Model-based Fatigue Risk Management

Fatigue in operational settings has many facets, as is discussed in various other contributions in this volume. One of the most pervasive manifestations of fatigue in today’s 24/7 economy is in the form of human impairment resulting from extended work hours and night and shift work. Such work schedules lead to sleep insufficiency and temporal misalignment relative to the biological clock (i.e., circadian misalignment). These neurophysiological challenges promote fatigue and cognitive deficits (Åkerstedt, 1995) and lead to accidents (Folkard & Åkerstedt, 2004) and increased operational costs (Rosekind, 2005; Ricci et al., 2007). There is a well-established neurobiology underlying such operationally important aspects of work scheduling, and understanding the dynamics of how this neurobiology drives fatigue1 is important for effectively managing fatigue risk. Figure 30.1 illustrates the two main neurobiological processes driving fatigue in the context of extended or shifted work schedules. They are a homeostatic process and a circadian process, both of which are fundamental to sleep/wake regulation (Borbély, 1982; Banks, Jackson & Van Dongen, Chapter 11, this volume). The homeostatic process seeks to balance the amounts of wakefulness and sleep, and extended wakefulness therefore results in a progressive build-up of pressure for sleep. If this pressure for sleep is not met – i.e., if a person is sleep-deprived – fatigue results (Van Dongen & Dinges, 2005). Thus, fatigue is regulated by the homeostatic process as a function of sleep/wake history. The homeostatic process operates on short timescales (hours to days), as well as on longer timescales (days to weeks). As such, both acute