Short-term high-intensity interval exercise training attenuates oxidative stress responses and improves antioxidant status in healthy humans

Highlights

• Training reduced oxidative stress markers during high intensity exercise.

• Training induced a marked elevation of antioxidant status indices.

• These adaptations were attained after a total of 22 min of high intensity training.

Abstract

This study investigated the changes in oxidative stress biomarkers and antioxidant status indices caused by a 3-week high-intensity interval training (HIT) regimen. Eight physically active males performed three HIT sessions/week over 3 weeks. Each session included four to six 30-s bouts of high-intensity cycling separated by 4 min of recovery. Before training, acute exercise elevated protein carbonyls (PC), thiobarbituric acid reactive substances (TBARS), glutathione peroxidase (GPX) activity, total antioxidant capacity (TAC) and creatine kinase (CK), which peaked 24 h post-exercise (252 ± 30%, 135 ± 17%, 10 ± 2%, 85 ± 14% and 36 ± 13%, above baseline, respectively; p < 0.01), while catalase activity (CAT) peaked 30 min post-exercise (56 ± 18% above baseline; p < 0.01). Training attenuated the exercise-induced increase in oxidative stress markers (PC by 13.3 ± 3.7%; TBARS by 7.2 ± 2.7%, p < 0.01) and CK activity, despite the fact that total work done was 10.9 ± 3.6% greater in the post- compared with the pre-training exercise test. Training also induced a marked elevation of antioxidant status indices (TAC by 38.4 ± 7.2%; CAT by 26.2 ± 10.1%; GPX by 3.0 ± 0.6%, p < 0.01). Short-term HIT attenuates oxidative stress and up-regulates antioxidant activity after only nine training sessions totaling 22 min of high intensity exercise, further supporting its positive effect not only on physical conditioning but also on health promotion.

Introduction

Low-volume, high-intensity interval training (HIT) has recently gained popularity as an effective method of improving anaerobic as well as aerobic fitness (Burgomaster et al., 2005, Burgomaster et al., 2006) in only a few sessions. This type of training has not only been used in healthy trained individuals, but also in patient populations with metabolic disorders such as obesity and type II diabetes (Gibala et al., 2012). The effectiveness of this type of training stems from a combination of high anaerobic demand, mainly in the first bouts and an increasingly high aerobic contribution as the high intensity bouts are repeated (Bogdanis et al., 1996, Parolin et al., 1999). As a result, adaptations include rapid increases in muscle oxidative capacity, as reflected by key mitochondrial enzymes, glucose transporters, and muscle membrane lactate transporters (Burgomaster et al., 2007). The key factor for the success of this exercise model is the combination of high intensity, corresponding to >200% of the power output eliciting maximal oxygen uptake and resulting in large changes in ATP:ADP/AMP ratio and the activation of 5′-adenosine monophosphate-activated protein kinase (AMPK) and peroxisome-proliferator activated receptor γ coactivator (PGC)-1α (Gibala et al., 2009, Gibala et al., 2012).

The large increase in metabolism during this type of exercise may cause increased production of reactive oxygen and reactive nitrogen species (RONS) that may not be counteracted by antioxidant defense systems, causing oxidative stress (Powers et al., 2011a, Powers et al., 2011b, Powers and Jackson, 2008). The sources of RONS production during or after HIT may be both the high oxygen consumption, as well as the high anaerobic metabolism inducing RONS production from xanthine and NADPH oxidase, ischemic reperfusion conditions, altered calcium homeostasis and induced muscle damage (Bloomer and Goldfarb, 2004, Hellsten, 1994, Nikolaidis et al., 2007, Nikolaidis et al., 2008, Powers et al., 2011a, Powers et al., 2011b). Although HIT is becoming a popular training modality for athletes as well as for the general population, there is very little and conflicting information regarding oxidative stress after an acute session (Bloomer et al., 2006, Deminice et al., 2010, Farney et al., 2012) or short-term training (Fisher et al., 2011, Hellsten et al., 1996). Bloomer et al. (2006) found that there was no increase in protein carbonyls (PC) and malondialdehyde (MDA), a lipid peroxidation marker, after six 10 s sprints with 3 min recovery in anaerobically trained men. However, Shing et al. (2007) found significant increases in MDA when trained cyclists performed nine bouts lasting 30 s each at 150% of power output eliciting maximal oxygen consumption (VO_2max). The only study that examined oxidative stress and antioxidant enzyme activity [glutathione peroxidase (GPX), superoxide dismutase (SOD) and catalase (CAT) activities] using the most popular protocol of HIT (i.e. repeated 30 s sprints) has followed individuals for only three sessions over one week period (Fisher et al., 2011). Antioxidant enzyme activity, measured in lymphocytes, was increased immediately after each exercise session, but returned to resting levels after 3–24 h post exercise, showing no significant training effect over the three sessions. However, oxidative stress measured indirectly in plasma as thiobarbituric acid reactive substances (TBARS) was attenuated after the third exercise session (Fisher et al., 2011). Therefore, the purpose of the present study was to investigate the acute (one session of four 30 s high intensity bouts) and the long-term changes in oxidative stress biomarkers and antioxidant status indices caused by a 3-week HIT regimen.