The implications of emerging technology on military human performance research priorities.

OBJECTIVES: To demonstrate the need for the military human performance research community to anticipate and evolve with the emergence of new and disruptive battlefield technologies that are changing the fundamental role of the human combatant. METHODS: An international team of military performance researchers drew on relevant literature and their individual national perspectives and experiences to provide an integrated forecast of research priorities and needs based on current trends. RESULTS: Rapid advances and convergence in fields such as robotics, information technology and artificial intelligence will continue to have a revolutionary impact on the battlefield of the future. The disruption associated with these technologies will most acutely be experienced by the human combatant at the tactical level, with increasing cognitive demands associated with the employment and use of new capabilities. New research priorities may include augmented performance of humans-machine teams, enhanced cognitive and immunological resilience based on exercise neurobiology findings, and psychophysiological stress tolerance developed in realistic but safe synthetic training environments. Solving these challenges will require interdisciplinary research teams that have the capacity to work across the physical, digital and biological boundaries whilst collaborating seamlessly with end-users, human combatants. New research methodologies taking full advantage of sensing technologies will be needed to provide rigorous, evidence-based data in real and near-real world environments. Longer term research goals involving biological manipulation will be shaped by moral, legal and ethical considerations and evolving concepts of what it means to be human. CONCLUSION: This paper outlines key recommendations to assist military human performance researchers to adapt their practice in order to match the increasing pace of military modernisation. By anticipating technological change and forecasting possible emerging technologies the military human performance research community can manoeuvre to prioritise research activities today in line with future needs and requirements.

Breathing 40% O(2) can attenuate postcontraction hyperaemia or muscle fatigue caused by static forearm contraction, depending on timing.

Little is known of the role of O(2)-dependent mechanisms in the hyperaemia associated with static muscle contraction or recovery from fatigue. Thus, in recreationally active, young, male subjects, forearm contraction was performed twice at 100% maximal voluntary effort until exhaustion, with a 7 min recovery period, whilst 40% O(2) (hyperoxia) was breathed during the contractions only, or during recovery only, or room air (normoxia) was breathed throughout. When hyperoxia was limited to the contractions, postcontraction increases in forearm blood flow, measured by venous occlusion plethysmography, were ∼25% lower (P < 0.05, n = 10) than during normoxia throughout. Furthermore, the postcontraction increase in venous lactate and fall in pH were attenuated (P < 0.05, n = 8). However, there was no effect on fatigue; time to voluntary exhaustion of contraction 2 was ∼25% less than for contraction 1 in both conditions. By contrast, when hyperoxia was limited to recovery (n = 10), there was no effect on postcontraction increases in forearm blood flow, but fatigue was ameliorated; time to voluntary exhaustion of contraction 2 was comparable to that of contraction 1. These results allow the novel conclusions that, even during static forearm contraction at 100% maximal voluntary effort, additional O(2) dissolved in plasma can attenuate the contribution made by O(2)-dependent dilator substances to postcontraction hyperaemia and that these substances may be released from the muscle fibres or blood vessel wall. Furthermore, they indicate that even in recreationally active individuals, recovery from fatigue can be improved by additional O(2) made available during recovery, and the O(2)-dependent mechanisms that contribute to fatigue are different from those that induce postcontraction hyperaemia.