Muscle-damaging Exercise Research Articles

Effect of Branched-Chain Amino Acid Supplementation on Recovery Following Acute Eccentric Exercise.

This study investigated the effect of branched-chain amino acid (BCAA) supplementation on recovery from eccentric exercise. Twenty males ingested either a BCAA supplement or placebo (PLCB) prior to and following eccentric exercise. Creatine kinase (CK), vertical jump (VJ), maximal voluntary isometric contraction (MVIC), jump squat (JS) and perceived soreness were assessed. No significant (p > 0.05) group by time interaction effects were observed for CK, soreness, MVIC, VJ, or JS. CK concentrations were elevated above baseline (p < 0.001) in both groups at 4, 24, 48 and 72 hr, while CK was lower (p = 0.02) in the BCAA group at 48 hr compared to PLCB. Soreness increased significantly from baseline (p < 0.01) in both groups at all time-points; however, BCAA supplemented individuals reported less soreness (p < 0.01) at the 48 and 72 hr time-points. MVIC force output returned to baseline levels (p > 0.05) at 24, 48 and 72 hr for BCAA individuals. No significant difference between groups (p > 0.05) was detected for VJ or JS. BCAA supplementation may mitigate muscle soreness following muscle-damaging exercise. However, when consumed with a diet consisting of ~1.2 g/kg/day protein, the attenuation of muscular performance decrements or corresponding plasma CK levels are likely negligible.

Investigation of Circulating Extracellular Vesicle MicroRNA Following Two Consecutive Bouts of Muscle-Damaging Exercise.

Background: Extracellular vesicles (EVs) are nano-sized vesicles that are known to be powerful mediators of intercellular communication via their microRNA (miR) content. A paucity of information on EV-mediated communication arising from skeletal muscle (SkM) in response to exercise-induced muscle damage is present in the published literature. Lack of such information inhibits our understanding of muscle injury and repair processes.Aims: To assess circulating EV levels and selected miR content within them, in response to two consecutive bouts of muscle-damaging exercise.Methods: Serum creatine kinase activity (CK) and EVs were analyzed from the blood of 9 healthy, untrained males at baseline, and at 2 and 24 h post-exercise. The exercise regimen consisted of a combination of plyometric jumping and downhill running. Perceived muscle pain (PMP) was assessed on a scale from 1 to 10. Plasma EVs were isolated using size exclusion columns and visualized with transmission electron microscopy (TEM). EV size and number were quantified using nanoparticle tracking analysis (NTA). miR expression was quantified using qPCR, with normalization to an exogenous control (cel-miR-39).Results: PMP and CK were significantly elevated post-exercise compared to baseline levels, providing indirect evidence for muscle damage. EV visualization using TEM revealed an abundant and heterogeneously sized pool of intact particles within the exosome size range (30–150 nm). No significant change in mean EV size or number was seen over time. The SkM-specific miR-206 in EVs was found to be variable among participants and no significant change occurred in SkM-important miRs; 1, 133a, 133b, 486, and 499a. However, EV miR-31 decreased from baseline to 24 h post-exercise (p = 0.027).Conclusion: Mild to moderate exercise-induced muscle damage altered the miR-31 profile of circulating EVs within the first 24 h post-exercise, but not that of myomiRs in EVs. These data demonstrate that EVs carry selectively packaged cargo which can be affected by exercise. Future research into the total miR content of EVs in response to exercise-induced muscle damage may reveal other miRs responsive to this relatively mild perturbation. More time points post-muscle-damaging exercise would provide a better understanding of the temporal EV myomiR response.

Creatine supplementation does not alter the creatine kinase response to eccentric exercise in healthy adults on atorvastatin

Serum creatine kinase (CK) levels are higher after eccentric, muscle-damaging exercise in statin-treated patients. This could contribute to the increased statin-associated muscle symptoms reported in physically active individuals. We tested the hypothesis in this pilot study that creatine (Cr) monohydrate supplementation would reduce the CK response to eccentric exercise in patients using statins to determine if Cr supplementation could be a strategy to mitigate statin-associated muscle symptoms in physically active individuals. Healthy, nonsmoking men (n=5) and women (n=14) were randomized to Crmonohydrate=atorvastatin 80mg+10g Cr monohydrate (n=10, age=60 ± 7years) or to placebo (PL)=atorvastatin 80mg+PL (n=9, age=52 ± 6years). After 4weeks of treatment, subjects performed 45minutes of eccentric exercise (downhill walking at a -15% grade). Serum CK levels, muscle soreness (visual analog scale after two squats), and muscle pain severity and interference (using the brief pain inventory) were measured before and after 4weeks of treatment, and then for 4 consecutive days after downhill walking. Vitamin D, or serum 25(OH)D, was also measured at baseline. The PL group was younger (P=.01) but not otherwise different in blood lipids, vitamin D, CK, muscle visual analog scale, and pain scores before (all P>.21) or after (all P>.12) treatment. CK increased in all subjects after downhill walking (P<.01), but neither the relative peak change (expressed as group mean difference with 95% confidence intervals: 43.52% [-196.41, 283.45]) nor the absolute peak change (67.38 U/L [-121.55, 256.31]) relative to baseline was different between groups (P=.46 and .71, respectively). A similar lack of treatment effect was observed for muscle soreness (11.03mm [-9.49, 31.55]), pain severity (0.77 pts [-0.95, 2.50]), and pain interference (1.02 pts [-1.25, 3.29]) with P-values for group comparisons=0.27, 0.36, and 0.35, respectively. However, subjects with "insufficient" Vitamin D<30ng/mL (n=10) had an ∼2-fold greater CK increase with eccentric exercise (nominal P-value=.04) than subjects with higher vitamin D levels. Cr monohydrate did not reduce CK increases after exercise in statin-treated subjects. We did observe that low vitamin D levels are associated with a greater CK response to eccentric exercise in statin-treated subjects.

Hormonal Responses after Exercise-induced Muscle Damage in Healthy Humans

Mechanically overloaded muscle and its subsequent damage are strong stimuli for eliciting acute hormonal changes, and muscle adaptation following exercise- induced muscle damage may involve complex hormonal responses before the completion of muscle regeneration. PURPOSE: This study investigated systemic responses of thyroid-stimulating hormone (TSH), free thyroxine (fT4) and prolactin (PRL) for several days after eccentric exercise-induced muscle damage in humans. METHODS: Nine healthy men (age 25.7 ± 1.7 years, height 180.4 ± 1.7 cm, body mass 77.2 ± 2.7 kg, body mass index 23.7 ± 0.6) performed 50 maximal eccentric muscle actions using the knee extensor muscles of both legs on an isokinetic dynamometer. Blood samples were withdrawn before and at 6, 48 and 120 hrs post-exercise, and serum levels of TSH, fT4) and PRL were measured by ELISA using commercially available kits. Myoglobin (Mb) concentration and lactate dehydrogenase (LDH) activity were also evaluated as indirect markers of muscle damage. One-way ANOVA was used for statistics. RESULTS: Significant alterations in Mb and LDH were observed over time after eccentric exercise (p<0.05-0.001). Serum fT4 levels exhibited a gradual increase reaching statistical significance at 48 and 120 hrs following the muscle damaging exercise (1.20±0.05 ng/dl, 1.29±0.04 ng/dl, and 1.26±0.05 ng/dl, at 6, 48 and 120 hours after exercise, respectively, compared to 1.13±0.02 ng/dl at baseline; mean±SE, p<0.05). Both PRL and TSH showed also a gradual increase up to 33% at 48 hrs and 120 hrs post exercise, respectively, however they failed to reach statistical significance due to a large variability shown between the subjects’ responses (PRL: 23.4±3.1 ng/ml, 28.1±4.7 ng/ ml, 30.2±4.1 ng/ml and 25.7±4.6 ng/ml; TSH: 1.09±0.14 μIU/ml, 1.27±0.15 μIU/ml, 1.17±0.20 μIU/ml, and 1.33±0.17 μIU/ml, at baseline, 6, 48 and 120 hours post- exercise, respectively, mean±SE, p>0.05). CONCLUSION: The late elevated levels of TSH and PRL, and particularly of fT4, during the recovery period after muscle damage may suggest functional interactions between those hormones and muscle regeneration. Further studies are needed to characterize the mechanisms by which those hormonal responses are triggered and regulated at the systemic level during recovery after exercise-induced muscle damage.

Using Multiplex and Single-Molecule Bead-Based Technologies to Assess Inflammatory Changes Following Skeletal Muscle Injury

Abstract Inflammation is a key component in the healing and recovery of injured skeletal muscle. Despite the known importance of inflammation, its response has not been consistently demonstrated in human experimental model systems. One plausible explanation for the inconsistent outcomes in human skeletal muscle injury models may be caused by the analytical methods selected. Traditional methods (i.e. ELISA, Western Blotting, etc.) used to measure serum inflammatory/muscle damage biomarkers lack the bandwidth and/or sensitivity to measure multiple biomarkers or femtomolar changes. The purpose of this investigation was to describe a comprehensive method for the measurement of serum inflammatory biomarkers in a human skeletal muscle injury model. To accomplish this objective, we combined 384-well, bead-based multiplex assays (MILLIPLEX® and Luminex® FM3D) with a novel, bead-based single molecule detection technology (MilliporeSigma SMCxPro). The samples used in the present investigation were collected from an IRB-approved study and consented subjects (in accordance with the latest Declaration of Helsinki). Subjects completed a muscle damage exercise session and blood samples were collected at 0, 24, 48, and 72-h after muscle damage. We observed a significant change in inflammation post-damage using both detection technologies. Combining multiplexing with the precise, single molecule counting detection method allowed for a better clarification and description of the inflammatory response in otherwise undetectable sample concentrations. More research is needed to demonstrate repeatability for this assay approach as well as validation for other inflammatory states (i.e. chronic inflammatory disease).

The influence of capillarization on satellite cell pool expansion and activation following exercise-induced muscle damage in healthy young men.

Skeletal muscle stem cells (satellite cells) play a crucial role in repair and remodelling of muscle in response to exercise. Satellite cells are in close spatial proximity to muscle capillaries and therefore may be influenced by them. In this study, we describe the activation and expansion of the satellite cell pool in response to eccentric contraction-induced muscle damage in individuals with significantly different levels of muscle capillarization. Individuals with greater capillarization and capacity for muscle perfusion demonstrated enhanced activation and/or expansion of the satellite cell pool allowing for an accelerated recovery of muscle function. These results provide insight into the critical relationship between muscle capillarization and satellite cells during skeletal muscle repair. Factors that determine the skeletal muscle satellite cell (SC) response remain incompletely understood. It is known, however, that SC activation status is closely related to the anatomical relationship between SCs and muscle capillaries. We investigated the impact of muscle fibre capillarization on the expansion and activation status of SCs following a muscle-damaging exercise protocol in healthy young men. Twenty-nine young men (21±0.5years) performed 300 unilateral eccentric contractions (180degs-1 ) of the knee extensors. Percutaneous muscle biopsies from the vastus lateralis and blood samples from the antecubital vein were taken prior to (Pre) exercise and at 6, 24, 72 and 96h of post-exercise recovery. A comparison was made between subjects who had a relative low mixed muscle capillary-to-fibre perimeter exchange index (CFPE; Low group) and high mixed muscle CFPE index (High group) at baseline. Type I and type II muscle fibre size, myonuclear content, capillarization, and SC response were determined via immunohistochemistry. Overall, there was a significant correlation (r=0.39; P<0.05) between the expansion of SC content (change in total Pax7+ cells/100 myofibres) 24h following eccentric exercise and mixed muscle CFPE index. There was a greater increase in activated SCs (MyoD+ /Pax7+ cells) in the High as compared to the Low CFPE group 72h following eccentric exercise (P<0.05). The current study provides further evidence that muscle fibre capillarization may play an important role in the activation and expansion of the SC pool during the process of skeletal muscle repair.

Hormonal responses following eccentric exercise in humans.

Mechanically overloaded muscle and its subsequent damage are strong stimuli for eliciting acute hormonal changes, while the muscle adaptation which occurs following exercise-induced muscle damage may involve complex hormonal responses before the completion of muscle regeneration. The purpose of this study was to investigate systemic responses of various hormones, as well as secreted proteins that are exercise-regulated and associated with muscle adaptation, for several days after eccentric exercise-induced muscle damage in humans. Nine young male volunteers performed 50 maximal eccentric muscle actions using the knee extensor muscles of both legs. Blood samples were drawn before and at 6, 48 and 120 hours post exercise and serum levels of growth hormone (GH), insulin-like growth factor binding protein-3 (IGFBP-3), cortisol, prolactin, thyroid-stimulating hormone (TSH), free thyroxine (fT4), irisin, follistatin and sclerostin were measured. Myoglobin (Mb) concentration and lactate dehydrogenase (LDH) activity were also evaluated as indirect markers of muscle damage. Significant alterations in Mb and LDH were observed over time after eccentric exercise (p=0.039-0.001). A late serum increase in fT4 and decrease in irisin levels, along with an early and persistent decrease in IGFBP-3 levels, were observed following the muscle-damaging exercise (p=0.049-0.016). GH, cortisol, prolactin, TSH, follistatin and sclerostin exhibited moderate changes during the recovery period after exercise, though without reaching statistical significance (p>0.05), while correlational analyses revealed significant associationsbetween GH and IGFBP-3, prolactin and sclerostin over time (p=0.049-0.001). The significant hormonal responses observed in this study may indicate their involvement in the regenerative mechanisms following muscle damage, potentially as part of a regulatory network to support a normal adaptation process after muscle-damaging exercise.

Systemic Responses of Inflammation-Related Factors Following Eccentric Exercise in Humans

Background: Exercise-induced muscle damage is followed by muscle adaptation which has been associated with an inflammatory response and is influenced by a crucial balance between pro- and anti-inflammatory cytokines. This study investigated the pattern of systemic cytokine responses for several hours after muscle-damaging exercise. Methods: Nine healthy, young men volunteers performed 50 maximal eccentric muscle actions with each leg using the knee extensors. Serum levels of interleukin (IL)-1α, IL-2, IL-6 and IL-10, transforming growth factor (TGF)-β1 and tumor necrosis factor (TNF)-α were measured by ELISA before and at 6, 48 and 120 hours post-exercise. Results: Volunteers reported significant muscle soreness and their serum creatine kinase (CK) activity increased gradually up to 120 hrs post-exercise (p<0.05). Circulating levels of IL-1a remained unaltered and TGF-β1 increased slightly over time, while IL-2 showed a moderate increase 48 hrs following eccentric exercise (p>0.05). Levels of TNF-α and IL-10 exhibited a similar pattern of response over time, showing a nearly 50% and 100% increase, respectively, 6 hrs post-exercise, while IL-6 increase significantly 6 and 48 hrs post-exercise (p<0.05). Conclusion: These findings suggest that eccentric exercise might trigger a systemic, predominantly anti-inflammatory, acute cytokine response as part of the adaptation process to muscle damage, where IL-6 may be especially involved.

Egzersize bağlı iskelet kası hasarının güç, sürat ve denge performansına zamana bağlı etkisinin incelenmesi

The purpose of this study was to investigate the time-course effects of an exercise that creates muscle damage on muscle strength, power, speed and balance performance of young male subjects. Ten male subjects (age mean 21.1 ± 3.4 years, height 171.2 ± 6.1 cm, body weight 64.1 ± 4.7 kg) voluntarily participated in the study. On the first day of the study, participants’ height and body weight measurements and muscle pain, Creatine Kinase (CK), balance, power and speed test baseline values obtained. On the second day, a training protocol was performed and the muscle pain, balance, power and speed tests, and CK values were measured at 1, 24, 48 and 72 hours after the protocol. SPSS 19 package program was used to analyze the data. The data were evaluated using the ANOVA test for repeated measures. CK and muscle pain values at 1, 24, 48 and 72 hours after exercise protocol were significantly higher than baseline (p 0.05). The speed values were statistically significantly higher at 24 and 72 hours after exercise compared to the baseline values (p<0.05). As a result; muscle damage exercise protocol, increased CK and muscle pain scores, adversely affected the speed performance but had no effect on balance and power performance of the subjects

The Effects of 10 Days of a Multi- Ingredient Supplement on Performance Lactate during Exercise and Post Exercise Muscle Damage, Oxidative Stress and Inflammation

Intense and prolonged bouts of intense exercise can cause metabolic acidosis due to the accumulation of intramuscular hydrogen ions. The purpose of the investigation was to assess the efficacy of a calcium bicarbonate sport supplement to enhance exercise performance and recovery. Sixteen healthy, active, college-aged males were recruited to participate in the investigation. Participants in this cross-over study had two tendaysupplementation periods separated by a ten-day washout period. Performance measures were tested and recorded via graded exercise tests on a cycle ergometer at baseline, as well as after both supplementation periods. Blood samples were acquired at baseline as well as pre- and post-exercise after both trial periods to assess levels of ammonia, 8-OHdG, creatine kinase, lactate dehydrogenase, and C-reactive proteins, IL-2, IL-6, and TNF-Alpha markers. ANOVA revealed significantly lower levels (treatment vs. placebo) by time (baseline, day ten) for 8-OHdG post exercise (main effect F=6.98, p=0.013). Creatine kinase levels demonstrated a significant interaction effect (main effect F=0.267, p=0.608; treatment * time: F=3.05, p=0.04). Additionally, a significant difference in peak lactate was noted by treatment (t=1.67, p=0.05, 3.8 mmol supplement vs. 4.8 mmol placebo). Significant differences were not found for aerobic performance measures, ammonia, C-reactive proteins, Interleukin-2, Interleukin-6, or TNF-alpha. The results of the present investigation provided initial evidence for the use of the multiingredient supplements. This preliminary evidence suggests the supplement may blunt lactate response to exercise and help provide some protection from muscle damage and oxidative stress.

THE EFFECT OF DIFFERENT DOSE OF DROP JUMPING ON SYMPTOMS OF MUSCLE DAMAGE

Background. The aim of this study was to follow symptoms of exercise induced muscle damage in response to 50, 100 and 200 drop jumps with maximal intensity. Methods. Three groups of young healthy men (n = 10 in each group) performed a bout of mechanically demanding stretch shortening cycle exercise consisting of 50, 100 and 200 drop jumps. Voluntary and electrically induced knee extension torque, creatine kinase, muscle soreness were measured before and 24 h after exercise. Results. Indirect symptoms of exercise induced damage were dependent on DJs volume: the higher the numbers of jumps, the more symptoms were observed. Only after 200 DJs compared to 50-100 DJ there was decrease of CAR and H of DJ, and 24 h after 200 DJs CK was greater than after 50-100 DJs. Conclusion. In response to acute severe muscle-damaging exercise (after 200 DJs), indirect symptoms of exercise-induced muscle damage occurred.

Murine myoblast migration: influence of replicative ageing and nutrition

Cell migration is central to skeletal muscle repair following damage. Leucine and β-Hydroxy β-methylbutyric acid (HMB) are supplements consumed for recovery from muscle damaging exercise in humans, however, their impact on muscle cell migration with age is not yet understood. We hypothesised that replicatively aged (“aged”; P46–P48) myoblasts would be less efficient at basal and supplemented repair versus parental controls (“control”; P12–P16). Aged and control myoblasts were scratch-damaged and migration velocity, directionality and distance assessed over 48 h in the absence and presence of leucine (10 mM) or HMB (10 mM) ± PI3K/Akt (LY294002 10 μM), ERK (PD98059 5 μM) or mTOR (rapamycin 0.5 μM) inhibition. Opposing our hypothesis, aged cells displayed increased velocities, directionality and distance migrated (P < 0.001) versus control. Leucine and HMB significantly increased (P < 0.001) the same parameters in control cells. The supplements were with smaller, albeit significant impact on aged cell velocity (P < 0.001) and in the presence of HMB only, distance (P = 0.041). Inhibitor studies revealed that, PI3K and ERK activation were essential for velocity, directionality and migration distance of aged cells in basal conditions, whereas mTOR was important for directionality only. While PI3K activation was critical for all parameters in control cells (P < 0.001), inhibition of ERK or mTOR improved, rather than reduced, control cell migration distance. Enhanced basal velocity, directionality and distance in aged cells required ERK and PI3K activation. By contrast, in control cells, basal migration was underpinned by PI3K activation, and facilitated by leucine or HMB supplementation, to migration levels seen in aged cells. These data suggest that replicatively aged myoblasts are not anabolically resistant per se, but are capable of efficient repair, underpinned by altered signaling pathways, compared with unaged control myoblasts.

5주간 전해질 음료 섭취가 고온 환경에서 일회성 운동 시 혈중 전해질 농도, 심근손상지표 및 운동수행력에 미치는 영향

5주간 전해질 음료 섭취가 고온 환경에서 일회성 운동 시 혈중 전해질 농도, 심근손상지표 및 운동수행력에 미치는 영향

Effect of timing of whey protein supplement on muscle damage markers after eccentric exercise

Whey protein is a nutritional supplement commonly ingested for recovery following exercise. However, the timing when whey protein supplement must be ingested after muscle-damaging exercise is debatable. Therefore, the present study investigated the effects of the timing of supplement ingestion on muscle damage markers after eccentric or muscle-damaging exercise. In total, 32 collegiate male students participated in this study; they were randomly assigned to control group (n=8), before supplement group (n=8), after supplement group (n=8), or before and after supplement group (n=8). Eccentric exercise was performed using elbow flexors with a modified preacher curl machine. Subsequently, maximal isometric strength, muscle soreness, range of motion (relaxed and flexed arm angle), and blood markers (creatine kinase and aspartate transaminase) were measured before and after exercise. Repeated-measure analysis of variance was used to analyze the effects of timing of supplement. No significant group by time effects were noted in maximal isometric strength, muscle soreness, range of motion, and blood markers (P>0.05). The timing of whey protein supplement did not affect reduction of muscle damage or recovery following eccentric exercise.

Activating transcription factor 3 regulates chemokine expression in contracting C2C12 myotubes and in mouse skeletal muscle after eccentric exercise

Activating transcription factor (ATF) 3 regulates chemokine expression in various cell types and tissues. Herein, we studied this regulation in contracting muscle cells in vitro, and in skeletal muscle after muscle-damaging exercise in vivo. C2C12 myotubes with normal or low ATF3 levels (atf3_siRNA) were electrically stimulated (EPS). Also, ATF3-knockout (ATF3-KO) and control mice ran downhill until exhaustion, and muscles were analyzed post-exercise. EPS increased ATF3 levels in myotubes (P < 0.01). Chemokine C-C motif ligand (ccl) 2 mRNA increased post-EPS, but atf3_siRNA attenuated the response (P < 0.05). Atf3_siRNA up-regulated ccl6 basal mRNA, and down-regulated ccl9 and chemokine C-X-C motif ligand (cxcl) 1 basal mRNAs. Post-exercise, ATF3-KO mice showed exacerbated mRNA levels of ccl6 and ccl9 in soleus (P < 0.05), and similar trends were observed for ccl2 and interleukin (il) 1β (P < 0.09). In quadriceps, il6 mRNA level increased only in ATF3-KO (P < 0.05), and cxcl1 mRNA showed a similar trend (P = 0.082). Cluster of differentiation-68 (cd68) mRNA, a macrophage marker, increased in quadriceps and soleus independently of genotype (P < 0.001). Our data demonstrate that ATF3 regulates chemokine expression in muscle cells in vitro and skeletal muscle in vivo, but the regulation differs in each model. Cells other than myofibers may thus participate in the response observed in skeletal muscle. Our results also indicate that ATF3-independent mechanisms would regulate macrophage infiltration upon muscle-damaging exercise. The implications of chemokine regulation in skeletal muscle remain to be determined.

Serum brain-derived neurotrophic factor and interleukin-6 response to high-volume mechanically demanding exercise.

The aim of this study was to follow circulating brain-derived neurotrophic factor (BDNF) and interleukin-6 (IL-6) levels in response to severe muscle-damaging exercise. Young healthy men (N = 10) performed a bout of mechanically demanding stretch-shortening cycle exercise consisting of 200 drop jumps. Voluntary and electrically induced knee extension torque, serum BDNF levels, and IL-6 levels were measured before and for up to 7 days after exercise. Muscle force decreased by up to 40% and did not recover by 24 hours after exercise. Serum BDNF was decreased 1 hour and 24 hours after exercise, whereas IL-6 increased immediately and 1 hour after but recovered to baseline by 24 hours after exercise. IL-6 and 100-Hz stimulation torque were correlated (r = -0.64, P < 0.05) 24 hours after exercise. In response to acute, severe muscle-damaging exercise, serum BDNF levels decrease, whereas IL-6 levels increase and are associated with peripheral fatigue. Muscle Nerve 57: E46-E51, 2018.

The Potential Of Omega 3 Supplementation To Reduce Muscle-inflammation After Muscle-damaging Exercise

Muscle inflammation which follows exercise-induced muscle damage (EIMD) relates to strength loss, muscle-soreness and impaired recovery (Lynn and Morgan, 1994). It remains unclear whether omega-3 fatty acids (O-3) supplementation blunts the exercise-induced inflammation associated with EIMD. PURPOSE: Following supplementation with O-3, indirect markers of muscle damage were examined after EIMD to determine if supplementation had any beneficial effect in reducing muscle inflammation. METHODS: Eight healthy, recreationally active caucasian males (28.13 ± 3.4 yrs) were randomly allocated to a supplementation group (SUP, n = 4) to receive 2.85g/day O-3 supplementation or a placebo group (CON, n = 4) for three weeks. After three-weeks, participants performed a bout of EIMD, which consisted of performing 10 sets of 15 repetitions of leg extension on a Rating of Perceived Exertion (RPE) of 7/10 (Borg, 1982). Creatine Kinase (CK) from venous blood samples, isometric right-leg strength, squat-jump test and perceived soreness were determined, as indirect markers of muscle-damage at Baseline, immediately after EIMD (POST) and 48 hours after EIMD to coincide with the delayed muscle inflammatory response. RESULTS: No differences were found between Baseline and POST. There was a trend for smaller increase of CK levels (pre vs 48-h post EIMD) on the SUP group (38.8% increase) compared with the CON group (105.6% increase; P = 0.051). There was no significant effect (baseline vs. 48-h post EIMD) on muscle strength between SUP and CON group (P > 0.05), however, CON showed a larger decrease in strength compared to SUP (>6.3% vs SUP). No differences in jump height were found between SUP and CON (P > 0.05). There was no significant difference in muscle soreness at 48-h post EIMD between SUP and CON group (P = 0.171). CONCLUSION: Three weeks of O-3 supplementation decreased exercise-induced muscle inflammation after eccentric exercise. The encouraging results from this pilot study have led to designing further work related to this topic. The lack of statistical significance may be adduced to the limitations of the study design. Supplementation with O-3 can be beneficial in sedentary individuals re-starting physical activity and in athletes undergoing heavy exercise regimes, decreasing the exercise related muscle inflammation.

Recovery is Not Facilitated with Protein Supplementation Following Muscle-Damaging Concurrent Exercise

Recovery is Not Facilitated with Protein Supplementation Following Muscle-Damaging Concurrent Exercise

Curcumin Reduces Muscle Damage and Soreness Following Muscle‐Damaging Exercise

The training of novice and competitive athletes involves the incorporation of unaccustomed exercise, likely to result in skeletal muscle tissue damage. The initial response, known to result in muscle soreness and swelling, and decreased forced production, is followed by a secondary inflammatory response integral in the skeletal muscle repair and recovery response. Athletes may benefit from a dampening of muscle damage and an accelerated recovery period, to support the performance of consequent bouts at maximal intensity. The antioxidant curcumin is able to counteract the two leading causes of muscle damage, oxidative stress and inflammation, as it interacts with multiple inflammatory pathways. This current study sought to examine the effect of differing doses of a highly bioavailable form of curcumin (CurcuWIN®, OmniActive) on muscle damage and recovery following a bout of muscle damaging exercise by assessing plasma cytokines (IL‐6, IL‐10, and TNF‐alpha), creatine kinase (CK), and perception of muscle soreness (VAS), before, immediately post, 1 hour post, and 24, 48, and 72 hours after a downhill running protocol. Fifty‐nine moderately trained men (n=30; 21±2 years; 173.8±20.0 cm; 79.4±11.0 kg) and women (n=29; 21±2 years; 164.9±6.5 cm; 60.1±8.0 kg) were randomly assigned to ingest 50 mg Curcuminoids (in the form of 250 mg CurcuWIN®), 200 mg Curcuminoids (in the form of 1,000 mg CurcuWIN®), or placebo (PLA) for eight weeks in a double‐blind, randomized, placebo controlled parallel design. Statistical analysis was performed using NCSS (NCSS 10 Statistical Software (2015); NCSS, LLC. Kaysville, Utah, USA). Statistical models specific to the evaluation of each outcome variable were formulated. 200 mg of Curcuminoids significantly reduced VAS pain scores, reflecting a subjects perception of pain in the thigh area, 24 hours post muscle damaging exercise (−1.74, p=0.03), and showed a trend one hour post exercise (−1.44, p=0.07), and non‐significant improvements at 48 (−0.94, p=0.24) and 72 hours (−0.41, p=0.60). Creatine kinase, a marker of muscle damage, increased immediately following the muscle damaging exercise bout and remained elevated for 48 hours post (p&lt;0.001). Curcuminoids supplementation significantly reduced the increase in CK levels over the placebo group when the baseline CK value is held constant at the mean (−19.0 U•L−1, p=0.04 (200mg), and = −27.2 U•L−1, p=0.03 (50mg) respectively), with treatment effects being most pronounced in males. No significant differences were observed between treatments for cytokines at both doses. These data demonstrate curcuminoids reduce muscle damage and improve muscle soreness in healthy young subjects following a bout of muscle damaging exercise. Faster recovery allows for consistent training at competition intensity and might lead to enhanced adaptation rate and performance.Support or Funding InformationThis work was supported by OmniActive Health Technologies Ltd., Mumbai, India.

The efficacy of protein supplementation during recovery from muscle-damaging concurrent exercise.

This study investigated the effect of protein supplementation on recovery following muscle-damaging exercise, which was induced with a concurrent exercise design. Twenty-four well-trained male cyclists were randomised to 3 independent groups receiving 20 g protein hydrolysate, iso-caloric carbohydrate, or low-calorific placebo supplementation, per serve. Supplement serves were provided twice daily, from the onset of the muscle-damaging exercise, for a total of 4 days and in addition to a controlled diet (6 g·kg-1·day-1 carbohydrate, 1.2 g·kg-1·day-1 protein, remainder from fat). Following the concurrent exercise session at time-point 0 h, comprising a simulated high-intensity road cycling trial and 100 drop-jumps, recovery of outcome measures was assessed at 24, 48, and 72 h. The concurrent exercise protocol was deemed to have caused exercise-induced muscle damage (EIMD), owing to time effects (p < 0.001), confirming decrements in maximal voluntary contraction (peaking at 15% ± 10%) and countermovement jump performance (peaking at 8% ± 7%), along with increased muscle soreness, creatine kinase, and C-reactive protein concentrations. No group or interaction effects (p > 0.05) were observed for any of the outcome measures. The present results indicate that protein supplementation does not attenuate any of the indirect indices of EIMD imposed by concurrent exercise, when employing great rigour around the provision of a quality habitual diet and the provision of appropriate supplemental controls.