Prefrontal cortex hemodynamics and marksmanship accuracy following cold stress exposure

Military operations require performance in extreme environments, where cold stress exposure (CSE) may compromise safety and mission success. Using functional near-infrared spectroscopy (fNIRS), we examined the effects of CSE on marksmanship performance and prefrontal cortex (PFC) cerebral hemodynamics. We hypothesized that CSE will decrease performance and increase oxygenated (O₂Hb) and deoxygenated (HHb) hemoglobin under cold stress.

Thirteen participants (24.3 ± 3.2 years) completed thermoneutral (TN, 24 °C air, no water immersion) and CSE (0 °C air, 15 °C water) visits. Before (pre-) and after (post-) exposure, participants completed simple marksmanship and shoot/no-shoot tasks. The PFC O₂Hb and HHb were measured via fNIRS. Repeated-measures ANOVAs assessed condition and time-course effects on marksmanship performance, core (T_C) and skin temperature (T_SK). A general linear model evaluated differences in β-values between conditions.

Simple marksmanship HHb decreased after CSE (p = 0.001). Simple marksmanship post-TN saw a decrease in HHb compared to pre (p = 0.004), but no change in O₂Hb (p = 0.060). Shoot/no-shoot score increased across TN (p = 0.005). Shoot/no-shoot score decreased after CSE (p = 0.005) with an increase in no-shots (p = 0.027). Both shoot/no-shoot score (p = 0.008) and no-shots (p = 0.006) were worse at post-CSE compared to post-TN. During shoot/no-shoot a decrease in O₂Hb (p = 0.003) and HHb (p = 0.013) was observed across TN. Both O₂Hb (p = 0.003) and HHb (p = 0.013) were greater at post-CSE than post-TN.

Acute CSE does not affect low-difficulty static marksmanship but does impair high-difficulty dynamic marksmanship tasks, potentially due to reduced cognitive reserve after CSE. Neurophysiological mechanisms underlying decrements in tactical performance are effectively evaluated using fNIRS.