Characterizing Hyperoxia-Induced Alterations in Muscular Physiology: Part 2
Abstract
Hyperoxia causes oxidative stress, which potentially disrupts mitochondrial processes; however, there are scarce data in skeletal muscle following hyperoxic environments. Ten subjects completed 6-hour dry dives on three consecutive days while breathing 100 oxygen at 1.35 atmospheres absolute (ATA). Muscle biopsy samples were collected before diving and post-dive 3 for measurements of messenger ribonucleic acid (mRNA) associated with mitochondrial function, mitochondrial biogenesis and dynamic regulation, antioxidants, mitophagy, and proteomics. Aerobic performance with surface electromyography (sEMG) devices on the lower limb muscles were completed before diving, post-dive 3, and 48 hr after dive 3. sEMG measurements consisted of burst duration, cycle duration, interburst interval, amplitude, and time to peak amplitude. There were no changes in mitochondrial mRNA measurements (p > .050). However, 144 proteins were differentially expressed after hyperoxic diving; 122 proteins were up-regulated (p < .050 and difference >0.585(fold change >1.5) and 22 were down-regulated (p < .050 and log2 fold change <-0.585(fold change < 1/1.5). There were no changes in any sEMG measurements (p > .050). These findings suggest that skeletal muscle mitochondria mRNA markers associated with stress and lower body neuromuscular fatigue are unlikely to be causes of hyperoxia-induced decreases in aerobic exercise performance. However, the proteomics analysis provides novel data on how hyperoxia influences the skeletal muscle proteome, which can be leveraged in future research.
Document Details
- Document Type
- Technical Report
- Publication Date
- Nov 01, 2022
- Accession Number
- AD1196109
Entities
People
- Alex O. Klemp
- Mitchell D. Reed
Organizations
- United States Navy Experimental Diving Unit