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Altitude exposure impairs exercise performance, while altitude acclimatization partially mitigates performance decrements. Non-acclimatization means to improve performance are presented. Acute exposure to terrestrial altitude (hypobaric hypoxia) causes decrements in endurance performance relative to sea level. Altitude acclimatization consistently results in partial attenuation of these decrements, but due to logistical challenges, it is not readily implemented. We discuss mechanisms and impact (or lack thereof) of other non-acclimatization interventions to improve endurance performance and provide suggestions for future research directions. [ABSTRACT FROM AUTHOR]

Wet clothing is less insulative than dry clothing and consequently increases heat loss in cold air. Tactical necessity can render removal of wet clothing impossible and/or require Warfighters to remain static to avoid detection, limiting heat production and posing a threat of hypothermia (core temperature <35 °C). This study aimed to characterize body temperatures and evaluate hypothermia risk while statically exposed to 5 °C air wearing three wet military uniforms. Further, low-speed loaded walking was evaluated as a strategy to raise end-static temperatures. Twelve adults (11 M, 1 F) randomly completed three wet-cold trials wearing either the Improved Hot Weather Combat Uniform (IHWCU), Army Combat Uniform (ACU), or ACU with silk-weight base layer (ACU+). Each trial involved 180 min of cold air (5.3 ± 0.3 °C, 0.8 m·s−1) exposure after a clothed 2 min head-out immersion (34.0 ± 0.2 °C). Volunteers were static for 60 min followed by 120 min of walking with a rucksack. Rectal temperature (Tre) area under the curve did not differ among the three wet uniforms when static (p = 0.431) with Tre increasing, rather than decreasing, across the 60 min (IHWCU: +0.26 ± 0.19 °C, ACU: +0.37 ± 0.21 °C, ACU+: +0.36 ± 0.20 °C). Hypothermia risk with 60 min static wet-cold exposure therefore appears minimal, regardless of the military uniform worn, in an otherwise low stress cohort. End-static finger temperatures (IHWCU: 9.48 ± 2.30 °C, ACU: 9.99 ± 1.82 °C, ACU+: 9.27 ± 1.66 °C, p > 0.999) were reduced by ∼20–23 °C posing a considerable dexterity concern. Heat production of ∼210 W·m2 appeared sufficient to begin to reverse negative cumulative heat storage and initiate slight elevations of rectal and peripheral temperatures, although finger temperatures increased <2 °C after 120 min. ClinicalTrials.gov ID: NCT05409937. [ABSTRACT FROM AUTHOR]

Ischemic preconditioning (IPC) involves brief, repeated bouts of limb occlusion and reperfusion capable of improving exercise performance at least partially by enhancing local skeletal muscle oxygenation. This study sought to investigate the effect of a lower limb IPC protocol, with either a 5-min or 45-min post-application delay, on vastus lateralis tissue saturation index (TSI) and systemic cardiac hemodynamics at rest and during short-duration intense cycling. Twelve young adults randomly completed four interventions: IPC (at 220 mmHg) with 5-min delay (IPC5), IPC with 45-min delay (IPC45), SHAM (at 20 mmHg) with 5-min delay (SHAM5), and SHAM with 45-min delay (SHAM45). Following IPC intervention and recovery delay, participants completed 5, 60-s high-intensity (100% Wpeak) cycle sprints separated by 120-sec of active recovery (30% Wpeak). Compared to baseline, TSI immediately following IPC5, but pre-exercise, remained lower than the equivalent for IPC45 (−5.9 ± 1.5%, p =.002). IPC, imposed at least 45-min before the completion of five 60-s sprint cycling efforts, significantly enhanced TSI during active recovery between sprint intervals compared to a 5-min delay (6.6 ± 2.4%, p =.021), and identical SHAM conditions (SHAM5: 5.8 ± 2.2%, p =.024; SHAM45: 6.2 ± 2.5%, p =.029). A 45-min delay following IPC appears to provide heightened skeletal muscle metabolic rebound prior to intense sprint cycling as compared to a 5-min delay. Furthermore, IPC followed by a 45-min delay enhanced recovery of skeletal muscle oxygenation during low intensity active sprint recovery, despite an unchanged decline in skeletal muscle oxygenation during near-maximal sprinting efforts. [ABSTRACT FROM AUTHOR]

Habituation is an adaptation seen in many organisms, defined by a reduction in the response to repeated stimuli. Evolutionarily, habituation is thought to benefit the organism by allowing conservation of metabolic resources otherwise spent on sub-lethal provocations including repeated cold exposure. Hypermetabolic and/or insulative adaptations may occur after prolonged and severe cold exposures, resulting in enhanced cold defense mechanisms such as increased thermogenesis and peripheral vasoconstriction, respectively. Habituation occurs prior to these adaptations in response to short duration mild cold exposures, and, perhaps counterintuitively, elicits a reduction in cold defense mechanisms demonstrated through higher skin temperatures, attenuated shivering, and reduced cold sensations. These habituated responses likely serve to preserve peripheral tissue temperature and conserve energy during non-life threatening cold stress. The purpose of this review is to define habituation in general terms, present evidence for the response in non-human species, and provide an up-to-date, critical examination of past studies and the potential physiological mechanisms underlying human cold habituation. Our aim is to stimulate interest in this area of study and promote further experiments to understand this physiological adaptation. [ABSTRACT FROM AUTHOR]