African Americans have a greater prevalence of hypertension and diabetes compared with white Americans, and both autonomic dysregulation and inflammation have been implicated in the etiology of these disease states. The purpose of this study was to examine the cardiac autonomic and systemic inflammatory response to resistance training in young African-American and white men. Linear (time and frequency domain) and nonlinear (sample entropy) heart rate variability, baroreflex sensitivity, tonic and reflex vagal activity, and postexercise heart rate recovery were used to assess cardiac vagal modulation. C-reactive protein (CRP) and white blood cell count were used as inflammatory markers. Twenty two white and 19 African-American men completed 6 wk of resistance training followed by 4 wk of exercise detraining (Post 2). Sample entropy, tonic and reflex vagal activity, and heart rate recovery were increased in white and African-American men following resistance training (P < 0.05). Following detraining (Post 2), sample entropy, tonic and reflex vagal activity, and heart rate recovery returned to baseline values in white men but remained above baseline in African-American men. While there were no changes in white blood cell count or CRP in white men, these inflammatory markers decreased in African-American men following resistance training, with reductions being maintained following detraining (P < 0.05). In conclusion, resistance training improves cardiac autonomic function and reduces inflammation in African-American men, and these adaptations remained after the cessation of training. Resistance training may be an important lifestyle modification for improving cardiac autonomic health and reducing inflammation in young African-American men.
- heart rate variability
- heart rate recovery
african americans have a greater prevalence of hypertension and diabetes compared with their white American counterparts, and racial differences in the onset of these diseases may manifest as early as within the first decade of life (7, 9, 13). Thus the burden of cardiovascular/metabolic disease-related comorbidities, such as fatal and nonfatal stroke, sudden cardiac death, and end-organ damage (i.e., left ventricular hypertrophy, carotid hypertrophy), is greater in African Americans (12, 21, 33, 56). African Americans also have higher levels of inflammatory markers compared with white Americans, and this too may contribute to the greater cardiovascular disease and metabolic burden in this population (30). Elevated C-reactive protein (CRP), a marker of systemic low-grade inflammation, is associated with an increased risk of stroke (41), hypertension (44), end-organ damage (63), and diabetes (50) and predicts cardiovascular disease independent of traditional risk factors (40).
The cholinergic anti-inflammatory pathway (51) fosters communication between the immune and autonomic nervous systems whereby vagal stimulation by inflammatory cytokines produces reflexive anti-inflammatory effects. Acetylcholine released from the vagus binds to nicotinic receptors on macrophages, halting proinflammatory cytokine production (51). Conversely, reduced vagal tone directly contributes to a heightened inflammatory state and end-organ damage (57) and is associated with the development of hypertension, stroke, and diabetes (1, 26, 31, 43). Interventions that increase cardiac vagal modulation and reduce inflammation may therefore have significant clinical utility for preventing future cardiovascular disease, particularly among African Americans.
Both aerobic/endurance exercise training and resistance exercise training are currently recommended for health promotion and primary/secondary disease prevention (15, 55). According to a recent meta-analysis, aerobic/endurance exercise training may not significantly reduce CRP (27). The effect of resistance training on inflammation is far less studied and has yet to be explored in young African-American men. Resistance exercise training can improve measures of vagal modulation in young white men (17, 19). Interestingly, African Americans have augmented autonomic responses (4, 11, 54) and possibly augmented inflammatory responses (38) to various acute physiological and psychological perturbations. Thus it is possible that there may be racial differences in the cardiac autonomic and inflammatory response to repeated resistance exercise bouts (i.e., resistance training).
The purpose of this investigation was to assess the effect of resistance training on noninvasive indexes of cardiac vagal modulation and systemic low-grade inflammation (white blood cell count and CRP) in young healthy African-American compared with white men. We hypothesized that resistance training would increase vagal modulation, and this change would be associated with concomitant reductions in inflammatory markers in both white and African-American men, that is, the increase in vagal modulation stemming from resistance training may be anti-inflammatory. Several different measures of heart rate dynamics at rest and following maximal exercise were determined and inferences regarding cardiac autonomic activity made in an attempt to provide a comprehensive examination of cardiac vagal modulation with race and exercise training.
Forty-four young healthy men (22 African American and 22 white) volunteered for this study. All subjects were free of cardiovascular, metabolic, or respiratory disease, and none smoked. Subjects did not take medication of any kind, including over-the-counter pain/anti-inflammatory medication. Subjects were self-defined as African American if reporting that both parents were of African descent. All subjects were recruited from the local university student population. All subjects gave written consent. This study was approved by the Institutional Review Board of the University of Illinois at Urbana-Champaign.
Measurements were made in each subject at baseline (Pre 1), following a 6-wk resistance training intervention (Post 1), and following a 4-wk detraining period (Post 2). We have previously shown this length of training and detraining sufficient to see transient increases in cardiac autonomic modulation (i.e., heart rate recovery and heart rate complexity) with subsequent return to baseline in a slightly older white male population (17). During the resistance training component of the study, subjects were instructed to refrain from any structured aerobic/endurance exercise. Subjects were then asked to resume their previous lifestyle and refrain from all forms of structured exercise for the detraining component of the study. At baseline, subjects completed a blood test after an overnight fast (minimum 12 h fasting). Immediately following the blood test, subjects underwent body composition assessment. During a second visit, conducted 24–48 h after the blood draw, subjects underwent resting electrocardiogram (ECG) measurement, blood pressure measurement, maximal aerobic exercise testing, and one-repetition-maximum bench press testing (in that order). All within-subject sessions were conducted at the same time of day to reduce possible diurnal variations in physiological signals. Subjects were tested in the postprandial state (∼3 h) and asked to refrain from caffeine and alcohol ingestion for 24 h before testing.
To assess the stability of our cardiac autonomic measures over time, a subset of subjects (n = 25) volunteered to complete a time-control period before initiation of the resistance exercise training. In this subset, all autonomic measures were made at baseline and following 4 wk of time control. Subjects were instructed to maintain their current lifestyle during this time and asked not to make any diet and/or exercise modifications. For all measures, baseline values obtained on the two separate days were not statistically different according to paired-sample t-tests, and intraclass correlation coefficients (ICC) were high and consistent with previous reports (42).
Body composition was determined using whole body air displacement plethysmography (Bod Pod, Life Measurement, Concord, CA). This technique has been shown to be valid in both African-American and white populations (5). Height was measured using a stadiometer (to the nearest 0.5 cm). Weight was measured using an electronic scale that was calibrated before each measurement (Bod Pod; Life Measurement). Body mass index was calculated as weight (kg) divided by height (m) squared.
Brachial artery blood pressure assessment.
Blood pressure was measured at baseline following 15 min of quiet supine rest and used for screening purposes to ensure all participants were not hypertensive. Resting systolic blood pressure and diastolic blood pressure were measured using an automated oscillometric cuff. All brachial blood pressure measurements were made in duplicate. The average of the two values was recorded and used for subsequent analysis. If values were not within 5 mmHg, a third measure was taken, and the two closest values were averaged (34).
ECG signal acquisition.
Following the 15-min quiet rest period, heart rate was recorded continuously for 15 min using ECG with a single lead CM5 configuration with the subjects still in the supine position in a dimly lit, climate-controlled room (Biopac Systems, Santa Barbara, CA). Lead site preparation and placement were standardized (10). Breathing was paced with a metronome at 12 breaths/min. The ECG was collected online at a sampling rate of 1,000 Hz, in real time, and stored on a computer. All data were stored and analyzed off-line. Subsequent off-line signal processing was performed using commercially available software (WinCPRS, Turku, Finland). Data were visually and automatically inspected for ectopic beats (premature, supraventricular, ventricular) and interpolated in accordance with previous suggestions to provide a continuous data stream (54). An R-R interval (RRI) time event series was generated from successive heart rate peaks. The time series was detrended and resampled at 5 Hz. A stable 220- to 260-s epoch was used for all subsequent analysis.
Heart rate variability in the time domain was assessed using the following dispersion statistics. The square root of the mean of the sum of the squares of differences between adjacent RRI was calculated as the square root of the mean of terms Sqr [RRI(i + 1) − RRI(i)]. The number of pairs of adjacent normal-to-normal (NN) RRI differing by >50 ms divided by the total number of all NN intervals was calculated as the percentage of those NN intervals where Abs [RRI(i + 1) − RRI(i)] > 50 ms. The weighted mean of RRI was calculated as the mean of RRI weighted by beat lengths.
Heart rate variability was assessed in the frequency domain using power spectral analysis as previously described (17). The power was calculated by measuring the area under the peak of the power spectra density curve and corresponding bandwidths. High-frequency oscillations of heart rate variability (0.15–0.40 Hz), as determined by spectral decomposition, are thought to be mediated almost entirely by the vagus nerve and thus represent tonic cardiac vagal nervous modulation (48a). The low-frequency region (0.04–0.15 Hz) is mediated by both the sympathetic and parasympathetic arms of the autonomic nervous system (48a). The power spectra were calculated in both absolute and normalized units to represent the relative value of each power component as a proportion of the total power (48a). All data acquisition and postacquisition analyses were carried out in accordance with standards put forth by the Task Force of the European Society of Cardiology and North American Society of Pacing and Electrophysiology (48a). All analyses were carried out using WinCPRS software. ICC attained in our laboratory have previously shown to be high (20), stable over time (17), and consistent with previous findings for short-term measures of heart rate variability in the frequency domain (42).
Sample entropy was used to quantify the nonlinear complexity of the RRI time event series and was calculated as originally described by Richman and Moorman (39). Sample entropy determines the probability of finding specific patterns in a short time series. A highly regular signal such as a sine wave will have a value close to zero. In contrast, a highly irregular signal will have a value close to two. The embedding dimension m (length of sequences to be compared) may range from 2 to 10 while the filter parameter r (tolerance for accepting matches) may range from 0.10 to 0.50. In the present investigation, m was fixed at two while the filter parameter r was set at 20% of the standard deviation of the time series, based on previous criteria (28).
We verified the stationarity of the signal at each time point. Stationarity refers to a signal's deviation from baseline. To quantify this, the heart rate signal was divided into twelve 20-data point (RRI) subepochs. The mean of each RRI subepoch was calculated. Stationarity was calculated as the ratio of the SD of the subepoch means to the SD of the whole time series (28). A stationarity value near zero means the signal is stationary, and an increased value is reflective of increased nonstationarity.
Cardiovagal baroreflex sensitivity.
With the subject still in the supine position, finger plethysmography was used to capture beat-to-beat blood pressure oscillations for a 5-min epoch (Finometer). The spontaneous baroreflex response was determined from the instantaneous and reflexive changes in interbeat intervals and systolic pressure (16). Activation of arterial baroreceptors via alterations in systemic arterial pressure results in reflexive changes in heart rate. A decrease in systemic arterial pressure initiates reflexive withdrawal of cardiac vagal tone, which increases heart rate, whereas an increase in pressure yields reflexive increases in cardiac vagal tone that decrease heart rate. Baroreflex sensitivity (BRS) thus represents reflex cardiac vagal nervous modulation. Any episodes of three or more consecutive heart beats in which the interbeat intervals and the corresponding systolic pressure changed in the same direction (either up or down) were recorded. The slope of the regression line for each episode was calculated (WinCPRS). Up and down sequences were separated to provide indexes of BRS during hypertensive (BRSup-up) and hypotensive (BRSdown-down) changes in systolic pressure, respectively.
A composite index of cardiac tonic and reflex vagal activity was calculated from aforementioned variables as (high-frequency power of heart rate variability/low-frequency power of heart rate variability) × BRS (52). This was done separately for hypertensive (up-up) and hypotensive (down-down) sequences.
Maximal oxygen uptake and heart rate recovery.
Peak oxygen consumption was assessed using a graded cycle ergometry protocol, as previously described (19, 21). Heart rate recovery was calculated as the difference between maximum heart rate during the test and heart rate 1 min after cessation of exercise. Postexercise recovery of heart rate is mediated by both branches of the autonomic nervous system. The initial decrease in heart rate is mediated via prompt vagal reactivation with later reductions due to both continued vagal reactivation and sympathetic withdrawal (35). Although high-frequency power of heart rate variability more aptly reflects phasic fluctuations in vagal efferent activity (i.e., tonic vagal modulation), heart rate recovery is an index of mean cholinergic signaling at the level of the sinoatrial node (i.e., vagal tone) (3, 8). The recovery protocol consisted of 2 min of light cycling (50 revolutions/min and 0 watts) followed by 1 min of quiet sitting on the cycle. The ICC attained in our laboratory have previously shown to be high and stable over time (17, 18).
Fasting blood chemistries.
Fasting glucose was assessed by an oxygen rate method using a Beckman Coulter oxygen electrode (Beckman Coulter, Villapointe, France). Total cholesterol, high-density lipoprotein cholesterol, and triglycerides were measured using standard enzymatic techniques. Low-density lipoprotein cholesterol was calculated using the Friedewald formula. White blood cell count, hematocrit, and hemoglobin were measured using a quantitative automated hematology analyzer (Sysmex XE-2100; Sysmex, Kobe, Japan). Circulating levels of CRP were measured by enzyme-linked immunosorbent assay using a commercially available kit (Diagnostic Automation, Calabasas, CA). The intra-assay and interassay coefficient of variation is 2.3–7.5% and 2.5–4.1%, respectively. Samples with absorbance values exceeding the standard curve were rerun on a separate plate following appropriate dilution. The intraclass correlation between two CRP measurements during the same study visit for all subjects was 0.99. The ICC in a subset of subjects (n = 25; 10 African American, 15 white) collected on two separate days over the time control was 0.92. According to paired-samples t-test, CRP values were not significantly different following the time control (group as a whole: 3.31 vs. 3.35 mg/l, P > 0.05). According to paired-samples t-test, in the African-American men only, there was no difference in CRP following the time control (6.80 vs. 6.52 mg/l, P > 0.05).
One-repetition-maximum bench press.
One repetition maximum (defined as the maximum amount of weight lifted with proper form through a full range of motion for a single repetition) for the bench press was ascertained as previously described (17). The one-repetition-maximum value was then divided by lean body mass to express muscular strength relative to lean mass. The relative one-repetition-maximum value was taken as a measure of upper body strength and used to gauge effectiveness of the resistance training intervention (i.e., documentation of a training effect).
Training sessions were carried out 3 days/wk (∼60 min/session). All sessions were supervised by personal trainers/strength and conditioning specialists. The resistance training protocol used was a two-way body part split (muscles of the legs, back, and biceps were stressed one day; muscles of the chest, shoulders, and triceps were stressed on a separate day, and this was repeated in an alternating fashion), and each session consisted of five exercises. Sessions were rotated in the order shown in Table 1. For week 1, the first three sessions were completed. Week 2 began with session 4, proceeding then to sessions 1 and 2. Week 3 began with session 3, proceeding to session 4 and then 1, and so on. Exercises were selected to stress all major muscle groups of the upper and lower body using both multijoint and single-joint exercises. Each session began with a brief warm-up consisting of 1 set of 15 repetitions of the first exercise to be performed during that session using a submaximal load. Three sets of each exercise were performed with 1–2 min of rest between each set. During the initial 2 wk, load was selected to ensure fatigue was reached between 12 and 15 repetitions. During the final 4 wk, load was adjusted to ensure fatigue was reached between 8 and 12 repetitions. As strength increased, load was progressively increased to ensure fatigue occurred within the desired repetition schema with proper form.
A two by three ANOVA with repeated measures was used to compare variables in both groups over three time points [(African American × white) × (Pre 1 × Post 1 × Post 2)]. When a significant main effect was detected at a significance level of P < 0.05, t-tests were used for post hoc comparisons. Adjustment for multiple comparisons was made with Bonferonni's correction. Statistical significance was set at P < 0.01 for all pairwise comparisons. Total power, absolute low-frequency power, absolute high-frequency power, low-frequency-to-high-frequency ratio, tonic and reflexive vagal activity, and CRP were not normally distributed (determined from Shapiro-Wilk and Kolmogorov-Smirnov tests as well as analysis of histograms and Q-Q plots). Therefore, these values were log transformed to meet assumptions for parametric statistical analysis. Given the lack of clear clinical utility of log-transformed CRP, we also present absolute CRP values. Pearson's correlation coefficients were calculated to examine the association between main outcome variables of interest. All results are presented as means ± SE. Data analyses were carried out using the Statistical Package for the Social Sciences (version 12.0.1; SPSS, Chicago, IL).
Twenty-two white and 19 African-American subjects completed the study. Two African-American subjects dropped out during training. One African-American subject was not included in final data analyses because of poor training compliance. Compliance was 100% in all remaining subjects. If subjects missed a session, the session was rescheduled for another day that same week to ensure that three training sessions were completed per week. One white subject and one African-American subject were not included in data analyses because of arrhythmia. Therefore, all analysis was completed on 18 African-American and 21 white participants.
White subjects were slightly older than African-American subjects (P < 0.05, Table 2). African-American and white subjects had similar body mass index, body fat, systolic and diastolic blood pressure, blood lipids, and fasting glucose.
There was no change in body fat, maximal oxygen consumption, hemoglobin, or hematocrit following resistance training and detraining (Table 3). There was a time effect for body weight. Although there was no change in body weight in the white subjects, there was a slight increase in body weight following both training and detraining in African-American subjects (P < 0.05, Table 3). There was a time effect for relative one-repetition-maximum bench press, with both groups increasing relative one-repetition maximum following training (P < 0.05, Table 3).
There was no significant change in BRS (up-up) or (down-down) or any time/frequency domain measure of heart rate variability with training (Tables 4 and 5). There was an increase in ln tonic and reflexive vagal activity(up-up) following training in both groups (P < 0.05, Table 5). Following detraining (Post 2) ln tonic and reflexive vagal activity(up-up) returned to baseline values in the white group but remained above baseline in the African-American group. There was no change in ln tonic and reflexive vagal activity(down-down) in either group (Table 5, P > 0.05). There was an increase in heart rate recovery following training in both groups (P < 0.05, Table 4). Following detraining (Post 2), heart rate recovery returned to baseline values in the white group but remained above baseline in the African-American group. There was an increase in sample entropy following training in both groups (P < 0.05, Table 5). Following detraining (Post 2), sample entropy returned to baseline values in the white group but remained above baseline in the African-American group.
Interaction for CRP and logCRP were detected (Table 3, P < 0.05). CRP was significantly higher in African-American men at baseline compared with white men (P < 0.05). While there was no change in CRP in white men following training, CRP was reduced following training in African-American men. Following detraining (Post 2), CRP in the African-American men remained significantly lower than baseline (P < 0.05). An interaction for white blood cell count was detected (Table 3, P < 0.05). Although there was no change in white blood cell count in white men following training, white blood cell count was reduced following training in African-American men. Following detraining (Post 2), white blood cell count remained significantly lower than baseline in the African-American men (P < 0.05).
When examining the group as a whole, a negative correlation was found between change in heart rate recovery and change in white blood cell count following resistance training (r = −0.36, P < 0.05). A negative correlation was found between change in ln tonic and reflexive vagal activity and change in white blood cell count following detraining (−0.28, P < 0.05). A negative correlation was also found between change in ln tonic and reflexive vagal activity and logCRP following resistance training (−0.32, P < 0.05) and change in ln tonic and reflexive vagal activity and logCRP following detraining (−0.45, P < 0.05). There were no significant correlations between change in sample entropy and inflammatory markers.
The novel finding of this study was that short-term resistance training had no effect on CRP or white blood cell count in white men, although it significantly reduced these inflammatory markers in African-American men. There were no changes in cardiorespiratory fitness and/or body fatness, suggesting that changes in inflammation were not secondary to these factors. Short-term resistance exercise training increased postexercise heart rate recovery, nonlinear heart rate complexity, and tonic and reflexive vagal activity similarly in white and African-American men, suggesting comparable improvements in tonic and reflex cardiac vagal modulation between races. However, improvements in cardiac vagal modulation were sustained following 4 wk of detraining in young African-American men, whereas they returned to pretraining values in young white men. Thus African-American men may experience an additive benefit from resistance training by maintaining cardiac autonomic and immune adaptations for a longer period of time.
The fact that we noted no change in CRP in young white men with resistance exercise training may be related to their initial low inflammatory state. Previous research has found that exercise training has no effect on CRP levels in men with values <3 mg/l (29). At baseline, CRP values were significantly higher in African-American men. It has previously been reported that ∼40% of African-American men have CRP values >3.0 mg/l (30). No study has yet to examine the role of exercise training in modulating CRP in young African Americans. We noted an ∼60% reduction in CRP in young African-American men following resistance training. This is comparable to the 58% reduction in CRP reported following the combination of aerobic and resistance exercise training in healthy older men (53). Thus the reduction in CRP in African-American men may be a function of their initially higher starting values. Resistance exercise training also reduced white blood cell count in African-American men while having no effect on this inflammatory marker in young white men. Elevated white blood cell count is associated with the incidence of hypertension (45) and mortality independent of traditional cardiovascular risk factors (46). Thus the incorporation of resistance exercise to lifestyle modifications may have significant clinical utility for reducing inflammation in young African-American men.
We noted no racial differences in baseline heart rate variability or BRS. Although some studies have shown reduced high-frequency power of heart rate variability and lower BRS in African Americans (58), this is not a universal finding, with several studies noting no racial differences (14, 30, 47). Since within single individual markers of tonic vs. reflex vagal activity could have variable predictive power, Vanoli et al. (52) have recently proposed a composite index derived from heart rate variability and BRS that gives equal weight to both the tonic and reflexive nature of cardiac autonomic physiology. Although no change was evident in heart rate variability or BRS when examined separately, and this is similar to previous reports (7, 18), we noted a significant increase in the tonic and reflex vagal activity index in white and African-American men following resistance training. Thus this measure may hold promise in revealing information about cardiac autonomic physiology that traditional measures cannot.
We have previously shown that nonlinear means of assessing heart rate variability provide additional information regarding cardiac autonomic fluctuations following exercise training that is neglected by conventional spectral methods (17). Both branches of the autonomic nervous system contribute to nonlinear oscillations in heart rate kinetics, and it has been proposed that complexity measures of heart rate variability are a reflection of a general sympathovagal balance (36), that is, a reduction in sample entropy is due to sympathoexcitation and/or vagal withdrawal and can occur despite no change in traditional heart rate variability parameters (53). There were no racial differences in heart rate complexity at baseline, and resistance training increased heart rate complexity similarly in both white and African-American men. This is consistent with recent findings noting improvements in sympathovagal balance following endurance exercise training in young African-American men (2).
Previous exercise interventions have noted that reductions in CRP are not related to improvement in cardiorespiratory fitness or reduction in body fat (29), and our results support this. A potential mechanism explaining reductions in inflammatory markers in African-American men following resistance training may be improved vagal activity. Numerous studies now acknowledge a relationship between inflammation and vagal modulation (25, 51, 59). Acetylcholine released from the vagus can act on nicotinic receptors located on macrophages, deactivating the macrophage and halting cytokine production (32). Inflammatory markers may also directly affect autonomic nervous activity via activation of the vagus and/or direct central activation of the brain (32). We noted an inverse association between inflammatory markers and measures of vagal modulation following resistance training. These findings support the possibility that improved vagal modulation in African-American men stemming from resistance training may have had an anti-inflammatory effect. Given that young white men initially presented with low CRP levels, a further improvement in vagal activity likely had negligible effects on inflammatory status in this cohort.
Effect of resistance exercise detraining.
Cardiac autonomic adaptations were maintained in African-American men following exercise detraining. The reason for these changes is unknown but may be related to racial differences in the response to acute stressors. African-American men have an augmented pressor response to various laboratory tests (such as cold pressor testing and psychological stress) as well as during static and submaximal dynamic exercise (4, 12, 61). The greater subacute pressor responses to resistance exercise may result in a more favorable resetting of the baroreflex (49), augmenting vagal outflow for a longer stay of time. Resetting with resistance training may occur with no change in BRS at the new operating point (49).
Reductions in inflammatory markers were also maintained following exercise detraining in the young African-American men. There was also an inverse association between tonic and reflex vagal activity following detraining and change in inflammatory markers. This would support the possibility that augmented tonic and reflex vagal activity following detraining may continue to exert anti-inflammatory effects.
Perspectives and Significance
Slow heart rate recovery after exercise is associated with impaired fibrinolysis, increased inflammation, increased target organ damage, and mortality (23–25). Loss of cardiac complexity has also been shown to be associated with inflammation and cardiovascular disease burden (37, 48). Lifestyle modification in the form of dietary alteration and exercise is currently recommended as a means of primary cardiovascular disease prevention in African Americans (12). A reduction in CRP of 1–2 μg/dl can significantly reduce risk of cardiovascular disease and associated mortality in individuals with high CRP levels (>3 μg/dl) (22). Given that resistance training increases various measures of vagal modulation and reduces inflammatory markers, and these adaptations are maintained even in the absence of continued training, this may have favorable cardiovascular health implications in African America men.
We did not follow our subjects for a greater length of time; thus, we do not know how long these favorable adaptations prevailed. The lack of information on the length of the cardiac autonomic return to baseline for African-American men is also a limitation of the study. We did not control for subject stress levels, and this may have influenced overall findings. Although it may be argued that, since all subjects were university students, stressors would be uniform (i.e., exams), there are known racial differences in stress responses. Whether racial differences are truly biological or merely reflect differences in environmental factors (i.e., diet, social support) and/or psychosocial factors (i.e., perceived stress, discrimination, coping ability, locus of control) is beyond the scope of this study. Finally, our study design cannot determine if change in autonomic function truly drive reductions in inflammation but only suggests an association between change in autonomic function and change in inflammation. Thus there may be other unforeseen and currently unrecognized factors that are responsible for both reductions in inflammation and improvements in autonomic function with exercise training.
In conclusion, resistance exercise training improves heart rate recovery, heart rate complexity, and tonic and reflex vagal activity in white and African-American men and reduces white blood cell count and CRP in African-American men. These adaptations remain after the cessation of training in African-American men. Resistance exercise training may be an important lifestyle modification for improving cardiac autonomic health and reducing inflammation in young African-American men.
This study was supported in by a predoctoral research grant from the American College of Sports Medicine and a predoctoral fellowship from the American Heart Association Greater Midwest Affiliate.
We thank all subjects for their time and effort.
The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked “advertisement” in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.
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