Exaggerated exercise pressor reflex in male UC Davis type 2 diabetic rats is due to the pathophysiology of the disease and not aging

Introduction: Studies in humans and animals have found that type 2 diabetes mellitus (T2DM) exaggerates the blood pressure (BP) response to exercise, which increases the risk of adverse cardiovascular events such as heart attack and stroke. T2DM is a chronic disease that, without appropriate management, progresses in severity as individuals grow older. Thus, it is possible that aging may also exaggerate the BP response to exercise. Therefore, the purpose of the current study was to determine the effect of the pathophysiology of T2DM on the exercise pressor reflex independent of aging. Methods: We compared changes in peak pressor (mean arterial pressure; delta MAP), BP index (delta BPi), heart rate (delta HR), and HR index (delta HRi) responses to static contraction, intermittent contraction, and tendon stretch in UCD-T2DM rats to those of healthy, age-matched Sprague Dawley rats at three different stages of the disease. Results: We found that the delta MAP, delta BPi, delta HR, and delta HRi responses to static contraction were significantly higher in T2DM rats (delta MAP: 29 +/- 4 mmHg; delta BPi: 588 +/- 51 mmHg center dot s; delta HR: 22 +/- 5 bpm; delta HRi: 478 +/- 45 bpm center dot s) compared to controls (delta MAP: 10 +/- 1 mmHg, p < 0.0001; delta BPi: 121 +/- 19 mmHg center dot s, p < 0.0001; delta HR: 5 +/- 2 bpm, p = 0.01; delta HRi: 92 +/- 19 bpm center dot s, p < 0.0001) shortly after diabetes onset. Likewise, the delta MAP, delta BPi, and delta HRi to tendon stretch were significantly higher in T2DM rats (delta MAP: 33 +/- 7 mmHg; delta BPi: 697 +/- 70 mmHg center dot s; delta HRi: 496 +/- 51 bpm center dot s) compared to controls (delta BPi: 12 +/- 5 mmHg, p = 0.002; delta BPi: 186 +/- 30 mmHg center dot s, p < 0.0001; delta HRi: 144 +/- 33 bpm center dot s, p < 0.0001) shortly after diabetes onset. The delta BPi and delta HRi, but not delta MAP, to intermittent contraction was significantly higher in T2DM rats (delta BPi: 543 +/- 42 mmHg center dot s; delta HRi: 453 +/- 53 bpm center dot s) compared to controls (delta BPi: 140 +/- 16 mmHg center dot s, p < 0.0001; delta HRi: 108 +/- 22 bpm center dot s, p = 0.0002) shortly after diabetes onset. Discussion: Our findings suggest that the exaggerated exercise pressor reflex and mechanoreflex seen in T2DM are due to the pathophysiology of the disease and not aging.