Background and ObjectivesIncreased central arterial stiffness is an emerging risk factor for cardiovascular disease. Acute aerobic exercise reduces arterial stiffness, while acute resistance exercise may increase arterial stiffness, but this is not a universal finding. We tested whether an acute resistance exercise program was associated with an increase in arterial stiffness in healthy young men.Subjects and MethodsThirteen healthy subjects were studied under parallel experimental conditions on 2 separate days. The order of experiments was randomized between resistance exercise (8 resistance exercises at 60% of 1 repeated maximal) and sham control (seated rest in the exercise room). Carotid-femoral pulse wave velocity (PWV) and aortic augmentation index as indices of aortic stiffness were measured using applanation tonometry. Measurements were made at baseline before treatments, 20 minutes, and 40 minutes after treatments (resistance exercise and sham control).ResultsThere was no difference in resting heart rate or in arterial stiffness between the two experimental conditions at baseline. At 20 minutes after resistance exercise, heart rate, carotid-femoral PWV and augmentation index@75(%) were significantly increased in the resistance exercise group compared with the sham control (p<0.05). Brachial blood pressure, central blood pressure and pulse pressure were not significantly increased after resistance exercise.ConclusionAn acute resistance exercise program can increase arterial stiffness in young healthy men. Further studies are needed to clarify the effects of long-term resistance training on arterial stiffness.

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We examined changes in central blood pressure (BP) following resistance exercise training (RET) in men and women with prehypertension and never-treated hypertension. Both Windkessel theory and wave theory were used to provide a comprehensive examination of hemodynamic modulation with RET. Twenty-one participants (age 61±1 years, n=6 male; average systolic blood pressure (SBP)/diastolic blood pressure (DBP)=138/84 mm Hg) were randomized to either 12 weeks of RET (n=11) or an inactive control group. Central BP and augmentation index (AIx) were derived from radial pressure waveforms using tonometry and a generalized transfer function. A novel reservoir-wave separation technique was used to derive excess wave pressure (related to forward and backward traveling waves) and reservoir pressure (related to the capacitance/Windkessel properties of the arterial tree). Wave separation using traditional impedance analysis and aortic flow triangulation was also applied to derive forward wave pressure (Pf) and backward wave pressure (Pb). There was a group-by-time interaction (P<0.05) for central BP as there was a significant ~6 mm Hg reduction in SBP and ~7 mm Hg reduction in DBP following RET with no change in the control condition. There were also group-by-time interactions (P<0.05) for Pf, excess wave pressure and reservoir pressure attributable to reductions in these parameters in the RET group concomitant with slight increases in the control group. There was no change in AIx or Pb (P>0.05). RET may reduce central BP in older adults with hypertension and prehypertension by lowering Pf and reservoir pressure without affecting pressure from wave reflections.

Although studies have shown an inverse association between cardiorespiratory fitness (CRF) and C-reactive protein (CRP) levels, the underlying mechanisms are not fully understood. There is emerging evidence that autonomic nervous system function is related to CRP levels. Because high CRF is related to improved autonomic function, we hypothesized that the association between high CRF and low CRP levels would be affected by autonomic nervous system function. Cross-sectional analyses were conducted on 2,456 asymptomatic men who participated in a medical screening program. Fasting blood samples for cardiovascular disease risk factors were analyzed, and CRF was measured by maximal exercise treadmill test with expired gas analysis. We used an index of cardiac autonomic imbalance defined as the ratio of resting heart rate to 1 min of heart rate recovery after exercise (RHR/HRR). CRF was significantly correlated with CRP (r = -0.16, P < 0.05), and RHR/HRR (r = -0.48, P < 0.05), while RHR/HRR was significantly correlated with CRP (r = 0.25, P < 0.05). In multivariable linear regression models that adjusted for age, body mass index, smoking, disease status, medications, lipid profiles, glucose, and systolic blood pressure, CRF was inversely associated with CRP (β = -0.09, P < 0.05). However, this relationship was no longer significant after adjusting for RHR/HRR in a multivariable linear regression model (β = -0.03, P = 0.29). These results suggest that autonomic nervous system function significantly affects the relationship between CRF and inflammation in middle-aged men. Thus, physical activity or exercise training may favorably affect the cholinergic antiinflammatory pathway, but additional research is needed to confirm this finding.

We tested the hypothesis that acute inflammation may cause arterial stiffening in older adults. We further explored if high cardiorespiratory fitness may partially prevent the unfavorable effect of arterial stiffening produced by acute systemic inflammation in older adults. Using a randomized double-blind sham placebo-controlled design, forty healthy older adults were assigned to receive either an influenza vaccine or a sham vaccine. C-reactive protein and interleukin 6 (IL-6) were measured as markers of inflammation. Carotid-femoral pulse wave velocity (PWV) and augmentation index (AIX) as indices of arterial stiffness and wave reflection were assessed at baseline and 24 and 48 h after each vaccination. When compared with sham placebo, the influenza vaccination caused a significant increase in CRP (p < 0.05) and IL-6 (p < 0.05). Carotid-femoral PWV, but not AIX was significantly increased after influenza vaccination (p < 0.05), but not sham vaccination. The high cardiorespiratory fitness group had an attenuated increase in PWV as compared to the low cardiorespiratory fitness group after acute inflammation (p < 0.05). These findings show that acute inflammation may cause significant increases in arterial stiffness in older adults, but these increases were attenuated in the high cardiorespiratory fitness group as compared to the low cardiorespiratory fitness group.