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Although we experience thousands of distinct events on a daily basis, relatively few are committed to memory. The human capacity to intentionally control which events will be remembered has been demonstrated using learning procedures with instructions to purposely avoid committing specific items to memory. In this study, we used a variant of the item-based directed-forgetting procedure and instructed participants to memorize the location of some images but not others on a grid. These instructions were conveyed using a set of auditory cues. Then, during an afternoon nap, we unobtrusively presented a cue that was used to instruct participant to avoid committing the locations of some images to memory. After sleep, memory was worse for to-be-forgotten image locations associated with the presented sound relative to those associated with a sound that was not presented during sleep. We conclude that memory processing during sleep can serve not only to secure memory storage but also to weaken it. Given that intentional suppression may be used to weaken unpleasant memories, such sleep-based strategies may help accelerate treatments for memory-related disorders such as post-traumatic stress disorder.

We sought to delineate the effects of acute and chronic exercise on the regulation of intracellular nitric oxide (N[O.sub.i]) production in putative endothelial progenitor cells (EPCs). Putative EPC colony-forming units (CFU-EC) were cultured from blood drawn before and after 30 min of treadmill exercise at 75% of maximal oxygen uptake in active (n = 8) and inactive (n = 8) men. CFU-EC were similar between groups at baseline, but increased after exercise in active men only (P = 0.04). CFU-EC expressed Dower NADPH oxidase subunit [gp91.sup.phox] mRNA and elevated endothelial nitric oxide synthase mRNA in active relative to inactive men at baseline (P < 0.05). Acute exercise reduced [gp91.sup.phox] mRNA in CFU-EC of both groups (P < 0.05), whereas [p47.sup.phox] mRNA levels were reduced in the inactive group only (P = 0.02). There were no differences between groups or with acute exercise in xanthine oxidase, superoxide dismutase isoforms, or gluthathione peroxidase-1 mRNA levels. N[O.sub.i] was significantly greater in CFU-EC of active men at baseline (P = 0.004). N[O.sub.i] increased in CFU-EC of inactive men with acute exercise, and in vitro experiments with apocynin indicated the increased N[O.sub.i] production was caused by suppression of NADPH oxidase. However, the increases in N[O.sub.i] with the different treatments in the inactive group did not reach the baseline levels in the active group (P < 0.05). We conclude that acute exercise increases N[O.sub.i] in cells generated by the CFU-EC assay through an NADPH oxidase-inhibition mechanism in sedentary men. However, differences due to chronic exercise must involve additional factors. Our findings support exercise as a means to improve putative EPC function and suggest a novel mechanism that may explain this effect. physical activity; angiogenesis; oxidative stress doi: 10.1152/ajpheart.00347.2009.

We tested the hypothesis that women have blunted sympathetic neural responses to orthostatic stress compared with men, which may be elicited under hypovolemic conditions. Muscle sympathetic nerve activity (MSNA) and hemodynamics were measured in eight healthy young women and seven men in supine position and during 6 rain of 60[degrees] head-up tilt (HUT) under normovolemic and hypovolemic conditions (randomly), with ~4-wk interval. Acute hypovolemia was produced by diuretic (furosemide) administration ~2 h before testing. Orthostatic tolerance was determined by progressive lower body negative pressure to presyncope. We found that furosemide produced an ~13% reduction in plasma volume, causing a similar increase in supine MSNA in men and women (mean [+ or -] SD of 5 [+ or -] 7 vs. 6 [+ or -] 5 bursts/min; P = 0.895). MSNA increased during HUT and was greater in the hypovolemic than in the normovolemic condition (32 [+ or -] 6 bursts/min in normovolemia vs. 44 [+ or -] 15 bursts/min in hypovolemia in men, P = 0.055; 35 [+ or -] 9 vs. 45 [+ or -] 8 bursts/min in women, P < 0.001); these responses were not different between the genders (gender effect: P = 0.832 and 0.814 in normovolemia and hypovolemia, respectively). Total peripheral resistance increased proportionately with increases in MSNA during HUT; these responses were similar between the genders. However, systolic blood pressure was lower, whereas diastolic blood pressure was similar in women compared with men during HUT, which was associated with a smaller stroke volume or stroke index. Orthostatic tolerance was lower in women, especially under hypovolemic conditions. These results indicate that men and women have comparable sympathetic neural responses during orthostatic stress under normovolemic and hypovolemic conditions. The lower orthostatic tolerance in women is predominantly because of a smaller stroke volume, presumably due to less cardiac filling during orthostasis, especially under hypovolemic conditions, which may overwhelm the vasomotor reserve available for vasoconstriction or precipitate neurally mediated sympathetic withdrawal and syncope. muscle sympathetic nerve activity; vascular resistance; arterial pressure; head-up tilt

The aim of this study was to determine whether inhibition of nitric oxide synthase (NOS) alters dynamic cerebral autoregulation in humans. Beat-to-beat blood pressure (BP) and cerebral blood flow (CBF) velocity (transcranial Doppler) were measured in eight healthy subjects in the supine position and during 60[degrees] head-up tilt (HUT). NOS was inhibited by intravenous [N.sup.G]-monomethyl-L-arginine (L-NMMA) infusion. Dynamic cerebral autoregulation was quantified by transfer function analysis of beat-to-beat changes in BP and CBF velocity. Pressor effects of L-NMMA on cerebral hemodynamics were compared with those of phenylephrine infusion. In the supine position, L-NMMA increased mean BP from 83 [+ or -] 3 to 94 [+ or -] 3 mmHg (P < 0.01). However, CBF velocity remained unchanged. Consequently, cerebrovascular resistance index (CVRI) increased by 15% (P < 0.05). BP and CBF velocity variability and transfer function gain at the low frequencies of 0.07-0.20 Hz did not change with L-NMMA infusion. Similar changes in mean BP, CBF velocity, and CVRI were observed after phenylephrine infusion, suggesting that increase in CVRI after L-NMMA was mediated myogenically by increase in arterial pressure rather than a direct effect of cerebrovascular NOS inhibition. During baseline tilt without L-NMMA, steady-state BP increased and CBF velocity decreased. BP and CBF velocity variability at low frequencies increased in parallel by 277% and 217%, respectively (P < 0.05). However, transfer function gain remained unchanged. During tilt with L-NMMA, changes in steady-state hemodynamics and BP and CBF velocity variability as well as transfer gain and phase were similar to those without L-NMMA. These data suggest that inhibition of tonic production of NO does not appear to alter dynamic cerebral autoregulation in humans. cerebral blood flow; head-up tilt; transcranial Doppler

Cui, Jian, Rong Zhang, Thad E. Wilson, Sarah Witkowski, Craig G. Crandall, and Benjamin D. Levine. Nitric oxide synthase inhibition does not affect regulation of muscle sympathetic nerve activity during head-up tilt. Am J Physiol Heart Circ Physiol 285: H2105-H2110, 2003. First published July 3, 2003; 10.1152/ajpheart.01076.2002.--To test the hypothesis that systemic inhibition of nitric oxide (NO) synthase does not alter the regulation of sympathetic outflow during head-up tilt in humans, in eight healthy subjects NO synthase was blocked by intravenous infusion of [N.sup.G]-monomethyl-L-arginine (L-NMMA). Blood pressure, heart rate, cardiac output, total peripheral resistance (TPR), and muscle sympathetic nerve activity (MSNA) were recorded in the supine position and during 60[degrees] head-up tilt. In the supine position, infusion of L-NMMA increased blood pressure, via increased TPR, and inhibited MSNA. However, the increase in MSNA evoked by head-up tilt during L-NMMA infusion (change in burst rate: 24 [+ or -] 4 bursts/min; change in total activity: 209 [+ or -] 36 U/min) was similar to that during head-up tilt without L-NMMA (change in burst rate: 23 [+ or -] 4 bursts/ min; change in total activity: 251 [+ or -] 52 U/min, n = 6, all P > 0.05). Moreover, changes in TPR and heart rate during head-up tilt were virtually identical between the two conditions. These results suggest that systemic inhibition of NO synthase with L-NMMA does not affect the regulation of sympathetic outflow and vascular resistance during head-up tilt in humans. baroreceptors; nervous system; autonomic; orthostatic; microneurography

ABSTRACT Objective Methods Results Conclusion Hot flashes (HFs) are experienced as sudden sensations of heat. We hypothesized that brown adipose tissue (BAT) activation could increase the likelihood of HFs in winter. The aim of this study was to test whether women with more BAT activity were more likely to experience self‐reported or biometrically measured HFs.Women aged 45–55 years (n = 270) participated in face‐to‐face interviews and anthropometric and ambulatory measures. Level of BAT activity was estimated from the difference in supraclavicular skin temperature measured by infrared thermography before and after cooling. Logistic regressions were applied to examine whether bothersome HFs (yes/no) during the past 2 weeks were associated with BAT activity, adjusting for menopausal status, childhood exposure to cold, waist/hip ratio, and self‐reported health. Linear regressions were used to examine the frequency of self‐reported and biometrically measured HFs during the study period and BAT activity, adjusting for potential confounders.Menopausal status, childhood exposure to cold, waist‐to‐hip ratio (WHR), and self‐reported health were associated with both BAT activity and HFs. After adjusting for potential confounders, an increase in BAT activity almost tripled the likelihood of bothersome HFs (OR 2.84, 95% CI 1.26–6.43). In linear regressions, BAT activity was not associated with frequency of subjective or objective HFs during the study period, but childhood exposure to cold was associated with subjective HF report (β = 0.163, p = 0.010).To our knowledge, this is the first study of BAT activation and HFs. Our results support a role for BAT activity in HF experience. Therefore, we encourage further examination of the role of BAT, as well as childhood exposure to cold, in HFs. [ABSTRACT FROM AUTHOR]