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Virtual Environment Usage Protocols
Published in Waldemar Karwowski, Anna Szopa, Marcelo M. Soares, Handbook of Standards and Guidelines in Human Factors and Ergonomics, 2021
Kay M. Stanney, David A. Graeber, Robert S. Kennedy
The factors reviewed in Table 29.2 can be used to characterize the intensity of a VE stimulus. The technological factors (e.g., system consistency, lag, update rate, mismatched IPDs, and unimodal and intersensorial distortions) are system-specific and may be resolved—to some extent—as technology progresses, whereas the system design (e.g., DOF of user control, scene complexity), usage (e.g., exposure duration, intersession interval), and individual factors (e.g., susceptibility, gender) are not dependent on technological progress and will likely have an enduring influence on human–VE interaction. Among these factors, exposure durations of 15 min or more, very short (<2 days) or extended (>5 days) intersession intervals, high DOF of user control, and complex visual scenes are all known to lead to a more intense VE stimulus. In terms of user control, Held (1965) and Reason (1978) provided evidence that suggests that motion sickness can be overcome if users have control over their movements and receive an appropriate sensory response (e.g., visual, vestibular, or proprioceptive) to their actions. Essentially, in response to a neural mismatch (i.e., sensory conflict), users create a new “neural store” with which incoming sensory information is compared, eventually resulting in a new neural match (i.e. the reafference copy resulting from effector stimulation [i.e. stimuli resulting from one’s own muscular activity] overwrites the efference copy [i.e. motor impulses]). However, Stanney and Hash (1998) found that high DOF of motion, although being superior to passive motion in minimizing cybersickness, may not be the best solution to the sickness problem. Under such conditions, VE users may not be able to efficiently update the neural store with the abundant amount of sensory information resulting from their unrestricted movements. Thus, by allowing users streamlined control (i.e. only those DOF necessary for supporting an activity) within a VE, the neural store may be updated quickly in response to streamlined reafference.
The ‘sensory tolerance limit’: A hypothetical construct determining exercise performance?
Published in European Journal of Sport Science, 2018
Thomas J. Hureau, Lee M. Romer, Markus Amann
Neuromuscular fatigue develops during strenuous physical activities and causes a temporary reduction in the force or power generating capacity of a muscle or muscle group. This impairment stems from a decrease in neural activation of muscle (i.e. central fatigue) and/or biochemical changes at or distal to the neuromuscular junction that cause an attenuated contractile response to neural input (i.e. peripheral fatigue) (Bigland-Ritchie, Jones, Hosking, & Edwards, 1978). Despite this differentiation, exercise-induced fatigue needs to be viewed as an integrative phenomenon since interactions between central and peripheral fatigue can occur via humoral and non-humoral processes (Taylor, Amann, Duchateau, Meeusen, & Rice, 2016), with the latter including neural feedforward and feedback mechanisms. Although the significance of group III/IV muscle afferents is well described for the circulatory and ventilatory control during exercise, their role in the development of muscle fatigue and the interaction between central and peripheral fatigue is less well-recognised. Specifically, the neural feedforward component, which refers to corollary discharge (also called ‘efferent copy’) related to central motor command (Sperry, 1950; Wolpert, Ghahramani, & Jordan, 1995), is a neural signal generated in motor centres of the brain that is not directly involved in the ongoing motor activity (Poulet & Hedwig, 2007). Corollary discharges activate sensory areas within the cortex and thereby influence effort perception and ultimately the development of central fatigue during exercise (Gallagher et al., 2001; Liu et al., 2005). With progressive increases in peripheral fatigue during exercise at a fixed work rate, increases in central motor command are necessary to compensate for fatigued motor units. This increase in central command also increases corollary discharge (Eldridge, Millhorn, & Waldrop, 1981; Williamson et al., 2001) and likely central fatigue (Liu et al., 2005). Therefore, the increase in central command and subsequently central fatigue secondary to the increase in peripheral fatigue highlights the link between the two components of fatigue via a feedforward mechanism. While corollary discharges and associated anatomical structures are difficult to study in humans, related pathways have been identified, to a cellular level, in animals (Poulet & Hedwig, 2006, 2007). The neural feedback component entails afferent feedback (which increases with the development of peripheral fatigue) from contracting muscles to the CNS, the associated activation of sensory areas within the brain, and the subsequent facilitation of effort perception and central fatigue (Amann et al., 2011; Taylor et al., 2016). This interaction highlights the link between peripheral and central fatigue via a feedback mechanism.