Total peripheral resistance fine-tunes mean arterial pressure to a set level induced by isometric handgrip.

We quantified, using a new method, the contribution of heart rate (HR), stroke volume (SV) and total peripheral resistance (TPR) to the increase in mean arterial pressure (MAP), expressed as % of baseline during a 3-min static handgrip (HG) performed at 30% of maximum voluntary contraction by 11 subjects. Arterial pressure was measured noninvasively with Finapres Nova, SV with Doppler imaging. The increase in MAP was greater at the end of HG than at the end of the first minute of HG, the maximum individual increases in MAP ranged from 0% to 33%; the HR contribution was mostly positive, the SV contribution was mostly negative. The magnitude of the HR contribution was similar at the beginning and end of the HG both in subjects who experienced high and low MAP increases; a similar observation applies to the SV contribution. Only the TPR contribution was significantly correlated with the individual MAP increase. Assuming that the individual level of MAP is set during HG, the contribution of TPR by taking positive or negative values plays a main role as an adjustment factor that brings MAP to set level; compensating for insufficient or excessive contributions from HR and SV. Our results question the use of changes in MAP or TPR as an indicator of sympathetic reactivity; the increase in MAP is determined by the individual change in set level induced by HG, whereas the magnitude of the change in sympathetic activity is such as needed to achieve the desired increase in MAP.