Epidemiological evidence indicates that physical activity is associated with a reduced risk of coronary heart disease (7,63,80). A number of mechanisms may be responsible for this effect of physical activity. One such mechanism may involve cardiac vagal tone. Links between aerobic exercise, cardiac vagal tone, and cardiovascular disease are suggested by findings from two lines of research. First, evidence from several studies suggests that reduced cardiac vagal tone and/or impaired vagal function is a risk factor for hypertension (20,35,36,40,98), coronary artery disease (1,45,46), episodes of myocardial ischemia (94), and sudden cardiac death (47). Second, the findings of a number of studies have provided support for the association of higher aerobic fitness and enhanced resting cardiac vagal tone relative to lower levels of fitness (5,15,32,33,59,69,74,82,86,90), although not all of the studies are in agreement (19,37,44,58,68,81). If enhanced cardiac vagal tone is, in fact, an adaptation of chronic aerobic exercise involvement, then it may partially account for the exercise-related reductions in the risk of heart disease.
One specific way that exercise-related increases in cardiac vagal tone may reduce the risk of heart disease is by attenuating cardiac reactivity to psychological stressors, as it is hypothesized that cardiovascular hyperreactivity to real-life stressors contributes to the development of cardiovascular disease (60,70). It is well documented that heart rate and blood pressure increase during stressful psychological challenges in both the laboratory (3,66) and real-life situations (67,99). Such changes in heart rate are typically attributed to increases in sympathetic influence on the heart (34,75); however, a withdrawal of cardiac vagal tone may also contribute to the increased cardiac activation (3,42,89). In light of the fact that vagal influences on the heart can offset those of the sympathetic nervous system, the maintenance of higher cardiac vagal tone may attenuate the increases in heart rate that occur during stress (40) and thereby attenuate the associated increases in cardiac output and blood pressure (56,84).
In light of the evidence that aerobically fit individuals exhibit greater cardiac vagal tone at rest than those who are less fit, it is possible that aerobically fit individuals also tend to exhibit greater vagal tone during psychological stress and recovery. Although Hatfield et al. (44) did not find differences between trained and untrained men on respiratory sinus arrhythmia (RSA), an index of cardiac vagal tone, during ergogenic stress, it is possible that group differences in the parasympathetic response to psychogenic stressors may emerge in light of the possibility of specific cardiovascular response patterns to ergogenic versus psychogenic challenges (24,57). Beyond the possibility of higher vagal tone levels during psychological stress, aerobically fit individuals may also exhibit a smaller phasic vagal withdrawal than less fit individuals, and they may restore vagal tone more rapidly during recovery. Concomitantly, we would expect aerobically fit individuals to exhibit longer heart periods (HP) and smaller phasic changes in HP during stress and recovery than less fit individuals.
Although the relationship between aerobic fitness and heart rate reactivity has been examined extensively (e.g., see 27), relatively little attention has been devoted to the specific issue of whether parasympathetic regulation of the heart during psychological stress and recovery differs between individuals who vary on aerobic fitness levels. To date, only three studies have appeared in the literature on this issue, and the results are mixed. In the first such study de Geus et al. (29) compared young men who were randomly assigned to either a brief aerobic training program or a wait-listed control group, on phasic RSA responses to two reaction time tasks and recovery. Cardiac vagal reactivity was assessed in both groups before and after the training program. When the data were analyzed with analysis of variance (ANOVA) procedures, it was found that the trained and control groups did not differ at posttest on phasic RSA withdrawal during the challenges or on the reengagement of RSA during recovery. However, when the data were subjected to correlational analysis, the investigators found, consistent with their expectations, that 1) higher aerobic fitness levels were associated with smaller phasic RSA responses (i.e., smaller withdrawal of RSA) to the tasks at pretraining and that 2) among the trained subjects, greater improvements in aerobic fitness were associated with less vagal withdrawal at the posttraining assessment. The contradictory findings yielded by the ANOVA and correlational analyses may be explained by the fact that the different statistical procedures were sensitive to different aspects of the data structure. In a preliminary report of another investigation, Nurhayati and Boutcher (74) presented findings that trained postmenopausal women maintained longer HP and higher RSA than their sedentary counterparts before, during, and after a Stroop test. However, when phasic changes in RSA were examined, they found no group difference during or after the challenge. Lastly, Boutcher and colleagues (17) examined trained young men and two groups of their untrained counterparts, one group with low resting heart rates (i.e., <62 beats·min−1) and another with typical resting heart rates (i.e., >67 beats·min−1), for differences in RSA levels as well as phasic changes in RSA during mental arithmetic and a Stroop test. There were no group differences on RSA levels during either task, nor were there any differences between the groups on phasic RSA responses to mental arithmetic. However, the trained and untrained men with low resting heart rates did exhibit a greater phasic decrease in RSA during the first half of the Stroop test than did the untrained controls with normal resting heart rates. As the trained and untrained men with low resting heart rates had higher RSA at baseline than the controls, it is possible that the group differences in phasic responses to the Stroop were simply due to the effects of the Law of Initial Values (LIV;101,102). In accordance with the LIV, individuals with higher baseline RSA would be expected to exhibit a larger decrease in RSA during stress than individuals with a lower baseline RSA. In light of the absence of appropriate tests and adjustments for the effects of the LIV, the results obtained by Boutcher et al. (17) remain equivocal.
Thus, the evidence regarding the relationship between aerobic fitness and cardiac vagal reactivity and recovery is mixed. The mixed findings may be partially explained by the different methods used to quantify RSA. de Geus et al. (29) used the peak-to-trough method (43) to quantify RSA, whereas Boutcher and colleagues (17,74) used Porges’ (77) method. Estimates of vagal tone derived with the peak-to-trough method may be influenced by changes in ventilatory activity and trends in heart rate (i.e., slow aperiodic and periodic shifts in heart rate) (23,41), which was not controlled in the study by de Geus et al. (29). In contrast, Porges’ method is robust to the influence of changes in ventilatory activity and the HP slope and is, therefore, appropriate for assessing RSA across conditions in which ventilatory activity may vary substantially. In light of the potential importance of cardiac vagal tone in moderating the effects of reactivity on the risk of cardiovascular disease, and the equivocal findings, there is a need to reexamine the association between aerobic fitness and cardiac vagal reactivity using methods which are appropriate for assessing RSA under conditions characterized by variable ventilatory activity and which account for the effects of the LIV, if present. In the present study we compared endurance-trained and untrained young men on RSA and HP during rest, three contiguous psychological challenges, and subsequent recovery. Porges’ (77) method was used to estimate RSA and tests for the effects of the LIV were made when appropriate. We predicted that trained men, as compared with untrained men, would 1) have longer HP and higher RSA levels at rest and during psychological stress and recovery, 2) have smaller phasic reductions in HP and RSA during psychological stress, and 3) show a more rapid return of HP and RSA to resting levels during recovery.
The subjects were 10 endurance-trained men recruited from running and cycling clubs in a major metropolitan area and 10 untrained male undergraduate students recruited from a large university in the same area. Subjects ranged in age from 19 to 26 yr. All subjects completed a brief health questionnaire to screen for a history of cardiovascular disease and the use of tobacco products and any medications as well as a physical activity questionnaire (4). Runners reported averaging approximately 40 miles per week for an average of 4.5 yr, and cyclists reported averaging approximately 300 miles per week for an average of 3.3 yr. In contrast, the untrained men indicated that they did not regularly participate in any form of aerobic or endurance activity. Subject characteristics are provided in Table 1. Group differences on all subject characteristics except maximal oxygen consumption (O2max) were evaluated with separate two-tailed t-tests for independent groups. The group difference on O2max was evaluated with a one-tailed t-test. Trained subjects had a significantly higher aerobic capacity and weighed less than the untrained. However, the groups did not differ on age, height, blood pressure, trait anxiety, or state anxiety associated with exposure to the laboratory setting before the psychological stress testing.
The experiment involved tests on two separate days. A test of aerobic capacity was conducted on the first day and stress reactivity was assessed on a second day. On the first visit to the laboratory subjects were provided with a brief description of the study and signed a consent form approved by the university’s human subjects research review board. Height, weight, and resting blood pressure were obtained. Subjects then completed a graded exercise test on a treadmill (Quinton Treadmill System, model 18–60, Quinton Instrument Company, Seattle, WA) to determine aerobic capacity. Subjects were tested after abstaining from food for 2–3 h and from exercise participation earlier in the day. The exercise test began with a warm-up period during which the subject walked on the treadmill for 2 min at a level grade and a speed of 3 mph. The treadmill speed was then increased until the subject reached 75% of his age-predicted maximal heart rate and remained constant thereafter. Subjects then continued exercising for 4 min, after which the treadmill grade was increased to 4%. At the end of each minute thereafter the grade was increased by 2% until the subject reached voluntary exhaustion. Throughout the test, the electrocardiogram (ECG) was monitored via pregelled, disposable electrodes attached to the subject in a CM5 configuration. Expired gases were analyzed with a calibrated Beckman Metabolic Measurement Cart (Beckman Instruments, Inc., Fullerton, CA) to obtain 30-s averages of minute volume and fractional gas concentrations of oxygen and carbon dioxide. The assessment of O2max was deemed valid if the following three criteria were met: 1) heart rate equaled the age-predicted maximum ± 10 bpm, 2) the increase in oxygen consumption was less than 150 mL with an increase in workload, and 3) the respiratory quotient exceeded 1.10 (97). All subjects met these criteria. The O2max (mL·kg−1·min−1) reported was the highest 30-s value obtained.
On the second day, after arriving at the laboratory, subjects first completed the Spielberger State and Trait Anxiety Inventories (93). Sensors were then attached for the measurement of the ECG. During testing subjects were seated in a thickly padded reclining chair in the upright position in a dimly lit room adjacent to the ECG monitoring equipment. The experimental protocol consisted of a 15-min rest period, three contiguous psychological challenges presented in fixed order as described in previous studies (87,88), and a 3-min recovery period. The psychological tasks included mental arithmetic, a 14-item general knowledge and logic quiz, and a modified version of the Stroop color-word test (95). To standardize procedures, the instructions and tasks were presented to subjects via a videotape player. Subjects were instructed to respond verbally to the tasks and, in order to increase the stressfulness of the challenges, they were told that their responses would be recorded for subsequent evaluation. The mental arithmetic task was 2.5 min in duration and consisted of five 20-s serial subtraction problems and an additional six arithmetic problems. Each serial subtraction problem involved subtracting sequentially by a new one- or two-digit subtrahend starting from 100 or 425. Subjects were required to report aloud the result of each subtraction. Each of the six remaining arithmetic problems involved two operations (e.g., 8 × 9 + 13). Subjects were required to answer aloud within 5 s after the presentation of each problem. The order of presentation was two serial subtraction problems, six arithmetic problems, and three additional serial subtraction problems. The quiz was 2 min in duration and consisted of 14 general knowledge, logic, and analogy problems. In this condition, subjects were also required to answer aloud within 5 s after presentation of a problem. The Stroop test involved the presentation of specific color words (i.e., red, green, blue, and yellow) that were displayed individually in an incongruous color on the videotape monitor at a rate of one per second for 2.5 min. Audio presentation of conflicting color names were made concurrently with video presentation of the color words in order to increase the difficulty of the task. Subjects were asked to report the color in which the word was printed. The Stroop test was immediately followed by a 3-min recovery period, during which subjects were instructed to relax with their eyes closed. The ECG was recorded during the last 3 min of the initial rest period (baseline) and throughout the challenge and recovery periods and was obtained via pregelled, disposable electrodes attached to the skin over the sternum and over the sixth intercostal space on the midaxillary line of the left side of the chest. A small transmitter (Transkinetics, Model TXM-205, Canton, MA) attached to the subject’s chest relayed the ECG to a Transkinetics Telemetry receiver (Model TXE-206) which filtered and amplified the signal. The analog ECG was recorded on tape with an FM cassette recorder (A.R. Vetter, Inc., model C-4, Rebersburg, PA) for off-line analysis.
Ratings of perceived stress were obtained for each condition of the experiment with a visual analog scale (VAS) and were used to determine if the groups experienced similar levels of subjective stress throughout the experiment. The VAS consisted of a 100-mm line that was anchored on the left end by the words “completely relaxed” and on the other by the words “highly stressed.” Subjects were instructed that the scale represented the full range of feelings from being completely relaxed to being highly stressed and that, when prompted, they were to place a vertical mark at a point along the line corresponding to their level of perceived stress at the moment. Visual analog scale measures were obtained at the end of the rest period, at the midpoint of each stressor condition, and at 30 s into the recovery. Scores for each condition were obtained by measuring the distance in mm from the left end of the line to the mark made by the subject. VAS scores could range from 0 to 100, with a higher score representing a higher level of perceived stress. Previous investigators have employed this methodological approach for the assessment of psychological states (13,38).
Quantification of heart period and RSA.
Heart period was quantified off-line from the recorded ECG as the time in ms between consecutive R-waves. To quantify HP, the analog ECG signal was digitally converted at a sampling rate of 1 kHz and the digitized ECG data were then processed by software on a minicomputer (PDP 11/34, Digital Equipment Inc., Maynard, MA) to detect R-wave peaks and calculate the time between R-waves. Heart period series were generated for 30-s epochs within the baseline, task, and recovery periods for each subject, and mean HP was calculated for each 30-s epoch.
Respiratory sinus arrhythmia was also obtained for 30-s epochs within the baseline, task, and recovery periods and was estimated from the HP series for each epoch using MXedit software (Delta-Biometrics, Bethesda, MD) and procedures described by Porges (77). To quantify RSA, the HP data were first displayed graphically and manually edited to remove artifacts. Editing involved adding adjacent HP that appeared to be short relative to intervals typical for the subject being examined or dividing excessively long HP by the number of cardiac cycles surmised to be contributing to them. The edited HP series were then time sampled to obtain estimates of instantaneous HP at 500-ms intervals (79). This step yielded series of HP estimates that were equally spaced in time, which is a requirement of time series analysis methods utilized in a subsequent step to filter the data. In the absence of time-sampling the HP series may be characterized as realizations of a point process (i.e., based on a physiological process in which an R-wave peak occurs or does not occur), which consists of data points that are spaced irregularly in time and, as such, are not amenable to analysis with conventional time series techniques that assume equally spaced data. Sources of nonstationarity in the data (i.e., aperiodic trends and slow periodicities) were then modeled with a 21-point moving polynomial and removed from the HP series. The resulting stationary HP series was then band-pass filtered (0.12–0.40 Hz) to exclude variance outside of the respiratory frequencies that are typical for adults at rest and during psychological stress (i.e., 7.2–24 breaths·min−1). The variance of the band-passed data was then calculated and RSA was estimated as the natural logarithmic transformation of the variance. The natural log transform was necessary to normalize the distribution. Respiratory sinus arrhythmia values can range from 0 to approximately 10. A number of previous studies have shown that RSA is a valid measure of cardiac vagal tone. Electrical and pharmacological manipulations to evoke increased baroreceptor reflex inhibition of the heart via the vagus were shown to increase RSA in anesthetized cats (71) and rabbits (72). In these studies, the RSA response was abolished by the infusion of atropine, a cholinergic blocker, and was unaffected by beta-adrenergic blockade. Similarly, in a study of alert and ambulatory rats, the infusion of atropine eliminated the RSA, saline produced no effect, and phenylephrine-induced hypertension increased the amplitude of RSA (103). In humans, a monotonic increase in the dose of atropine has been shown to produce a monotonic decrease in RSA (31,78).
Analyses were conducted on absolute levels and change scores for mean HP and RSA as well as VAS scores. Mean HP was estimated for the baseline (i.e., last 3 min of the initial rest period), each psychological challenge, and each minute of recovery by averaging HP means for 30-s epochs contained within each of the seven respective periods. Similarly, mean RSA was estimated for the same periods by averaging RSA across the 30-s epochs contained within each respective period. Change scores were calculated as the mean task (or recovery) level minus the mean baseline level. Group differences in baseline HP and RSA were evaluated with separate one-tailed t-tests for independent groups. The group difference in baseline VAS scores was examined with a two-tailed t-test. To determine whether the groups differed on activity levels across the experiment, HP and RSA values were subjected to separate 2 (group: trained vs untrained) × 7 (condition: baseline, mental arithmetic, quiz, Stroop, and recovery minutes 1, 2, and 3) mixed ANOVA with repeated measures on condition. Similarly, VAS scores were subjected to a 2 (group: trained vs untrained) × 5 (condition: baseline, mental arithmetic, quiz, Stroop, and recovery) mixed ANOVA with repeated measures on condition. Additionally, to determine whether the groups differed on phasic responses to the challenges and recovery HP and RSA change scores were subjected to separate 2 (group: trained vs untrained) × 6 (condition: mental arithmetic, quiz, Stroop, and recovery min 1, 2, and 3) mixed ANOVA with repeated measures on condition. Also, VAS change scores were subjected to a 2 (group: trained vs untrained) × 4 (condition: mental arithmetic, quiz, Stroop, and recovery) mixed ANOVA with repeated measures on condition. A Huynh-Feldt (54) adjustment was applied to the degrees of freedom for all tests of within-subjects effects to correct bias introduced by violation of the sphericity assumption. When it was appropriate, post hoc analyses were conducted using the student Newman-Keuls method. Last, for each group, O2max was correlated with absolute levels and change scores for HP and RSA, respectively, for each challenge and each 1-min epoch of recovery.
Group comparisons on baseline levels.
Resting HP was greater for the trained subjects ( = 1133.0, SEM = 61.8) than the untrained ( = 900.8, SEM = 43.9), one-tailed t (18) = −3.06, P < 0.007. However, the relative bradycardia exhibited by the trained men was not associated with higher RSA. Resting RSA was similar for trained ( = 6.64, SEM = 0.37) and untrained men ( = 6.92, SEM = 0.34). There was no significant difference in the levels of subjective stress at rest; mean baseline VAS scores were 8.3 mm (SEM = 1.5) for trained and 13.9 mm (SEM = 2.9) for untrained men.
Test for LIV effects.
The significant group difference in baseline HP raised the possibility that the group comparisons on HP responses to the challenges could be affected by the LIV. As the trained men had a longer baseline HP than the untrained, they may, in accordance with the LIV, exhibit a greater phasic shortening of HP during stress than the untrained men. The effect of the LIV, if present, may therefore confound and obscure the true differences in reactivity between the groups. To exclude this possibility tests were conducted to determine whether HP responses to the psychological challenges were dependent on baseline levels. Myrtek and Foerster’s (73) procedure was used to test for LIV effects. This procedure involves estimating the slope of the principal component, bpc, from baseline and task values. They proposed testing the hypothesis that bpc differs significantly from 1. If bpc is significantly less than 1, then an LIV effect is present. The estimate proposed by Myrtek and Foerster (73) is superior to more traditional estimates of LIV effects (e.g., see 6, 61) because it is not biased by the x(y − x) effect. This effect occurs for correlations between two values that share a common term (i.e., x, the baseline value) and will bias the correlation of baseline values and change scores toward being negative whenever the correlation between baseline and task values is less than 1.00. As this latter correlation is almost always less than 1.00, the correlation of initial values and change scores are biased toward supporting the LIV effect (39,55). As HP was assessed across a short interval, it was assumed that the error variances of baseline and task HP measures were equal (55). Therefore, bpc was calculated for each challenge under the assumption that the ratio of the error variances was 1. The hypothesis that bpc ≠ 1 was tested with a t statistic (see in 55), which follows a Student’s t distribution with n − 2 degrees of freedom. The two prerequisites for the test were satisfied (55): 1) that the correlation between baseline and task HP values was significant for mental arithmetic (r (18) = 0.62, P = 0.003), the quiz (r (18) = 0.80, P < 0.001), and the Stroop test (r (18) = 0.78, P < 0.001); and 2) that the mean change score was significantly different from 0 for all three challenges, all t ’s(19) ≤ −5.1, P ’s ≤ 0.0001. The analyses revealed that the estimates of bpc for mental arithmetic (0.79), the quiz (0.79), and the Stroop test (0.73) were not significantly different from 1.0, all t’ s(18) ≤ 1.4. Therefore, it was concluded that HP responses were not dependent on baseline HP levels for any of the challenges in this study. Consequently, it was not deemed necessary to adjust task HP levels or change scores for differences in baseline levels in subsequent analyses.
Group comparisons on responses to tasks and recovery.
Mean (and SEM) HP and HP change scores for trained and untrained subjects as well as groups combined are presented in Figure 1A and B, respectively. The ANOVA on HP levels revealed that trained men exhibited longer HP ( = 1008.1, SEM = 23.6) than the untrained men ( = 822.2, SEM = 17.2) throughout the experiment (F (1,18) = 8.7, P < 0.01). Also, the analysis of HP levels revealed a significant main effect for condition (F (6,108) = 29.7, ε = 0.32, P < 0.001). Heart period was significantly shorter during each of the tasks as compared with baseline, indicating that the psychological challenges produced chronotropic cardiac activation. However, the quiz was not as effective as the Stroop or mental arithmetic tasks in producing activation, as HP was significantly longer during the quiz than during the Stroop and mental arithmetic tasks, which did not differ. After the last challenge HP recovered to baseline levels within the first min. The group × condition interaction for HP levels was not significant. The lack of an interactive effect for HP levels indicates that the trained and untrained men did not differ on phasic changes in HP during stress or recovery. With respect to HP change scores, the ANOVA failed to reveal a significant group main effect or group × condition interaction, again indicating that the groups did not differ on phasic changes in HP during stress or recovery. However, a significant condition main effect was observed (F (5,90) = 27.5, ε = 0.34, P < 0.0001). The post hoc analysis revealed that HP shortened less during the quiz than during mental arithmetic or the Stroop test, which did not differ. Also, the shortening of HP was significantly greater during the challenges than during recovery.
Mean (and SEM) RSA and RSA change scores for trained and untrained subjects, as well as groups combined, are presented in Figure 2A and B. The ANOVA failed to reveal a significant group main effect or group x condition interaction for either variable.1 The overall mean RSA levels and change scores were 6.57 (SEM = 0.16) and −0.08 (SEM = 0.18), respectively, for the trained and 6.54 (SEM = 0.12) and −0.45 (SEM = 0.12), respectively, for untrained subjects. ANOVA revealed a significant condition main effect for both RSA levels (F (6,108) = 4.4, ε = 0.84, P = 0.001) and RSA change scores (F (5,90) = 5.5, ε = 0.75, P < 0.001). Post hoc analysis of RSA levels revealed that RSA was significantly lower during mental arithmetic and the Stroop test than during the baseline. However, the Quiz did not differ from the baseline. Also, RSA for mental arithmetic and the Stroop test returned to baseline level within the 1st minute of recovery. Post hoc analysis of RSA change scores revealed that the challenges did not differ. Although RSA change scores for mental arithmetic and the Stroop test differed from those of recovery, change scores for the Quiz did not.
Mean (and SEM) VAS and VAS change scores for trained and untrained subjects as well as groups combined are presented in Figure 3A and B, respectively. The ANOVA failed to reveal a significant group main effect or group × condition interaction for either variable. Overall, mean VAS level and change scores were 49.2 mm (SEM = 3.8) and 44.2 (SEM = 3.3), respectively, for the untrained and 36.9 mm (SEM = 3.3) and 35.8 (SEM = 3.0), respectively, for trained subjects. The analysis revealed that VAS levels were significantly different across conditions (F (4,72) = 60.3, ε = 0.91, P < 0.001). Scores were greater for each of the tasks than for the baseline, indicating that subjects perceived the psychological challenges as stressful, and they were greater for the Stroop test than for either mental arithmetic or the quiz, which did not differ. Also, the VAS scores were significantly greater at recovery than at the baseline, indicating that the recovery of perceived stress was not complete 30 s after the last stressor. Finally, a significant condition main effect was also observed for VAS change scores (F (3,54) = 17.8, ε = 1.00, P < 0.0001). The post hoc analysis revealed that the change in VAS scores from baseline was greater for the Stroop test than for mental arithmetic and the quiz, which did not differ. Visual analog change scores were significantly greater for the challenges than for recovery.
Within-group Pearson correlation coefficients calculated for O2max with absolute levels and change scores for HP and RSA, respectively, for each condition of the experiment are presented in Table 2. The 52 correlations obtained were variable in sign and, except for three instances, were not significant. In one case, aerobic capacity was negatively correlated with phasic changes in RSA in the untrained subjects during the second min of recovery. However, significant correlations were not observed for the other min of recovery in this group. In the other two instances, aerobic capacity was negatively correlated with HP change scores for the untrained men in the mental arithmetic and Stroop conditions indicating that, for these subjects and conditions, lower aerobic capacity was associated with a greater shortening of HP. The corresponding correlations were not significant for the trained men. In general, individual differences in aerobic capacity were not associated with absolute levels or phasic changes in HP or RSA during psychological challenge or recovery for either group.
In this study, RSA and HP were examined at rest and during psychological stress and recovery in two groups of healthy young men that differed substantially on aerobic capacity (O2max = 67.0 ± 5.7 and 45.5 ± 6.7 mL·kg−1·min−1 for the trained and untrained, respectively) and a similar sample size was employed to those reported in other investigations of aerobic fitness and RSA reactivity to psychological stress (17,29). It was hypothesized that the trained men would have greater cardiac vagal tone and lower chronotropic cardiac arousal during stress and recovery than the untrained. This hypothesis was based on a model specifying that 1) the trained men would exhibit greater cardiac vagal tone at rest than the untrained and that 2) the training-related enhancement of vagal tone manifested at rest would generalize to periods of psychological stress and recovery and, thereby, moderate cardiac arousal. However, the requisite group difference in resting cardiac vagal tone was not observed. Although the trained men in this study did have longer resting HP than the untrained, they did not differ from the untrained on RSA at rest. Therefore, the relative bradycardia observed at rest for the trained men was not due to enhanced parasympathetic influences on the heart. These results are consistent with those of previous cross-sectional studies (44,58,68,81). Other investigators, however, have found evidence of enhanced cardiac vagal tone at rest for high-fit subjects relative to less fit ones (5,15,17,59,74,86,90). The mixed findings may be due to genetically determined differences in the constitutions of the samples examined in the different studies. Twin studies and studies of relatives indicate that between 30% and 40% of maximal aerobic power and between 25% and 31% of resting RSA are heritable (12,14,91). Boutcher et al. (17) also found evidence that is consistent with a genetic basis for resting RSA. They found that untrained men with low resting heart rates did not differ from trained men on resting RSA or HP. It is possible that the significant fitness-related differences in resting RSA observed in some studies were due to chance differences in the samples of individuals examined. Therefore, the groups in these studies may have been composed of individuals who differed significantly on genetically determined factors affecting aerobic capacity and cardiac vagal tone. Additionally, it is also possible that a self-selection bias was operating in those investigations such that subjects who had higher established levels of cardiac vagal tone may have been more likely to have engaged in exercise than those who had lower vagal tone. Furthermore, the results of training studies, which are not subject to the influences of constitutional factors and selection bias, are also mixed. A number of investigators have shown that resting cardiac vagal tone is enhanced following a brief aerobic exercise training program (2,32,82,83,85), whereas other investigators have reported no posttraining improvements (19,29,37,68). Therefore, the role of cardiac vagal tone in maintaining resting bradycardia in trained individuals remains equivocal. Alternatively, the relative bradycardia observed among trained individuals at rest may be due to reduced sympathetic influences on the heart (37,90) and/or a lower intrinsic heart rate (58,64,96).
Importantly, a group difference in chronotropic cardiac arousal was observed during stress and recovery in the present study. Higher aerobic fitness was associated with a moderation of cardiac arousal during stress and recovery as the trained men maintained longer HP during both phases of the experiment than the untrained. However, the groups did not differ on phasic changes in HP during the psychological challenges or recovery. As such, the groups exhibited similar phasic HP responses, but their phasic responses were superimposed on different HP levels. These findings replicate those of many previous investigations which have also shown that higher aerobic fitness or posttraining improvements in fitness were associated with lower heart rates during psychological stress and/or recovery but were not associated with an alteration in phasic cardiac responses (9–11,16–18,21,25,30,49,62,74,76,87,88,92).
Of central interest in this study was the question of whether higher aerobic fitness is associated with enhanced vagal moderation of chronotropic cardiac arousal during psychological stress and recovery. Lower chronotropic cardiac arousal was observed during stress and recovery for the trained men, but it was not associated with higher cardiac vagal tone, as the trained and untrained men did not differ on RSA. This finding is not surprising in light of the absence of a group difference in resting RSA. Furthermore, the trained and untrained men in this study did not differ on phasic change in RSA during stress and recovery. In general, O2max was not correlated with absolute levels or phasic changes in RSA during psychological stress or recovery for either group. The present results obtained for psychogenic stress extend the findings of Hatfield et al. (44), who found that trained and untrained healthy young men exhibited similar cardiac vagal responses to ergogenic stress as well as a similar pattern of vagal recovery. Additionally, the present results are consistent with the findings from previous investigations that also examined young men for both RSA levels (17) and phasic changes in RSA (17,29,74) during psychological stress and recovery. Contrary to the negative findings in the literature and the expectations following from the model presented herein, however, Boutcher et al. (17) did find that trained men exhibited a greater phasic decrease in RSA than untrained controls in the first half of a Stroop test. This finding may be explained by the LIV. Accordingly, the trained men in Boutcher et al.’s (17) study had higher resting RSA than untrained controls. Therefore, in accordance with the LIV, the trained men would have been expected to exhibit a greater decrease in RSA during stress than the untrained. In the absence of a test to exclude the effects of the LIV, the results of Boutcher et al. (17) remain equivocal.
In contrast to the findings for young men, Nurhayati and Boutcher (74) found that aerobically trained postmenopausal women did exhibit higher RSA levels during and after a Stroop test than their untrained counterparts. Two implications are suggested by this finding. First, the failure to observe fitness-related differences in cardiac vagal tone during stress for young men may be due to the fact that young individuals, regardless of their aerobic fitness levels, have healthy, robust parasympathetic nervous systems. Second, aerobic exercise may not have an impact on parasympathetic regulation of the heart during stress until later in life when normal aging, in the absence of habitual aerobic exercise involvement, has produced decrements in parasympathetic function as cardiac vagal tone is known to decline with age (22,48). In one study, the decline was estimated to be approximately 10% per decade (52). In light of these latter findings, the results of Nurhayati and Boutcher (74) suggest that exercise-related modifications of cardiac vagal tone during stress may be confined to older populations.
In studies such as the present one, it is common for trained and untrained subjects to differ at baseline on HP and other cardiovascular parameters. When a group difference on baseline values is observed for a particular variable, the group comparison on reactivity scores for that measure is potentially compromised by the LIV. There is some recognition that the statistical treatment of LIV effects has been problematic in many studies of aerobic fitness and cardiovascular reactivity (28,51,100). One concern is that the employment of ANCOVA or regression techniques to remove LIV effects from reactivity scores has typically been based on the presence of fitness group differences at baseline rather than on evidence of a relationship between response magnitudes and baseline values (100). It cannot be automatically assumed that LIV effects will be present when groups are different at baseline. The likelihood of observing LIV effects for HP will depend on whether the functional origin of baseline differences is neural or nonneural (8). For example, if fitness group differences in baseline HP are due to differences in intrinsic heart rate (nonneural), and there is evidence to indicate that they may be (58,64,96), then the likelihood of observing LIV effects will be reduced. This is because the groups would likely have similar neural response ranges or functions but the neural regulation of the heart for each group would be superimposed on different basal heart rate levels. Hence, groups could have different baseline HP but, because their neural response functions are similar, their HP responses would be independent of initial HP levels. As it usually is not known whether group differences in baseline values are due to neural or nonneural factors, it is important to test for the effects of the LIV before adjusting reactivity scores for differences in baseline values. In the present study, the groups were different on resting HP, but phasic HP responses were not dependent on baseline values. Hence, the use of ANCOVA would have been inappropriate in this study. ANCOVA or regression methods may have been inappropriately applied in a number of previous studies in which a priori tests for LIV effects were not made (10,11,26,50,51,62,65,76,84,92). In contrast, other investigators have ignored initial group differences in the analysis of their cardiac and vagal tone reactivity data (17,21,53). In these studies, investigators would have failed to appropriately adjust reactivity scores if the LIV was operative. The failure to test for LIV effects and to make appropriate adjustments, if needed, casts doubt on the conclusions of the above cited studies.
Lastly, ratings of perceived stress were obtained in this study via a minimally obtrusive instrument (i.e., VAS) before, during, and after psychological challenge. Trained and untrained men were not different on ratings of perceived stress during the experiment, indicating that high aerobic fitness, as compared with lower fitness, did not confer any benefits in terms of reducing subjective stress during rest, psychological challenge, or recovery. Therefore, the results of this study do not support the proposition that trained individuals experience less subjective stress than untrained ones when exposed to a laboratory setting and psychological challenge.
In summary, 20 healthy young men who differed substantially on aerobic fitness (trained: 67.0 mL·kg−1·min−1 vs untrained: 45.4) and exercise history were examined for differences in HP, RSA, and subjective stress during rest, three contiguous psychological challenges, and subsequent recovery. Although reporting similar levels of subjective stress, trained men exhibited bradycardia throughout the experiment relative to the untrained men, but the group difference in HP level was not associated with a difference in cardiac vagal tone. Furthermore, although the groups differed on HP level, they did not differ on phasic HP responses to any of the psychological challenges or recovery, nor did they differ on RSA reactivity or recovery.
1 To reduce the variability of RSA values and, thereby, improve statistical power, RSA levels were also averaged across the three cognitive challenges and the three 1-min recovery epochs, respectively, and analyzed in separate one-tailed t-tests for independent means. RSA change scores were analyzed similarly. These analyses confirmed that the groups did not differ on RSA levels or change scores during stress or recovery (−1.29 ≥ all t ’s(18) ≤ 0.40, P > 0.05).
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