The purpose of this study was to examine heart rate recovery (HRR) and linear/nonlinear heart rate variability (HRV) before and after resistance training. Fourteen young men (25.0 ± 1.1 yr of age) completed a crossover design consisting of a 4-wk time-control period, 6 wk of resistance training (3 days/wk), and 4 wk of detraining. Linear HRV was spectrally decomposed using an autoregressive approach. Nonlinear dynamics of heart rate complexity included sample entropy (SampEn) and Lempel-Ziv entropy (LZEn). HRR was calculated from a graded maximal exercise test as maximal heart rate attained during the test minus heart rate at 1 min after exercise (HRR). There was no change in SampEn, LZEn, or HRR after the time-control portion of the study ( P > 0.05). SampEn ( P < 0.05), LZEn ( P < 0.05), and HRR ( P < 0.05) increased after resistance training and returned to pretraining values after detraining. There was no change in spectral measures of HRV at any time point ( P > 0.05). These findings suggest that resistance exercise training increases heart rate complexity and HRR after exercise but has no effect on spectral measures of HRV in young healthy men. These autonomic changes regress shortly after cessation of training.

Background: Carotid-femoral pulse wave velocity (cfPWV), the referent measure of aortic stiffness, is an established measure of vascular aging. In studies where cfPWV cannot be measured, alternative methods are needed to help promote research on vascular aging. This study examines the construct validity of a measure of PWV estimated from age and blood pressure (ePWV). The specific aims of the study are to: 1) explore the strength of association between ePWV, cfPWV, and other established measures of vascular aging; 2) examine the sensitivity and specificity of elevated ePWV (≥10m/s) in relation to elevated cfPWV (≥10m/s). Methods: We measured cfPWV in two-hundred and fifty-two adults (mean age 57±12 years, 48% female) and calculated each participant’s ePWV from their age and brachial blood pressure. Additional measures of vascular aging included: carotid intima-media thickness (cIMT); carotid stiffness measured as elastic modulus (cEp); and carotid augmentation index (cAIx). Results: The correlations between cfPWV and measures of vascular aging were: cEp (r = 0.36), cIMT (r = 0.49), and cAIx (r = 0.04). The correlations between ePWV and measures of vascular aging were: cEp (r = 0.45), cIMT (r = 0.60), and cAIx (r = 0.24). The correlation between ePWV and cfPWV was (r = 0.67). The sensitivity and specificity of elevated ePWV (≥ 10 m/s) for concomitantly identifying high cfPWV (≥ 10 m/s) were 85.4% and 73.0% respectively. Conclusion: ePWV is associated with established measures of vascular aging, such as carotid thickness, carotid stiffness and carotid augmentation index. ePWV may be a useful tool to help promote research on vascular aging.

The kinetics of parasympathetic reactivation after dynamic endurance exercise have been well elucidated. However, autonomic recovery of cardiac function after resistance exercise is not known. The purpose of this study was to assess cardiac autonomic modulations during recovery from acute resistance exercise versus acute endurance exercise. Electrocardiogram readings were collected before and 30 min after a single bout of endurance or resistance exercise in 14 male participants (aged 25.3+/-2.5 years). Heart rate (HR) variability was spectrally decomposed using an autoregressive approach. High frequency (HF) power was considered representative of vagal modulation. All values were expressed in both absolute and normalized units (normalized for change in total power). A mode-by-time interaction (P<0.05) was detected for HR, which remained elevated to a greater extent after resistance exercise. Total power was significantly reduced after resistance exercise (P<0.05) but not endurance exercise. An interaction (P<0.05) was also detected for both a change in absolute natural log function HF power and natural log function low frequency (LF) power (P<0.05), as both variables decreased more after resistance exercise. When normalized for changes in total power, interactions in LF and HF power were lost. The LF/HF ratio was significantly increased after both resistance and endurance exercise (P<0.05). Greater elevations in HR after acute resistance exercise versus acute endurance exercise may be related to greater reductions in cardiac parasympathetic tone.

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.

Increased aortic stiffness, assessed as carotid-femoral pulse wave velocity (cfPWV), contributes to cerebrovascular damage and is predictive of cerebrovascular events. We sought to examine the association between estimated pulse wave velocity (ePWV), a proxy of carotid-femoral pulse wave velocity, and stroke and its subtypes (ischemic and hemorrhagic) in a prospective cohort of 2666 men (aged mean 53.1, range 42–61 years) enrolled in the Kuopio Ischemic Heart Disease cohort study. During a median 28-year follow-up, 471 incident stroke (397 ischemic and 94 hemorrhagic) events occurred. After adjusting for several established and emerging risk factors including age and pulse pressure, comparing the p versus bottom quartiles of ePWV, there was an increased risk of stroke (hazard ratio [HR] 2.37, 95% Confidence Interval [CI]: 1.57–3.58), ischemic stroke (HR 2.23, 95% CI, 1.42–3.50), and hemorrhagic stroke (HR 3.57, 95% CI, 1.45–8.76). These findings demonstrate that ePWV is independently associated with the risk of stroke in middle-aged men.