Search

High salt consumption increases blood pressure (BP) and cardiovascular disease risk by altering autonomic function and increasing inflammation. However, it is unclear whether salt manipulation alters resting and exercising heart rate variability (HRV), a noninvasive measure of autonomic function, in healthy young adults. The purpose of this investigation was to determine whether short-term high-salt intake 1) alters HRV at rest, during exercise, or exercise recovery and 2) increases the circulating concentration of the inflammatory biomarker monocyte chemoattractant protein 1 (MCP-1). With the use of a randomized, placebo-controlled, crossover study, 20 participants (8 females; 24 ± 4 yr old, 110 ± 10/64 ± 8 mmHg) consumed salt (3,900 mg sodium) or placebo capsules for 10 days each separated by ≥2 wk. We assessed HRV during 10 min of baseline rest, 50 min of cycling (60% V̇o2peak), and recovery. We quantified HRV using the standard deviation of normal-to-normal RR intervals, the root mean square of successive differences (RMSSD), and additional time and frequency domain metrics of HRV. Plasma samples were collected to assess MCP-1 concentration. No main effect of high salt or condition × time interaction was observed for HRV metrics. However, acute exercise reduced HRV (e.g., RMSSD time: P < 0.001, condition: P = 0.877, interaction: P = 0.422). High salt elevated plasma MCP-1 (72.4 ± 12.5 vs. 78.14 ± 14.7 pg/mL; P = 0.010). Irrespective of condition, MCP-1 was moderately associated ( P values < 0.05) with systolic ( r = 0.32) and mean BP ( r = 0.33). Short-term high-salt consumption does not affect HRV; however, it increases circulating MCP-1, which may influence BP in young adults.

The importance of nitric oxide (NO) in regulating cerebral blood flow (CBF) remains unresolved, due in part to methodological approaches, which lack comprehensive assessment of both global and regional effects. Importantly, NO synthase (NOS) expression and activity appear greater in some anterior brain regions, suggesting region-specific NOS influence on CBF. We hypothesized that NO contributes to basal CBF in healthy adults, in a regionally distinct pattern that predominates in the anterior circulation. 14 healthy adults (7 females; 24±5 years) underwent two magnetic resonance imaging (MRI) study visits with saline (placebo) or the NOS inhibitor, L-NMMA, administered in a randomized, single-blind approach. 4D Flow MRI quantified total and regional macrovascular CBF, whereas arterial spin labeling (ASL) MRI quantified total and regional microvascular perfusion. L-NMMA (or volume-matched saline) was infused intravenously for 5 minutes prior to imaging. L-NMMA reduced CBF (L-NMMA: 722±100 vs. placebo: 771±121 mL/min, p = 0.01) with similar relative reductions (5–7%) in anterior and posterior cerebral circulations, due in part to reduced cross sectional area of 9 of 11 large cerebral arteries. Global microvascular perfusion (ASL) was reduced by L-NMMA (L-NMMA: 42±7 vs. placebo: 47±8 mL/100g/min, p = 0.02), with 7–11% reductions in both hemispheres of frontal, parietal, and temporal lobes, and in the left occipital lobe. We conclude NO contributes to macrovascular and microvascular regulation including larger artery resting diameter. Contrary to our hypothesis, the influence of NO on cerebral perfusion appears regionally uniform in healthy young adults.

Traumatic brain injury (TBI) is known to be associated with poor sleep. In this report, we aimed to identify associations between differences in cortical volume and sleep quality post-TBI. MRI anatomical scans from 88 cases with TBI were analyzed in this report. Subjective sleep quality was assessed using the Pittsburgh Sleep Quality Index (PSQI). Voxel Based Morphometry (VBM), was used to obtain statistical maps of the association between PSQI and cortical volume in gray matter and white matter voxels. Higher PSQI total scores (poor sleep quality) were strongly associated with smaller gray matter volume in the cerebellum. White matter volume was not associated with total PSQI. The sleep disturbance subcomponent showed a significant association with gray and white matter volumes in the cerebellum. Although not significant, cortical areas such as the cingulate and medial frontal regions were associated with sleep quality. The cerebellum with higher contribution to motor and autonomic systems was associated strongly with poor sleep quality. Additionally, regions that play critical roles in inhibitory brain function and suppress mind wandering (i.e., default mode network including medial frontal and cingulate regions) were associated (although to a lesser extent) with sleep. Our findings suggest that poor sleep quality following TBI is significantly associated with lower cerebellar volume, with trending relationships in regions associated with inhibitory function.