DTIC ADA600954: Evaluation Of The Human/Extreme Environment Interaction: Implications For Enhancing Operational Performance And Recovery - Info and Reading Options
By Defense Technical Information Center
"DTIC ADA600954: Evaluation Of The Human/Extreme Environment Interaction: Implications For Enhancing Operational Performance And Recovery" and the language of the book is English.
“DTIC ADA600954: Evaluation Of The Human/Extreme Environment Interaction: Implications For Enhancing Operational Performance And Recovery” Metadata:
- Title: ➤ DTIC ADA600954: Evaluation Of The Human/Extreme Environment Interaction: Implications For Enhancing Operational Performance And Recovery
- Author: ➤ Defense Technical Information Center
- Language: English
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- Internet Archive ID: DTIC_ADA600954
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"DTIC ADA600954: Evaluation Of The Human/Extreme Environment Interaction: Implications For Enhancing Operational Performance And Recovery" Description:
The Internet Archive:
The purpose of this research determines how hypoxia interacts with exercise and recovery to yield various metabolic responses that may affect performance and performance at high-altitude critical to mission success. Participants completed a maximal exercise test under normoxic conditions (975 m). Four experimental trials were completed including 60 minutes of cycling (70% of Wmax) followed by 6 h of recovery at four different simulated altitudes (0 m, 1667 m, 3333 m, or 5000 m) using a randomized, counterbalanced, cross-over design over the span of 4 weeks, with a minimum of 7 days between trials. Blood O2 saturation was measured via pulse oximetry every hour during the 6 h recovery period. Muscle biopsies were obtained from the vastus lateralis pre- and 6 h post-exercise for analysis of mitochondrial related gene expression. Blood O2 saturation decreased with each increase in simulated altitude during recovery (0 m: 98 1%; 1667 m: 94 1%; 3333 m: 90 1%; 5000 m: 79 2%; p 0.05). Expression of PGC-1 , HK, and SOD increased significantly with exercise (p 0.05), but were not different between trials. Similarly, markers of oxidative stress indicated a time-dependent response following exercise for all variables (p0.05), but the two highest recovery altitudes (3333m and 5000m) demonstrated a partially attenuated this response for LOOH (p0.001). These data demonstrate no dose-response relationship between magnitude of hypoxic exposure and mitochondrial gene expression yet minor alterations in oxidative stress. Therefore, the paradox of mitochondrial function in response to acute and chronic exposure to hypoxia cannot be explained by the magnitude of hypoxia. Of additional interest in year three of this project series related to the evaluation of advanced instrumentation to determine changes in hydration status in parallel to established markers from urine and isotopic enrichment methodologies.
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