Exercise-induced oxidative stress and hypoxic exercise recovery

Abstract

Hypoxia due to altitude diminishes performance and alters exercise oxidative stress responses. While oxidative stress and exercise are well studied, the independent impact of hypoxia on exercise recovery remains unknown. Accordingly, we investigated hypoxic recovery effects on post-exercise oxidative stress. Physically active males (n = 12) performed normoxic cycle ergometer exercise consisting of ten high:low intensity intervals, 20 min at moderate intensity, and 6 h recovery at 975 m (normoxic) or simulated 5,000 m (hypoxic chamber) in a randomized counter-balanced cross-over design. Oxygen saturation was monitored via finger pulse oximetry. Blood plasma obtained pre- (Pre), post- (Post), 2 h post- (2Hr), 4 h post- (4Hr), and 6 h (6Hr) post-exercise was assayed for Ferric Reducing Ability of Plasma (FRAP), Trolox Equivalent Antioxidant Capacity (TEAC), Lipid Hydroperoxides (LOOH), and Protein Carbonyls (PC). Biopsies from the vastus lateralis obtained Pre and 6Hr were analyzed by real-time PCR quantify expression of Heme oxygenase 1 (HMOX1), Superoxide Dismutase 2 (SOD2), and Nuclear factor (euthyroid-derived2)-like factor (NFE2L2). PCs were not altered between trials, but a time effect (13 % Post-2Hr increase, p = 0.044) indicated exercise-induced blood oxidative stress. Plasma LOOH revealed only a time effect (p = 0.041), including a 120 % Post-4Hr increase. TEAC values were elevated in normoxic recovery versus hypoxic recovery. FRAP values were higher 6Hr (p = 0.045) in normoxic versus hypoxic recovery. Exercise elevated gene expression of NFE2L2 (20 % increase, p = 0.001) and SOD2 (42 % increase, p = 0.003), but hypoxic recovery abolished this response. Data indicate that recovery in a hypoxic environment, independent of exercise, may alter exercise adaptations to oxidative stress and metabolism.

Acute Hypoxia and Exercise-Induced Blood Oxidative Stress

“…A follow-up study by our group was performed where subjects exercised at 975m with recovery in a hypoxic environment. Findings from the follow-up investigation reveal that normoxic exercise followed by hypoxic recovery attenuate the post exercise peak in plasma LOOH (Ballmann et al, 2014). Further investigation using multiple recovery altitudes confirmed that this finding in recovery is altitude-dependent (unpublished).…”

“…Other studies investigating ultra-marathon distances support an increase in plasma FRAP postexercise (Nieman et al, 2003;Quindry et al, 2008). Interestingly, current findings from our laboratory show that recovery from an identical exercise protocol, when performed in a hypoxic environment (5000 m) resulted in a decrease in plasma FRAP and TEAC compared with normoxic recovery (Ballmann et al, 2014). …”

Nrf2 mediates redox adaptations to exercise

“…Gene expression of Nrf2 and target SOD2 were shown to increase significantly in skeletal muscle of young fit males following an acute bout of cycling exercise lasting 90-min in normoxic recovery conditions [47]. Interestingly, these responses were not seen when recovery was performed under hypoxic conditions [47]. Similarly Nrf2 mRNA was significantly increased at 2-h post 30-min of moderate treadmill exercise in middle-aged women who were regular exercisers; however, sedentary women showed no change in gene expression for Nrf2 or targets in response to the exercise bout [48], suggesting that fitness may play a role in maintaining the acute Nrf2 response with aging.…”

“…Gene expression of Nrf2 and target SOD2 were shown to increase significantly in skeletal muscle of young fit males following an acute bout of cycling exercise lasting 90-min in normoxic recovery conditions [47]. Interestingly, these responses were not seen when recovery was performed under hypoxic conditions [47].…”

Use of Saliva Biomarkers to Monitor Efficacy of Vitamin C in Exercise-Induced Oxidative Stress

“…Blood is the most common for exercise-induced oxidative stress and biomarker extraction. Biomarkers present in blood include protein carbonyls [83,84,85,86]; total antioxidant capacity [87,88]; F 2 -isoprostanes [89,90]; malondialdehyde [91]; and Thiobarbituric Acid-Reactive Substances (TBARS), of malondialdehyde [92,93]. The presence of such blood biomarkers does not necessarily indicate damage is occurring in the surrounding cells/tissues; malondialdehyde, for instance, can be a product of actual damaged-tissue but also a product of reactive species.…”