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Previous studies suggest that sleep deprivation (SD) decreases glucose tolerance in humans. The present study examined the ability of 10 males to process a glucose load during two conditions separated by at least 10 d. Condition I consisted of sedentary daily activity and sleep deprivation (SDS). Condition II consisted of daily physical activity and sleep deprivation (SDX). In both the SDS and SDX conditions, subjects were sleep deprived for 60 h followed by 7 h of normal sleep. An oral glucose tolerance test (OGTT) was administered at 10 and 60 h of SD, and after a night of recovery sleep in each condition, and plasma glucose and insulin concentrations were measured. No differences in the total plasma glucose response to the OGTT were observed over the total experimental period during Conditions I and II. However, the insulin response to the OGTT was elevated in the two conditions after 60 h of SD. Furthermore, the sedentary Condition I (SDS) resulted in higher insulin responses at all times compared to exercise Condition II (SDX). It is suggested that SD contributes to the development of an insulin resistance that can be partially reversed by physical activity. The results support the suggestion that SD results in decreased insulin sensitivity at peripheral receptor sites which can eventually lead to insulin exhaustion at pancreatic sites after longer periods of SD.

Sleep deprivation or partial sleep loss are common in work conditions as rotating shifts and prolonged work hours, in sustained military operations and in athletes competing in events after crossing several time zones or engaged in ultramarathon or triathlon events. Although it is well established that sleep loss has negative effects on mental performance, its effects on physical performance are equivocal. This review examines the latter question in light of recent studies published on this problem. Sleep deprivation of 30 to 72 hours does not affect cardiovascular and respiratory responses to exercise of varying intensity, or the aerobic and anaerobic performance capability of individuals. Muscle strength and electromechanical responses are also not affected. Time to exhaustion, however, is decreased by sleep deprivation. Although ratings of perceived exertion always increased during exercise in sleep-deprived (30 to 60 hours) subjects compared with normal sleep, this is not a reliable assessment of a subject's ability to perform physical work as the ratings of perceived exertion are dissociated from any cardiovascular changes in sleep deprivation. Examination of the various hormonal and metabolic parameters which have been measured in the studies reviewed reveals that the major metabolic perturbations accompanying sleep deprivation in humans are an increase in insulin resistance and a decrease in glucose tolerance. This may explain the reduction in observed time to exhaustion in sleep-deprived subjects. The role of growth hormone in mediating altered carbohydrate metabolism may be of particular relevance as to how sleep deprivation alters the supply of energy substrate to the muscle.

The effect of 60 h of sleep deprivation (SD) upon physical performance and physiological responses to exercise was examined in 11 male subjects. The experiment consisted of two conditions separated by at least 10 d. In the experimental condition (E) subjects remained awake for 60 h and in the control condition (C) the same subjects had 7 h of sleep per night. In both conditions subjects reported to the laboratory on the evening prior to d 1 and slept for 7 h. Physical performance testing was carried out on d 1 and again on d 3 after either two nights of sleep or two nights of SD. Results obtained on d 3 are expressed relative to d 1, the control day. Maximal isometric and isokinetic muscular strength and endurance of selected upper and lower body muscle groups, performance of the Wingate Anaerobic Power Test, simple reaction time, the blood lactate response to cycle exercise at 70% VO2max, and most of the cardiovascular and respiratory responses to treadmill running at 70% and 80% VO2max, were not significantly altered as a result of SD. These results suggest that sleep loss of up to 60 h will not impair the capability for physical work, a finding of considerable importance in sustained military operations which frequently involve the combination of both physical and mental tasks.

New methods for chronic instrumentation of the newborn piglet are described, which allow continuous monitoring of not only pressures in the pulmonary artery and aorta but also in the left and right atria, pulmonary vein, as well as main branch pulmonary artery flows. Changes in pulmonary vascular tone to short-acting vasoactive agents can be recognized by redistribution of flow between lungs and localized to the precapillary vessels or pulmonary veins. Furthermore, vasoactive response in small pulmonary veins may be investigated as well as selective metabolic studies across the right lung. Methods are also described for the chronic cannulation of the neck vessels permitting repeated introduction of catheters on separate study days in the conscious piglet. The pulmonary circulation of the piglet constricts briskly to moderate hypoxemia ([Formula: see text], 1 Torr = 133.32 Pa) with little change in cardiac output or systemic resistance. The piglet demonstrated responses to dilator and constrictor prostaglandins generally similar to the lambs and other species. None of these agents significantly affect pulmonary venous tone.

This study examined the effect of 60 h of sleep deprivation (SD) on electromechanical response times (EMRT), maximal voluntary isometric contraction (MVC), rate of force development (RFD), and times required to reach various percentages of MVC, during a maximal voluntary isometric contraction of both the forearm flexors and leg extensors. Eleven male subjects were either sleep deprived for 60 h (E) or performed similar daily activities and slept 7 h per night (C). Performance variables were evaluated at the same time intervals during both conditions. No significant differences were observed between the E and C conditions for EMRT (pre-motor time, electro-mechanical delay, total reaction time) or muscular performance (MVC, RFD). The results suggest that subjects who have undergone 60 h of SD can react as fast, and with as much force, as those who have had 7 h of sleep per night.

Sleep deprivation or partial sleep loss are common in work conditions as rotating shifts and prolonged work hours, in sustained military operations and in athletes competing in events after crossing several time zones or engaged in ultramarathon or triathlon events. Although it is well established that sleep loss has negative effects on mental performance, its effects on physical performance are equivocal. This review examines the latter question in light of recent studies published on this problem. Sleep deprivation of 30 to 72 hours does not affect cardiovascular and respiratory responses to exercise of varying intensity, or the aerobic and anaerobic performance capability of individuals. Muscle strength and electromechanical responses are also not affected. Time to exhaustion, however, is decreased by sleep deprivation. Although ratings of perceived exertion always increased during exercise in sleep-deprived (30 to 60 hours) subjects compared with normal sleep, this is not a reliable assessment of a subject's ability to perform physical work as the ratings of perceived exertion are dissociated from any cardiovascular changes in sleep deprivation. Examination of the various hormonal and metabolic parameters which have been measured in the studies reviewed reveals that the major metabolic perturbations accompanying sleep deprivation in humans are an increase in insulin resistance and a decrease in glucose tolerance. This may explain the reduction in observed time to exhaustion in sleep-deprived subjects. The role of growth hormone in mediating altered carbohydrate metabolism may be of particular relevance as to how sleep deprivation alters the supply of energy substrate to the muscle.

Persistent fetal circulation may be primary or secondary to other causes. Apart from treating the underlying cause, its management may include ventilatory support and the use of vasodilators, whose value may be limited by marked systemic hypotension. Milrinone is a new cardiotonic agent with smooth muscle-relaxant properties. Unlike its predecessor amrinone, milrinone is less likely to be limited by tachyphylaxis. We evaluated the effect of Milrinone on the neonatal pulmonary circulation in conscious newborn lambs; in particular, on the pulmonary arteriolar constrictor effect of leukotriene D4 (LTD4) during normoxia and hypoxia.