Athanasios Chatzinikolaou

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.

Strength training and detraining effects on muscular strength, anaerobic power, and mobility of inactive older men are intensity dependent

Background: Although strength training (ST) enhances physical function in the elderly, little is known about the effect of training intensity on training and detraining adaptations in musculoskeletal fitness. Objective: To determine the effect of exercise intensity on strength, anaerobic power, and mobility of older men subjected to a 24 week ST protocol followed by prolonged detraining. Methods: Fifty two healthy but inactive older men (mean (SD) age 71.2 (4.1) years) were assigned to a control (n  =  14), low intensity training (LIST; n  =  18; 55% 1RM), or high intensity training (HIST; n  =  20; 82% 1RM) group. They carried out a 24 week, whole body (10 exercises, two to three sets/exercise) ST programme followed by a 48 week detraining period. Upper and lower body strength, anaerobic power (Wingate testing), and mobility (timed up and go, walking, climbing stairs) were measured at baseline and immediately after training and during detraining. Results: Although low intensity training improved (p<0.05) strength (42–66%), anaerobic power (10%), and mobility (5–7%), high intensity training elicited greater (p<0.05) gains (63–91% in strength, 17–25% in anaerobic power, 9–14% in mobility). All training induced gains in the LIST group had been abolished after four to eight months of detraining, whereas in the HIST group strength and mobility gains were maintained throughout detraining. However, anaerobic power had returned to baseline levels after four months of detraining in both groups. Conclusions: Higher intensity training protocols induce greater gains in strength, anaerobic power, and whole body physical function of older men. Moreover, higher intensity training may maintain the gains for more prolonged periods after training ceases.

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.

Resistance training and detraining effects on flexibility performance in the elderly are intensity-dependent.

The present investigation attempted to determine whether resistance exercise intensity affects flexibility and strength performance in the elderly following a 6-month resistance training and detraining period. Fifty-eight healthy, inactive older men (65–78 yrs) were randomly assigned to 1 of 4 groups: a control group (C, n = 10), a low-intensity resistance training group (LI, n = 14, 40% of 1 repetition maximum [1RM]), a moderate-intensity resistance training group (MI, n = 12, 60% of 1RM), or a high-intensity resistance training group (HI, n = 14, 80% of 1RM). Subjects in exercise groups followed a 3 days per week, whole-body (10 exercises, 3 sets per exercise) protocol for 24 weeks. Training was immediately followed by a 24-week detraining period. Strength (bench and leg press 1RM) and range of motion in trunk, elbow, knee, shoulder, and hip joints were measured at baseline and during training and detraining. Resistance training increased upper-(34% in LI, 48% in MI, and 75% in HI) and lower-body strength (38% in LI, 53% in MI, and 63% in HI) in an intensity-dependent manner. Flexibility demonstrated an intensity-dependent enhancement (3–12% in LI, 6–22% in MI, and 8–28% in HI). Detraining caused significant losses in strength (70–98% in LI, 44–50% in MI, and 27–29% in HI) and flexibility (90–110% in LI, 30–71% in MI, and 23–51% in HI) in an intensity-dependent manner. Results indicate that resistance training by itself improves flexibility in the aged. However, intensities greater than 60% of 1RM are more effective in producing flexibility gains, and strength improvement with resistance training is also intensity-dependent. Detraining seems to reverse training strength and flexibility gains in the elderly in an intensity-dependent manner.

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.

Thiol-based antioxidant supplementation alters human skeletal muscle signaling and attenuates its inflammatory response and recovery after intense eccentric exercise

BACKGROUND The major thiol-disulfide couple of reduced glutathione (GSH) and oxidized glutathione is a key regulator of major transcriptional pathways regulating aseptic inflammation and recovery of skeletal muscle after aseptic injury. Antioxidant supplementation may hamper exercise-induced cellular adaptations. OBJECTIVE The objective was to examine how thiol-based antioxidant supplementation affects skeletal muscles performance and redox-sensitive signaling during the inflammatory and repair phases associated with exercise-induced microtrauma. DESIGN In a double-blind, crossover design, 10 men received placebo or N-acetylcysteine (NAC; 20 mg · kg(-1) · d(-1)) after muscle-damaging exercise (300 eccentric contractions). In each trial, muscle performance was measured at baseline, after exercise, 2 h after exercise, and daily for 8 consecutive days. Muscle biopsy samples from vastus lateralis and blood samples were collected before exercise and 2 h, 2 d, and 8 d after exercise. RESULTS NAC attenuated the elevation of inflammatory markers of muscle damage (creatine kinase activity, C-reactive protein, proinflammatory cytokines), nuclear factor κB phosphorylation, and the decrease in strength during the first 2 d of recovery. NAC also blunted the increase in phosphorylation of protein kinase B, mammalian target of rapamycin, p70 ribosomal S6 kinase, ribosomal protein S6, and mitogen activated protein kinase p38 at 2 and 8 d after exercise. NAC also abolished the increase in myogenic determination factor and reduced tumor necrosis factor-α 8 d after exercise. Performance was completely recovered only in the placebo group. CONCLUSION Although thiol-based antioxidant supplementation enhances GSH availability in skeletal muscle, it disrupts the skeletal muscle inflammatory response and repair capability, potentially because of a blunted activation of redox-sensitive signaling pathways. This trial was registered at clinicaltrials.gov as NCT01778309.

Age-dependent changes in 8-oxoguanine-DNA glycosylase activity are modulated by adaptive responses to physical exercise in human skeletal muscle

8-Oxo-7,8-dihydroguanine (8-oxoG) accumulates in the genome over time and is believed to contribute to the development of aging characteristics of skeletal muscle and various aging-related diseases. Here, we show a significantly increased level of intrahelical 8-oxoG and 8-oxoguanine-DNA glycosylase (OGG1) expression in aged human skeletal muscle compared to that of young individuals. In response to exercise, the 8-oxoG level was lastingly elevated in sedentary young and old subjects, but returned rapidly to preexercise levels in the DNA of physically active individuals independent of age. 8-OxoG levels in DNA were inversely correlated with the abundance of acetylated OGG1 (Ac-OGG1), but not with total OGG1, apurinic/apyrimidinic endonuclease 1 (APE1), or Ac-APE1. The actual Ac-OGG1 level was linked to exercise-induced oxidative stress, as shown by changes in lipid peroxide levels and expression of Cu,Zn-SOD, Mn-SOD, and SIRT3, as well as the balance between acetyltransferase p300/CBP and deacetylase SIRT1, but not SIRT6 expression. Together these data suggest that that acetylated form of OGG1, and not OGG1 itself, correlates inversely with the 8-oxoG level in the DNA of human skeletal muscle, and the Ac-OGG1 level is dependent on adaptive cellular responses to physical activity, but is age independent.

The effects of aging, physical training, and a single bout of exercise on mitochondrial protein expression in human skeletal muscle.

Aging results in a significant decline in aerobic capacity and impaired mitochondrial function. We have tested the effects of moderate physical activity on aerobic capacity and a single bout of exercise on the expression profile of mitochondrial biogenesis, and fusion and fission related genes in skeletal muscle of human subjects. Physical activity attenuated the aging-associated decline in VO2 max (p<0.05). Aging increased and a single exercise bout decreased the expression of nuclear respiratory factor-1 (NRF1), while the transcription factor A (TFAM) expression showed a strong relationship with VO(2max) and increased significantly in the young physically active group. Mitochondrial fission representing FIS1 was induced by regular physical activity, while a bout of exercise decreased fusion-associated gene expression. The expression of polynucleotide phosphorylase (PNPase) changed inversely in young and old groups and decreased with aging. The A2 subunit of cyclic AMP-activated protein kinase (AMPK) was induced by a single bout of exercise in skeletal muscle samples of both young and old subjects (p<0.05). Our data suggest that moderate levels of regular physical activity increases a larger number of mitochondrial biogenesis-related gene expressions in young individuals than in aged subjects. Mitochondrial fission is impaired by aging and could be one of the most sensitive markers of the age-associated decline in the adaptive response to physical activity.

Adipose Tissue Lipolysis Is Upregulated in Lean and Obese Men During Acute Resistance Exercise

OBJECTIVE—To investigate the effect of acute resistance exercise on adipose tissue triacylglycerol lipase activity (TGLA) in lean and obese men. RESEARCH DESIGN AND METHODS—Nine lean and eight obese men performed 30 min of circuit resistance exercise. Adipose tissue and blood were sampled during exercise for TGLA, metabolite, and hormone determinations. Respiratory exchange ratio (RER) was measured throughout exercise. RESULTS—Energy expenditure of exercise relative to body mass was higher in the lean and RER was higher in the obese men, suggesting lower fat oxidation. TGLA increased 18-fold at 5 min of exercise in the lean men and 16-fold at 10 min of exercise in the obese men. The delayed lipolytic activation in the obese men was reflected in serum nonesterified fatty acid and glycerol concentrations. Plasma insulin increased in the obese but did not change in the lean men. CONCLUSIONS—Resistance exercise upregulated adipose tissue lipolysis and enhanced energy expenditure in lean and obese men, with a delayed lipolytic activation in the obese men.

Muscle damage, inflammatory, immune and performance responses to three football games in 1 week in competitive male players

PurposeWe examined effects of a three-game, 1-week microcycle (G1, G2, G3) on recovery of performance and inflammatory responses in professional male footballers.MethodsPlayers were randomized into an experimental (EXP; N = 20) and a control group (CON; N = 20). Blood was drawn and repeated sprint ability (RSA), muscle soreness and knee range of motion (KJRM) were determined pre- and post-games and during recovery.ResultsHigh-intensity running during G2 was 7–14 % less compared to G1 and G3. RSA declined in EXP by 2–9 % 3 days post-game with G2 causing the greatest performance impairment. In EXP, game play increased muscle soreness (~sevenfold) compared to CON with G2 inducing the greatest rise, while KJRM was attenuated post-game in EXP compared to CON (5–7 %) and recovered slower post G2 and G3 than G1. CK, CRP, sVCAM-1, sP-Selectin and cortisol peaked 48 h post-games with G2 eliciting the greatest increase. Leukocyte count, testosterone, IL-1β and IL6 responses, although altered 24 h post each game, were comparable among games. Plasma TBARS and protein carbonyls rose by ~50 % post-games with G2 eliciting the greatest increase 48 h of recovery. Reduced to oxidized glutathione ratio declined for 24 h post all games with G2 displaying the slowest recovery. Total antioxidant capacity and glutathione peroxidase activity increased (9–56 %) for 48 h in response to game play.ConclusionIn summary, post-game performance recovery and inflammatory adaptations in response to a three-game weekly microcycle displayed a different response pattern, with strong indications of a largest physiological stress and fatigue after the middle game that was preceded by only a 3-day recovery.