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. 2002 Apr 15;540(Pt 2):701–706. doi: 10.1113/jphysiol.2001.013664

Is autonomic support of arterial blood pressure related to habitual exercise status in healthy men?

Pamela Parker Jones 1, Linda F Shapiro 1, Gretchen A Keisling 1, Robert A Quaife 1, Douglas R Seals 1
PMCID: PMC2290253  PMID: 11956356

Abstract

We determined if the tonic autonomic nervous system (ANS) contribution to arterial blood pressure (BP) maintenance in humans is related to habitual endurance exercise status. Twenty-three healthy young (age 18–31 years) males, 11 endurance exercise-trained and 12 untrained, were studied. Maximal oxygen consumption was higher (P < 0.001) and resting heart rate and body fatness were lower (P < 0.05) in the exercise-trained men. Plasma noradrenaline concentrations and BP decreased from baseline levels in response to ganglionic blockade (intravenous trimethaphan) in both groups (all P < 0.001). The absolute (ΔmmHg: systolic = −35 ± 2 vs. − 32 ± 4; diastolic = −13 ± 2 vs. − 10 ± 2; mean = −21 ± 2 vs. − 17 ± 3) and relative (Δ%: systolic = −35 ± 2 vs. − 31 ± 3; diastolic = −26 ± 3 vs. − 20 ± 3; mean = − 31 ± 2 vs. − 26 ± 3) decreases in BP were not significantly different between the endurance-trained and untrained men. There were no significant group differences in the heart rate, stroke volume, cardiac output or systemic vascular resistance (conductance) responses to trimethaphan. Systemic vascular α-adrenergic sensitivity (slope of the increase in mean BP with incremental phenylephrine infusion during ganglionic blockade) also did not differ in the two groups (endurance-trained: 3.2 ± 0.5; untrained: 3.2 ± 0.7 mmHg (ng phenylephrine)−1 (ml plasma)−1). In the pooled sample, the decrease in mean BP during trimethaphan was related to baseline and changes in plasma noradrenaline concentrations (r = 0.58–0.65, P < 0.001) and α-adrenergic sensitivity (r = 0.49, P < 0.02). Our results suggest that the endurance exercise-trained state is not obviously associated with altered ANS support of BP in healthy young men. Basal sympathetic nervous system (SNS) activity and α-adrenergic vascular sensitivity are significant physiological correlates of ANS support of BP in this population.

The autonomic nervous system (ANS), via its sympathetic (SNS) and parasympathetic branches, is critically involved in the tonic maintenance of arterial blood pressure (BP). The ANS contribution to the tonic support of BP can be determined with acute systemic infusion of drugs that block the transmission of neural signalling at the autonomic ganglia (Santajuliana et al. 1996; Jordan et al. 2000; Shannon et al. 2000; Jones et al. 2001). The decrease in BP during this ‘ganglionic blockade’ is determined by the strength of the cardiac parasympathetic inhibition of heart rate and cardiac output, and by the SNS stimulation of the heart and vasculature (i.e. the net effect of basal SNS activity and the associated tissue adrenergic responsiveness).

The endurance exercise-trained state has been reported to influence both the acute and chronic regulation of BP in humans (Davy et al. 1996, 1998; Seals et al. 1999; Monahan et al. 2000; Fagard, 2001). Moreover, habitual endurance exercise may affect one or more of the determinants of ANS support of BP described above (Meredith et al. 1991; Svendenhag et al. 1991; Davy et al. 1996; Hopkins et al. 1996; Davy et al. 1998). As such, one might hypothesize that the endurance exercise-trained state may be associated with altered ANS support of BP in humans. However, currently there is no information on this question.

Thus, the primary experimental aim of this study was to determine the decrease in BP in response to acute ganglionic blockade (Jordan et al. 2000; Shannon et al. 2000; Jones et al. 2001) in untrained and endurance exercise-trained healthy young adults. A secondary aim was to determine the systemic haemodynamic mechanisms contributing to the reductions in BP during ganglionic blockade in these two populations, as well as the potential modulatory influences of the ANS and α-adrenergic vascular sensitivity. Because ANS support of BP may be influenced by the sex of the subject and correlates with baseline BP (Jones et al. 2001), these factors were controlled in order to experimentally isolate the relation to habitual endurance exercise status as much as is possible.

METHODS

Subjects

Twenty-three non-obese men 18–31 years of age were studied: 11 endurance exercise-trained and 12 untrained. Untrained subjects had not performed any type of regular exercise for at least 2 years. Endurance exercise-trained subjects were top finishers in local endurance events including running, cycling and triathlons. They performed at least 40 min of vigorous aerobic exercise four or more times per week for at least the preceding 2 years. Subjects were normotensive, non-smokers and not taking any medications. All were free of overt cardiovascular disease and were otherwise healthy as assessed by a medical history, physical exam, urinalysis and blood chemistries. Written, informed consent was obtained from all subjects, the experimental protocol was approved by the Colorado Multiple Institutional Review Board and the University of Colorado at Boulder Human Research Committee and studies were performed according to the Declaration of Helsinki.

Experimental procedures

Maximal oxygen consumption was measured using on-line computer-assisted open circuit spirometry during incremental treadmill exercise (Tanaka et al. 2000). Body composition was determined using dual energy X-ray absorptiometry (Lunar Radiation).

The procedures for the main ganglionic blockade protocol have been described in detail recently (Jones et al. 2001). Subjects were admitted to the University of Colorado Adult General Clinical Research Center the prior evening. For the preceding 48 h, subjects consumed a eucaloric, controlled sodium (150 mequiv day−1) and potassium (70 mequiv day−1) diet. All were studied in the supine position beginning at 0800 h. Radial artery catheterization (20G, 5 cm catheter; Arrow, Reading, PA, USA) was performed under local anaesthesia (1 % lidocaine) using standard aseptic procedures, and flushed with heparinized saline (2 U ml−1) at 3 ml h−1. Two intravenous catheters were placed in the contralateral arm for drug infusions.

Measurements

Plasma volume was measured by a modified Evans Blue dye technique (New World Trading, DeBary, FL, USA), with total blood volume calculated from simultaneous measurements of plasma volume and haematocrit in triplicate (Greenleaf et al. 1979; Jones et al. 1997). During pharmacological testing, BP was continually monitored by a pressure transducer connected to the arterial catheter and heart rate by ECG (Hewlett-Packard Merlin Patient Monitoring System, Palo Alto, CA, USA). The ECG, BP and respiratory signals were digitized (CODAS, Dataq Instruments, Akron, OH, USA) at 500 Hz for later computer analysis.

Heart rate variability (HRV) was determined as described previously by our laboratory (Davy et al. 1996, 1998). Heart rate, mean heart period (R-R interval), and the standard deviation of the R-R intervals (HRVS.D.(R-Rinterval), time domain measure of HRV) were computed from the beat-to-beat R-R intervals, whereas frequency domain measures of HRV were obtained using power spectral analysis.

Cardiac output was measured as previously described (Huntsman et al. 1983; Chandraratna et al. 1984; Jones et al. 2001) using 2-D echocardiography (Hewlett-Packard ultrasonography 2500) with a 3.5 Mz phased-array transducer using the parasternal short axis view. Care was taken to measure the maximal flow velocity of the left ventricular outflow tract (LVOT) parallel to the flow envelope. The velocity envelope was integrated over time (velocity time integral) and corrected for the orifice size (2πr2, with the LVOT as the radius). A total of three cardiac cycles were averaged to yield a mean cardiac output. All measurements were made by a certified echotechnician according to the American Association of Echocardiography. Systemic vascular resistance and systemic vascular conductance were calculated as the quotients of mean BP/cardiac output and cardiac output/mean BP, respectively.

Plasma samples were analysed for both catecholamine (Peuler & Johnson, 1977) and arginine vasopressin (Robertson et al. 1973) concentrations.

Protocol

After a stable 30 min baseline, 10 min measurements of heart rate, BP, and cardiac output were obtained. NN-cholinergic receptors were blocked by continuous intravenous infusion of trimethaphan (Cambridge Laboratories Limited, UK). Infusions started at 2 mg min−1 and increased by 2 mg min−1 at 6 min intervals up to 6 mg min−1 or until blockade was established by no fluctuations of heart rate and BP with respiration. In every subject, complete cardiovascular-autonomic blockade was documented by heart rate changes of < 5 beats min−1 with a 25 mmHg increase in systolic BP resulting from a bolus injection (< 1 s) of phenylephrine (25, 50, and/or 100 μg). After a 20 min washout period, measurements of heart rate, BP and cardiac output were repeated under ANS blockade. Arterial blood samples were drawn at rest and during ANS blockade. Differences between baseline and trimethaphan were taken as the measure of ANS support. To determine vascular α-adrenergic sensitivity, while still under ganglionic blockade, phenylephrine was infused intravenously in 6 min steady-state doses (0.02, 0.04, 0.08, 0.16 μg kg−1 min−1) until mean BP increased 25 mmHg above baseline. Vascular α-adrenergic sensitivity is expressed as the slope of the change in blood pressure per unit plasma concentration of phenylephrine (ng ml−1). Upon completion of all measurements, trimethaphan infusion was stopped and subjects were monitored until completely recovered.

Statistical analyses

Group comparisons for baseline characteristics were made using unpaired t tests. Responses to trimethaphan were analysed using a two-way analysis of variance with repeated measures [group × condition (baseline vs. autonomic blockade)]. Relations of interest were determined using univariate correlations. The slope of the increase in mean BP with incremental phenylephrine infusion was used to determine α-adrenergic vascular responsiveness. All data are reported as mean ±s.e.m.

RESULTS

Subject characteristics (Table 1)

Table 1.

Baseline subject characteristics

Sedentary Trained P value (two-tailed)
n 12 11
Age (years) 23 ± 1 26 ± 1 0.20
Height (cm) 177 ± 1 179 ± 1 0.42
Body mass (kg) 74.8 ± 2.9 76.4 ± 1.6 0.64
Body mass index (kgm−2) 23.8 ± 0.8 23.8 ± 0.4 0.96
%Body fat 19.2 ± 1.7 10.9 ±.1.3 0.0001
Fat-free mass 58.0 ± 2.0 64.5 ± 1.1 0.01
V̇O2,max (ml kg−1 min−1) 44.6 ± 1.3 56.5 ± 0.7 0.0001
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V̇O2,max = maximal oxygen consumption. Values are means ±s.e.m.

Maximal oxygen consumption (P < 0.001) and fat-free mass (P < 0.05) were greater and % body fat was lower (P < 0.05) in the endurance exercise-trained men compared with the untrained controls. There were no other significant differences between the groups.

Baseline cardiovascular and neurohumoral function (Table 2)

Table 2.

Supine baseline cardiovascular and neurohumoral function

Sedentary Trained P value (two-tailed)
Systolic blood pressure (mmHg) 125 ± 2 128 ± 3 0.46
Diastolic blood pressure (mmHg) 66 ± 1 67 ± 2 0.80
Mean blood pressure (mmHg) 86 ± 1 87 ± 2 0.58
Cardiac output (l min−1) 4.8 ± 0.4 4.6 ± 0.1 0.54
Systemic vascular resistance (a.u.) 18.6 ± 1.7 19.2 ± 0.7 0.74
Systemic vascular conductance (a.u.) 0.057 ± 0.005 0.053 ± 0.002 0.22
Stroke volume (ml) 83 ± 6 87 ± 3 0.53
Heart rate (beats min−1) 61 ± 3 53 ± 1 0.02
HRVhfp (ms2 Hz−1) 110 ± 21 152 ± 41 0.13
HRVlfp (ms2 Hz−1) 533 ± 230 550 ± 158 0.95
HRVs.d. (R-R interval) (ms) 72 ±.7 75 ± 6 0.70
Total blood volume (ml kg−1) 94 ± 6 104 ± 4 0.24
Plasma noradrenaline (nmol l−1) 1.486 ± 0.134 1.657 ± 0.182 0.49
Plasma vasopressin (ngl −1) 0.97 ±.0.39 0.57 ± 0.10 0.27
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HRVhfp = high frequency power of heart rate variability; HRVlfp = low frequency power of heart rate variability; HRVs.d. (R-R interval) = heart rate variability by standard deviation of the R-R interval; a.u. = arbitrary unit. Values are means ±s.e.m.

Supine resting heart rate was lower in the endurance-trained compared with the untrained men (P < 0.05). No other significant differences were observed.

Responses to ganglionic blockade

Systolic, diastolic, and mean BP decreased from baseline levels in response to trimethaphan in both groups (all P < 0.001). The absolute (Δ mmHg, Fig. 1) and relative (Δ%: systolic = −35 ± 2 vs. −31 ± 3; diastolic = −26 ± 3 vs. −20 ± 3; mean = −31 ± 2 vs. −26 ± 3) decreases were not significantly different (all P > 0.3) between the endurance-trained and untrained men, respectively. Consistent with this, there were no statistical differences in the systemic haemodynamic responses to trimethaphan between the two groups (all P > 0.2, Fig. 1). Plasma noradrenaline concentration decreased and plasma vasopressin concentration increased from baseline during trimethaphan in both groups (P < 0.001); the changes were not significantly different (endurance exercise-trained vs. untrained: noradrenaline = −0.622 ± 0.088 and −0.609 ± 0.098 nmol l−1; vasopressin = 22 ± 13 and 8 ± 4 ng l−1, respectively; P > 0.38).

Figure 1. Haemodynamic responses to ganglionic blockade.

Figure 1

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Responses to ganglionic blockade in untrained (n = 12) and endurance exercise-trained (n = 11) healthy young men. There were no significant differences (all P > 0.2) between groups in any of the responses. Systolic (SBP); diastolic (DBP); and mean (MAP) arterial blood pressure; systemic vascular resistance (SVR); and conductance (SVC). Values are means ±s.e.m.

Vascular α-adrenergic sensitivity

The slope of the increase in mean BP in response to incremental plasma concentrations of phenylephrine during ganglionic blockade was not different between the two groups (endurance-trained: 3.2 ± 0.5; untrained: 3.2 ± 0.7 mmHg (ng phenylephrine)−1 (ml plasma)−1).

Physiological correlates of ANS support of BP

In the pooled sample of endurance-trained and untrained men, the decrease in mean BP from baseline during trimethaphan was related to baseline plasma noradrenaline concentrations (r = 0.58, P < 0.001), the decrease in plasma noradrenaline concentrations from baseline during ganglionic blockade (r = 0.65, P < 0.001), and the slope of the increase in mean BP in response to phenylephrine (r = 0.49, P < 0.02).

DISCUSSION

The primary new finding from this investigation is that the endurance exercise-trained state is not obviously associated with altered ANS support of BP, at least in healthy young men. Consistent with this, we found no significant differences in the systemic cardiovascular adjustments to acute ganglionic blockade. Finally, we identified basal SNS activity and α-adrenergic vascular sensitivity as significant physiological correlates of ANS support of BP among the individual subjects.

The ability of the ANS to provide tonic support of BP is determined by a complex interaction involving parasympathetic and SNS influences on cardiac chronotrophy and inotrophy, as well as SNS input to and responsiveness of the vasculature. Ganglionic blockade is an experimentally effective model with which to discern condition or population differences in ANS support of BP in both human and animal subjects (Santajuliana et al. 1996; Jordan et al. 1998; Shannon et al. 2000; Jones et al. 2001). However, this approach does not provide definitive insight into each specific mechanism involved in these interactive ANS effects on BP: cardiac vagus and sympathetic nerve discharge; muscarinic and adrenergic receptor properties and post-receptor signalling; and sympathetic vasoconstrictor nerve discharge and receptor/post-receptor influences in the vasculature. In the present study, we attempted to offset these limitations by acquiring as much complementary mechanistic data as possible. Nevertheless, we can only speculate as to why no group differences in ANS support of BP were observed.

Examination of the significant ANS-cardiovascular correlates of ANS support of BP may provide some clues. In our recent investigation of the effects of primary ageing on ANS support of BP (Jones et al. 2001), we found that measures of SNS activity and α-adrenergic vascular sensitivity were the strongest determinants of the decrease in mean BP with ganglionic blockade. Consistent with these previous observations, in the present study baseline plasma noradrenaline concentrations (and the decreases in those concentrations during ganglionic blockade) and the slope of the increase in mean BP in response to phenylephrine infusion were significantly related to the reduction in mean BP in response to trimethaphan among the individual subjects. Neither of these correlates of ANS support of BP was different between the sedentary and endurance exercise-trained subjects. Moreover, the increases in heart rate and reductions in left ventricular stroke volume with ganglionic blockade were not different between the two groups. Thus, key determinants of both cardiac output support of BP and SNS support of systemic vascular resistance did not differ in our sedentary and exercising men.

Several issues related to our study may deserve comment. First, heart rate variability is generally believed to reflect cardiac parasympathetic modulation of heart rate (Katona & Jih, 1975; Eckberg, 1983). In the present study, the two expressions of HRV, HRVS.D.(R-Rinterval) and HRVHFP, were not significantly different between the endurance-trained and untrained men. These data suggest that there were no marked differences in cardiac parasympathetic modulation of heart rate in our endurance-trained and untrained subjects. Although higher HRV has been reported in the endurance exercise-trained compared with the untrained state in adult humans (Katona et al. 1982; Demeersman, 1993), lack of differences have also been observed in several previous investigations (Maciel et al. 1985; Reiling & Seals, 1988; Furlan et al. 1993). We speculate that cardiac parasympathetic modulation of heart rate is quite strong, even in untrained healthy young males, thus making it difficult to demonstrate consistently an independent (additive) influence of habitual endurance exercise in this population. Had our control population been extremely sedentary and mildly obese, we probably would have observed greater differences at baseline in both sympathetic and parasympathetic measures of the ANS.

Figure 2. Relation between the change in plasma noradrenaline and ANS support of BP.

Figure 2

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The relation between the change in plasma noradrenaline concentration with ganglionic blockade and the change in mean arterial blood pressure (MAP) with ganglionic blockade in the pooled population of untrained (n = 12) and endurance exercise-trained (n = 11) healthy young men.

Second, in rat, the reduction in BP with trimethaphan is greater in the presence of a vasopressin receptor antagonist (Santajuliana et al. 1996), suggesting that vasopressin is partially counteracting the fall in BP and causing ANS support to be underestimated. Whether trimethaphan-evoked vasopressin release modulates the BP response to ganglionic blockade in humans is unknown. In the present study, the increases in plasma vasopressin concentrations during ganglionic blockade were not significantly different between the two groups, nor did the responses correlate with the corresponding reductions in mean BP among the pooled individual subjects (r = 0.20, P = 0.27). As such, we do not believe that the arginine vasopressin ‘counter-regulatory’ response to the acute hypotension produced by trimethaphan influenced the interpretation of our group comparisons.

Third, although mean baseline stroke volume and blood volume were ∼5–10 % higher in the endurance exercise-trained compared with the sedentary men in the present study, these differences were not statistically significant. We believe that this was probably related to the fact that body mass and body surface area were similar in both groups.

Finally, we should emphasize the cross-sectional approach employed in the present investigation and the well-known limitations associated with this study design. However, we have previously used this approach successfully to gain initial insight into the possible effects of habitual endurance exercise on ANS and cardiovascular function in humans (Davy et al. 1996, 1998; Hunt et al. 1997; Jones et al. 1997; Seals et al. 1999; Desouza et al. 2000; Monahan et al. 2000; Tanaka et al. 2000). The concept is that differences between sedentary and endurance-trained populations provide initial evidence for a possible influence of regular exercise that can then be more definitively determined in a follow-up, intervention study. However, as was the case in the present study, if no differences are found it suggests the absence of any significant effect, thus avoiding the substantial time, effort and resources required to conduct an exercise intervention trial.

In summary, the present results support the conclusion that, at least among healthy young males, the endurance exercise-trained state is not obviously related to ANS support of BP or the systemic cardiovascular adjustments to acute removal of ANS input to the heart and vasculature. Our findings also confirm the observations of our recent work (Jones et al. 2001) suggesting that basal SNS activity and α-adrenergic vascular sensitivity are important physiological determinants of ANS support of BP among healthy men.

Acknowledgments

This work was supported by National Institutes of Health Awards HL39966, AG13038, AG06537, AG00828, RR-00051, and by American Heart Association CWFW-02–98.

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