Antioxidant and redox status after maximal aerobic exercise at high altitude in acclimatized lowlanders and native highlanders

Abstract

Exercise-induced increase in oxygen consumption leads to oxidative stress. On the contrary, hypoxia triggers oxidative stress despite decreased oxygen flux. Therefore, exercise under hypoxia may aggravate oxidative damage. Highlanders are expected to have better antioxidant capacity than lowlanders as a result of adaptation to hypoxia. The present study was undertaken to investigate the effect of exercise on antioxidant system in lowlanders and highlanders at high altitudes (HA). This study was conducted on active male volunteers, randomly selected and categorized into three groups, i.e., lowlanders tested at sea level (LL-SL, n = 35), lowlanders tested at altitude of 4560 m (LL-HA, n = 35) and native highlanders tested (HAN, n = 20) at the same height. Volunteers performed maximal exercise until exhaustion. Blood samples were collected before and after exercise. Both LL-SL and HAN had shown similar VO2max, which was significantly higher than LL-HA. GSH/GSSG ratio significantly increased in LL-SL and decreased in HAN after exercise. With exercise there were a decrease in superoxide dismutase and increase in glutathione peroxidase and catalase activities in HAN. Therefore, the results have suggested that HAN are more susceptible to oxidative stress when subjected to high-intensity exercise than lowlanders. The cumulative effect of higher VO2max and longer duration of exercise in hypoxia may be the reason of higher level of oxidative insult among HAN. Comparatively better management of antioxidant system observed in lowlanders at HA may be explained by the lower VO2max and shorter duration of exercise in hypoxia.

Antioxidant and oxidative stress responses of sojourners at high altitude in different climatic temperatures

“…In agreement with previous studies (Blatteis and Lutherer 1976;Robinson and Haymes 1990), the greater fall in VO 2max after hypoxia and cold exposure may be explained by the fall in maximum heart rate and tighter binding of oxygen to hemoglobin due to a drop in core body temperature which will ultimately impair oxygen supply to the active muscle (Bergh and Ekblom 1979;Bhaumik et al 2008). Our previous study had shown that reduction in VO 2max and duration of maximal exercise facilitates lowlanders to maintain better antioxidant status at HA as compared to native highlanders with higher VO 2max and greater performance duration (Sinha et al 2009). In the present study, the effect of unequal VO 2max levels between SOJ 1 and SOJ 2 on antioxidant system at HA can be nullified because both groups had followed submaximal exercise as a part of their daily routine fitness schedule.…”

Phenotypic plasticity and genetic adaptation to high-altitude hypoxia in vertebrates

“…This might be caused by a single amino acid substitution in subunit 3 of the protein that alters inter-subunit interactions (Scott et al, 2010). The importance of reducing ROS production in preventing oxidative damage is emphasized by studies comparing high-and low-altitude human populations: oxidative damage at high altitudes is generally less in highlanders even though most (but not all) antioxidant enzyme levels are reduced (Gelfi et al, 2004;Sinha et al, 2009a;Sinha et al, 2009b;Sinha et al, 2010). It is presently unclear how these evolutionary changes relate to the ancestral acclimatization response, but they should nonetheless be important for improving cell function at high altitudes.…”

Heightened Exercise-Induced Oxidative Stress at Simulated Moderate Level Altitude vs. Sea Level in Trained Cyclists

“…Many of the studies assessing oxidative stress and exercise under hypoxic conditions have examined the effects of high altitude (i.e., 3000m) in field-based studies, with prior exposure of the participants commonly not reported (Joanny et al, 2001;Miller et al, 2013;Sanchari et al, 2010;Sinha et al, 2009). At rest, the ascent (Møller et al, 2001;Siervo et al, 2014;Taylor et al, 2012) and descent (González et al, 2005) from altitude has been shown to cause marked increases in lipid peroxidation.…”

“…At rest, the ascent (Møller et al, 2001;Siervo et al, 2014;Taylor et al, 2012) and descent (González et al, 2005) from altitude has been shown to cause marked increases in lipid peroxidation. The participants in the current study had not been exposed to altitude for at least 4 months, minimizing the impact of prior exposure perturbing basal or exercise-induced redox state, which has previously been demonstrated in active individuals (Sanchari et al, 2010;Sinha et al, 2009). Our findings show that only selective biomarkers of oxidative stress were exaggerated following exercise under hypoxic conditions relative to normoxia.…”

“…Many of the studies in the literature investigating acute hypoxic exercise have not reported whether participants have been previously exposed to altitude or not, a factor that appears to markedly influence acute redox responses following exercise. Translation of previous studies conducted at high altitude (3000 m above sea level) (Joanny et al, 2001;Siervo et al, 2014;Sinha et al, 2009;Vij et al, 2005) is therefore difficult, given that competitive athletes are typically not exposed to elevations above 2500 m. Furthermore, because V O2max is reduced at altitude (Ferretti et al, 1997), cycling at the same absolute power output in hypoxia will result in higher relative exercise intensity (% V O2max). To determine whether differences in responses are due to hypoxia per se, rather than an increase in relative exercise intensity, trials can be instead matched based on a fraction of altitude-specific V O2max.…”