The Impact of Melatonin, Melatonin Analogues, Caffeine, and Bright Light on Sleep and Thermoregulatory Physiology

doses under controlled conditions during the daytime, when endogenous levels are low. Study findings have demonstrated that exogenous melatonin improves sleep, increases peripheral heat loss, and decreases core body temperature (CBT). These thermoregulatory adjustments mimic those that occur around habitual bedtime, when endogenous melatonin levels are high. The emergences of artificial light and stimulants i.e., caffeine have impacted the behavior and physiology that normally precede sleep. Caffeine may independently impact sleep/wakefulness, or in conjunction with the thermoregulatory system. Bright light during the biological night suppresses melatonin and changes the thermoregulatory pattern that precedes nocturnal sleep; these changes may ultimately impact the sleep/wakefulness system. To improve our understanding of physiological mechanisms promoting and disrupting sleep/wakefulness, it is important to examine the connection between melatonin and the sleep/wakefulness and thermoregulatory systems, and the impact of environmental and behavioral factors on these systems. Therefore, the aims of this dissertation were to: 1) determine the effect of a melatonin receptor analogue ramelteon, on daytime sleep and body temperature, and the relationship between the two variables; 2) determine the effect of daytime exogenous melatonin on resting energy expenditure, (REE); and 3) determine the individual and compound effects of caffeine and bright light on thermoregulatory and sleep physiology at night. Consistent with our hypotheses, 1) ramelteon significantly improved daytime sleep, lowered CBT, and increased peripheral heat loss 2) exogenous melatonin decreased REE during the daytime, and 3) caffeine delayed the nocturnal rise in peripheral heat loss, attenuated the fall in CBT, while the combination of caffeine and bright light decreased slow wave sleep and increased sleep onset latency. These findings suggest that melatonin may play an important role in the regulation of sleep/wakefulness as evidenced by the effect of daytime ramelteon administration on sleep and thermoregulatory physiology and the effect of daytime exogenous melatonin on REE. Finally, caffeine and bright light had a negative impact on nocturnal sleep and these effects may be mediated in part by their impact on the thermoregulatory system

Small arms combat modeling: a superior way to evaluate marksmanship data

Purpose – Marksmanship data is a staple of military and law enforcement evaluations. This ubiquitous nature creates a critical need to use all relevant information and to convey outcomes in a meaningful way for the end users. The purpose of this study is to demonstrate how simple simulation techniques can improve interpretations of marksmanship data. Design/methodology/approach – This study uses three simulations to demonstrate the advantages of small arms combat modeling, including (1) the benefits of incorporating a Markov Chain into Monte Carlo shooting simulations; (2) how small arms combat modeling is superior to point-based evaluations; and (3) why continuous-time chains better capture performance than discrete-time chains. Findings – The proposed method reduces ambiguity in low-accuracy scenarios while also incorporating a more holistic view of performance as outcomes simultaneously incorporate speed and accuracy rather than holding one constant. Practical implications – This process determines the probability of winning an engagement against a given opponent while circumventing arbitrary discussions of speed and accuracy trade-offs. Someone wins 70% of combat engagements against a given opponent rather than scoring 15 more points. Moreover, risk exposure is quantified by determining the likely casualties suffered to achieve victory. This combination makes the practical consequences of human performance differences tangible to the end users. Taken together, this approach advances the operations research analyses of squad-level combat engagements. Originality/value – For more than a century, marksmanship evaluations have used point-based systems to classify shooters. However, these scoring methods were developed for competitive integrity rather than lethality as points do not adequately capture combat capabilities. The proposed method thus represents a major shift in the marksmanship scoring paradigm

Leaning in to Address Sleep Disturbances and Sleep Disorders in Department of Defense and Defense Health Agency

Letter to the Editor, Military Medicine, 187, 5/6:155, 202217 USC 105 interim-entered record; under review.The article of record as published may be found at http://dx.doi.org/10.1177/0018720820906050In their article entitled, “Engaging Stakeholders to Optimize Sleep Disorders Management in the U.S. Military: A Qualitative Analysis,” Abdelwadoud and colleagues conducted focus groups of service members, primary care managers (PCMs), and administrative stakeholders about their perceptions, experiences, roles in sleep management, stated education needs, and management of sleep disorders.1 The qualitative methods are rigorous, and the findings reinforce and nuance prior results, especially regarding key requirements from PCMs. We feel compelled, however, to further nuance the authors’ conclusion that “current military sleep management practices are neither satisfactory nor maximally effective” and offer specific examples of actions taken by the Department of Defense (DoD) and Defense Health Agency (DHA) in recognition of the significance of optimal sleep in combat readiness and overall health of service members. We offer here a succinct list of concrete efforts to support and implement substantial clinical, operational, research, or educational efforts by the DoD or DHA to improve sleep in service members and associated clinical challenges in this unique population.Identified in text as U.S. Government work

Combined inhibition of nitric oxide and vasodilating prostaglandins abolishes forearm vasodilatation to systemic hypoxia in healthy humans

Abstract  We tested the hypothesis that nitric oxide (NO) and vasodilating prostaglandins (PGs) contribute independently to hypoxic vasodilatation, and that combined inhibition would reveal a synergistic role for these two pathways in the regulation of peripheral vascular tone. In 20 healthy adults, we measured forearm blood flow (Doppler ultrasound) and calculated forearm vascular conductance (FVC) responses to steady-state (SS) isocapnic hypoxia (O2 saturation ∼85%). All trials were performed during local α- and β-adrenoceptor blockade (via a brachial artery catheter) to eliminate sympathoadrenal influences on vascular tone and thus isolate local vasodilatory mechanisms. The individual and combined effects of NO synthase (NOS) and cyclooxygenase (COX) inhibition were determined by quantifying the vasodilatation from rest to SS hypoxia, as well as by quantifying how each inhibitor reduced vascular tone during hypoxia. Three hypoxia trials were performed in each subject. In group 1 (n= 10), trial 1, 5 min of SS hypoxia increased FVC from baseline (21 ± 3%;P \u3c 0.05). Infusion of NG-nitro-l-arginine methyl ester (l-NAME) for 5 min to inhibit NOS during continuous SS hypoxia reduced FVC by −33 ± 3% (P \u3c 0.05). In Trial 2 with continuous NOS inhibition, the increase in FVC from baseline to SS hypoxia was similar to control conditions (20 ± 3%), and infusion of ketorolac for 5 min to inhibit COX during continuous SS hypoxia reduced FVC by −15 ± 3% (P \u3c 0.05). In Trial 3 with combined NOS and COX inhibition, the increase in FVC from baseline to SS hypoxia was abolished (∼3%; NS vs. zero). In group 2 (n= 10), the order of NOS and COX inhibition was reversed. In trial 1, five minutes of SS hypoxia increased FVC from baseline (by 24 ± 5%;P \u3c 0.05), and infusion of ketorolac during SS hypoxia had minimal impact on FVC (−4 ± 3%; NS). In Trial 2 with continuous COX inhibition, the increase in FVC from baseline to SS hypoxia was similar to control conditions (27 ± 4%), and infusion of l-NAME during continuous SS hypoxia reduced FVC by −36 ± 7% (P \u3c 0.05). In Trial 3 with combined NOS and COX inhibition, the increase in FVC from baseline to SS hypoxia was abolished (∼3%; NS vs. zero). Our collective findings indicate that (1) neither NO nor PGs are obligatory to observe the normal local vasodilatory response from rest to SS hypoxia; (2) NO regulates vascular tone during hypoxia independent of the COX pathway, whereas PGs only regulate vascular tone during hypoxia when NOS is inhibited; and (3) combined inhibition of NO and PGs abolishes local hypoxic vasodilatation (from rest to SS hypoxia) in the forearm circulation of healthy humans during systemic hypoxia