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Graduation date: 1993

Introduction: Studies reveal differential cognitive effects of alcohol use, with moderate to heavy alcohol having some beneficial effects in older adults, whereas in young adulthood, heavier alcohol use produces deficits. The aim of the research was to investigate the relationship between patterns of alcohol use and the cognitive and symptomatic functioning of university students over one year, and to discern which demographic, clinical and alcohol factors might moderate cognitive outcomes. Method: The sample included undergraduate Psychology students from a South African University, aged 18 to 23 years (n = 86). The sample was divided into two alcohol use groups based on four categories from the Alcohol Use Disorders Identification Test (AUDIT) (Babor et al., 2001), including a lighter drinking group (Safe/Hazardous, n = 74) and a heavier drinking group (Harmful/Dependent, n = 12). The two drinking groups were statistically equivalent for distribution of age, gender, English first language, race groups, history of neurological or psychiatric vulnerability, a measure of initial intelligence/cognitive reserve (Peabody Picture Vocabulary Test: PPVT-4) (Dunn & Dunn, 2007) and for a measure of test-taking validity (Immediate Postconcussion Assessment and Cognitive Test: ImPACT Impulse Control) (p = < 0.05 in all instances). Participants were tested on the computerized ImPACT battery (ImPACT, 2007) at three intervals over an academic year (May, August, October 2012). Repeated measures ANOVAs were used to investigate cognitive and symptomatic differences between the two alcohol use groups, in association with moderating factors. Results: The heavier drinking group revealed: (i) poorer performance on ImPACT Visual Motor Speed, Reaction Time and Cognitive Efficiency Index scores, including less ability to benefit from practice over time; (ii) symptom reports of severe Numbness/Tingling, Balance problems and Dizziness. Deleterious cognitive outcome was exacerbated by longer lifetime duration of alcohol use, passing out monthly, beer or wine drinking, smoking or substance use. Conclusion: Deleterious cognitive and symptomatic effects of heavy alcohol use are in evidence for undergraduate university students implicating current and/or cumulative alcohol induced brain impairment. The results of the study are of concern for optimal academic performance of students at an early stage of university level study, who engage in heavier (Harmful/Dependent) drinking patterns, with negative implications for future career attainment.

The detrimental effect of ethanol on coordinated movement and the similarity of this effect to that of pathological damage to the cerebellum or the inferior olive (10) suggests that ethanol profoundly effects the olivocerebellar system. Each cerebellar Purkinje cell (PC) displays two distinct action potential responses: the simple spike (SS), evoked intrinsicly and via the parallel fibres, and the complex spike (CS), evoked via a solitary climbing fibre (CF) which originates from the 10. Ethanol (1.5 g/kg, i.v.) was found to have no significant effect on the CS activity evoked by direct electrical activation of CFs, while it significantly reduced, in parallel, that evoked by cerebral cortex stimulation and that occurring spontaneously. In addition, ethanol, applied both systemically and locally by micropressure, reduced the spontaneous activity of inferior olive (10) neurones. These results strongly suggest an action of ethanol local to the 10 nucleus, perhaps by a direct action on the 10 neurones themselves. Elimination of spontaneous CS activity by the electrolytic lesioning of the contralateral 10 did not significantly alter spontaneous SS firing rate. However, subsequent administration of ethanol i.v. did produce a significant increase of SS rate, indicating that only part of ethanol-evoked SS rate increase is dependant upon the reduction of CS activity. Simple spike regularity was not significantly altered by either 10 lesioning or i.v. ethanol. Ethanol applied locally to PC's by micropressure was found to reduce the period of inhibition evoked by local stimulation of the cerebellar cortex in the majority of the cells tested. This result is in agreement with the previously reported effects of intravenous ethanol on this inhibition, thought to be mediated by gamma-aminobutyric acid (GABA). Both intravenously and locally applied ethanol antagonized the inhibition of PC's evoked by locally applied GABA. These results, while in agreement, are contrary to the reported effects of ethanol in other systems. Intravenously administered ethanol did not significantly alter Golgi cell spontaneous firing, while it did significantly reduce the period of inhibition of Golgi cell firing evoked by 10 stimulation. / Pharmaceutical Sciences, Faculty of / Graduate

The purpose was to examine the effect of chronic alcohol abuse on the androgen receptor content (AR) in skeletal muscle, and to determine if this effect was influenced by resistance training. Thirty-four male rats (456 ± 1 g; mean ± SE) were divided into 4 groups: Sham exercise-Ethanol, Sham exercise-Normal diet, Exercise-Ethanol, and Exercise-Normal diet. Both Exercise groups underwent a 6-week "squat" resistance training protocol and both Ethanol groups received an alcohol-rich diet throughout the 6-week period. Western blot analysis showed no effect of alcohol or resistance training on the AR of the extensor digitorum longus. For the rectus femoris, alcohol caused a decline in the AR (p=0.01). This reduction was not attenuated by resistance training. The AR of the soleus was not affected by chronic alcohol abuse alone; however, the resistance training induced increase in the AR was prevented by chronic alcohol abuse (p=0.03).

This study explored the possibility that some individuals with alcohol and amphetamine addictions are initially motivated to use alcohol and amphetamines because of underlying issues involving body dissatisfaction and weight reduction associated with Anorexia and Bilimia Nervosa. Current literature reveals similarities among chemical dependencies and eating disorders.

The purpose of this study was to examine the effect of post-resistance exercise alcohol ingestion on LPS-stimulated production of IFNγ, TNF-α, IL-1β, IL-6, IL-8, and IL-10. Recreationally resistance-trained men (n = 10, 25 ± 3 yr, 177 ± 7 cm, 83.8 ± 15.7 kg, 14.8 ± 8.5% body fat) and women (n = 8, 23 ± 2 yr, 161 ± 3 cm, 59.5 ± 6.0 kg, 26.5 ± 3.0% body fat) completed the study. Participants visited the laboratory for an initial visit at which time they were screened, familiarized with procedures, and had their 1-repetition maximum (1RM) back squat tested. Subsequently, participants visited the laboratory 2 more times and completed 2 identical heavy resistance exercise bouts (6 sets of 10 repetitions of 80% 1RM back squat) after which a beverage, either containing alcohol (alcohol condition, ALC; 1.09 g EtOH per kg fat free mass) or water (placebo condition, PLA), was administered. Blood samples were collected before exercise (PRE), and at 3 hours (3h) and 5 hours (5h) after exercise. Samples were stimulated with lipopolysaccharide (LPS) and cultured overnight. Supernatant was collected and analyzed for IFNγ, TNF-α, IL-1β, IL-6, IL-8, and IL-10. A significant (p < 0.05) main effect for time was found for IFNγ, TNF-α, and IL-1β (5h greater than PRE) and for IL-10 (5h less than PRE and 3h, 3h less than PRE). An interaction effect was found for IL-8 (ALC less than PLA at 5h) and for IL-6 (ALC greater than PLA at PRE and ALC less than PLA at 3h). For IL-6, ALC was less at 3h than at PRE, and PLA was greater at 3h than at PRE. Overall, the LPS-stimulated cytokine response was pro-inflammatory by 5h. Alcohol consumed after heavy resistance exercise reduced LPS-stimulated production of IL-6 and IL-8 but not of IFNγ, TNF-α, IL-1β, or IL-10. These data indicate that alcohol affected inflammatory capacity but that the potential effect of alcohol on the production of cytokines in response to LPS was largely overwhelmed by the resistance exercise bout.

The purpose of this project was to further elucidate the effects post-exercise alcohol ingestion. This project had many novel aspects including using a resistance exercise (RE) only exercise design and the inclusion of women. To our knowledge, we are the first to investigate the effect of post-RE alcohol ingestion in women. In the first chapter of this project, information on the prevalence of alcohol use and the importance of skeletal muscle as a dynamic and metabolic tissue was provided. In chapter two, the effects of post-RE alcohol ingestion in men and women are detailed. The major findings of this study was that although RE elicited similar mTORC1 signaling both in men and in women, alcohol ingestion appeared to only attenuate RE-induced phosphorylation of the mTORC1 signaling pathway in men. The third chapter focused on examining the effects of post-RE alcohol ingestion on acute testosterone bioavailability. The primary findings of this study was that alcohol substantially elevated serum total and free testosterone concentrations during recovery from a bout of resistance exercise. The fourth chapter detailed factors that contribute to bone density in men. The major findings of this study was that young adult male long-distance runners who participated in resistance training at least once per week had greater bone mineral density than their non-resistance trained and non-exercise trained peers.

Evidence linking the development of chronic alcoholism with endogenous opioid peptides is reviewed. Particular emphasis is placed on enkephalin metabolism with respect to its involvement in the development of addiction and stress-related psychophysiological changes. The study was concerned with enkephalin hydrolysing activity (EHA) in chronic alcoholism as well as the mood changes that reportedly accompany alcoholism. Also of interest was the relationship of enkephalin degradation to voluntary relaxation.