Handgrip contraction induces a linear increase in arterial pressure by peripheral vasoconstriction, increased heart rate and a decrease in stroke volume
The hypothesis that isometric handgrip induces a progressive increase in arterial pressure and a linear increase in setpoint for arterial pressure control was tested. Methods:
The continuous time course of changes in heart rate (HR), stroke volume (SV) and mean arterial pressure (MAP) was recorded during a 2-min handgrip contraction of 40% of maximal voluntary contraction force. Twice during the development of the handgrip-induced, gradual pressure increase of ∼25 mmHg, additional, transient changes in arterial pressure were mechanically induced. The subsequent baroreflex responses to these additional pressure changes were studied. The additional steep increase in arterial pressure (∼10 mmHg) was induced both after 70 and 100 s of handgrip contraction, by inflating bilateral thigh cuffs to suprasystolic pressure. Cuff pressure was released after 10 s, thus introducing a steep decrease in MAP. Results:
During the development of the handgrip-induced pressure increase, HR increased, SV decreased, cardiac output (CO) increased slightly and total peripheral conductance (TPC = CO/MAP) increased (i.e. peripheral vasoconstriction). The circulatory responses to the additional, sudden increase and subsequent decrease in arterial pressure after 70 and 100 s perfectly adjusted arterial pressure back to the linear increase in MAP, indicating an effective baroreflex response. Conclusion:
The increase in MAP which characterizes handgrip-induced pressure response can be regarded as a result of a gradual increase in the set point of the arterial baroreflexes, with no change in the time course and magnitude of the baroreflex responses to additional, induced changes in MAP.