A model for the genesis of arterial pressure Mayer waves from heart rate and sympathetic activity

Both theoretic models and cross-spectral analyses suggest that an oscillati ng sympathetic nervous outflow generates the low-frequency arterial pressur e fluctuations termed Mayer waves. Fluctuations in heart rate also have bee n suggested to relate closely to Mayer waves, but empiric models have not a ssessed the joint causative influences of heart rate and sympathetic activi ty. Therefore, we constructed a model based simply upon the hemodynamic equ ation derived from Ohm's Law. With this model, we determined time relations and relative contributions of heart rate and sympathetic activity to the g enesis of arterial pressure Mayer waves. We assessed data from eight health y young volunteers in the basal state and in a high sympathetic state known to produce concurrent increases in sympathetic nervous outflow and Mayer w ave amplitude. We fit the Mayer waves (0.05-0.20 Hz) in mean arterial press ure by the weighted sum of leading oscillations in heart rate and sympathet ic nerve activity. This model of our data showed heart rate oscillations le ading by 2-3.75 s were responsible for almost half of the variance in arter ial pressure (basal R-2 = 0.435 +/- 0.140, high sympathetic R-2 = 0.438 +/- 0.180). Surprisingly, sympathetic activity (lead 0-5 s) contributed only m odestly to the explained variance in Mayer waves during either sympathetic state (basal: Delta R-2 = 0.046 +/- 0.026; heightened: DeltaR(2) = 0.085 +/ - 0.036). Thus, it appears that heart rate oscillations contribute to Mayer waves in a simple linear fashion, whereas sympathetic fluctuations contrib ute little to Mayer waves in this way. Although these results do not exclud e an important vascular sympathetic role, they do suggest that additional f actors, such as sympathetic transduction into vascular resistance, modulate its influence. (C) 2001 Elsevier Science B.V. All rights reserved.