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Comparative Study
. 2005 Apr 1;564(Pt 1):321-7.
doi: 10.1113/jphysiol.2004.079665. Epub 2005 Feb 10.

Neurovascular responses to mental stress

Collaborators, Affiliations
Comparative Study

Neurovascular responses to mental stress

Jason R Carter et al. J Physiol. .

Abstract

The effects of mental stress (MS) on muscle sympathetic nerve activity (MSNA) and limb blood flows have been studied independently in the arm and leg, but they have not been studied collectively. Furthermore, the cardiovascular implications of postmental stress responses have not been thoroughly addressed. The purpose of the current investigation was to comprehensively examine concurrent neural and vascular responses during and after mental stress in both limbs. In Study 1, MSNA, blood flow (plethysmography), mean arterial pressure (MAP) and heart rate (HR) were measured in both the arm and leg in 12 healthy subjects during and after MS (5 min of mental arithmetic). MS significantly increased MAP (Delta15 +/- 3 mmHg; P < 0.01) and HR (Delta19 +/- 3 beats min(-1); P < 0.01), but did not change MSNA in the arm (14 +/- 3 to 16 +/- 3 bursts min(-1); n = 6) or leg (14 +/- 2 to 15 +/- 2 bursts min(-1); n = 8). MS decreased forearm vascular resistance (FVR) by -27 +/- 7% (P < 0.01; n = 8), while calf vascular resistance (CVR) did not change (-6 +/- 5%; n = 11). FVR returned to baseline during recovery, whereas MSNA significantly increased in the arm (21 +/- 3 bursts min(-1); P < 0.01) and leg (19 +/- 3 bursts min(-1); P < 0.03). In Study 2, forearm and calf blood flows were measured in an additional 10 subjects using Doppler ultrasound. MS decreased FVR (-27 +/- 10%; P < 0.02), but did not change CVR (5 +/- 14%) as in Study 1. These findings demonstrate differential vascular control of the arm and leg during MS that is not associated with muscle sympathetic outflow. Additionally, the robust increase in MSNA during recovery may have acute and chronic cardiovascular implications.

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Figures

Figure 1
Figure 1. Heart rate (HR) and mean arterial pressure (MAP) responses to 5 min of mental stress (Study 1; n= 12)
B, baseline; R, recovery. Mental stress elicited significant increases in HR and MAP. *Significantly different from baseline (P < 0.05)
Figure 2
Figure 2. Muscle sympathetic nerve activity (MSNA) responses to 5 min of mental stress in the arm (n= 6) and leg (n= 8; Study 1)
B, baseline; R, recovery. Mental stress failed to elicit significant increases in MSNA. However, MSNA was significantly elevated after mental stress in both limbs. *Significantly different from baseline (P < 0.05)
Figure 3
Figure 3. Muscle sympathetic nerve activity (MSNA; burst frequency, left; total activity, right) responses after mental stress
Total activity has been normalized with the baseline value being 100%. MSNA was significantly elevated after mental stress. Arm MSNA, n= 6; leg MSNA, n= 8. *Significantly different from baseline (P < 0.05)
Figure 4
Figure 4. Changes (Δ) in forearm (left panel) and calf (right panel) blood flow (BF), vascular resistance (VR) and vascular conductance (VC) during mental stress
Changes as measured by venous occlusion plethysmography (PLETH; Study 1; arm, n= 8; leg, n= 11) and Doppler ultrasound (DOPPLER; Study 2; arm, n= 10; leg, n= 10). Mental stress vasodilated the forearm, but not the calf. Results were not different between techniques (plethysmography versus Doppler ultrasound). *Significantly different from baseline (P < 0.05)
Figure 5
Figure 5. Simultaneous neurograms of muscle sympathetic nerve activity (MSNA) recorded from the radial (arm) and peroneal (leg) nerves in a subject before, during and after mental stress
A temporal patterning of MSNA burst frequency was observed between the arm and leg

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