The positive influence of animal-based protein supplementation during muscle-damaging exercise has been widely studied. However, the effects of plant-based proteins remain unclear and require further clarification. This study investigated the protective role of oat protein against exercise induced muscle damage (EIMD), subsequent inflammation, and loss of performance induced by downhill running. Subjects consumed either oat protein (25 g protein) or a placebo for 14 days prior to a downhill running test and then for 4 days thereafter. Treatments with oat protein for 19 days markedly alleviated eccentric exercise induced skeletal muscle soreness, and reduced the elevation of plasma IL-6 concentrations and serum creatine kinase, myoglobin and C reactive protein contents. In addition, oat protein supplementation significantly inhibited limb edema following damaging exercise, and the adverse effects on muscle strength, knee-joint range of motion, and vertical jump performance were lessened. Furthermore, the administration of oat protein facilitated recovery from exhaustive downhill running in this study. These findings demonstrated that oat protein supplementation has the potential to alleviate the negative effects of eccentric exercise in untrained young males.

We investigated whether low-level laser therapy (LLLT) prior to or post resistance exercise could attenuate muscle damage and inflammation. Female Wistar rats were assigned to non-LLLT or LLLT groups. An 830-nm DMC Laser Photon III was used to irradiate their hind legs with 2J, 4J, and 8J doses. Irradiations were performed prior to or post (4J) resistance exercise bouts. Resistance exercise consisted of four maximum load climbs. The load work during a resistance exercise bout was similar between Control (non-LLLT, 225 ± 10 g), 2J (215 ± 8 g), 4J (210 ± 9 g), and 8J (226 ± 9 g) groups. Prior LLLT did not induce climbing performance improvement, but exposure to 4J irradiation resulted in lower blood lactate levels post-exercise. The 4J dose decreased creatine kinase and lactic dehydrogenase levels post-exercise regardless of the time of application. Moreover, 4-J irradiation exposure significantly attenuated tumor necrosis factor alpha, interleukin-6, interleukin-1β, cytokine-induced neutrophil chemoattractant-1, and monocyte chemoattractant protein-1. There was minor macrophage muscle infiltration in 4J-exposed rats. These data indicate that LLLT prior to or post resistance exercise can reduce muscle damage and inflammation, resulting in muscle recovery improvement. We attempted to determine an ideal LLLT dose for suitable results, wherein 4J irradiation exposure showed a significant protective role.

Souglis, A, Bogdanis, GC, Chryssanthopoulos, C, Apostolidis, N, and Geladas, ND. Time course of oxidative stress, inflammation and muscle damage markers for 5 days after a soccer match: Effects of sex and playing position. J Strength Cond Res 32(7): 2045-2054, 2018-This study examined the influence of sex and playing position on the time course of selected oxidative stress, inflammation, and muscle damage markers after an official soccer match. Sixty professional soccer players (30 men and 30 women) were divided into 3 groups, according to their playing position: defenders, midfielders, and attackers. Each group consisted of 10 male and 10 female players. Sixty healthy volunteers (30 men and 30 women) served as control. Blood samples were taken before and after the match and daily for 5 days after the match. Analysis of variance revealed different responses over time between sex and playing positions, as shown by the 3-way interaction, for creatine kinase (CK), protein carbonyls (PCs), catalase, fibrinogen, uric acid (UA), lactate dehydrogenase, reduced glutathione, C-reactive protein, and interleukin 6 (p < 0.01). Male players had higher values compared with women of the same playing position, for all oxidative, inflammatory, and muscle damage indices (p < 0.01). Also, in both sexes, midfielders had higher peaks in all indices compared with defenders (p < 0.05). Five days after the game CK and UA concentrations had not returned to pregame levels in any exercise group, whereas PCs were still elevated in male midfielders and attackers (p < 0.05). These results show that sex and playing position influence the time course of selected oxidative stress, inflammation, and muscle damage markers after an official soccer game. This information should be taken into account by practitioners for the design of training programs after match play.

BACKGROUND:

The effects of a multi-ingredient performance supplement (MIPS) on markers of inflammation and muscle damage, perceived soreness and lower limb performance are unknown in endurance-trained female athletes. The purpose of this study was to determine the impact of MIPS (NO-Shotgun®) pre-loaded 4 weeks prior to a single-bout of downhill running (DHR) on hsC-Reactive Protein (hsCRP), interleukin (IL)-6, creatine kinase (CK), muscle soreness, lower limb circumferences and performance.

METHOD:

Trained female runners (n = 8; 29 ± 5.9 years) (VO_2max: ≥ 50 ml^-1.kg^-1.min^-1, midfollicular phase (7-11 days post-menses) were randomly assigned in a double-blind manner into two groups: MIPS (n = 4) ingested one serving of NO Shotgun daily for 28 days prior to DHR and 30 min prior to all post-testing visits; Control (CON) (n = 4) consumed an isocaloric maltodextrin placebo in an identical manner to MIPS. hsCRP, IL-6, CK, perceived soreness, limb circumferences, and performance measures (flexibility, squat jump peak power) were tested on 5 occasions; immediately before (PRE), immediately post-DHR, 24, 48 and 72 h post-DHR.

RESULTS:

There were main effects of time for CK (p = 0.05), pain pressure threshold (right tibialis anterior (p = 0.010), right biceps femoris (p = 0.01), and left iliotibial band (ITB) (p = 0.05) across all time points), and maximum squat jump power (p = 0.04). Compared with 24 h post-DHR, maximum squat jump power was significantly lower at 48 h post-DHR (p = 0.05). Lower body perceived soreness was significantly increased at 24 h (p = 0.02) and baseline to 48 h (p = 0.02) post DHR. IL-6 peaked immediately post-DHR (p = 0.03) and hsCRP peaked at 24 h post-DHR (p = 0.06). Calculation of effect sizes indicated a moderate attenuation of hsCRP in MIPS at 72 h post-DHR.

CONCLUSIONS:

Consumption of MIPS for 4 weeks prior to a single bout of DHR attenuated inflammation three days post, but did not affect perceived soreness and muscle damage markers in endurance trained female runners following a single bout of DHR.

BACKGROUND:

The purpose of the present study was to evaluate the effects of PCSO-524®, a marine oil lipid and n-3 LC PUFA blend, derived from New Zealand green- lipped mussel (Perna canaliculus), on markers of muscle damage and inflammation following muscle damaging exercise in untrained men.

METHODS:

Thirty two untrained male subjects were randomly assigned to consume 1200 mg/d of PCSO- 524® (a green-lipped mussel oil blend) or placebo for 26 d prior to muscle damaging exercise (downhill running), and continued for 96 h following the muscle damaging exercise bout. Blood markers of muscle damage (skeletal muscle slow troponin I, sTnI; myoglobin, Mb; creatine kinase, CK), and inflammation (tumor necrosis factor, TNF-α), and functional measures of muscle damage (delayed onset muscle soreness, DOMS; pressure pain threshold, PPT; knee extensor joint range of motion, ROM; isometric torque, MVC) were assessed pre- supplementation (baseline), and multiple time points post-supplementation (before and after muscle damaging exercise). At baseline and 24 h following muscle damaging exercise peripheral fatigue was assessed via changes in potentiated quadriceps twitch force (∆Qtw,pot) from pre- to post-exhaustive cycling ergometer test in response to supra-maximal femoral nerve stimulation.

RESULTS:

Compared to placebo, supplementation with the green-lipped mussel oil blend significantly attenuated (p < 0.05) sTnI and TNF-α at 2, 24, 48, 72 and 96 h., Mb at 24, 48, 72, 96 h., and CK-MM at all-time points following muscle damaging exercise, significantly reduced (p < 0.05) DOMS at 72 and 96 h post-muscle damaging exercise, and resulted in significantly less strength loss (MVC) and provided a protective effect against joint ROM loss at 96 h post- muscle damaging exercise. At 24 h after muscle damaging exercise perceived pain was significantly greater (p < 0.05) compared to baseline in the placebo group only. Following muscle damaging exercise ∆Qtw,pot was significantly less (p < 0.05) on the green-lipped mussel oil blend compared to placebo.

CONCLUSION:

Supplementation with a marine oil lipid and n-3 LC PUFA blend (PCSO-524®), derived from the New Zealand green lipped mussel, may represent a useful therapeutic agent for attenuating muscle damage and inflammation following muscle damaging exercise.

The purpose of this study was to examine the effects of anatabine supplementation in conjunction with unilateral, maximal eccentric isokinetic muscle actions on serum markers of muscle damage and pro-inflammatory cytokines in humans. Seventeen men (mean ± S.D. age = 22.4 ± 3.2 yrs) participated in this double-blinded, placebo-controlled, crossover study. Participants were randomly assigned to two 10-day conditions (anatabine and placebo) separated by a 2-4 week washout period. After seven days of supplementation, blood was sampled immediately prior to PRE, immediately following POST, and 24, 48, and 72 h after 6 sets of 10 repetitions of unilateral, maximal eccentric isokinetic forearm flexion exercise. Concentrations of serum creatine kinase, lactate dehydrogenase, myoglobin, high sensitivity c-reactive protein, and TNF-α were measured. Creatine kinase, myoglobin, and lactate dehydrogenase increased (P<0.05), while high sensitivity c-reactive protein and TNF-α did not change (P>0.05) after the eccentric exercise during both conditions. Lactate dehydrogenase was higher (P<0.05) during the anatabine condition. The primary findings of this study were two-fold: (a) anatabine had no beneficial effects on traditional markers of muscle damage (creatine kinase, lactate dehydrogenase, and myoglobin) compared to placebo after the eccentric exercise protocol, and (b) the eccentric exercise protocol did not elicit increase in the pro-inflammatory cytokines (c-reactive protein and TNF-α). Future studies are needed to examine the effects of anatabine on naturally-occurring inflammation that is common with aging or obesity. Furthermore, additional research is needed to examine the relationship between muscle damage and inflammation after eccentric exercises of different modes, durations, and intensities.

The purpose of this study was to determine if a moderate intensity whole-body vibration (WBV) body mass resistive exercise session causes additional muscle damage, soreness, and inflammation compared with the same exercise session without vibration (NoV). Ten recreationally active male university students completed 2 separate 24-hour study periods incorporating an exercise session with WBV or NoV. Muscle torque was measured (at 0, 60, and 240°·s-1 angular velocities), soreness (10-point scale) in the upper (UE [triceps]) and lower (LE [quadriceps]) extremities, and muscle inflammation markers (interleukin [IL]-1β, IL-6, IL-10) were measured at 4 time points (preexercise, immediately postexercise, 4 hours post, and 24 hours post). Diet was controlled. Compared with NoV, WBV increased (p < 0.01) muscle soreness at 24 hours postexercise in both the UE (2.2 ± 1.7 vs. 0.6 ± 0.9) and LE (2.0 ± 1.5 vs. 0.7 ± 0.7). Muscle torque was decreased immediately postexercise (p < 0.05) in the UE and LE at 0°·s and in the UE at 240°·s, but there was no difference between exercise treatments. The exercise session caused significant but small increases in IL-1β and IL-6 but with no differences between exercise treatments. Interleukin-10 was increased with WBV (2.9 ± 2.0 to 3.6 ± 1.9 pg·ml-1; p < 0.03). These data suggest that the addition of WBV to exercise has little effect on muscle function and damage, soreness, or inflammation.

The flavonoid quercetin is purported to have potent antioxidant and anti-inflammatory properties. This study examined if quercetin supplementation attenuates indicators of exercise-induced muscle damage in a double-blind laboratory study. Thirty healthy subjects were randomized to quercetin (QU) or placebo (PL) supplementation and performed 2 separate sessions of 24 eccentric contractions of the elbow flexors. Muscle strength, soreness, resting arm angle, upper arm swelling, serum creatine kinase (CK) activity, plasma quercetin (PQ), interleukin-6 (IL-6), and C-reactive protein (CRP) were assessed before and for 5 d after exercise. Subjects then ingested nutrition bars containing 1,000 mg/d QU or PL for 7 d before and 5 d after the second exercise session, using the opposite arm. PQ reached 202 ± 52 ng/ml after 7 d of supplementation and remained elevated during the 5-d postexercise recovery period (p < .05). Subjects experienced strength loss (peak = 47%), muscle soreness (peak = 39 ± 6 mm), reduced arm angle (-7° ± 1°), CK elevations (peak = 3,307 ± 1,481 U/L), and arm swelling (peak = 11 ± 2 mm; p < .0001), indicating muscle damage and inflammation; however, differences between treatments were not detected. Eccentric exercise did not alter plasma IL-6 (peak = 1.9 pg/ml) or CRP (peak = 1.6 mg/L) relative to baseline or by treatment. QU supplementation had no effect on markers of muscle damage or inflammation after eccentric exercise of the elbow flexors.

The purpose of this investigation was to determine whether Panax ginseng extract intake would influence exercise-induced muscle damage and inflammation responses. Eighteen male college students were randomly assigned to either an RG intake group (RG, n = 9) or a placebo group (P, n = 9). All subjects performed a high-intensity uphill treadmill running task (two rounds of 45 min at 10 km/h speed with a 15 degree uphill slope separated by 5 min of rest). The RG group ingested 20 g/day of Korean red ginseng extract (mixed with 200 ml of water) three times/day for seven days prior to performing the uphill treadmill exercise test and for four days after the treadmill test, while the P group ingested 200 ml of water containing Agastachis Herba on the same schedule. Plasma creatine kinase activity (CK) and interlukin-6 (IL-6) levels were measured at pre-exercise and 24, 48, 72, and 96 h post-exercise; the IL-6 level was also measured at 1 and 2 h post-exercise. To evaluate insulin sensitivity, the oral glucose tolerance test (OGTT) was performed 24 h post-exercise. Plasma CK level in RG was significantly lower than that in P 72 h post-exercise (p < 0.05), and IL-6 level was significantly decreased in RG during the 2 h and 3 h recovery period compared to that of P (p < 0.05). Plasma glucose and insulin responses in RG were significantly reduced compared to those of P (p < 0.05). The results of this study suggest that RG supplementation could reduce exercise-induced muscle damage and inflammatory responses, resulting in improvements in insulin sensitivity.

In this study, we investigated the effect of the supplementation with the dipeptide L-alanyl-L-glutamine (DIP) and a solution containing L-glutamine and L-alanine on plasma levels markers of muscle damage and levels of pro-inflammatory cytokines and glutamine metabolism in rats submitted to prolonged exercise. Rats were submitted to sessions of swim training for 6 weeks. Twenty-one days prior to euthanasia, the animals were supplemented with DIP (n = 8) (1.5 g.kg(-1)), a solution of free L-glutamine (1 g.kg(-1)) and free L-alanine (0.61 g.kg(-1)) (G&A, n = 8) or water (control (CON), n = 8). Animals were killed at rest before (R), after prolonged exercise (PE-2 h of exercise). Plasma concentrations of glutamine, glutamate, tumour necrosis factor-alpha (TNF-alpha), prostaglandin E2 (PGE2) and activity of creatine kinase (CK), lactate dehydrogenase (LDH) and muscle concentrations of glutamine and glutamate were measured. The concentrations of plasma TNF-alpha, PGE2 and the activity of CK were lower in the G&A-R and DIP-R groups, compared to the CON-R. Glutamine in plasma (p < 0.04) and soleus muscle (p < 0.001) was higher in the DIP-R and G&A-R groups relative to the CON-R group. G&A-PE and DIP-PE groups exhibited lower concentrations of plasma PGE2 (p < 0.05) and TNF-alpha (p < 0.05), and higher concentrations of glutamine and glutamate in soleus (p < 0.001) and gastrocnemius muscles (p < 0.05) relative to the CON-PE group. We concluded that supplementation with free L-glutamine and the dipeptide LL-alanyl-LL-glutamine represents an effective source of glutamine, which may attenuate inflammation biomarkers after periods of training and plasma levels of CK and the inflammatory response induced by prolonged exercise.

Downhill running is associated with fiber damage, inflammation, delayed-onset muscle soreness, and various functional deficits. Curcumin, a constituent of the Indian spice turmeric has been investigated for its anti-inflammatory activity and may offset some of the damage and functional deficits associated with downhill running. This study examined the effects of curcumin on inflammation and recovery of running performance following downhill running in mice. Male mice were assigned to downhill placebo (Down-Plac), downhill curcumin (Down-Cur), uphill placebo (Up-Plac), or uphill curcumin (Up-Cur) groups and run on a treadmill at 22 m/min at -14% or +14% grade, for 150 min. At 48 h or 72 h after the up/downhill run, mice (experiment 1) underwent a treadmill performance run to fatigue. Another subset of mice was placed in voluntary activity wheel cages following the up/downhill run (experiment 2) and their voluntary activity (distance, time and peak speed) was recorded. Additional mice (experiment 3) were killed at 24 h and 48 h following the up/downhill run, and the soleus muscle was harvested for analysis of inflammatory cytokines (IL-1beta, IL-6, and TNF-alpha), and plasma was collected for creatine kinase analysis. Downhill running decreased both treadmill run time to fatigue (48 h and 72 h) and voluntary activity (24 h) (P < 0.05), and curcumin feedings offset these effects on running performance. Downhill running was also associated with an increase in inflammatory cytokines (24 h and 48 h) and creatine kinase (24 h) (P < 0.05) that were blunted by curcumin feedings. These results support the hypothesis that curcumin can reduce inflammation and offset some of the performance deficits associated with eccentric exercise-induced muscle damage.

PURPOSE:

This study examined the effects of a 7-d repeated maximal isokinetic eccentric training period on the indicators of muscle damage and inflammatory response.

METHODS:

Twenty-two college-age males were randomly assigned to eccentric training (ET) (N = 12) and control groups (CON) (N = 10). The initial exercise was 30 repetitions of maximal voluntary isokinetic eccentric contraction (ECC1) on nondominant elbow flexors with Cybex 6000 at 60 degrees.s-1 angular velocity. The ET group performed the same exercise for the following 6 consecutive days (referred to as ECC2 to ECC7) after ECC1. Upper arm circumference (CIR), range of motion (ROM), and maximal isometric force (MIF) were measured before, immediately after, and every 24 h for 7 consecutive days after ECC1. Plasma creatine kinase (CK), lactate dehydrogenase (LDH), glutamic oxaloacetate transaminase (GOT), leukocyte counts, and serum interleukin-1beta and -6 (IL-1beta, IL-6) levels were assessed before; at 2 h; and at 1, 3, 4, 6, and 7 d after ECC1. Muscle soreness was measured before and for 7 consecutive days after ECC1.

RESULTS:

The ECC1 produced significant changes in most of the measures for both groups (P < 0.05), with the exception of leukocyte counts (P > 0.05). No indicators of increased damage (P > 0.05) were found from ECC2 to ECC7 for the ET group.

CONCLUSION:

Continuous intensive isokinetic eccentric training performed with damaged muscles did not exacerbate muscle damage and inflammation after ECC1. In addition, a muscular "adaptation effect" may occur as early as 24 h after ECC1, as shown by the ET group's performance for 6 consecutive days after ECC1.

Information suggests that there may be gender-based differences in skeletal muscle responses to damaging exercise. Evidence demonstrates that estrogen has strong antioxidant properties and may be an important factor in maintaining postexercise membrane stability and limiting creatine kinase (CK) leakage from damaged muscle in female animals. Research demonstrates effects of estrogen and possible gender differences in other morphological and biochemical indices of postexercise muscle damage and leukocyte invasion. Nevertheless, there are conflicting findings suggesting that in some in vivo exercise models, estrogen administration has limited ability to affect exercise-induced oxidative stress and muscle damage and may cause loss of tissue vitamin C. Gender differences appear to exist in tissue levels of other important antioxidants such as vitamin E and glutathione. More research is needed to fully define the potential for estrogen to influence postexercise muscle damage and the inflammatory response and to determine the mechanisms by which it may operate.