Effects Of Exercise-induced Muscle Damage Research Articles

The Impact of Exercise-Induced Muscle Damage on Various Cycling Performance Metrics: A Systematic Review and Meta-Analysis.

Devantier-Thomas, B, Deakin, GB, Crowther, F, Schumann, M, and Doma, K. The impact of exercise-induced muscle damage on various cycling performance metrics: a systematic review and meta-analysis. J Strength Cond Res 38(1): 196-212, 2024-This systematic review and meta-analysis examined the impact of exercise-induced muscle damage (EIMD) on cycling performance. The primary outcome measure was cycling performance, whereas secondary outcome measures included creatine kinase (CK), delayed-onset muscle soreness (DOMS), and muscular contractions. Data were extracted and quantified through forest plots to report on the standardized mean difference and p values. The meta-analysis showed no significant change in oxygen consumption at 24-48 hours (p > 0.05) after the muscle damage protocol, although ventilation and rating of perceived exertion significantly increased (p < 0.05) during submaximal cycling protocols. Peak power output during both sprint and incremental cycling performance was significantly reduced (p < 0.05), but time-trial and distance-trial performance showed no change (p > 0.05). Measures of CK and DOMS were significantly increased (p < 0.05), whereas muscular force was significantly reduced following the muscle-damaging protocols (p < 0.05), confirming that cycling performance was assessed during periods of EIMD. This systematic review showed that EIMD affected both maximal and submaximal cycling performance. Therefore, coaches should consider the effect of EIMD on cycling performance when implementing unaccustomed exercise into a cycling program. Careful consideration should be taken to ensure that additional training does not impair performance and endurance adaptation.

Acute effects of exercise-induced muscle damage on sprint and change of direction performance: A systematic review and metaanalysis

Acute effects of exercise-induced muscle damage on sprint and change of direction performance: A systematic review and metaanalysis

The effects of exercise-induced muscle damage on varying intensities of endurance running performance: A systematic review and meta-analysis

The effects of exercise-induced muscle damage on varying intensities of endurance running performance: A systematic review and meta-analysis

The Effects of Exercise-Induced Muscle Damage on Antagonist Muscles in Upper Limb Reaching Tasks

Coordination and control of multiple muscle groups are critical when adapting to movement disruptions, such as altered goals or pathways. Humans use sensory information from internal and external sources to engage in online movement control. Proprioception, mainly obtained from sensors in the muscles such as muscle spindles, is an important source of sensory information. After intense or unusual exercise, exercise-induced muscle damage (EIMD) can occur within 24 to 48 hours. EIMD can also increase noise in the signals generated by the sensory organs in the muscles and may influence online movement control.&#x0D; The objective of the study is to investigate the effects of EIMD on upper-limb movement control.&#x0D; Four right-handed, neurologically healthy, female participants (aged 20-21, M = 0.5) took part in the pilot experiment, they had normal, or corrected-to-normal vision, and participated in less than 5 hours of structured strength training weekly. The study consisted of familiarization and baseline testing, an exercise protocol, and a muscle damage assessment. In each session, a maximal voluntary contraction of the biceps brachii was assessed using a dynamometer. This dynamometer was also used for the EIMD-inducing protocol. To test the effects of EIMD on online control, participants completed a series of reaching tasks using the Kinarm Exoskeleton Robot. During some reaches, participants were required to correct their movement to either a force or target perturbation.&#x0D; Our pilot data shows that our protocol successfully induced muscle damage, as well as less antagonistic muscle (bicep) activation during reaching tasks. This suggests reduced biceps muscle contribution to movement control post-exercise. A decrease in movement time could signify learning and requires further exploration. We are hopeful that with further data collection, we will establish that participants are less accurate and have reduced flexor muscle activity in responses to both types of perturbations, compared to baseline.

Exercise induced muscle damage and repeated bout effect: an update for last 10 years and future perspectives

Exercise-induced muscle damage (EIMD) and repeated bout effect (RBE) are widely researched across various populations. EIMD is the muscle damage occurring after one bout of unaccustomed exercise while RBE is the attenuation of the same muscle damage in subsequent second bout. RBE seems to have significant implications for exercise prescription. Despite existence of vast literature, there is lack of clarity on the effects of EIMD and RBE in a healthy population. The purpose of this study is to review the literature on EIMD and RBE in healthy participants published during the last 10 years. The search of major databases (including Scopus, Google Scholar and PubMed) was conducted using specific keywords ‘Exercise induced muscle damage’, ‘Repeated bout effect’, ‘Healthy participants’ ‘Pre-conditioning’, ‘Eccentric exercise’. Studies published from 2011 onwards which included EIMD and RBE assessment in healthy participants were included in this review. Database searching revealed a total of 38 studies on EIMD and RBE in healthy participants. Three major themes of papers were identified that focused on EIMD and RBE along with (1) age related differences, (2) sex-based differences, and (3) response in athletes. Findings of this comprehensive review suggests that both EIMD and RBE are age, and sex specific. Delayed onset muscle soreness played a major role in both EIMD and RBE in all the population types. Female participants are less susceptible to EIMD as compared to age-matched male counterparts. Moreover, both EIMD and RBE are more elicited in middle aged and younger adults as compared to children and older adults while the magnitude of RBE turns out to be minimal in trained individuals due to persisting adaptations.

The combined effects of exercise-induced muscle damage and heat stress on acute kidney stress and heat strain during subsequent endurance exercise.

The purpose of the study was to investigate the combined effect of downhill running and heat stress on muscle damage, as well as on heat strain and kidney stress during subsequent running in the heat. In a randomized cross-over study, ten non-heat-acclimated, physically active males completed downhill running in temperate (EIMD in Temp) and hot (EIMD in Hot) conditions followed by an exercise-heat stress (HS) test after 3-h seated rest. Blood and urine samples were collected immediately pre- and post-EIMD and HS, and 24h post-EIMD (post-24h). Core temperature and thermal sensation were measured to evaluate heat strain. Serum creatine kinase (CK), maximal voluntary isometric contraction of the quadriceps (MVC) and perceived muscle soreness were measured to evaluate muscle damage. Urinary neutrophil gelatinase-associated lipocalin (NGAL) and kidney injury molecule-1 (KIM-1) levels were measured to indicate acute kidney stress. CK, MVC and perceived soreness were not different between conditions at any timepoints. In the EIMD in Hot condition, urinary NGAL was significantly elevated from pre- to post-HS (pre-HS: 6.56 {1.53-12.24}ng/min, post-HS: 13.72 {7.67-21.46}ng/min, p = 0.034). Such elevation of NGAL or KIM-1 was not found in the EIMD in Temp condition. As compared with downhill running in a temperate environment, downhill running in a hot environment does not appear to aggravate muscle damage. However, elevated NGAL levels following EIMD in a hot environment suggest such exercise may increase risk of mild acute kidney injury during subsequent endurance exercise in the heat.

Preliminary Investigations Into the Effect of Exercise-Induced Muscle Damage on Systemic Extracellular Vesicle Release in Trained Younger and Older Men.

Background: Exercise-induced muscle damage (EIMD) results in transient muscle inflammation, strength loss, and muscle soreness and may cause subsequent exercise avoidance. Research has recently proven that skeletal muscle can also release extracellular vesicles (EVs) into the circulation following a bout of exercise. However, EV’s potential role, including as a biomarker, in the response to eccentric resistance exercise stimulus remains unclear.Methods: Twelve (younger, n=7, 27.0±1.5years and older, n=5, 63.0±1.0years) healthy, physically active males, undertaking moderate, regular physical activity (3–5 times per week) performed a unilateral high intensity eccentric exercise protocol. Venous plasma was collected for assessment of EVs and creatine kinase (CK) prior to EIMD, immediately after EIMD, and 1–72h post-EIMD, and maximal voluntary isometric contraction (MVIC) and delayed onset muscle soreness (DOMS) were assessed at all time points, except 1 and 2h post-EIMD.Results: A significant effect of both time (p=0.005) and group (p<0.001) was noted for MVIC, with younger participants’ MVIC being higher throughout. Whilst a significant increase was observed in DOMS in the younger group (p=0.014) and in the older group (p=0.034) following EIMD, no significant differences were observed between groups. CK was not different between age groups but was altered following the EIMD (main effect of time p=0.026), with increased CK seen immediately post-, at 1 and 2h post-EIMD. EV count tended to be lower in older participants at rest, relative to younger participants (p=0.056), whilst EV modal size did not differ between younger and older participants pre-EIMD. EIMD did not substantially alter EV modal size or EV count in younger or older participants; however, the alteration in EV concentration (ΔCount) and EV modal size (ΔMode) between post-EIMD and pre-EIMD negatively associated with CK activity. No significant associations were noted between MVIC or DOMS and either ΔCount or ΔMode of EVs at any time point.Conclusion: These findings suggest that profile of EV release, immediately following exercise, may predict later CK release and play a role in the EIMD response. Exercise-induced EV release profiles may therefore serve as an indicator for subsequent muscle damage.

Effect of Exercise-Induced Muscle Damage on Bowling-Specific Motor Skills in Male Adolescent Cricketers.

The current study examined the acute effects of a bout of resistance training on cricket bowling-specific motor performance. Eight sub-elite, resistance-untrained, adolescent male fast bowlers (age 15 ± 1.7 years; height 1.8 ± 0.1 m; weight 67.9 ± 7.9 kg) completed a bout of upper and lower body resistance exercises. Indirect markers of muscle damage (creatine kinase [CK] and delayed onset of muscle soreness [DOMS]), anaerobic performance (15-m sprint and vertical jump), and cricket-specific motor performance (ball speed, run-up time, and accuracy) were measured prior to and 24 (T24) and 48 (T48) hours following the resistance training bout. The resistance training bout significantly increased CK (~350%; effect size [ES] = 1.89–2.24), DOMS (~240%; ES = 1.46–3.77) and 15-m sprint times (~4.0%; ES = 1.33–1.47), whilst significantly reducing vertical jump height (~7.0%; ES = 0.76–0.96) for up to 48 h. The ball speed (~3.0%; ES = 0.50–0.61) and bowling accuracy (~79%; ES = 0.39–0.70) were significantly reduced, whilst run-up time was significantly increased (~3.5%; ES = 0.36–0.50) for up to 24 h. These findings demonstrate that a bout of resistance training evokes exercise-induced muscle damage amongst sub-elite, adolescent male cricketers, which impairs anaerobic performance and bowling-specific motor performance measures. Cricket coaches should be cautious of incorporating bowling sessions within 24-h following a bout of resistance training for sub-elite adolescent fast bowlers, particularly for those commencing a resistance training program.

Effectiveness of a combined New Zealand green-lipped mussel and Antarctic krill oil supplement on markers of exercise-induced muscle damage and inflammation in untrained men

Green-lipped mussel oil (PCSO-524®) has been shown to attenuate signs and symptoms of exercise-induced muscle damage (EIMD), and krill oil has been shown to have a protective effect against cytokine-induced tissue degradation. The purpose of this study was to compare the effects of PCSO-524® and ESPO-572® (75% PCSO-524® and 25% krill oil) on signs and symptoms of EIMD. Fifty-one untrained men consumed 600 mg/d of PCSO-524® (n = 24) or ESPO-572® (n = 27) for 26 d prior to and 72 h following a downhill running bout. Delayed onset muscle soreness (DOMS), pressure pain threshold, limb swelling, range of motion (ROM), isometric torque, and blood markers of inflammation and muscle damage were assessed at baseline, 24, 48 and 72 h post-eccentric exercise. ESPO-572® was ‘at least as good as’ PCSO-524® and both blends were superior (p < 0.05) to placebo in lessening the increase in DOMS at 24, 48, 72 h. ESPO-572® and PCSO-524® were protective against joint ROM loss compared to placebo (p < 0.05) at 48 and 72 h. Notably, at 24 and 48 h, joint ROM was higher in the ESPO-572® compared to the PCSO-524® group (p < 0.05). No differences between the two blends for the other markers were found. ESPO-572® is ‘at least as good’ as PCSO-524® in reducing markers of muscle damage and soreness following eccentric exercise and was superior to PCSO-524® in protecting against the loss in joint ROM during recovery. Our data support the use of ESPO-572®, a combination of green-lipped mussel and krill oil, in mitigating the deleterious effects of EIMD.

Erythroferrone as a sensitive biomarker to detect stimulation of erythropoiesis.

Erythroferrone (ERFE) is a glycoprotein hormone secreted by erythroblasts in response to erythropoietin stimulation. ERFE suppresses the hepatic synthesis of the master iron-regulatory hormone, hepcidin. The impact of erythropoiesis stimulation on ERFE secretion in humans is poorly understood. This paucity of information is due in part to the lack of available means for ERFE quantification in serum samples. The present study tested a new sensitive sandwich immunoassay for human ERFE. This assay was used to demonstrate that injection of various erythropoiesis stimulating agents (ESAs) increased the blood ERFE levels in healthy volunteers. After exogenous stimulation of erythropoiesis, ERFE increased up to 8-fold with a detection window of 13 days. The impact of one unit of blood withdrawal on erythropoiesis stimulation of ERFE was also tested. ERFE significantly increased after blood withdrawal in subjects injected with both iron and saline solution, suggesting that iron supplementation did not mask the ERFE increase after blood withdrawal. The effects of exercise-induced muscle damage on ERFE was assessed by comparing ERFE levels with creatine kinase levels in samples from subjects with heavy exercise loads, and determined that this was not a confounder. The ERFE assay is a sensitive means to investigate the connection between iron metabolism and erythropoiesis in humans, and to detect ESA abuse in the antidoping field.

Irisin response to downhill running exercise in humans.

[Purpose]To determine the effects of exercise-induced muscle damage, we examined irisin responses during level running (LR), with less muscle damage, and downhill running (DHR), with greater muscle damage under equivalent exercise duration and oxygen consumption (⩒O2) conditions.[Methods]Fifteen healthy men (age: 21.6 ± 2.0 y, height: 170 ± 1.3 cm, weight: 64.8 ± 2.7 kg) were randomly assigned to either the LR group (n = 8) or the DHR group (n = 7). Subjects in the LR group performed treadmill running at 70% of maximum oxygen uptake (⩒O2max) for 30 min on a 0% gradient. In contrast, subjects in the DHR group performed the same exercise on a –10% gradient. Blood samples were collected before exercise, immediately after exercise, and 1, 3, and 24 h after exercise.[Results]No significant interaction (group × time) or main effect of group or time was observed for changes in plasma irisin concentrations over time (P > 0.05). However, the area under the curve of plasma irisin concentrations during a 3-h post-exercise period was significantly greater in the DHR (239,197 ± 8,166 ng/mL) group than in the LR (92,293 ± 8,755 ng/ml) group (P < 0.05). The blood lactate, serum cortisol, myoglobin, and plasma interleukin-6 concentrations were significantly higher in the DHR group than in the LR group after exercise (P < 0.05 for all variables).[Conclusion]DHR associated with marked muscle damage promoted a greater increase in exercise-induced irisin did LR after the same duration under identical VO2 conditions.

Effects of Exercise-Induced Muscle Damage in Well-Trained Cyclists' Aerobic and Anaerobic Performances.

Karasiak, FC and Guglielmo, LGA. Effects of exercise-induced muscle damage in well-trained cyclists' aerobic and anaerobic performances. J Strength Cond Res 32(9): 2632-2640, 2018-The purpose of this study was to analyze the effect of exercise-induced muscle damage (EIMD) in gross efficiency and in aerobic and anaerobic cycling performances. Nine well-trained cyclists (30.8 ± 6.4 years, cycling experience 8.4 ± 5.6 years) visited the laboratory 5 times. During the first visit, they performed a maximal incremental test on a cycle ergometer, to identify V[Combining Dot Above]O2max (55.2 ± 4.9 ml·kg·min) and maximum aerobic power (Pmax; 327.0 ± 28.5 W). During the second visit (control), they cycled 5 minutes at 60% of Pmax, 5 minutes at 70% of Pmax, 5-minute time trial, and Wingate test. During the third visit, the athletes performed 10 sets of 10 countermovement jumps, to generate EIMD. The athletes repeated the second visit tests (control) 30 minutes, 48 hours (fourth visit), and 96 hours (fifth visit) after the jumps. The rated perceived exertion values increased 48 hours after EIMD (3.8 vs. 3.1) at 60% of Pmax. The ventilation and respiratory exchange ratio increased at 60% of Pmax (up to 4.3 L·min and 0.04, respectively) and at 70% of Pmax (up to 5.4 L·min and 0.05, respectively), mainly after 96 hours. There was no significant difference in V[Combining Dot Above]O2, V[Combining Dot Above]CO2, and heart rate in submaximal exercises, neither in time trial. No differences were observed in the Wingate tests. In conclusion, the EIMD did not impair gross efficiency, nor aerobic and anaerobic performances in trained cyclists. However, despite the benefits of strength training to improve cyclists' performance, coaches must be cautious to the days after the strength training sessions because EIMD may change the perception of maintaining a given submaximal intensity during training or competition.

The effects of exercise-induced muscle damage on critical torque

Exercise-induced muscle damage (EIMD) has been shown to reduce endurance exercise performance. This study examined the effects of EIMD on critical torque (CT) and the sum of the torque integral above CT during (∫ T total) during a 5-min all-out, intermittent isometric knee extension exercise. CT was determined in eight participants prior to and 48-h following EIMD. EIMD was induced using electrically stimulated eccentric knee extensions until maximal voluntary strength (MVC) was reduced by 40%. EIMD was assessed by changes in MVC and ratings of muscle soreness using a VAS scale. EMG and near-infrared spectroscopy (NIRS) were collected from the vastus lateralis and vastus medialis, respectively, during the CT test to assess neuromuscular electrical activity and microvascular circulation. MVC decreased 22% (p=0.006) and soreness increased from 2.1±1.9 to 50.4±31.5mm (p=0.002) 48-h following eccentric exercise. CT declined from 61.6±17.8 to 52.0±14.1Nm (-14%; p=0.005) post-EIMD. ∫ T total declined 33% (p=0.0006) post-EIMD. No changes were observed in neuromuscular electrical activity (p=0.95 for EMG RMS and p=0.57 for EMG median frequency) or any parameter of microvascular circulation (p=0.60 for tissue saturation index, p=0.27 for total hemoglobin and myoglobin, p=0.51 for oxyhemoglobin, and p=0.26 for deoxyhemoglobin) between conditions. Our finding that EIMD-reduced CT may explain the decrements in endurance performance following EIMD observed in the previous studies. The disproportionate reduction in ∫ T total compared to MVC and CT is suggestive of a more rapid depletion of anaerobic energy stores and/or accumulation of metabolic by-products leading to fatigue following EIMD.

Supplementation Strategies to Reduce Muscle Damage and Improve Recovery Following Exercise in Females: A Systematic Review.

Exercise-induced muscle damage (EIMD) caused by unaccustomed or strenuous exercise can result in reduced muscle force, increased muscle soreness, increased intramuscular proteins in the blood, and reduced performance. Pre- and post-exercise optimal nutritional intake is important to assist with muscle-damage repair and reconditioning to allow for an accelerated recovery. The increased demand for training and competing on consecutive days has led to a variety of intervention strategies being used to reduce the negative effects of EIMD. Nutritional intervention strategies are largely tested on male participants, and few report on sex-related differences relating to the effects of the interventions employed. This review focuses on nutritional intervention strategies employed to negate the effects of EIMD, focussing solely on females.

Effect of exercise-induced muscle damage on vascular function and skeletal muscle microvascular deoxygenation.

This paper investigated the effects of unaccustomed eccentric exercise‐induced muscle damage (EIMD) on macro‐ and microvascular function. We tested the hypotheses that resting local and systemic endothelial‐dependent flow‐mediated dilation (FMD) and microvascular reactivity would decrease, V˙O2max would be altered, and that during ramp exercise, peripheral O2 extraction, evaluated via near‐infrared‐derived spectroscopy (NIRS) derived deoxygenated hemoglobin + myoglobin ([HHb]), would be distorted following EIMD. In 13 participants, measurements were performed prior to (Pre) and 48 h after a bout of knee extensor eccentric exercise designed to elicit localized muscle damage (Post). Flow‐mediated dilation and postocclusive reactive hyperemic responses measured in the superficial femoral artery served as a measurement of local vascular function relative to the damaged tissue, while the brachial artery served as an index of nonlocal, systemic, vascular function. During ramp‐incremental exercise on a cycle ergometer, [HHb] and tissue saturation (TSI%) in the m. vastus lateralis were measured. Superficial femoral artery FMD significantly decreased following EIMD (pre 6.75 ± 3.89%; post 4.01 ± 2.90%; P < 0.05), while brachial artery FMD showed no change. The [HHb] and TSI% amplitudes were not different following EIMD ([HHb]: pre, 16.9 ± 4.7; post 17.7 ± 4.9; TSI%: pre, 71.0 ± 19.7; post 71.0 ± 19.7; all P > 0.05). At each progressive increase in workload (i.e., 0–100% peak), the [HHb] and TOI% responses were similar pre‐ and 48 h post‐EIMD (P > 0.05). Additionally, V˙O2max was similar at pre‐ (3.0 ± 0.67 L min−1) to 48 h post (2.96 ± 0.60 L min−1)‐EIMD (P > 0.05). Results suggest that moderate eccentric muscle damage leads to impaired local, but not systemic, macrovascular dysfunction.

Effect of damaging exercise on electromechanical delay.

In this study we aimed to quantify the effect of exercise-induced muscle damage on both the electrochemical and mechanical components of electromechanical delay using very-high-frame-rate ultrasound. Fifteen participants underwent electrically evoked contractions of the medial gastrocnemius muscle with an ultrasound transducer on the muscle belly and on the myotendinous junction, before, 1 hour, and 48 hours after eccentric exercise of the plantar flexor muscles. Maximal isometric plantar flexor torque was significantly lower at 1 hour (-41.1 ± 14.9%; P = 0.0001) and 48 hours (-11.9 ± 14.9%; P = 0.038) post-exercise compared with pre-exercise. However, the delay between electrical stimulation and the onset of muscle activation, the delay between electrical stimulation and myotendinous junction motion, and the electromechanical delay were not altered significantly by eccentric exercise (P = 0.063). These findings suggest that moderate muscle damage does not affect the time for the electrochemical or mechanical components of electromechanical delay. Muscle Nerve 54: 136-141, 2016.

Effect of exercise-induced muscle damage on muscle hardness evaluated by ultrasound real-time tissue elastography.

PurposeTo assess the effect of exercise-induced muscle damage on muscle hardness and evaluate the relationship between muscle hardness and muscle damage indicators.MethodsSeven men (mean 25.3 years; 172.7 cm; 66.8 kg) performed the single-leg ankle plantar flexion exercise involving both concentric and eccentric contractions (10 sets of 40 repetitions). The hardness of the medial gastrocnemius (MG) was evaluated using ultrasound real-time tissue elastography before, from day 1 to 4, and day 7 after exercise. The strain ratio between the MG and a reference material was calculated. Simultaneously, we evaluated the magnetic resonance T2 value (an index of edema) of the triceps surae, the ankle dorsiflexion range of motion (ROM), and calf muscle soreness. Serum creatine kinase activity was assessed before, 2 and 4 h, and from day 1 to 4 after exercise.ResultsThe MG showed lower strain ratio, indicating increased muscle hardness, on day 4 post-exercise (P < 0.01) and higher T2 values on days 1–7 post-exercise (P < 0.01) relative to each pre-exercise value. The ankle dorsiflexion ROM was lower on days 2–4 post-exercise (P < 0.01). The serum creatine kinase markedly increased on days 3 and 4 post-exercise (not significant). The degree of muscle soreness among the post-exercise time points was similar. The decreased strain ratio did not correlate with the increased T2, the decreased joint ROM or muscle soreness.ConclusionMuscle hardness increased after strenuous resistance exercise, but the change was not related with muscle edema, decreased joint ROM, or muscle soreness resulting from muscle damage.

Effect of a carbohydrate-protein multi-ingredient supplement on intermittent sprint performance and muscle damage in recreational athletes.

Carbohydrate-protein-based multi-ingredient supplements have been proposed as an effective strategy for limiting the deleterious effects of exercise-induced muscle damage. This study compares the effects of a commercially available carbohydrate-protein supplement enriched with l-glutamine and l-carnitine-l-tartrate to carbohydrate alone or placebo on sprint performance, muscle damage markers, and recovery from intermittent exercise. On 3 occasions, 10 recreationally trained males ingested a multi-ingredient, a carbohydrate supplement, or a placebo before, during, and immediately after a 90-min intermittent repeated sprint test. Fifteen-metre sprint times, creatine kinase, myoglobin, and interleukin-6 were assessed before (pre), immediately after (post), 1 h after (1h), and 24 h after (24h) exercise. Total sprint time measured during the intermittent protocol was not different between conditions. Fifteen-metre sprint time was slower (p < 0.05) at post, 1h and 24h compared with pre without differences between conditions (p > 0.05). Creatine kinase at 24h was lower (p < 0.05) in the multi-ingredient (461.8 ± 271.8 U·L) compared with both carbohydrate and placebo (606 ± 314.5 U·L and 636 ± 344.6 U·L, respectively). Myoglobin increased (p < 0.05) in all 3 conditions at post and 1h compared with pre, showing lower values at 1h (p < 0.05) for the carbohydrate and a trend (p = 0.060) for multi-ingredient compared with the placebo condition (211.4 ± 127.2 ng·mL(-1) and 239.4 ± 103.8 ng·mL(-1) vs. 484.6 ± 200.0 ng·mL(-1), respectively). Interleukin-6 increased at both post and 1h compared with pre (p < 0.05) with no differences between conditions. In conclusion, ingesting a multi-ingredient supplement before, during, and immediately after a 90-min intermittent sprint test resulted in no effects on performance and fatigue while the accumulation of some biomarkers of muscle damage could be attenuated.

Effects of Air-Pulsed Cryotherapy on Neuromuscular Recovery Subsequent to Exercise-Induced Muscle Damage

Background: Localized cooling has been proposed as an effective strategy to limit the deleterious effects of exercise-induced muscle damage on neuromuscular function. However, the literature reports conflicting results. Purpose: This randomized controlled trial aimed to determine the effects of a new treatment, localized air-pulsed cryotherapy (–30°C), on the recovery time-course of neuromuscular function following a strenuous eccentric exercise. Study Design: Controlled laboratory study. Methods: A total of 24 participants were included in either a control group (CONT) or a cryotherapy group (CRYO). Immediately after 3 sets of 20 maximal isokinetic eccentric contractions of elbow flexors, and then 1, 2, and 3 days after exercise, the CRYO group received a cryotherapy treatment (3 × 4 minutes at −30°C separated by 1 minute). The day before and 1, 2, 3, 7, and 14 days after exercise, several parameters were quantified: maximal isometric torque and its associated maximal electromyographic activity recorded by a 64-channel electrode, delayed-onset muscle soreness (DOMS), biceps brachii transverse relaxation time (T2) measured using magnetic resonance imaging, creatine kinase activity, interleukin-6, and C-reactive protein. Results: Maximal isometric torque decreased similarly for the CONT (–33% ± 4%) and CRYO groups (−31% ± 6%). No intergroup differences were found for DOMS, electromyographic activity, creatine kinase activity, and T2 level averaged across the whole biceps brachii. C-reactive protein significantly increased for CONT (+93% at 72 hours, P < .05) but not for CRYO. Spatial analysis showed that cryotherapy delayed the significant increase of T2 and the decrease of electromyographic activity level for CRYO compared with CONT (between day 1 and day 3) in the medio-distal part of the biceps brachii. Conclusion: Although some indicators of muscle damage after severe eccentric exercise were delayed (ie, local formation of edema and decrease of muscle activity) by repeated air-pulsed cryotherapy, we provide evidence that this cooling procedure failed to improve long-term recovery of muscle performance. Clinical Relevance: Four applications of air-pulsed cryotherapy in the 3 days after a strenuous eccentric exercise are ineffective overall in promoting long-term muscle recovery. Further studies taking into account the amount of exercise-induced muscle damage would allow investigators to make stronger conclusions regarding the inefficiency of this recovery modality.

Prior Eccentric Exercise Augments Muscle Pain and Perception of Effort During Cycling Exercise

This study examined the effects of exercise-induced muscle damage (EIMD) on the physiological and perceptual responses to 30 minutes of submaximal cycling at 60% of oxygen consumption (VO2 peak). Ten participants completed two 30-minute bouts of cycling, one before and one 48 hours after performance of strenuous (24 contractions with 120% of concentric 1-repeition maximum) eccentric exercise. Eccentric exercise resulted in a significant delayed-onset muscle pain (1.6±1.6 mm to 44.8±20 mm on a 100-mm visual analog scale; P<0.001) and a 15% (P<0.001) reduction in maximal strength 48 hours after exercise. Ratings of quadriceps muscle pain (1.99±0.42 vs. 3.30±0.56; P=0.003) and perceived exertion (RPE; 13.0±0.30 vs. 13.8±0.61; P=0.02) were elevated during cycling after EIMD at identical work rates. No changes were observed in VO2 (29.6±4.6 vs. 30.2±4.4 mL/kg/min; P=0.41), heart rate (154±15 vs. 155±9 beats/min; P=0.58), and ventilation (57.2±12.1 vs. 59.8±12.7 L/min; P=0.13) during exercise after EIMD. The mean change in RPE was significantly correlated (r=0.56; P<0.01) with the change in muscle pain during cycling and delayed-onset pain during resistance exercise (r=0.86; P<0.01), but did not correlate with changes in VO2, heart rate, ventilation, and maximal strength. These findings indicate the elevations in RPE after EIMD are likely a consequence of the EIMD with the most likely explanation being an increase in localized pain before and during cycling exercise.