Chronic ethanol exposure leads to divergent control of dopaminergic synapses in distinct target regions.

Neuroadaptations following chronic exposure to alcohol are hypothesized to play important roles in alcohol-induced alterations in behavior, in particular increased alcohol drinking and anxiety-like behavior. Dopaminergic signaling plays a key role in reward-related behavior, with evidence suggesting it undergoes modification following exposure to drugs of abuse. A large literature indicates an involvement of dopaminergic signaling in response to alcohol. Using a chronic inhalation model of ethanol exposure in mice, we have begun to investigate the effects of alcohol intake on dopaminergic signaling by examining protein levels of tyrosine hydroxylase and the dopamine transporter, as well as monoamine metabolites in three different target fields of three different dopaminergic nuclei. We have focused on the dorsal lateral bed nucleus of the stria terminalis because of the reported involvement of dorsal lateral bed nucleus of the stria terminalis dopamine in ethanol intake, and the nucleus accumbens and dorsal striatum because of their dense dopaminergic innervation. After either a chronic intermittent exposure or continuous exposure regimen, mice were killed, and tissue punches collected from the dorsal lateral bed nucleus of the stria terminalis, nucleus accumbens, and striatum for Western analysis. Strikingly, we found divergent regulation of tyrosine hydroxylase and dopamine transporter protein levels across these three regions that was dependent upon the means of exposure. These data thus suggest that distinct populations of catecholamine neurons may be differentially regulated by ethanol, and that ethanol and withdrawal interact to produce differential adaptations in these systems.

Body cooling between two bouts of exercise in the heat enhances subsequent performance.

The purpose was to assess whether body cooling between 2 bouts of exercise in the heat enhances performance during the second exercise session. Using a random, crossover design, 15 subjects (3 women, 12 men; 28 +/- 2 years, 180 +/- 2 cm, 69 +/- 2.3 kg) participated in all 3 trials. Subjects ran 90 minutes on hilly trails in a hot environment (approximately 27 degrees C) before 12 minutes of either cold water immersion (CWI; 13.98 degrees C), ice water immersion (IWI; 5.23 degrees C), or a mock treatment (MT) of sitting in a tub with no water (29.50 degrees C). After immersion, subjects ran a 2-mile race. CWI had faster (p < 0.05) performance time (725 seconds) than MT (769 seconds). CWI and IWI had significantly (p < 0.05) lower rectal temperatures postimmersion than MT as well as postrace (p < 0.05). Heart rate also remained significantly lower (p < 0.05) during the CWI and IWI trials for the first half of the race. In conclusion, CWI enhances performance (6% improvement in race time) in the second bout of exercise, supporting its potential role as an ergogenic aid in athletic performance.

Creatine use and exercise heat tolerance in dehydrated men.

CONTEXT: Creatine monohydrate (CrM) use is highly prevalent in team sports (eg, football, lacrosse, ice hockey) and by athletes at the high school, college, professional, and recreational levels. Concerns have been raised about whether creatine use is associated with increased cramping, muscle injury, heat intolerance, and risk of dehydration. OBJECTIVE: To assess whether 1 week of CrM supplementation would compromise hydration status, alter thermoregulation, or increase the incidence of symptoms of heat illness in dehydrated men performing prolonged exercise in the heat. DESIGN: Double-blind, randomized, crossover design. SETTING: Human Performance Laboratory. PATIENTS OR OTHER PARTICIPANTS: Twelve active males, age = 22 +/- 1 year, height = 180 +/- 3 cm, mass = 78.8 +/- 1.2 kg, body fat = 9 +/- 1%, V(O2)peak = 50.9 +/- 1 ml.kg(-1).min(-1). INTERVENTION(S): Subjects consumed 21.6 g.d(-1) of CrM or placebo for 7 days, underwent 48 +/- 10 days of washout between treatments, and then crossed over to the alternate treatment in the creatine group. On day 7 of each treatment, subjects lost 2% body mass by exercising in 33.5 degrees C and then completed an 80-minute exercise heat-tolerance test (33.5 degrees C +/- 0.5 degrees C, relative humidity = 41 +/- 12%). The test consisted of four 20-minute sequences of 4 minutes of rest, alternating a 3-minute walk and 1-minute high-intensity run 3 times, and walking for 4 minutes. MAIN OUTCOME MEASURES: Thermoregulatory, cardiorespiratory, metabolic, urinary, and perceptual responses. RESULTS: On day 7, body mass had increased 0.88 kg. No interaction or treatment differences for placebo versus CrM during the exercise heat-tolerance test were noted in thermoregulatory (rectal temperature, 39.3 +/- 0.4 degrees C versus 39.4 +/- 0.4 degrees C) cardiorespiratory (Vo(2), 21.4 +/- 2.7 versus 20.0 +/- 1.8 ml.kg(-1).min(-1); heart rate, 192 +/- 10 versus 192 +/- 11 beats.min(-1); mean arterial pressure, 90 +/- 9 versus 88 +/- 5 mm Hg), metabolic (lactate, 6.7 +/- 2.7 versus 7.0 +/- 3.0 mmol.L(-1)), perceptual thirst (thirst, 7 +/- 1 versus 7 +/- 1; thermal sensation, 8 +/- 2 versus 8 +/- 1; rating of perceived exertion, 17 +/- 3 versus 17 +/- 2), plasma glucose (0-20 minutes of exercise heat-tolerance, 6.5 +/- 1.2 versus 6.8 +/- 0.8 mmol.L(-1)), plasma (297 +/- 5 versus 300 +/- 4 mOsm.kg(-1)) and urine (792 +/- 117 versus 651 +/- 134 mOsm.kg(-1)), urine specific gravity (1.025 +/- 0.003 versus 1.030 +/- 0.005) and urine color (7 +/- 1 versus 6 +/- 1) measures were increased during CrM. Environmental Symptoms Questionnaire scores were similar between treatments. The levels of dehydration incurred during dehydration and the exercise heat-tolerance test were similar and led to similar cumulative body mass losses (-4.09 +/- 0.53 versus -4.38 +/- 0.58% body mass). CONCLUSIONS: Short-term CrM supplementation did not increase the incidence of symptoms or compromise hydration status or thermoregulation in dehydrated, trained men exercising in the heat.