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1 Departments of Medicine (Cardiology) and Cellular & Molecular Physiology, Pennsylvania State University College of Medicine, Hershey, PA 17033, USA
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Abstract |
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15 ± 3 mmHg; P < 0.01) and HR (19 ± 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.
(Received 19 November 2004;
accepted after revision 7 February 2005;
first published online 10 February 2005)
Corresponding author C. A. Ray: Division of Cardiology, H047, Penn State College of Medicine, 500 University Drive, Hershey, PA 17033-2390, USA. Email: caray{at}psu.edu
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Introduction |
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Most studies demonstrate a vasodilator response to mental stress in the forearm, but not the calf (Blair et al. 1959; Barcroft et al. 1960; Rusch et al. 1981; Halliwill et al. 1997). Early studies suggested that forearm vasodilatation during mental stress involved both neural and humoral mechanisms (Blair et al. 1959; Barcroft et al. 1960). A humoral mechanism is still widely accepted, but neurally mediated vasodilatation during mental stress has become controversial (Lindqvist et al. 1996; Halliwill et al. 1997). Using axillary blockade, Lindqvist et al. (1996) demonstrated that stress-induced forearm vasodilatation occurs in the absence of neurogenic control of the vascular bed. In contrast, Halliwill et al. (1997) reported significant reductions of muscle sympathetic nerve activity (MSNA) and peripheral resistance in the arm, and observed forearm vasodilatation after stellate blockade, suggesting that mental stress elicits a passive neurogenic vasodilatation. This finding by Halliwill et al. is in conflict with a study by Anderson et al. (1987) that demonstrated no change in arm MSNA during mental stress. The neurogenic role of forearm vasodilatation during mental stress remains unresolved. Furthermore, the effect of post-mental stress on neurovascular control, and its possible role in cardiovascular events, has not been adequately addressed in previous studies.
The goal of this study was to comprehensively examine concurrent neural and vascular responses to mental stress in both the arm and leg. We hypothesize that: (1) mental stress will increase MSNA in the leg, but not the arm; (2) mental stress will vasodilate the arm, but not the leg; and (3) marked increases of MSNA will occur to both limbs following mental stress.
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Methods |
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Twenty-two volunteers (17 men and 5 women; age 24 ± 1 year, height 177 ± 2 cm, weight 71 ± 3 kg) participated in this study. All subjects were normotensive, non-obese, non-smokers, not taking any medication, and had no history of autonomic dysfunction or cardiovascular diseases. Subjects arrived at the laboratory after abstaining from caffeine and exercise for at least 12 h. The experimental protocol was approved by the Institutional Review Board of Pennsylvania State University and all subjects gave written informed consent prior to the study.
Experimental design
In Study 1 (9 men and 3 women), we measured heart rate, arterial pressure, forearm (n = 8) and calf (n = 11) blood flows (venous occlusion plethysmography), and MSNA in both the arm (n = 6) and leg (n = 8) during 5 min of mental arithmetic in the prone position. High quality dual recordings of MSNA from the arm and leg were obtained in 6 of 12 subjects. During mental arithmetic, subjects continuously subtracted the number six or seven from a two or three digit number. The subtraction number, six or seven, was randomized. Subjects answered verbally and were encouraged by an investigator to subtract as fast as possible. An investigator provided a new number to subtract from every 5–10 s. Subjects were asked to rate perceived stress using a standard five-point scale of 0 (not stressful), 1 (somewhat stressful), 2 (stressful), 3 (very stressful), and 4 (very, very stressful) (Carter et al. 2002). Trials began with a 2 min baseline and ended with a 3 min recovery.
In Study 2, an additional 10 subjects (8 men and 2 women) were examined using the same protocol as Study 1, but with arm and leg blood flows measured using Doppler ultrasound. Neural responses were not examined in Study 2. In Study 1, the arm was positioned forward and slightly elevated to measure forearm blood flow using plethysmography. Although most had no difficulty with this position, a few subjects reported mild shoulder discomfort. Study 2 was performed to verify the blood flow results of Study 1 using a different technique which permitted the arm to remain at the subject's side.
Measurements
Multifibre recordings of MSNA were measured directly by inserting a tungsten microelectrode into the peroneal nerve in the popliteal region behind the left knee and the radial nerve in the lateral region of the humerus of the left arm. A reference electrode was inserted subcutaneously 2–3 cm from the recording electrode. Both electrodes were connected to a differential preamplifier and then to an amplifier where the nerve signal was band-pass filtered (700–2000 Hz) and integrated at a time constant of 0.1 s to obtain a mean voltage display of nerve activity. Satisfactory recordings of MSNA were defined by spontaneous, pulse-synchronous bursts that did not change during arousal or stroking of the skin.
In Study 1, forearm and calf blood flows were measured using venous occlusion plethysmography (Hokanson, Bellevue, WA, USA). Mercury-in-silastic strain gauges were placed around the maximal circumferences of the forearm and calf. Wrist and ankle cuffs were inflated to 220 mmHg to arrest circulation to the hand and foot. Blood flow was determined every 15 s during these trials. Vascular resistance was calculated as mean arterial pressure divided by limb blood flow, and vascular conductance was calculated as the reciprocal of vascular resistance.
In Study 2, Duplex ultrasound (HDI 5000, ATL Ultrasound, Bothell, WA, USA) was used to examine blood velocity and vessel diameter in the arm and leg. Briefly, two linear array L12–5 MHz Doppler probes with a 6.0 MHz pulsed Doppler frequency were used. The focal zone was at the depth of the brachial and peroneal artery. Cardiac cycle Doppler signals were analysed to determine the mean blood flow velocity. Each velocity measurement was normalized with a time constant of 1 s. For each data point, 15 s of data were averaged. Using vessel diameter to estimate area (
r2), mean blood flow was calculated by multiplying mean blood velocity by the area of the vessel.
Heart rate was continuously recorded using a 3-lead electrocardiogram. Arterial pressure was recorded using a Finapres (Ohmeda, Englewood, CO, USA) positioned on the middle digit of the subject's left hand.
Data analysis
Sympathetic bursts were identified from inspection of mean voltage neurograms displayed by a computer program (Peaks; ADInstruments). MSNA was expressed as burst frequency and total activity (the sum of bursts amplitude expressed in arbitrary units (a.u.)). Total activity was ignored in one subject's leg recording because of a recognized site shift. All data were analysed using a repeated-measures ANOVA. Planned comparisons were used to compare baselines. Perceived stress levels were compared using a Wilcoxon rank test. Vascular responses for the 5 min mental stress trial are presented as mean values because no time effect was observed. Significance was considered at a P value of < 0.05. Results are expressed as mean ± S.E.M.
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Results |
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Mental stress significantly increased heart rate (66 ± 2 versus 84 ± 4 beats min–1; P < 0.01; n = 12) and mean arterial pressure (101 ± 6 versus 115 ± 8 mmHg; P < 0.01; n = 12; Fig. 1). Heart rate returned to baseline, whereas mean arterial pressure remained elevated (110 ± 7 mmHg; P < 0.01) during recovery. MSNA did not change in the arm (14 ± 3 versus 16 ± 3 bursts min–1 and 229 ± 44 versus 268 ± 39 a.u.; n = 6) or leg (14 ± 2 versus 15 ± 2 bursts min–1 and 100 ± 18 versus 131 ± 36 a.u.; n = 8) during mental stress (Fig. 2), but did increase during recovery in both the arm (21 ± 3 bursts min–1 and 339 ± 26 a.u.; P < 0.01) and leg (19 ± 3 bursts min–1 and 153 ± 30 a.u.; P < 0.03; Fig. 3). Mental stress increased both forearm (67 ± 20%; P < 0.01; n = 8) and calf (26 ± 12%; P < 0.05; n = 11) blood flow. Although vascular resistance significantly decreased in the forearm (–27 ± 7%; P < 0.01), it did not change in the calf (–6 ± 5%; Fig. 4). Vascular conductance demonstrated similar physiological responses as vascular resistance by increasing in the forearm (47 ± 16%; P < 0.01) with no change in the calf (11 ± 8%; Fig. 4). All vascular responses remained at or returned to baseline during recovery. Perceived stress level during mental arithmetic was 2.7 ± 0.3.
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Mental stress increased heart rate (70 ± 3 versus 93 ± 5 beats min–1; P < 0.01; n = 10) and mean arterial pressure (93 ± 2 versus 118 ± 4 mmHg; P < 0.01; n = 10). During recovery, mean arterial pressure remained elevated (102 ± 3 mmHg; P < 0.05), while heart rate returned to baseline. Mental stress increased forearm (116 ± 39%; P < 0.02; n = 10) and calf (38 ± 17%; P < 0.05; n = 10) blood flow. Mental stress decreased forearm vascular resistance (–27 ± 10%; P < 0.02), with a corresponding increase in forearm vascular conductance (72 ± 34%; P < 0.05). Calf vascular resistance (5 ± 14%) and conductance (8 ± 13%) did not change during mental stress. All vascular responses remained at or returned to baseline during recovery. Figure 4 illustrates that mental stress yields similar responses with regard to vascular resistance using either plethysmography (Study 1) or Doppler ultrasound (Study 2). Perceived stress level during mental arithmetic was 2.5 ± 0.2.
Neural and vascular correlation between limbs
In six subjects, simultaneous arm and leg recordings of MSNA revealed no temporal difference in MSNA burst pattern before, during and after mental stress between limbs (Fig. 5). Total MSNA was significantly correlated between the arm and leg (r = 0.92; P < 0.01). MSNA was not correlated to vascular blood flow, resistance or conductance in either limb.
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Discussion |
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Mental arithmetic increases heart rate and arterial pressure, a response that is mediated, in part, by the release of noradrenaline (norepinephrine) (Hjemdahl et al. 1984; Esler et al. 1989; Tidgren & Hjemdahl, 1989). Noradrenaline release is dependent on the sampling site, with the greatest stress-induced increase of noradrenaline spillover at the heart (Esler et al. 1989). Although mental stress consistently increases noradrenaline levels, peripheral sympathetic neural responses remain equivocal. Classic studies by Blair et al. (1959) and Barcroft et al. (1960) demonstrated vasodilatation of the forearm during mental stress, and suggested that both humoral and neural mechanisms were responsible for the forearm vasodilatation. More recently, both nitric oxide and circulating adrenaline have been demonstrated to contribute to forearm vasodilatation during mental stress (Dietz et al. 1994; Lindqvist et al. 1996; Cardillo et al. 1997).
It is clear from previous investigations that endothelial- and smooth muscle-mediated vasodilatation of the forearm occurs during mental stress, but is there a neurally mediated response? An active neurogenic mechanism does not appear to contribute to forearm vasodilatation during mental stress (Lindqvist et al. 1996; Halliwill et al. 1997). However, passive vasodilatation due to sympathetic withdrawal in the forearm remains controversial. Anderson et al. (1987) measured MSNA responses to mental stress in both limbs and reported an increase in leg, but not the arm. Because blood flows were not measured simultaneously, the authors could only speculate that their observations contribute to previously reported differences in vascular responses in the forearm and calf. In contrast, Halliwill et al. (1997) reported a decrease in MSNA and peripheral resistance during mental stress, supporting the concept that passive sympathetic withdrawal contributes to stress-induced forearm vasodilatation. However, Halliwill et al. (1997) did not record neurovascular responses to mental stress in the lower extremities.
To our knowledge, this is the first study that has comprehensively examined neural and vascular responses to mental stress concurrently in the arm and leg. In contrast to the findings of Halliwill et al. (1997), our results demonstrate a significant reduction in forearm vascular resistance during mental stress that is not associated with a change in arm MSNA. Vasodilatation of the forearm during mental stress was not caused by a passive neurogenic mechanism (i.e. sympathetic withdrawal). These findings suggest that mental stress-induced forearm vasodilatation is mediated by non-neural mechanisms. Our design does not allow us to speculate on the non-neural mechanisms involved, but previous studies suggest that increased circulating adrenaline (Lindqvist et al. 1996) and flow-induced nitric oxide release (Dietz et al. 1994; Cardillo et al. 1997) may be of prime importance.
It is possible that the differences in our findings and those of Halliwill et al. (1997) are related to total magnitude of the dilatation. The dilatation demonstrated in the current study was modest compared with Halliwill et al. (1997) and others (Blair et al. 1959; Barcroft et al. 1960). Perhaps this ‘modest’ dilatation was because subjects did not experience the forearm sympathetic withdrawal observed by Halliwill et al. (1997). Furthermore, Halliwill et al. (1997) observed more dilatation when there was sympathetic withdrawal, but we did not observe a similar correlation. It is important to note that vascular responses to mental stress are highly variable, depending on technique and individual responsiveness (Roddie, 1977). Early studies by Blair et al. (1959) and Barcroft et al. (1960) used extreme stressors and reported very high blood flow values. Halliwill et al. (1997) used a Stroop-word colour conflict test, whereas we used mental arithmetic. It is possible that the different techniques contributed to differences between our findings and Halliwill et al. (1997). However, our subjects reported perceived stress levels between stressful and very stressful for both studies. It is possible that the highly variable individual responsiveness to mental stress may have contributed to differences between our findings and those of Halliwill et al. (1997).
The highly variable mental stress response was also observed in our leg MSNA data. In the current study, mental stress did not increase leg MSNA. This finding is consistent with previous studies demonstrating no change in leg MSNA burst frequency during mental stress (Hjemdahl et al. 1989; Wallin et al. 1992; Kamiya et al. 2000). In contrast, other studies report that mental stress significantly increases MSNA burst frequency in the leg (Anderson et al. 1987; Callister et al. 1992; Carter et al. 2002). Because stimulation of leg MSNA during mental stress has been reported to be primarily dependent on perceived stress (Callister et al. 1992), we asked our subjects to rate their perceived stress level during mental arithmetic. Perceived stress levels were rated between stressful and very stressful, but our data did not indicate any correlation between stress level and neurovascular responses in either limb. It is possible that mental stress only activates sympathetic outflow in certain individuals, but no studies have attempted to categorize subjects into responders and non-responders with regards to mental stress.
Anderson et al. (1987) suggested mental stress causes a dissociation of muscle sympathetic outflow to the arm and leg, and that this dissociation may be involved in the differential control of arm and leg blood flow during mental stress. Our results do not support this concept. Simultaneous recordings of MSNA reveal a similar pattern of sympathetic activity that did not increase during mental stress. Similarly, dual recording of arm and leg MSNA recordings have been shown to be comparable during other sympathetic stressors, including baroreceptor unloading (Rea & Wallin, 1989), exercise (Ray et al. 1992), post-exercise muscle ischaemia (Ray et al. 1992), and vestibular activation (Monahan & Ray, 2002). In contrast to the analogous neural responses, divergent vascular responses were observed in the forearm and calf. These findings indicate that vascular control of the arm and leg during mental stress is not associated with muscle sympathetic outflow.
The physiological responses after mental stress have not been thoroughly addressed. Our results demonstrate significant increases of MSNA in both the arm and leg following mental stress. One possible explanation for this rise in post-stress MSNA is a resetting of the baroreflex during mental stress. Mental stress resulted in significantly elevated blood pressures for a period of 5 min, a time period sufficient for resetting the baroreflex. However, we did not directly examine the baroreflex during this investigation.
It is unclear how long sympathetic activation persists after mental stress. MSNA has been shown to be significantly elevated during 10 min of recovery after 30 min of graded mental stress (Callister et al. 1992). In this study (Callister et al. 1992), post-stress elevation of MSNA was associated with a significant reduction of heart rate compared with pre-stress levels during the final minute of recovery, a finding that is of interest because myocardial ischaemia often occurs at low heart rates (Schang & Pepine, 1977; Deanfield et al. 1983). Our post-mental stress data did not show an increase in MSNA associated with bradycardia, but 3 min of recovery may not have been of sufficient length to observe such a reduction in heart rate. The findings of this paper suggest a need to investigate post-mental stress responses in more depth as it could be of prime importance in uncovering the mechanisms underlying mental stress-induced myocardial ischaemia.
It is reasonable to speculate that elevated sympathetic activity after mental stress may have cardiovascular implications. Rozanski et al. (1988) reported that 23 of 39 patients with coronary artery disease demonstrated wall abnormalities during periods of mental stress, indicating a causal association between myocardial ischaemia and mental stress in patients with coronary artery disease. Our post-mental stress data suggest a potentially new mechanistic link between mental stress and myocardial ischaemia in patients with coronary artery disease. A sudden surge in sympathetic activation to the heart during recovery from cognitive and emotional stress could lead to subsequent cardiac events. More recently, mental stress has been reported to induce prolonged endothelial dysfunction (Ghiadoni et al. 2000; Spieker et al. 2002), persisting for up to 4 h after 10 min of mental stress in one study (Ghiadoni et al. 2000). This is further support for our concept that it may be the recovery response that precipitates cardiovascular problems associated with mental stress.
In summary, the findings of the present study provide strong evidence that mental stress does not elicit divergent neural responses to the arm and leg. Furthermore, forearm vasodilatation during mental stress is not mediated via MSNA. Potent increases of MSNA are simultaneously elicited upon cessation of mental stress in both the upper and lower extremities. Post-mental stress activation of MSNA may have cardiovascular implications, but more research is needed in this area.
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References |
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