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Adaptation to military operational stress is a complex physiological response that calls upon the sympathetic nervous system (SNS), hypothalamic pituitary adrenal (HPA) axis and immune system, to create a delicate balance between anabolism and catabolism and meet the demands of an ever-changing environment. As such, resilience, the ability to withstand and overcome the negative impact of stress on military performance, is likely grounded in an appropriate biological adaptation to encountered stressors. Neuroendocrine [i.e. cortisol, epinephrine (EPI), norepinephrine (NE), neuropeptide-Y (NPY), and brain derived neurotropic factor (BDNF)], inflammatory [i.e. interleukin 6 (IL-6), IL-1β, IL-4, IL-10 and tumour necrosis factor (TNF)-α], as well as growth and anabolic [i.e. insulin-like growth factor-I (IGF-I), testosterone, and dehydroepiandrosterone (DHEA)] biomarkers independently and interactively function in stress adaptations that are associated with a soldier's physical and psychological performance. In this narrative review, we detail biomarkers across neuroendocrine, inflammatory, and growth stimulating domains to better elucidate the biological basis of a resilient soldier. The findings from the reviewed studies indicate that military readiness and resiliency may be enhanced through better homeostatic control, better regulated inflammatory responses, and balanced anabolic/catabolic processes. It is unlikely that one class of biomarkers is better for assessing physiological resilience. Therefore, a biomarker panel that can account for appropriate balance across these domains may be superior in developing monitoring frameworks. Real-time physiological monitoring to assess biomarkers associated with resilience will be possible pending more sophisticated technologies and provide a field-expedient application for early identification and intervention of at-risk soldiers to improve military resiliency.

Extracellular vesicles (EV) are established mediators of adaptation to exercise. Currently, there are no published data comparing changes in EVs between men and women after resistance exercise. PURPOSE: We tested the hypothesis that EV profiles would demonstrate a sex-specific signature following resistance exercise. METHODS: Ten men and 10 women completed an acute heavy resistance exercise test for back squats using 75% of their one-repetition maximum. Blood was drawn before and immediately after exercise. EVs were isolated from plasma using size exclusion chromatography and stained with antibodies associated with exosomes (CD63), microvesicles (VAMP3), apoptotic bodies (THSD1), and a marker for skeletal muscle EVs (SGCA). RESULTS: CD63+ EV concentration and proportion of total EVs increased 23% (p=0.006) and 113% (p=0.005) in both sexes. EV mean size declined in men (p=0.020), but not women, suggesting a relative increase in small EVs in men. VAMP3+ EV concentration and proportion of total EVs increased by 93% (p=0.025) and 61% (p=0.030) in men and women, respectively. SGCA+ EV concentration was 69% higher in women compared to men independent of time (p=0.007). Differences were also observed for CD63, VAMP3, and SGCA median fluorescence intensity, suggesting altered surface protein density according to sex and time. There were no significant effects of time or sex on THSD1+ EVs or fluorescence intensity. CONCLUSION: EV profiles, particularly among exosome-associated and muscle-derived EVs, exhibit sex-specific differences in response to resistance exercise which should be further studied to understand their relationship to training adaptations.