Over the past three decades, the investigation of oxidative stress has continued to gain popularity within the medical and exercise science community (14). Oxidative stress occurs when the body’s antioxidant defenses are unable to adequately combat reactive oxygen and nitrogen species (RONS), ultimately leading to the oxidation of lipids, proteins, DNA, and other biological molecules (2). Although the production of RONS is a normal physiological process and can occur with a variety of stressors (e.g., nutrient consumption, environmental toxins, and strenuous physical work), when produced in excess, RONS can be damaging to body tissues (30). In fact, extensive cellular oxidation can severely compromise cell viability and contribute to ill health and disease (11).
It has been reported that acute exercise of sufficient intensity (22,28) and duration (4) can lead to an increase in RONS and induce an acute state of oxidative stress (14). However, this finding is not ubiquitous, and the discrepancy may be at least partly related to differences in exercise intensity across study protocols. In addition, the vast differences in exercise training status of participants, ranging from sedentary to highly trained, may further the discrepancies among studies. Moreover, many studies involving the measure of blood oxidative stress have failed to correct for changes in plasma volume during the postexercise period, which may have provided erroneous inflation of postexercise data points. This failure ultimately may have led to inaccurate conclusions regarding the degree of oxidative stress during the postexercise period.
Participating in a regular exercise program is associated with a chronic increase in endogenous antioxidant enzyme activity (24,25,34), which may serve to provide protection against the exercise-induced increase in RONS (2). Exercise-induced RONS production leads to the activation of the redox-sensitive transcription factor known as nuclear factor-κB, which upon activation leads to the expression of antioxidant enzymes (16). Moreover, a decrease in RONS production may be apparent after repeated exposure to the same stressor, as well as increased activity of specific repair enzymes (30), such as oxoguanine DNA glycosylase (OGG1) and uracil DNA glycosylase. These adaptations and others are in accordance with the principle of hormesis, which states that in response to repeated exposure to various stressors, the body undergoes favorable adaptations that may result in enxhanced physiological protection, performance, and/or physical health (29).
Exercise-induced oxidative stress has been observed for all types of exercise, including aerobic (13,24,34) and anaerobic (6), with different mechanisms of RONS generation for each (20). In terms of aerobic exercise, most laboratory-based studies have used treadmill walking/running or stationary cycling performed for 30–60 min at 60%–80% V˙O2max (14). In terms of anaerobic exercise, protocols have involved dynamic resistance exercise (5,6,19), eccentric exercise (26), jumping (27), and sprinting (17). As regards anaerobic exercise, very few studies have compared intensity and duration within the same design.
To our knowledge, no study has compared both aerobic and anaerobic exercise bouts of different intensities and/or durations on biomarkers of oxidative stress within a sample of exercise-trained men. When concerned with identifying the magnitude of exercise-induced oxidative stress, attempting to generalize findings collected from sedentary or poorly trained subjects to those who are well trained may prove problematic. We included a sample of well-trained men and studied the change in oxidative stress biomarkers after 1) moderate-intensity and moderate-duration steady-state aerobic cycling exercise, 2) high-intensity and moderate-duration interval cycle sprints, and 3) maximal-intensity and short-duration interval cycle sprints. We hypothesized that because of adaptations specific to attenuation in RONS production, as well as heightened antioxidant status in our exercise-trained subjects, a small but significant oxidative stress would be observed after exercise, in an intensity-dependent manner (greatest for maximal-intensity sprints, lowest for aerobic exercise).
Twelve healthy, exercise-trained men between the ages of 21 and 35 yr were recruited to participate. All subjects completed a health history and physical activity questionnaire before enrollment, including training status classification. To be classified as “exercise trained” for the purposes of the study, subjects had to be participating in a structured exercise training program (including both aerobic and anaerobic) for the past 12 months, with each session lasting no less than 45 min per session, as well as no less than three sessions per week. Subjects’ exercise sessions had to be performed at a minimum average rating of 15 (i.e., hard) on the Borg RPE (6–20) scale. This training classification was documented with each subject by completing a detailed exercise training history in conjunction with personal interviews.
All experimental procedures were performed in accordance with the Declaration of Helsinki and approved by The University of Memphis Human Subjects Review Board. Subjects provided both verbal and written informed consent. Along with completing a health history and physical activity questionnaire, subjects underwent a physical examination that included hemodynamic and anthropometric testing. Body fat was estimated via seven-site skinfold determination and use of the Siri equation (33). Resting HR and blood pressure were recorded after a 10-min quiet rest period. Subjects were not obese (body mass index ≤30 kg·m−2) and were free of any diagnosed cardiovascular, metabolic, or pulmonary disease as defined by the American College of Sports Medicine (38). In addition, subjects were nonsmokers and did not use medications (e.g., anti-inflammatory or cardiovascular drugs) or nutritional supplements (e.g., antioxidants) during the study, because these might have effects to our outcome measures. Following all screening procedures, including the graded exercise test (GXT) as described in the next part of this article, subjects were scheduled for testing and given detailed instructions and data forms related to the recording of both dietary and physical activity data during the 48 h before the testing days. Subject characteristics are presented in Table 1.
A maximal GXT was conducted to determine aerobic capacity (V˙O2max) and maximal aerobic power output (W max) using a Lode Excalibur Sport™ cycle ergometer (Lode B.V., Groningen, The Netherlands). Expired gases were collected via facemask and analyzed using a SensorMedics Vmax 229™ metabolic cart system (SensorMedics, Inc., Yorba Linda, CA) for determination of maximal oxygen consumption (V˙O2max). This test was necessary for prescribing the intensity for the acute exercise sessions (moderate-intensity and moderate-duration steady-state aerobic exercise, high-intensity and moderate-duration interval sprints, and maximal-intensity and short-duration interval sprints, as described in the next part of this article). After warming up at 50 W for 3 min, the test began at 100 W and increased 25 W·min−1. The test was terminated once the participant was no longer able to continue because of fatigue (rpm drops below 50). The maximal wattage obtained during testing was used to calculate the workloads to be used during sprint intervals. During the final stage, subjects had to continue for a minimum of 30 s in order for the wattage to be considered their peak wattage, as has been done previously (7). Before and during the GXT, HR was continuously monitored via ECG tracings using a SensorMedics Max-1™ ECG unit. Expired oxygen and RER data were continuously monitored via breath-by-breath samples. Participant effort was monitored using the Borg scale of exertion. Subjects were allowed an active cool-down period (e.g., slow-speed cycling) for several minutes until their HR fell below 120 bpm or stabilized. Subjects were instructed not to perform any strenuous physical tasks during the 48-h period before the GXT.
Acute exercise sessions
Approximately 1 wk after the GXT, subjects participated in four additional sessions separated by 1 wk. Sessions were counterbalanced and included either a no-exercise condition or one of the three exercise conditions. For the no-exercise rest bout, subjects reported to the laboratory and simply rested for the entire period. As with the exercise bouts, four blood samples were obtained. The first was taken after a 10-min rest period (as was the case for all conditions). Subjects then rested for 20 min (the same duration as the sprint exercise bouts). A blood sample was collected at the end of the 20-min rest period (corresponding to the immediate postexercise blood samples) and 30 and 60 min after the 20-min rest period (corresponding to the postexercise blood samples).
All exercise bouts were performed on the same cycle ergometer used for the GXT, and subjects reported to the laboratory in the morning (0600–0900 h) after a minimum 10-h overnight fast. HR was continuously monitored via Polar™ HR monitors, and subjects received similar verbal encouragement by research assistants during all three exercise bouts. The exercise included one steady-state aerobic bout and two different intermittent anaerobic sprint bouts. The rationale for our use of the specific intensity and duration of the exercise bouts was based on recent literature demonstrating that low-volume, high-intensity “sprint”-type exercise elicits similar acute responses and chronic adaptations as compared with the more traditional high-volume aerobic exercise (8–10,35,36). It should be noted that the denotation of exercise as “moderate” or “short” duration was related to the specific type of exercise (i.e., 60 min was considered moderate duration for aerobic exercise, whereas 60 s was considered moderate duration for anaerobic sprint exercise). Pilot testing confirmed that the three bouts were challenging, yet subjects were able to complete all protocols. The exercise bouts were as follows:
- The moderate-intensity and moderate-duration steady-state aerobic exercise bout was performed at 70% of HR reserve for 60 min. This intensity corresponds to approximately 70% V˙O2max. HR and RPE were monitored continuously, and the workload (wattage) was adjusted every 5 min as necessary to maintain 70% of HR reserve. HR, RPE, and workload (wattage) were recorded every 5 min. The mean values for all variables were calculated and reported. A similar intensity and duration of exercise have been used in many other studies focused on exercise-induced oxidative stress (4,15,24).
- The high-intensity and moderate-duration interval sprints consisted of five 60-s sprints performed at a wattage equal to 100% of that at V˙O2max, followed by 225 s of recovery (1:3.75 work-to-rest ratio). Within each interval, subjects were instructed to pedal between 80 and 100 rpm for the first 45 s, and then for the final 15 s, subjects were instructed to pedal as fast as possible. Rate of perceived exertion was recorded twice during each interval: once at 45 s and again after the final 15 s of sprinting. The average of the two RPE values was used in the analysis (for comparison of RPE during the three different exercise bouts). HR was recorded at the cessation of each sprint. During the recovery periods, the subjects were encouraged to dismount the cycle and walk around in an attempt to reduce venous pooling in the lower extremities and to minimize feelings of light headedness or nausea. This protocol equated to 20 min. However, only 300 s of actual work was performed, but this was performed at half the intensity of the short intervals.
- The maximal-intensity and short-duration interval sprints consisted of ten 15-s sprints performed at a wattage equal to 200% of that at V˙O2max, followed by 116 s of recovery (1:7.7 work-to-rest ratio). After each sprint, HR and RPE were recorded. During the recovery periods, the subjects were encouraged to dismount the cycle and walk around in an attempt to reduce venous pooling in the lower extremities and to minimize feelings of light headedness or nausea. This protocol equated to 20 min. However, only 150 s of actual work was performed, but this was performed at double the intensity of the moderate duration intervals.
For all exercise conditions, blood was collected from subjects before exercise (after 10-min of quiet rest), immediately concluding exercise (0 min), and at 30 min and 60 min after exercise. The collection times for the no-exercise rest condition matched those of the sprint sessions. Subjects remained in the laboratory during this period and expended little energy (i.e., watched movies and worked on the computer). No meals or calorie-containing beverages were allowed during this period, but water was allowed ad libitum.
Blood collection and biochemistry
Blood samples were collected in vacuum tubes via venipuncture. Approximately 15 mL of blood was taken from subjects for all exercise modes (and for the no-exercise rest condition) at the following time points: before exercise, immediately after exercise, and 30 and 60 min after exercise. As measures of oxidative stress, samples were analyzed for malondialdehyde (MDA), hydrogen peroxide (H2O2), advanced oxidation protein products (AOPP), and nitrate/nitrite (NOx). As measures of antioxidant status, Trolox equivalent antioxidant capacity (TEAC), superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx) were measured. Blood lactate was also measured as an indicator of anaerobic metabolism.
Single samples were immediately analyzed (from EDTA-containing tubes) for whole-blood lactate using a Lactate Plus™ portable lactate analyzer (Nova Biomedical, Waltham, MA). The remainder of the whole blood collected into the EDTA tubes was centrifuged at 1500 rpm for 15 min at 4°C and then processed for plasma and stored at −70°C until analyzed. Whole blood collected into tubes containing no additive was allowed to clot for 30 min at room temperature, centrifuged at 1500 rpm for 15 min at 4°C, and then processed for serum and stored at −70°C until analyzed.
MDA was analyzed following the procedures of Jentzsch et al. (21) using commercially available reagents (Northwest Life Science Specialties, Vancouver, WA). Hydrogen peroxide was analyzed using the Amplex Red reagent method as described by the manufacturer (Molecular Probes, Invitrogen Detection Technologies, Eugene, OR). AOPPs were analyzed as previously described (39). Nitrate/nitrite was analyzed using a commercially available colorimetric assay kit (Cayman Chemical, Ann Arbor, MI) according to the procedures provided by the manufacturer. Antioxidant capacity was analyzed using the TEAC assay using procedures outlined by Sigma Chemical (St. Louis, MO). SOD activity was measured using enzymatic procedures as described by Cayman Chemical, where one unit of SOD is the amount of enzyme needed to exhibit 50% dismutation of the superoxide radical. CAT activity was measured using the Amplex Red reagent method as described by Molecular Probes, Invitrogen Detection Technologies. GPx activity was measured using enzymatic procedures as described by Cayman Chemical. Values for GPx were calculated using the NADPH extinction coefficient and are presented in nanomoles per minute per milliliter, where one unit is defined as the amount of enzyme needed to oxidize 1.0 nmol of NADPH to NADP+. Finally, hematocrit and hemoglobin were measured as part of a complete blood count using an automated cell counter (Coulter LH 750; Beckman Coulter, Brea, CA). Plasma volume was then corrected using the guidelines provided by Dill and Costill (12).
Dietary records and physical activity
All subjects were instructed to maintain their normal diet throughout the study period. Food logs during the day before each test day were maintained by subjects, analyzed by research staff, and returned to subjects so that they were able to mimic this intake during all subsequent days preceding testing. Nutritional records were analyzed for total calories, protein, carbohydrate, fat, and a variety of micronutrients (Food Processor SQL, version 9.9; ESHA Research, Salem, OR). Subjects were instructed to maintain their normal physical activity habits with the exception of specific instructions to abstain from alcohol consumption and strenuous exercise during the 48 h immediately preceding the test days to control for any acute effects of physical activity on oxidative stress and associated variables (e.g., inflammation). In addition, this potentially reduces undue fatigue by performing strenuous exercise during the hours before the actual test days.
The data obtained were analyzed using a four (condition)-by-four (time) repeated-measures ANOVA. Significant interactions and main effects were further analyzed for pairwise comparisons using Tukey post hoc tests. Dietary variables and all other data collected in relation to the exercise tests (e.g., mean HR and RPE) were compared using a one-way ANOVA. All analyses were performed using JMP statistical software (SAS Institute, Cary, NC). Statistical significance was set at P ≤ 0.05. The data are presented as mean ± SEM.
All 12 subjects completed all aspects of this study. Subject’s characteristics are presented in Table 1. As expected, a condition effect was noted for HR (P < 0.0001) and RPE (P < 0.0001), with HR and RPE values higher for all exercise conditions as compared with rest (P < 0.05). For HR, the 60-s sprint was greater than the 60-min aerobic and 15-s sprint (P < 0.05). For RPE, the 60-s sprint and the 15-s sprint were greater than the 60-min aerobic, and the 15-s sprint was greater than the 60-s sprint (P < 0.05). Also, as expected, a condition effect was noted for power (W) and total work (P < 0.0001), with values higher for all exercise conditions as compared with rest (P < 0.05). For power, values for the 60-s sprint and 15-s sprint were greater than those for the 60-min aerobic, whereas values for the 15-s sprint were greater than those for the 60-s sprint (P < 0.05). For total work, values for the 60-s sprint and 15-s sprint were less than those for 60-min aerobic (P < 0.05). Exercise test-related data are presented in Table 2. Dietary data during the 24 h before each test day were not different (P > 0.05). Dietary data are presented in Table 3.
As regards lactate, an interaction was noted (P < 0.0001). Values were higher at 0 and 30 min after exercise as compared with that before exercise for the 60-s sprint and the 15-s sprint (P < 0.05). Values were different between the two sprint exercise bouts and the rest and 60-min aerobic exercise conditions at the 0- and 30-min postexercise times (P < 0.05). A condition effect was noted (P < 0.0001), with values for the two sprint exercise bouts higher than those for the rest and 60-min aerobic exercise conditions (P < 0.05). A time effect was noted (P < 0.0001), with values higher at all times after exercise as compared with that before exercise, at 0 min after exercise as compared with 30 and 60 min after exercise, and at 30 min after exercise as compared with 60 min after exercise (P < 0.05). Data for lactate are presented in Table 4.
For TEAC, an interaction was noted (P = 0.0003) with values higher at 60 min after exercise as compared with that before and 0 min after exercise for the 15-s sprint (P < 0.05). A condition effect was noted (P = 0.004) with values higher for 60-s sprint and 15-s sprint as compared with 60-min aerobic (P < 0.05). A time effect was noted (P < 0.0001) with values higher at 30 and 60 min after exercise as compared with that before exercise and 0 min after exercise (P < 0.05). For SOD, no interaction was noted (P = 0.14). However, a condition effect was noted (P = 0.02) with values higher for 15-s sprint as compared with 60-min aerobic (P < 0.05). A time effect was noted (P = 0.0005) with values higher at 30 and 60 min after exercise as compared with 0 min after exercise (P < 0.05). For CAT, an interaction was noted (P = 0.003) with values lower at 0 min after exercise as compared with all other times for the 60-s sprint and 15-s sprint (P < 0.05). A condition effect was noted (P = 0.05) with values lower for 60-s sprint as compared with no exercise (P < 0.05). A time effect was noted (P < 0.0001) with values higher at all times as compared with 0 min after exercise (P < 0.05). GPx was not different between conditions or across time (P > 0.05). Antioxidant enzyme (SOD, CAT, and GPx) and TEAC data are presented in Table 4. No interactions, condition, or time effects were noted for MDA, H2O2, AOPP, or NOx (P > 0.05). Data for MDA and H2O2 are presented in Figure 1, whereas data for AOPP and NOx are presented in Figure 2.
The present study compared oxidative modification of blood lipids and proteins, as well as antioxidant capacity after both aerobic and anaerobic exercise bouts performed by exercise-trained men. To our knowledge, no study to date has compared both aerobic and anaerobic exercise bouts of different intensities and/or durations on biomarkers of oxidative stress—in particular, within a sample of exercise-trained men. Our data indicate that antioxidant capacity is generally highest at 30 and 60 min after exercise and lowest at 0 min after exercise. Moreover, a significant oxidative stress is not observed for any measured variable in response to the three exercise modes despite the great physical demand imposed by the exercise (cycle sprinting in particular).
Our findings support the notion that within a sample of well-trained men, there is minimal oxidative stress during the acute postexercise period. That being said, we did note a decrease in CAT activity during the immediate postexercise period, which may suggest an increase in RONS production (e.g., superoxide leading to H2O2) and subsequent use of CAT in defense. It is important to note a few limitations of this work in relation to our overall findings. First, we only measured selected biomarkers of oxidative stress and antioxidant activity and did not include an exhaustive list of potential markers. Although we believe that our array of biomarkers is well able to characterize the oxidative status during the postexercise period (and clearly equals or exceeds that of many similar investigations), the inclusion of additional biomarkers may have strengthened this study. Specifically, the measurement of glutathione (GSH) status (total, oxidized, and reduced) would have added to this work, because GSH is sacrificed in response to an increase in RONS and is viewed as both a reliable and sensitive indicator of redox status (32). Second, it is possible that oxidative stress may have occurred in tissues aside from blood, such as skeletal muscle, which may be the ideal tissue when studying exercise stress. Of course, biopsies are required for obtaining samples for analyses, which is likely the reason why so few human investigations include the analysis of oxidative stress biomarkers in skeletal muscle. As reported previously using an animal model, changes in oxidative stress observed during the postexercise period may not be the same when comparing blood and skeletal muscle (40). Third, although our time course of measurement is similar to that used in many other studies of exercise-induced oxidative stress, it is possible that an oxidative stress may have been observed at times distant to 1 h after exercise. Collectively, these limitations should be considered in relation to our overall findings.
The lack of a significant increase in oxidative stress biomarkers is interesting despite the very high intensity nature of the exercise protocols (significant postexercise increase in blood lactate, Table 4). These results are in accordance with other investigations that have found no significant rise in oxidative stress biomarkers despite large increases in lactate (3,31). However, our results contradict the work of others, including Lovlin et al. (22) who noted an association between MDA and lactate at maximal exertion. It is likely that difference in the assay techniques, the timing of sample collection, and the training status of subjects all may be responsible for the discrepancies in findings between the current investigation and that of Lovlin et al.
It is important to note that all postexercise blood samples herein were corrected for changes in plasma volume. Plasma volume decreases in response to exercise-induced dehydration (12), because solute-free, aqueous plasma diffuses into cells from the blood, in an attempt to maintain intracellular and extracellular ion concentrations. This change has not been corrected for in many studies of exercise-induced oxidative stress and may be one additional reason for conflicting findings.
Contrary to what we hypothesized, and possibly on the basis of factors discussed previously (e.g., plasma volume correction and use of exercise-trained men), our investigation failed to report a statistically significant increase in blood oxidative stress. Results from sprinting protocols have been mixed among the different biomarkers used to assess oxidative stress, and increases have been noted for lipid peroxidation (1,17,23). Marzatico et al. (23) investigated two different types of exercise involving either running a half marathon or a sprint exercise session of 6 × 150-m sprints (subjects were either marathon trained or sprint trained). On the one hand, the authors noted significant postexercise increases in MDA for both protocols—in opposition to the present findings. On the other hand, our findings are in accordance with other investigations that have failed to find significance regarding MDA after sprint exercise (5,17). Modality may be one discrepancy between our investigation and that of Marzatico et al. Running was used in the Marzatico et al. investigation, which when compared with cycling, involves more muscle groups and incorporates eccentric muscle actions. This may elicit greater muscular work and damage, potentially leading to increased RONS production. The significant findings regarding the aerobic bout in the Marzatico et al. may be due to intensity. For example, although the duration used in our investigation was 60 min, compared with the 68 min taken to run the half marathon in the Marzatico et al. (23) investigation, subjects likely were exercising at a higher intensity during the half marathon to complete a 13.1-mile run in such a short time.
Hydrogen peroxide is not a radical itself because it does not have any unpaired electrons. It is actually a relatively stable compound and is not very reactive in the absence of transition metal ions (18). In addition, H2O2 acts as either a mild oxidizing or weak reducing agent (18). Even though H2O2 itself is not very reactive, it can be converted into the hydroxyl radical, thus, becoming a reactive species. Hydrogen peroxide is reduced via the enzyme GPx by using the reduced GSH as the electron donor (32). Reduced GSH is then oxidized to GSH disulfide, and finally, GSH disulfide is reduced by GSH reductase. It is possible that because there was no significant increase in H2O2, GSH was available in abundant and/or GPx and CAT were efficient at reducing what H2O2 was actually produced. Our findings for a decrease in CAT (as well as TEAC) at the 0-min postexercise period lend some support to this hypothesis (i.e., increased consumption of CAT and circulating antioxidants).
As noted previously, we observed an increase in TEAC after exercise (in particular, sprint exercise), which may have counteracted the acute increase in RONS. Our findings demonstrate an acute decrease in TEAC (0 min after exercise), followed by an increase above basal levels at both the 30- and 60-min recovery period. A similar acute decrease in CAT was observed, with values rebounding to preexercise levels at 30 and 60 min after exercise. These findings are in accordance with the literature regarding the initial drop during and after exercise (34), as well as with the increase above basal levels at times distant to the immediate postexercise period (24,34). Others have failed to demonstrate an increase in TEAC after exercise (37); however, these investigations may have missed any potential increase in TEAC because of the failure to include sample measurement beyond the immediate postexercise period. Michailidis et al. (24) have shown that the collection schedule for blood samples analyzed for oxidative stress biomarkers may extend to 4 h after exercise. Our cessation of measurement at 60 min after exercise may be partly responsible for our lack of observed effect for all measures.
As stated earlier, engaging in a regular exercise program may be associated with an increase in endogenous antioxidant enzyme activity (24,25,34). This may serve endogenous biomolecules (e.g., lipids, proteins, and DNA) with protection against an exercise-induced increase in RONS. Exercise-induced RONS production leads to the activation of nuclear factor-κB, with its activation leading to the expression of antioxidant enzymes (16). These up-regulations are in accordance with the principle of hormesis (29) and may provide protection against future assaults of similar magnitude. These observations, coupled with the findings of the present study, should appease the concern of those suggesting that RONS resulting from strenuous exercise may pose health consequences. Our data demonstrate clearly that even extremely strenuous exercise (based on HR and lactate data) does not result in a blood oxidative stress in men who exercise regularly. It is important to keep in mind that our lack of findings regarding blood oxidative stress does not necessarily indicate that RONS were not produced. It is possible that RONS production simply did not overwhelm the antioxidant defense, in particular, within blood and during our time of collection. In much the same way as blood lactate may not accumulate despite a significant increase in lactate production, the oxidation of molecules may not occur despite the rise in RONS.
Exercise performed at very high intensity, yielding a high lactate response, does not result in a significant increase in blood oxidative stress during the 1-h postexercise period. This may be partly explained by an increase in antioxidant capacity and/or a decrease in RONS production as an adaptation to chronic exercise training, which may provide cellular protection against macromolecule oxidation. These findings are specific to the measurement of selected oxidative stress and antioxidant biomarkers only, using a sample of exercise-trained men. Future work is necessary to investigate the effect of other RONS generators, such as high-fat feedings, on providing cellular protection in accordance with the principal of hormesis—in particular, as related to the antioxidant defense system.
Funding for this work was provided by the University of Memphis.
No external funding was received to support the current investigation.
Appreciation is extended to Michael E. Dessoulavy for assistance in AOPP analysis.
The results of the present investigation do not constitute endorsement by the American College of Sports Medicine.
The authors declare no competing interests in relation to this work.
1. Baker JS, Bailey DM, Hullin D, Young I, Davies B. Metabolic implications of resistive force selection for oxidative stress and markers of muscle damage during 30 s of high-intensity exercise
. Eur J Appl Physiol
. 2004; 92 (3): 321–7.
2. Bloomer RJ. Effect of exercise
on oxidative stress biomarkers. Adv Clin Chem
. 2008; 46: 1–50.
3. Bloomer RJ, Cole BJ. Relationship between blood lactate and oxidative stress biomarkers following acute exercise
. Open Sports Med J
. 2009; 3: 39–43.
4. Bloomer RJ, Davis PG, Consitt LA, Wideman L. Plasma protein carbonyl response to increasing exercise
duration in aerobically trained men and women. Int J Sports Med
. 2007; 28 (1): 21–5.
5. Bloomer RJ, Falvo MJ, Fry AC, Schilling BK, Smith WA, Moore CA. Oxidative stress response in trained men following repeated squats or sprints. Med Sci Sports Exerc
. 2006; 38 (8): 1436–42.
6. Bloomer RJ, Goldfarb AH, Wideman L, McKenzie MJ, Consitt LA. Effects of acute aerobic and anaerobic exercise
on blood markers of oxidative stress. J Strength Cond Res
. 2005; 19 (2): 276–85.
7. Burgomaster KA, Hughes SC, Heigenhauser GJ, Bradwell SN, Gibala MJ. Six sessions of sprint interval training increases muscle oxidative potential and cycle endurance capacity in humans. J Appl Physiol
. 2005; 98 (6): 1985–90.
8. Christmass MA, Dawson B, Arthur PG. Effect of work and recovery duration on skeletal muscle oxygenation and fuel use during sustained intermittent exercise
. Eur J Appl Physiol Occup Physiol
. 1999; 80 (5): 436–47.
9. Christmass MA, Dawson B, Goodman C, Arthur PG. Brief intense exercise
followed by passive recovery modifies the pattern of fuel use in humans during subsequent sustained intermittent exercise
. Acta Physiol Scand
. 2001; 172 (1): 39–52.
10. Christmass MA, Dawson B, Passeretto P, Arthur PG. A comparison of skeletal muscle oxygenation and fuel use in sustained continuous and intermittent exercise
. Eur J Appl Physiol Occup Physiol
. 1999; 80 (5): 423–35.
11. Dalle-Donne I, Rossi R, Colombo R, Giustarini D, Milzani A. Biomarkers of oxidative damage in human disease. Clin Chem
. 2006; 52 (4): 601–23.
12. Dill DB, Costill DL. Calculation of percentage changes in volumes of blood, plasma, and red cells in dehydration. J Appl Physiol
. 1974; 37 (2): 247–8.
13. Fatouros IG, Jamurtas AZ, Villiotou V, et al.. Oxidative stress responses in older men during endurance training and detraining. Med Sci Sports Exerc
. 2004; 36 (12): 2065–72.
14. Fisher-Wellman K, Bloomer RJ. Acute exercise
and oxidative stress: a 30 year history. Dyn Med
. 2009; 8: 1.
15. Goldfarb AH, McKenzie MJ, Bloomer RJ. Gender comparisons of exercise
-induced oxidative stress: influence of antioxidant supplementation. Appl Physiol Nutr Metab
. 2007; 32 (6): 1124–31.
16. Gomez-Cabrera MC, Borras C, Pallardo FV, Sastre J, Ji LL, Vina J. Decreasing xanthine oxidase-mediated oxidative stress prevents useful cellular adaptations to exercise
in rats. J Physiol
. 2005; 567 (Pt 1): 113–20.
17. Groussard C, Rannou-Bekono F, Machefer G, et al.. Changes in blood lipid peroxidation markers and antioxidants after a single sprint anaerobic exercise
. Eur J Appl Physiol
. 2003; 89 (1): 14–20.
18. Halliwell B, Clement MV, Long LH. Hydrogen peroxide in the human body. FEBS Lett
. 2000; 486 (1): 10–3.
19. Hoffman JR, Im J, Kang J, et al.. Comparison of low- and high-intensity resistance exercise
on lipid peroxidation: role of muscle oxygenation. J Strength Cond Res
. 2007; 21 (1): 118–22.
20. Jackson MJ. Exercise
and oxygen radical production by muscle. In: Sen CK, Packer L, Hanninen O, editors. Handbook of Oxidants and Antioxidants in Exercise
. Amsterdam: Elsevier Science; 2000. pp. 57–68.
21. Jentzsch AM, Bachmann H, Furst P, Biesalski HK. Improved analysis of malondialdehyde in human body fluids. Free Radic Biol Med
. 1996; 20 (2): 251–6.
22. Lovlin R, Cottle W, Pyke I, Kavanagh M, Belcastro AN. Are indices of free radical damage related to exercise
intensity. Eur J Appl Physiol Occup Physiol
. 1987; 56 (3): 313–6.
23. Marzatico F, Pansarasa O, Bertorelli L, Somenzini L, Della Valle G. Blood free radical antioxidant enzymes and lipid peroxides following long-distance and lactacidemic performances in highly trained aerobic and sprint athletes. J Sports Med Phys Fitness
. 1997; 37 (4): 235–9.
24. Michailidis Y, Jamurtas AZ, Nikolaidis MG, et al.. Sampling time is crucial for measurement of aerobic exercise
-induced oxidative stress. Med Sci Sports Exerc
. 2007; 39 (7): 1107–13.
25. Nikolaidis MG, Kyparos A, Hadziioannou M, et al.. Acute exercise
markedly increases blood oxidative stress in boys and girls. Appl Physiol Nutr Metab
. 2007; 32 (2): 197–205.
26. Nikolaidis MG, Paschalis V, Giakas G, et al.. Decreased blood oxidative stress after repeated muscle-damaging exercise
. Med Sci Sports Exerc
. 2007; 39 (7): 1080–9.
27. Ortenblad N, Madsen K, Djurhuus MS. Antioxidant status and lipid peroxidation after short-term maximal exercise
in trained and untrained humans. Am J Physiol
. 1997; 272 (4 Pt 2): R1258–63.
28. Quindry JC, Stone WL, King J, Broeder CE. The effects of acute exercise
on neutrophils and plasma oxidative stress. Med Sci Sports Exerc
. 2003; 35 (7): 1139–45.
29. Radak Z, Chung HY, Koltai E, Taylor AW, Goto S. Exercise
, oxidative stress and hormesis. Ageing Res Rev
. 2008; 7 (1): 34–42.
30. Radak Z, Taylor AW, Ohno H, Goto S. Adaptation to exercise
-induced oxidative stress: from muscle to brain. Exerc Immunol Rev
. 2001; 7: 90–107.
31. Revan S, Balci SS, Pepe H, Kurtoglu F, Erol AE, Akkus H. Short duration exhaustive running exercise
does not modify lipid hydroperoxide, glutathione peroxidase and catalase. J Sports Med Phys Fitness
. 2010; 50 (2): 235–40.
32. Sen CK. Oxidants and antioxidants in exercise
. J Appl Physiol
. 1995; 79 (3): 675–86.
33. Siri WE. Body composition from fluid spaces and density: analysis of methods. 1961. Nutrition
. 1993; 9 (5): 480–91; discussion 480, 492.
34. Steinberg JG, Delliaux S, Jammes Y. Reliability of different blood indices to explore the oxidative stress in response to maximal cycling and static exercises. Clin Physiol Funct Imaging
. 2006; 26 (2): 106–12.
35. Tabata I, Irisawa K, Kouzaki M, Nishimura K, Ogita F, Miyachi M. Metabolic profile of high intensity intermittent exercises. Med Sci Sports Exerc
. 1997; 29 (3): 390–5.
36. Tabata I, Nishimura K, Kouzaki M, et al.. Effects of moderate-intensity endurance and high-intensity intermittent training on anaerobic capacity and VO2max. Med Sci Sports Exerc
. 1996; 28 (10): 1327–30.
37. Vincent HK, Morgan JW, Vincent KR. Obesity exacerbates oxidative stress levels after acute exercise
. Med Sci Sports Exerc
. 2004; 36 (5): 772–9.
38. Whaley MH. ACSM’s Guidelines for Exercise Testing and Prescription
. 7th ed. Philadelphia, PA: Lippincott Williams & Wilkins. 2005. pp. 19–30.
39. Witko-Sarsat V, Friedlander M, Capeillere-Blandin C, et al.. Advanced oxidation protein products as a novel marker of oxidative stress in uremia. Kidney Int
. 1996; 49 (5): 1304–13.
40. You T, Goldfarb AH, Bloomer RJ, Nguyen L, Sha X, McKenzie MJ. Oxidative stress response in normal and antioxidant supplemented rats to a downhill run: changes in blood and skeletal muscles. Can J Appl Physiol
. 2005; 30 (6): 677–89.
Keywords:©2012The American College of Sports Medicine
REACTIVE OXYGEN SPECIES; FREE RADICALS; EXERCISE; HIGH-INTENSITY SPRINTS