Key points: Non‐alcoholic fatty liver disease, characterized in part by elevated liver triglycerides (i.e. hepatic steatosis), is a growing health problem. In this study, we found that hepatic steatosis is associated with robust hepatic sympathetic overactivity. Removal of hepatic sympathetic nerves reduced obesity‐induced hepatic steatosis. Liver sympathetic innervation modulated hepatic lipid acquisition pathways during obesity. Non‐alcoholic fatty liver disease (NAFLD) affects 1 in 3 Americans and is a significant risk factor for type II diabetes mellitus, insulin resistance and hepatic carcinoma. Characterized in part by excessive hepatic triglyceride accumulation (i.e. hepatic steatosis), the incidence of NAFLD is increasing – in line with the growing obesity epidemic. The role of the autonomic nervous system in NAFLD remains unclear. Here, we show that chronic hepatic sympathetic overactivity mediates hepatic steatosis. Direct multiunit recordings of hepatic sympathetic nerve activity were obtained in high fat diet and normal chow fed male C57BL/6J mice. To reduce hepatic sympathetic nerve activity we utilized two approaches including pharmacological ablation of the sympathetic nerves and phenol‐based hepatic sympathetic nerve denervation. Diet‐induced NAFLD was associated with a nearly doubled firing rate of the hepatic sympathetic nerves, which was largely due to an increase in efferent nerve traffic. Furthermore, established high fat diet‐induced hepatic steatosis was effectively reduced with pharmacological or phenol‐based removal of the hepatic sympathetic nerves, independent of changes in body weight, caloric intake or adiposity. Ablation of liver sympathetic nerves was also associated with improvements in liver triglyceride accumulation pathways including free fatty acid uptake and de novo lipogenesis. These findings highlight an unrecognized pathogenic link between liver sympathetic outflow and hepatic steatosis and suggest that manipulation of the liver sympathetic nerves may represent a novel therapeutic strategy for NAFLD.

New Findings: What is the central question of this study? The purpose was to determine whether there is a difference between African Americans and Caucasians in cutaneous microvascular function and whether this difference is attributable to elevated oxidative stress. What is the main finding and its importance? The main finding is that African Americans have an attenuated cutaneous vasodilatation during local heating relative to Caucasians that is restored with local infusion of the superoxide dismutase mimetic, tempol. This suggests that superoxide mediates microvascular dysfunction and might contribute to the greater prevalence of cardiovascular disease in this population. African Americans (AA) have elevated risk for cardiovascular disease relative to other populations. We hypothesized that the cutaneous hyperaemic response to local heating is reduced in young AA relative to Caucasian Americans (CA) and that this is attributable to elevated oxidative stress. As such, ascorbic acid (a global antioxidant) and tempol (a superoxide dismutase mimetic) would improve this response in AA. Microdialysis fibres received lactated Ringer solution (control), 10 mm ascorbic acid or 10 μm 4‐hydroxy‐2,2,6,6‐tetramethylpiperidine‐1‐oxyl (tempol) at a rate of 2.0 μl min⁻¹. Cutaneous vascular conductance (CVC) was calculated as the red blood cell flux divided by mean arterial pressure. Data were presented as a percentage of maximal CVC (%CVC_max) induced by 44°C heating plus sodium nitroprusside. Twenty‐four (12 AA, 12 CA) young (23 ± 4 years old) subjects participated. During 39°C heating, the %CVC_max was lower in AA at the control (CA, 65 ± 20% versus AA, 47 ± 15%; P < 0.05) and ascorbic acid sites (CA, 73 ± 14% versus AA: 49 ± 17%; P < 0.01). At the tempol site, there were no differences between groups. This was followed by infusion of 10 mm l‐NAME at all sites to assess the contribution of nitric oxide to vasodilatation during local heating. The contribution of nitric oxide was lower in AA relative to CA at 39°C; however, this was restored with tempol. These data suggest that: (i) cutaneous vasodilatation in response to local heating is blunted in AA relative to CA; and (ii) elevated superoxide generation attenuates nitric oxide‐mediated cutaneous vasodilatation in AA.

Purpose: This study investigated the effects of 12 weeks of moderate intensity elastic band exercise (EBE) on functional fitness and blood pressure parameters in the elderly. Methods: 27 healthy older adults were randomly assigned to an exercise group (n = 15, age: 75.1 ± 1.4 years) and a control group (n = 12, age: 72.3 ± 1.4 years). Participants performed EBE for 60 min, three times a week, over the course of three months. The EBE consisted of incremental resistance and aerobic exercises designed to improve whole body fitness. Functional fitness and resting cardiovascular parameters were assessed before and after the exercise training program. Results: Grip strength, sit and reach, and one-leg stance improved significantly in the exercise group, while no significant improvements were found in chair stand and timed up and go (p < 0.05). Cardiovascular parameters including systolic blood pressure, diastolic blood pressure, mean arterial pressure, and pulse pressure significantly decreased in the exercise group relative to the control group (p < 0.05). Conclusions: Findings of the present study suggest that safe, inexpensive, and easily accessible EBE program with circuit training components play a significant role in improving upper and lower body fitness, as well as cardiovascular fitness, in the elderly.

New Findings: What is the central question of this study? The main purpose of this investigation is to determine whether there is a difference in cerebral vasodilatory capacity in response to rebreathing‐induced hypercapnia between African Americans and Caucasian Americans. What is the main finding and its importance? College‐aged African Americans have reduced cerebral vasodilatory capacity during hypercapnia when compared with Caucasian counterparts, a finding that suggests cerebral vascular dysfunction in this population. These findings may contribute to the understanding of the greater prevalence of cerebral vascular disease in this population. African Americans (AAs) have increased risk for cardiovascular, cerebral vascular and metabolic disease, including hypertension, stroke, coronary artery disease, metabolic syndrome and type II diabetes, relative to Caucasian Americans (CAs). While it is accepted that endothelial function is impaired in AAs, less is known regarding their cerebral vasodilatory capacity in response to hypercapnia. We hypothesized that AAs have a reduction in the total range of change in cerebral blood flow velocity (CBFV) measured in the middle cerebral artery and an index of cerebral vascular conductance (CVCI) in response to changes in the partial pressure of end‐tidal carbon dioxide () during rebreathing‐induced hypercapnia when compared with CAs. Twenty‐one healthy, college‐aged AA (10 male) and 21 age‐ and sex‐matched CA (10 male) subjects participated in this study. A four‐parameter logistic regression was used for curve fitting the responses of CBFV and CVCI relative to changes in . The total ranges of change in CBFV (101 ± 18 versus 69 ± 23%; P < 0.001) and CVCI (83 ± 21 versus 58 ± 21%; P < 0.001) as well as the maximal increase in CBFV (205 ± 24 versus 169 ± 24%; P < 0.001) and CVCI (188 ± 30 versus 154 ± 19%; P < 0.001) were reduced during hypercapnia in AAs relative to CAs despite a similar increase in (change, 15 ± 3 versus 15 ± 3 mmHg; P = 0.65). In conclusion, these data indicate that AAs have attenuated cerebral vascular capacity to respond to hypercapnia when compared with CAs.