Michalis G. Nikolaidis

Effect of supplementation with conjugated linoleic acid on human serum lipids and body fat

Conjugated linoleic acid (CLA) is a natural component of meat and dairy products with anticarcinogenic, fat lowering, antiatherogenic and anticatabolic activity in animals. The purpose of this study was to examine the effect of CLA supplementation to humans on body fat, certain biochemical parameters of serum, and the CLA content of serum lipids. Twenty-two volunteers were divided into a study group and a control group in a doubly blind design. The study group received 0.7 g of CLA for four weeks and 1.4 g of CLA for the next four weeks, while the control group received placebo. Diet was controlled and no significant differences in energy or macronutrient intake were found between the two groups. Measurements were taken at baseline, four weeks, and eight weeks. The sum of the thickness of ten skinfolds, percentage body fat calculated from it and fat mass was significantly reduced in the CLA group during the second period (P < 0.004) but not overall during the study. Serum HDL-cholesterol decreased significantly (P < 0.001) and triacylglycerols as well as total cholesterol tended to decrease in the CLA group during the first period. The CLA content of serum non-esterified fatty acids, triacylglycerols, phospholipids, and cholesteryl esters increased gradually with supplementation; the CLA content of total serum lipids doubled at the end of the study compared to baseline. Phospholipids had the highest CLA content regardless of supplementation. These data indicate that supplementation with 0.7-1.4 g CLA daily for 4-8 weeks may modulate body fat and serum lipids, as well as increase the CLA content of serum lipids in humans.

Time-course of changes in inflammatory and performance responses following a soccer game.

Objective:To study the effects of a single soccer game on indices of performance, muscle damage, and inflammation during a 6-day recovery period. Design:Participants were assigned to either an experimental group (E, played in the game; n = 14) or a control group (C, did not participate in the game; n = 10). Setting:Data were collected on a soccer field and at the Physical Education and Sports Science laboratory of the Democritus University of Thrace before and after the soccer game. Participants:Twenty-four elite male soccer players (age, 20.1 ± 0.8 years; height, 1.78 ± 0.08 m; weight, 75.2 ± 6.8 kg). Main Outcome Measurements:Muscle strength, vertical jumping, speed, DOMS, muscle swelling, leukocyte count, creatine kinase (CK), lactate dehydrogenase (LDH), C-reactive protein (CRP), cortisol, testosterone, cytokines IL-6 and IL-1b, thioburbituric acid-reactive substances (TBARS), protein carbnyls (PC), and uric acid (UA). Results:Performance deteriorated 1 to 4 days post-game. An acute-phase inflammatory response consisted of a post-game peak of leukocyte count, cytokines, and cortisol, a 24-hour peak of CRP, TBARS, and DOMS, a 48-hour peak of CK, LDH, and PC, and a 72-hour peak of uric acid. Conclusion:A single soccer game induces short-term muscle damage and marked but transient inflammatory responses. Anaerobic performance seems to deteriorate for as long as 72-hour post-game. The acute phase inflammatory response in soccer appears to follow the same pattern as in other forms of exercise. These results clearly indicate the need of sufficient recovery for elite soccer players after a game.

The Effect of Muscle-Damaging Exercise on Blood and Skeletal Muscle Oxidative Stress : Magnitude and Time-Course Considerations

The aim of this article is to present the effects of acute muscle-damaging exercise on oxidative stress/damage of animal and human tissues using a quantitative approach and focusing on the time-course of exercise effects. The reviewed studies employed eccentric contractions on a dynamometer or downhill running. The statistical power of each study to detect a 20% or 40% post-exercise change compared with pre-exercise value in each oxidative stress/damage biomarker was calculated. Muscle-damaging exercise can increase free radical levels and augment oxidation of lipids, proteins, glutathione and possibly DNA in the blood. In contrast, the effect of muscle-damaging exercise on concentration of antioxidants in the blood, except for glutathione, was little. Muscle-damaging exercise induces oxidative stress/damage in skeletal muscle, even though this is not fully supported by the original statistical analysis of some studies. In contrast, muscle-damaging exercise does not appear to affect — at least to similar extent as the oxidative stress/ damage markers — the levels of antioxidants in skeletal muscle. Based on the rather limited data available, the oxidative stress response of skeletal muscle to exercise was generally independent of muscle fibre type. Most of the changes in oxidative stress/damage appeared and were sustained for days after muscledamaging exercise. The major part of the delayed oxidative stress/damage production that follows muscle-damaging exercise probably comes from phagocytic cells that are activated and recruited to the site of the initial damage. A point that emerged and potentially explains much of the lack of consensus among studies is the low statistical power of many of them. In summary, muscle-damaging exercise can increase oxidative stress/damage in blood and skeletal muscle of rats and humans that may persist for and/or appear several days after exercise.

Blood as a reactive species generator and redox status regulator during exercise.

The exact origin of reactive species and oxidative damage detected in blood is largely unknown. Blood interacts with all organs and tissues and, consequently, with many possible sources of reactive species. In addition, a multitude of oxidizable substrates are already in blood. A muscle-centric approach is frequently adopted to explain reactive species generation, which obscures the possibility that sources of reactive species and oxidative damage other than skeletal muscle may be also at work during exercise. Plasma and blood cells can autonomously produce significant amounts of reactive species at rest and during exercise. The major reactive species generators located in blood during exercise may be erythrocytes (mainly due to their quantity) and leukocytes (mainly due to their drastic activation during exercise). Therefore, it is plausible to assume that oxidative stress/damage measured frequently in blood after exercise or any other experimental intervention derives, at least in part, from the blood.

Blood reflects tissue oxidative stress depending on biomarker and tissue studied

This study investigated whether selected oxidative stress markers measured in blood adequately reflect redox status in skeletal muscle, heart, and liver. Several markers were determined after implementing two treatments known to affect redox status, namely exercise and allopurinol administration. Xanthine oxidase, thiobarbituric acid-reactive substances (TBARS), protein carbonyls (PC), reduced glutathione (GSH), oxidized glutathione (GSSG), catalase, and total antioxidant capacity were determined in blood, skeletal muscle, heart, and liver. Correlation between blood and tissues in each marker was performed through the Spearman rank correlation coefficient. GSSG in erythrocytes was correlated with all tissues, ranging in the five experimental groups as follows: skeletal muscle r(s)=0.656-0.874, heart r(s)=0.742-0.981, liver r(s)=0.646-0.855. Xanthine oxidase and TBARS measured in blood satisfactorily described the redox status of the heart (0.753-0.964 and 0.705-1.000, respectively) and liver (0.755-0.902 and 0.656-1.000, respectively). Skeletal muscle and heart redox status can be adequately described by PC (0.652-1.000 and 0.656-0.964, respectively), GSH (0.693-1.000 and 0.656-1.000, respectively), and catalase (0.745-1.000 and 0.656-1.000, respectively) measured in blood. In conclusion, this study suggests that a combination of markers measured in blood provides a reliable indication about the redox status in skeletal muscle, heart, and liver.

No effect of antioxidant supplementation on muscle performance and blood redox status adaptations to eccentric training

BACKGROUND It was recently reported that antioxidant supplementation decreases training efficiency and prevents cellular adaptations to chronic exercise. OBJECTIVE This study aimed to investigate the effects of vitamin C and vitamin E supplementation on muscle performance, blood and muscle redox status biomarkers, and hemolysis in trained and untrained men after acute and chronic exercise. A specific type of exercise was applied (eccentric) to produce long-lasting and extensive changes in redox status biomarkers and to examine more easily the potential effects of antioxidant supplementation. DESIGN In a double-blinded fashion, men received either a daily oral supplement of vitamin C and vitamin E (n = 14) or placebo (n = 14) for 11 wk (started 4 wk before the pretraining exercise testing and continued until the posttraining exercise testing). After baseline testing, the subjects performed an eccentric exercise session 2 times/wk for 4 wk. Before and after the chronic eccentric exercise, the subjects underwent one session of acute eccentric exercise, physiologic measurements were performed, and blood samples and muscle biopsy samples (from 4 men) were collected. RESULTS The results failed to support any effect of antioxidant supplementation. Eccentric exercise similarly modified muscle damage and performance, blood redox status biomarkers, and hemolysis in both the supplemented and nonsupplemented groups. This occurred despite the fact that eccentric exercise induced marked changes in muscle damage and performance and in redox status after exercise. CONCLUSION The complete lack of any effect on the physiologic and biochemical outcome measures used raises questions about the validity of using oral antioxidant supplementation as a redox modulator of muscle and redox status in healthy humans.

Time course of changes in performance and inflammatory responses after acute plyometric exercise.

Chatzinikolaou, A, Fatouros, IG, Gourgoulis, V, Avloniti, A, Jamurtas, AZ, Nikolaidis, MG, Douroudos, I, Michailidis, Y, Beneka, A, Malliou, P, Tofas, T, Georgiadis, I, Mandalidis, D, and Taxildaris, K. Time course of changes in performance and inflammatory responses after acute plyometric exercise. J Strength Cond Res 24(5): 1389-1398, 2010-The objectives of the present investigation were to study the inflammatory and performance responses after an acute bout of intense plyometric exercise during a prolonged recovery period. Participants were randomly assigned to either an experimental group (P, n = 12) that performed intense plyometric exercises or a control group (C, n = 12) that rested. The delayed onset of muscle soreness (DOMS), knee range of motion (KROM), creatine kinase (CK) and lactate dehydrogenase (LDH) activities, white blood cell count, C reactive protein (CRP), uric acid (UA), cortisol, testosterone, IL-6, IL-1b strength (isometric and isokinetic), and countermovement (CMJ) and static (SJ) jumping performance were measured at rest, immediately postexercise and at 24, 48, 72, 96, and 120 hours of recovery. Lactate was measured at rest and postexercise. Strength remained unchanged throughout recovery, but CMJ and SJ declined (p < 0.05) by 8-20%. P induced a marked rise in DOMS, CK, and LDH (peaked 24-48 hours postexercise) and a KROM decline. An acute-phase inflammatory response consisting of leukocytosis (postexercise and at 24 hours), an IL-6, IL-1b, CRP, and cortisol elevation (during the first 24 hours of recovery) and a delayed increase of UA (peaked at 48 hours) and testosterone (peaked at 72 hours) was observed in P. The results of this investigation indicate that performing an acute bout of intense plyometric exercise may induce a short-term muscle damage and marked but transient inflammatory responses. Jumping performance seems to deteriorate for as long as 72 hours postexercise, whereas strength appears to remain unchanged. The acute-phase inflammatory response after a plyometric exercise protocol appears to follow the same pattern as in other exercise models. These results clearly indicate the need of sufficient recovery between successive plyometric exercise training sessions.

Redox biology of exercise: an integrative and comparative consideration of some overlooked issues

Summary The central aim of this review is to address the highly multidisciplinary topic of redox biology as related to exercise using an integrative and comparative approach rather than focusing on blood, skeletal muscle or humans. An attempt is also made to re-define ‘oxidative stress’ as well as to introduce the term ‘alterations in redox homeostasis’ to describe changes in redox homeostasis indicating oxidative stress, reductive stress or both. The literature analysis shows that the effects of non-muscle-damaging exercise and muscle-damaging exercise on redox homeostasis are completely different. Non-muscle-damaging exercise induces alterations in redox homeostasis that last a few hours post exercise, whereas muscle-damaging exercise causes alterations in redox homeostasis that may persist for and/or appear several days post exercise. Both exhaustive maximal exercise lasting only 30 s and isometric exercise lasting 1–3 min (the latter activating in addition a small muscle mass) induce systemic oxidative stress. With the necessary modifications, exercise is capable of inducing redox homeostasis alterations in all fluids, cells, tissues and organs studied so far, irrespective of strains and species. More importantly, ‘exercise-induced oxidative stress’ is not an ‘oddity’ associated with a particular type of exercise, tissue or species. Rather, oxidative stress constitutes a ubiquitous fundamental biological response to the alteration of redox homeostasis imposed by exercise. The hormesis concept could provide an interpretative framework to reconcile differences that emerge among studies in the field of exercise redox biology. Integrative and comparative approaches can help determine the interactions of key redox responses at multiple levels of biological organization.

Time-Course of Changes in Oxidative Stress and Antioxidant Status Responses Following a Soccer Game

Fatouros, IG, Chatzinikolaou, A, Douroudos, II, Nikolaidis, MG, Kyparos, A, Margonis, A, Michailidis, Y, Vantarakis, A, Taxildaris, K, Katrabasas, I, Mandalidis, D, Kouretas, D, and Jamurtas, AZ. Time-course of changes in oxidative stress and antioxidant status responses following a soccer game. J Strength Cond Res 24(12): 3278-3286, 2010-Exercise-induced muscle damage is associated with an acute-phase inflammatory response characterized by phagocyte infiltration into muscle and free radical production. Although soccer includes intense eccentric muscle actions that cause muscle damage, the oxidative stress responses after a soccer game are currently unknown. The present investigation attempted to determine the responses of circulating levels of oxidative stress and antioxidant status markers during recovery from a soccer game. Twenty soccer players (experimental group) were assigned to 2 different teams that competed against each other (2 × 45 minutes). Ten other players served as controls (rested). Creatine kinase (CK) activity, uric acid, leukocyte count, malondialdehyde (MDA), protein carbnyls (PC), reduced (GSH) and oxidized glutathione (GSSG), antioxidant capacity (TAC), catalase, glutathione peroxidase activity (GPX), delayed-onset of muscle soreness (DOMS), and anaerobic performance (speed, vertical jump performance) were measured before and following (immediately post, 24 hours, 48 hours, 72 hours) the game. Performance deteriorated (2-17%, p < 0.05) throughout recovery. Leukocytosis developed (p < 0.05) immediately following the game and at 24 hours. Both CK and DOMS (3-8-fold, p < 0.05) increased from baseline and remained elevated (p < 0.05) through 48 hours. Thiobarbituric acid reactive substances (TBARS), PC, uric acid, GPX, and TAC increased (13-67%, p < 0.05) throughout recovery, whereas catalase was elevated (38%, p < 0.05) only immediately after the game. GSH/GSSG declined (17-75%, p < 0.05) throughout recovery. Our results suggest that oxidative stress is markedly upregulated by a soccer game, probably as a part of the exercise-induced inflammatory response, and is accompanied by a marked deterioration of anaerobic performance for as long as 72 hours.

F2-isoprostane formation, measurement and interpretation: The role of exercise

The level of F₂-isoprostanes (F₂-IsoP) in blood or urine is widely regarded as the reference marker for the assessment of oxidative stress. As a result, nowadays, F₂-IsoP is the most frequently measured oxidative stress marker. Nevertheless, determining F₂-IsoP is a challenging task and the measurement is neither free of mishaps nor straightforward. This review presents for the first time the effect of acute and chronic exercise on F₂-IsoP levels in plasma, urine and skeletal muscle, placing emphasis on the origin, the methodological caveats and the interpretation of F₂-IsoP alterations. From data analysis, the following effects of exercise have emerged: (i) acute exercise clearly increases F₂-IsoP levels in plasma and this effect is generally short-lived, (ii) acute exercise and increased contractile activity markedly increase F₂-IsoP levels in skeletal muscle, (iii) chronic exercise exhibits trend for decreased F₂-IsoP levels in urine but further research is needed. Theoretically, it seems that significant amounts of F₂-IsoP can be produced not only from phospholipids but from neutral lipids as well. The origin of F₂-IsoP detected in plasma and urine (as done by almost all studies in humans) remains controversial, as a multitude of tissues (including skeletal muscle and plasma) can independently produce F₂-IsoP.