parasympathetic activity (PNS index: 4.2 ± 6.5), while T2DM’s autonomic response remained largely unchanged (PNS and SNS index were -4.7 ±2.3 and 9.7 ± 5.4, respectively). Combining hyperinsulinemia and hypoxia intensified the sympathetic surge, especially in HC (SNS index: 7.4 ±6.4). T2DM showed further parasympathetic suppression (-3.6 ± 5.2), while HC experienced increased parasympathetic activity (6.6 ±7.2). These autonomic changes, assessed via heart rate variability metrics, may impact the HVR. T2DM disrupted autonomic balance, leaning towards sympathetic dominance, and attenuated the hypoxic response. Conversely, HC maintained or enhanced their autonomic equilibrium and hypoxic sensitivity during hyperinsulinemia. These findings highlight T2DM’s significant influence on autonomic regulation and physiological responses to hyperinsulinemia and hypoxia. Hemodynamic parameters The effects of hyperinsulinemia on hemodynamic variables are given in Figure 5.4 on page 111. Sympathetic effects of hyperinsulinemia and hypoxia are reflected by an increase in diastolic blood pressure, systolic blood pressure, and cardiac index. The most distinguishing characteristic of T2DM is the elevated cardiac index (T2DM 2.71 ± 0.19 L.min-1.m-2 vs. HC 2.42 ± 0.13 L.min-1.m-2), which was most pronounced during the combination of hyperinsulinemia and hypoxia (T2DM 3.44 ± 0.18 L.min-1.m-2 vs. HC 2.67 ± 0.10 L.min-1.m-2; interaction diagnosis (T2DM or HC) and intervention (baseline or hyperinsulinemic hypoxia) p = 0.002). 110
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