mercodia, Sweden).
Overall cBRS during 10-minute baseline was significantly different between T1D and healthy adults (T1D = 16 ± 7 ms/mmHg, healthy = 23 ± 7 ms/mmHg, p = 0.
01).
During PEI following 30% HG, the cBRS remained unchanged from rest in T1D patients (PEI = 17 ± 8 ms/mmHg, p = 0.
79).
Similarly, during PEI following 40% HG, cBRS in T1D patients was preserved from baseline (PEI = 16 ± 6 ms/mmHg, p = 0.
91).
In addition, T1D patients had attenuated FMD% (T1D = 6 ± 3%, healthy = 10 ± 2%, p = 0.
002) and elevated oxLDL levels (T1D = 58.
9 x 103 ± 12.
8 x 103 U/L, healthy = 47.
3 x 103 ± 11.
2 x 103 U/L, p = 0.
04).
These preliminary results suggest high oxidative stress in T1D may, in part, contribute to reduced vascular function and resting spontaneous cardiac baroreflex sensitivity, however, the interaction between the muscle metaboreflex and arterial baroreflex remains preserved in T1D.
Funding sources: This research was funded by the 2025 College of Education Smart Research Grant at The University of Texas at Austin.
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.
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