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We hypothesized a sweet potato intervention would prevent high-fat (HF) diet-induced aortic stiffness, which would be associated with decreased arterial oxidative stress and increased mitochondrial uncoupling. Young (8-week old) C57BL/6J mice were randomly divided into 4 groups: low fat (LF; 10% fat), HF (60% fat), low-fat sweet potato (LFSP; 10% fat containing 260.3 μg/kcal sweet potato), or high-fat sweet potato diet (HFSP; 60% fat containing 260.3 μg/kcal sweet potato) for 16 weeks. Compared with LF and LFSP, HF- and HFSP-fed mice had increased body mass and percent fat mass with lower percent lean mass (all, P < 0.05). Sweet potato intervention did not influence body composition (all, P > 0.05). Arterial stiffness, assessed by aortic pulse wave velocity and ex vivo mechanical testing of the elastin region elastic modulus (EEM) was greater in HF compared with LF and HFSP animals (all, P < 0.05). Advanced glycation end products and nitrotyrosine abundance were greater in aortic segments from HF mice compared with LF and HFSP animals (all, P < 0.05). Aortic elastin and uncoupling protein 2 expressions, however, were reduced in HF compared with LF and HFSP mice (all, P < 0.05). Aortic segments cultured with 2,4-dinitrophenol (DNP), a mitochondrial uncoupler, for 72 h reduced the EEM of HF arteries compared with nontreated HF segments (P < 0.05). DNP had no effect on the EEM of aortic segments from HFSP mice. In conclusion, sweet potato attenuates diet-induced aortic stiffness independent of body mass and composition, which is associated with a normalization of arterial oxidative stress possibly due to mitochondrial uncoupling.

Higher body mass index (BMI) is associated with greater cardiovascular disease (CVD) risk, in part due to aortic stiffening assessed by carotid-femoral pulse wave velocity (cfPWV). Importantly, greater cardiorespiratory fitness (CRF; VO) decreases CVD risk, and is associated with reductions in aortic stiffness. We tested the hypothesis that young adult overweight (OW, n=17) compared with healthy-weight (HW, n=17) men will have greater resting aortic stiffness, reduced CRF and an impaired post-exercise hemodynamic response. Resting cfPWV was greater in OW versus HW individuals (5.81 ± 0.13 vs 4.81 ± 0.12 m/sec, p<0.05). Relative CRF (VO; mL/kg/min) was lower in OW compared with HW individuals (49.4 ± 1.3 vs 57.6 ± 1.0 mL/kg/min, p<0.05), and was inversely related with cfPWV (p<0.05). However, CRF as absolute VO (L/min) was not different between groups and there was no relation between cfPWV and absolute VO (L/min), indicating reduced relative CRF in OW men is due to greater body mass. Following the maximal treadmill exercise test, cfPWV was greater in OW compared with HW subjects from rest to 60 minutes post-exercise (p<0.05). Compared with HW, OW individuals had higher systolic blood pressure (main effect, p<0.05) and diastolic blood pressure was selectively increased for up to 60 minutes following exercise (p<0.05). Overweight individuals had an attenuated post-exercise decrease in mean arterial pressure (p<0.05). Collectively, these results indicate that young, apparently healthy, OW men have greater resting aortic stiffening and an impaired post-exercise hemodynamic response.

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