Previous research on adaptation to visual-motor rearrangement suggests that the central nervous system represents accurately only 1 visual-motor mapping at a time. This idea was examined in 3 experiments where subjects tracked a moving target under repeated alternations between 2 initially interfering mappings (the "normal" mapping characteristic of computer input devices and a 108 degree rotation of the normal mapping). Alternation between the 2 mappings led to significant reduction in error under the rotated mapping and significant reduction in the adaptation aftereffect ordinarily caused by switching between mappings. Color as a discriminative cue, interference versus decay in adaptation aftereffect, and intermanual transfer were also examined. The results reveal a capacity for multiple concurrent visual-motor mappings, possibly controlled by a parametric process near the motor output stage of processing.

Prior longitudinal work suggests that blood pressure (BP) reactivity to the cold pressor test (CPT) helps predict hypertension, yet the impact of age and sex on hemodynamic and neural responsiveness to CPT remain equivocal. Forty-three young (21±1yrs, mean±SEM) men (YM, n=20) and women (YW, n=23), and 16 older (60±1yrs) men (OM, n=9) and women (OW, n=7), participated in an experimental visit where continuous BP (finger plethysmography) and muscle sympathetic nerve activity (MSNA; microneurography) were recorded during a 3-5min baseline and 2-min CPT. Baseline mean arterial pressure (MAP) was greater in older men compared with young men, (92±4 vs. 77±1mmHg, p<0.01), but similar in women (p=0.12). Baseline MSNA incidence was greater in OM (69±6bursts/100hb) compared with OW (44±7bursts/100hb, p=0.02), and lower in young adults (YM: 17±3 vs. YW: 16±2bursts/100hb, p<0.01), but similar across sexes (p=0.83). However, when exposed to the CPT, MSNA increased more rapidly in OW (Δ43±6bursts/100hb; group×time, p=0.01) compared with OM (Δ15±3bursts/100hb), but was not different between YW (Δ30±3bursts/100hb) and YM (Δ33±4 bursts/100hb, p=1.0). There were no differences in MAP with CPT between groups (group×time, p=0.33). These findings suggest that OW demonstrate a more rapid initial rise in MSNA responsiveness to a CPT compared with OM. This greater sympathetic reactivity in OW may be a contributing mechanism to the increased hypertension risk in postmenopausal women.

Binge alcohol consumption elicits acute and robust increases of muscle sympathetic nerve activity (MSNA), yet the impact of evening binge drinking on morning-after MSNA is unknown. The present study examined the effects of evening binge alcohol consumption on polysomnographic sleep and morning-after MSNA. We hypothesized that evening binge drinking (i.e. 4-5 drink equivalent in <2hrs) would reduce sleep quality and increase morning-after blood pressure (BP) and MSNA. Following a familiarization night within the sleep laboratory, twenty-two participants (12 men, 10 women; 25±1 years) were examined after simulated binge drinking or fluid control (randomized, crossover design). Morning MSNA was successfully recorded across both conditions in 16 participants (8 men, 8 women) during a 10-minute baseline and three Valsalva's maneuvers (VM). Binge drinking reduced rapid eye movement (REM) sleep (15±1 vs. 20±1%; p=0.003), increased stage II sleep (54±1 vs. 51±1%; p=0.002), increased total urine output (2.9±0.2 vs. 2.1±0.1 liters; p<0.001), but did not alter morning-after urine specific gravity. Binge drinking increased morning-after heart rate (65 (54-72) vs. 58 (51-67) beats/min; p=0.013), but not resting BP or MSNA. Binge drinking elicited greater sympathoexcitation during VM (38±3 vs. 43±3 bursts/min, p=0.036). Binge drinking augmented heart rate (p=0.002), systolic BP (p=0.022) and diastolic (p=0.037) BP reactivity to VM phase IV, and blunted cardiovagal baroreflex sensitivity during VM phases II (p=0.028) and IV (p=0.043). In conclusion, evening binge alcohol consumption disrupted REM sleep and morning-after autonomic function. These findings provide new mechanistic insight into the potential role of binge drinking on cardiovascular risk.

Exercise-induced pulmonary haemorrhage (EIPH) occurs in horses performing high-intensity athletic activity. The application of physics principles to derive a ‘physical model’, which is coherent with existing physiology and cell biology data, shows that critical parameters for capillary rupture are cell–cell adhesion and cell stiffness (cytoskeleton organisation). Specifically, length of fracture in the capillary is a ratio between the energy involved in cell–cell adhesion and the stiffness of cells suggesting that if the adhesion diminishes and/or that the stiffness of cells increases EIPH is more likely to occur. To identify genes associated with relevant cellular or physiological phenotypes, the physical model was used in a post-genome-wide association study (GWAS) to define gene sets associated with the model parameters. The primary study was a GWAS of EIPH where the phenotype was based on weekly tracheal wash samples collected over a two-year period from 72 horses in a flat race training yard. The EIPH phenotype was determined from cytological analysis of the tracheal wash samples, by scoring for the presence of red blood cells and haemosiderophages. Genotyping was performed using the Illumina Equine SNP50 BeadChip and analysed using linear regression in PLINK. Genes within significant genome regions were selected for sets based on their GeneOntology biological process, and analysed using fastBAT. The gene set analysis showed that genes associated with cell stiffness (cytoskeleton organisation) and blood flow have the most significant impact on EIPH risk.

Epidemiological studies report a significant relationship between binge alcohol consumption and the incidence of hypertension and stroke. While sympathoexcitation is a suspected mechanism, this has not been definitively demonstrated. Acute consumption of alcohol has been shown to consistently activate the sympathetic nervous system, yet the impact of evening alcohol consumption on sympathetic activity the morning after consumption remains unknown. The purpose of the present study was to determine the impact of evening binge alcohol consumption on morning blood pressure and sympathetic neural activity. We hypothesized that blood pressure and neural activity would be augmented the morning after binge alcohol consumption. Using a randomized, crossover design, fifteen young adults (10 men, 5 women; 23±1 years, 27±1 kg/m2) were tested during both a binge alcohol condition and fluid control condition (one month apart). Participants arrived to the laboratory in the early evening for a standardized dinner and were instructed to relax in a semi‐recumbent position. Two beverages were administered to each participant over the course of two hours, designed to mimic an episode of binge drinking. Each alcohol dose was 1 g/kg or 0.85 g/kg in men and women, respectively (diluted in a 1:3 ratio with fruit juice), while fluid control was simply the fruit juice in similar volume. Participants were allotted 8 hours of polysomnography‐monitored sleep (data not included) prior to morning autonomic testing. Heart rate (HR), beat‐to‐beat blood pressure (NOVA, Finapres), and muscle sympathetic nerve activity (MSNA, microneurography) were recorded during a 10‐minute supine baseline and three 15‐second Valsalva maneuvers (VM). During VM, participants forcefully exhaled into a modified pressure manometer to 40 mmHg for 15 seconds and breathed normally during 1‐minute recovery period between each of the three VM strains. Statistical analysis included paired t‐tests across conditions (p<0.05). Baseline morning mean arterial pressure (81±2 vs. 80±2 mmHg) and MSNA (18±3 vs. 20±2 burst/min) were not different between alcohol and fluid control (p>0.05 for both). In contrast, HR was higher the morning after alcohol consumption compared to fluid control (64±3 vs. 59±2 beats/min, p=0.031). Increased sympathoexcitation (i.e. MSNA bursts/min) was exhibited during Phase II of VM strain after evening alcohol consumption when compared to fluid control (53±4 vs. 45±4 bursts/min, p=0.013). Cardiovagal baroreflex sensitivity (BRS) was assessed during Phase II and IV of VM strain, where phase II BRS was significantly blunted the morning after binge alcohol consumption (11±2 vs. 8±1 ms/mmHg, p=0.05). Phase IV BRS trended lower the morning after alcohol consumption (17±3 vs. 13±1 ms/mmHg, p=0.085). During Phase IV of the VM strain, systolic arterial pressure “overshoot” was augmented the morning after binge alcohol consumption compared to fluid control (Δ36±3 vs. Δ28±4 mmHg, p=0.021). These findings provide new mechanistic insight into the relation between bin...