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The LD(_50) of 10-day-old blowflies differed significantly in two different stocks, and were found to be 38.12 ± 0.07ºC for the Durham stock and 40.8 ± 0.18ºC for the Cambridge stock. A transitory increase in heat resistance occurred following the exposure of adult blowflies to a sublethal heat shock. This thermotolerance was apparent 1h after the application of heat shock, was maximal 2-3 h later and had disappeared after 6 h. Oxidative phosphorylation by flight muscle mitochondria from non-thermotolerant control flies was impaired by an LD(_50) dose in vivo. Respiration using glycerol-3- phosphate was more heat sensitive than that with pyruvate plus proline. State III respiration was markedly inhibited, acceptor control (RCI) was lost with (G 3P) as substrate and so ADP:0 ratios were not measurable; whereas with pyruvate + proline as substrates, although State III respiration was inhibited by 50% and acceptor control was significantly reduced, ADP:0 remained measurable. Uncoupling of oxidative phosphorylation was obvious only with pyruvate + proline where State IV was significantiy increased. The development of thermotolerance protected oxidative phosphorylation against heat damage. With G-3-P respiration State III was largely restored and acceptor control was not significantly different from controls, but ADP:0 remained lower. With pyruvate + proline as substrates State III respiration was inhibited, but State IV was also lower without evidence of uncoupling of oxidative phosphorylation. Acceptor control was restored to control levels but ADP:0 values were lower. The lower ADP:0 ratios indicate some impairment of mitochondrial function occurred. The effect of experimental temperature in vitro on respiratory performance of mitochondria from non-pretreated control and thermotolerant LD(_50) flies was also determined between 19 and 39ºC. State III respiration was markedly temperature- dependent in mitochondria from non-pretreated control flies with both substrates; it was maximal at 24-29ºC and fell progressively at higher measuring temperatures. In mitochondria from thermotolerant flies, State III respiration was less temperature dependent with both substrates, but this effect was more marked for G-3-P. The effect of experimental temperature on State IV respiration was similar in mitochondria from non- pretreated control and thermotolerant LD(_50) flies with the same substrate, but differed between the two substrates. With G 3P as substrate, respiration rate rose with temperature with a Q(_10) of approximately 1.5; however, with pyruvate + proline as substrate, the trend was for respiration rate to fall as experimental temperature rose. Differences in the temperature sensitivities of mitochondria from control and thermotolerant flies, in terms of acceptor control, were found. Using G-3-P, acceptor control was lost in mitochondria from control flies above 29ºC, but was still measurable at 34ºC in mitochondria from thermotolerant flies. With pyruvate + proline as substrate acceptor control was demonstrable in mitochondria from both non-pre-treated control and thermotolerant flies at all experimental temperatures. The thermal sensitivities of the respiratory complexes were studied using the inhibitors rotenone and antimycin A. In mitochondria from LD(_50) treated control flies respiration uncoupled with FCCP was not restored to State II levels. However, in LD(_50) treated mitochondria from thermotolerant flies respiration uncoupled with FCCP was not different from State III respiration. These data suggest that the reduction in State III respiration after heating is owing to an inhibition of oxidation rather than phosphorylation. Complex I, NADH coenzyme Q reductase, was shown to be the most temperature sensitive of the respiratory complexes.

Most sleep loss research has concentrated on long duration, repeated measures performance of low-level, monotonous tasks, such as vigilance and reaction time, in support of the theory that sleep loss induces a decline in Non-Specific arousal while having no specific effects on functioning. Numerous studies have shown the beneficial effects of caffeine on this type of performance measure. Recent studies have been conducted on executive functioning tasks that are short, novel, and stimulating. These measures display a sensitivity to sleep loss after 36h that is not compensated by waking countermeasures such as motivation and caffeine. These findings suggest Specific effects of sleep loss, contrary to the Non-Specific theory, particularly on tasks associated with frontal lobe activation. Similarities between performance deficits following brain lesions and those observed in sleep loss subjects form the basis of a neuropsychological model of sleep function. This thesis was an endeavour to document the findings of executive functioning sensitivity following 27 and 36 hours of sleep loss, testing the effect of two common countermeasures, caffeine and a nap. It was established that the critical period of sleep loss for executive functioning performance is at 36 hours. Sleep deprivation effects for periods shorter than 36 hours can be countered by a waking countermeasure, caffeine. It was further established that a 2-hour prophylactic nap opportunity inhibited sleep deprivation effects at 36-hr performance testing for executive functions. The systematic analysis of the effects of sleep loss on language skill, a complex task which is possibly an executive functioning task associated with frontal lobe activation but largely neglected in the literature, detected an increase in variability in language skill, and a propensity towards production errors in speech, but not writing, at 36 hours without sleep. This effect was not observed at 27 hours. The findings are discussed in support of a hypothetical consolidated model of Specific and Non-Specific Effects of sleep loss.

This thesis describes a study that aimed to assess the psychophysiological effects of offshore survival training, and to investigate whether responses of trainees differed according to age. A group of 99 subjects, randomly selected from across a wide age range, volunteered and subsequently were monitored during the training. The sample population were split into 2 groups according to the training course attended, refresher or combined survival and fire fighting course. Physiological and psychological measurements, chosen as indicators of stress, were performed on these subjects. Attention was centred on 4 particular events: helicopter underwater escape training (HUET); simulated platform abandonment using totally enclosed motor propelled survival craft; simulated platform abandonment into liferafts; and self rescue from a smoke filled room. State anxiety and urinary free cortisol were assessed early on each morning. Anxiety was also measured before the 4 chosen events. Early morning anxiety and urinary free cortisol were observed to peak on the first day of training, then each showed a very similar pattern of a decline to a plateau. On assessing all combined subjects' anxiety scores in sequence, values were found to be relatively lower towards the end of the course. These results suggested that subjects suffered from pre-course apprehensions that may have caused elevations in anxiety scores during the course. It was also found that subjects with high urinary free cortisol values on day 1, had relatively higher heart rates later in the course. Despite variation between the training courses, very similar mean heart rates were recorded in combined and refresher subjects. Relatively elevated heart rates were detected during the HUET brief. This was proposed to be the result of psychological activation, probably anxiety. Indicators of links among physiological and psychological measures were thus detected. Stronger and more consistent relationships may have been observed had more extensive data been available. Age effects were also detected, older refreshers had lower levels of anxiety, but found the course relatively more demanding. The lower anxiety levels were proposed to result from older refreshers having more training experience.

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