Pilot fatigue is a significant problem in modern aviation operations, largely because of the unpredictable work hours, long duty periods, circadian disruptions, and insufficient sleep that are commonplace in both civilian and military flight operations. The full impact of fatigue is often underappreciated, but many of its deleterious effects have long been known. Compared to people who are well-rested, people who are sleep deprived think and move more slowly, make more mistakes, and have memory difficulties. These negative effects may and do lead to aviation errors and accidents. In the 1930s, flight time limitations, suggested layover durations, and aircrew sleep recommendations were developed in an attempt to mitigate aircrew fatigue. Unfortunately, there have been few changes to aircrew scheduling provisions and flight time limitations since the time they were first introduced, despite evidence that updates are needed. Although the scientific understanding of fatigue, sleep, shift work, and circadian physiology has advanced significantly over the past several decades, current regulations and industry practices have in large part failed to adequately incorporate the new knowledge. Thus, the problem of pilot fatigue has steadily increased along with fatigue-related concerns over air safety. Accident statistics, reports from pilots themselves, and operational flight studies all show that fatigue is a growing concern within aviation operations. This position paper reviews the relevant scientific literature, summarizes applicable U.S. civilian and military flight regulations, evaluates various in-flight and pre-/postflight fatigue countermeasures, and describes emerging technologies for detecting and countering fatigue. Following the discussion of each major issue, position statements address ways to deal with fatigue in specific contexts with the goal of using current scientific knowledge to update policy and provide tools and techniques for improving air safety.

The phase advance from the combination of afternoon melatonin with next morning light is additive.

The dorsal and ventral aspects of the prefrontal cortex (PFC) are the two regions most consistently recruited in divergent thinking tasks. Given that frontal tasks have been shown to be vulnerable to sleep loss, we explored the impact of a single night of sleep deprivation on fluency (i.e., number of generated responses) and PFC function during divergent thinking. Participants underwent functional magnetic resonance imaging scanning twice while engaged in the Alternate Uses Task (AUT) – once following a single night of sleep deprivation and once following a night of normal sleep. They also wore wrist activity monitors, which enabled us to quantify daily sleep and model cognitive effectiveness. The intervention was effective, producing greater levels of fatigue and sleepiness. Modeled cognitive effectiveness and fluency were impaired following sleep deprivation, and sleep deprivation was associated with greater activation in the left inferior frontal gyrus (IFG) during AUT. The results suggest that an intervention known to temporarily compromise frontal function can impair fluency, and that this effect is instantiated in the form of an increased hemodynamic response in the left IFG.

Jet lag degrades performance and operational readiness of recently deployed military personnel and other travelers. The objective of the studies reported here was to determine, using a narrow bandwidth light tower (500 nm), the optimum timing of light treatment to hasten adaptive circadian phase advance and delay. Three counterbalanced treatment order, repeated measures studies were conducted to compare melatonin suppression and phase shift across multiple light treatment timings. In Experiment 1, 14 normal healthy volunteers (8 men/6 women) aged 34.9+/-8.2 yrs (mean+/-SD) underwent light treatment at the following times: A) 06:00 to 07:00 h, B) 05:30 to 07:30 h, and C) 09:00 to 10:00 h (active control). In Experiment 2, 13 normal healthy subjects (7 men/6 women) aged 35.6+/-6.9 yrs, underwent light treatment at each of the following times: A) 06:00 to 07:00 h, B) 07:00 to 08:00 h, C) 08:00 to 09:00 h, and a no-light control session (D) from 07:00 to 08:00 h. In Experiment 3, 10 normal healthy subjects (6 men/4 women) aged 37.0+/-7.7 yrs underwent light treatment at the following times: A) 02:00 to 03:00 h, B) 02:30 to 03:30 h, and C) 03:00 to 04:00 h, with a no-light control (D) from 02:30 to 03:30 h. Dim light melatonin onset (DLMO) was established by two methods: when salivary melatonin levels exceeded a 1.0 pg/ml threshold, and when salivary melatonin levels exceeded three times the 0.9 pg/ml sensitivity of the radioimmunoasssy. Using the 1.0 pg/ml DLMO, significant phase advances were found in Experiment 1 for conditions A (p < .028) and B (p < 0.004). Experiment 2 showed significant phase advances in conditions A (p < 0.018) and B (p < 0.003) but not C (p < 0.23), relative to condition D. In Experiment 3, only condition B (p < 0.035) provided a significant phase delay relative to condition D. Similar but generally smaller phase shifts were found with the 2.7 pg/ml DLMO method. This threshold was used to analyze phase shifts against circadian time of the start of light treatment for all three experiments. The best fit curve applied to these data (R(2) = 0.94) provided a partial phase-response curve with maximum advance at approximately 9-11 h and maximum delay at approximately 5-6 h following DLMO. These data suggest largest phase advances will result when light treatment is started between 06:00 and 08:00 h, and greatest phase delays will result from light treatment started between 02:00 to 03:00 h in entrained subjects with a regular sleep wake cycle (23:00 to 07:00 h).

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Appropriately timed 0.5 mg melatonin doses may avoid these problems.

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