Muscle-damaging Exercise Research Articles

Decreased eccentric exercise-induced macrophage infiltration in skeletal muscle after supplementation with a class of ginseng-derived steroids.

Dammarane steroids (DS) are a class of chemical compounds present in Panax ginseng. Here, we evaluated the effect of 10 weeks of DS supplementation on inflammatory modulation in the soleus muscle following eccentric exercise (EE)-induced muscle damage (downhill running). Eighty rats were randomized into 4 groups of DS supplementation (saline, 20, 60, 120 mg/kg body weight). Inflammatory markers were measured at rest and again 1 h after EE. At rest, NFκB signaling, TNF-alpha and IL-6 mRNAs, 3-nitrotyrosine, glutathione peroxidase, and GCS (glutamylcysteine synthetase) levels were significantly elevated in the skeletal muscle of DS-treated rats in a dose-dependent manner. Additionally, there were no detectable increases in the number of necrotic muscle fibers or CD68+ M1 macrophages. However, muscle strength, centronucleation, IL-10 mRNA expression, and the number of CD163+ M2 macrophages increased significantly over controls with DS treatment in rat soleus muscle. Under EE-challenged conditions, significant increases in muscle fiber necrosis, CD68+ M1 macrophage distribution, and 3-nitrotyrosine were absent in rats that received low and medium doses (20 and 60 mg/kg) of DS treatment, suggesting that DS possess anti-inflammatory action protecting against a muscle-damaging challenge. However, this protective activity was diminished when a high dose of DS (120 mg/kg) was administered, suggesting that DS possess hormetic properties. In conclusion, our study provides new evidence suggesting that DS is an ergogenic component of ginseng that potentiate inflammation at baseline but that produce anti-inflammatory effects on skeletal muscle following muscle-damaging exercise. Furthermore, high doses should be avoided in formulating ginseng-based products.

Changes in CEBPB expression in circulating leukocytes following eccentric elbow-flexion exercise.

In mouse models, CCAAT enhancer-binding protein beta (CEBPB) is necessary for M2 macrophage-mediated regeneration after muscle injury. In humans, CEBPB expression in blood was strongly associated with muscle strength. In this study we aimed to test whether CEBPB expression in blood in people is increased 2 days after exercise designed to induce muscle damage and subsequent repair. Sixteen healthy male volunteers undertook elbow flexor exercises designed to induce acute muscle micro-damage. Peripheral blood samples were collected at baseline and days 1, 2, 4 and 7 following exercise. Expression of CEBPB and related genes were analysed by qRT-PCR. Extent of muscle damage was determined by decline in maximal voluntary isometric torque and by plasma creatine kinase activity. Nine subjects had peak (day 4) creatine kinase activity exceeding 10,000 U/l. In this subgroup, CEBPB expression was elevated from baseline to 2 days post exercise (paired-samples t (1,8) = 3.72, p = 0.006). Related expression and selected cytokine changes after exercise did not reach significance. Muscle-damaging exercise in humans can be followed by induction of CEBPB transcript expression in peripheral blood. Associations between CEBPB expression in blood and muscle strength may be consistent with the CEBPB-dependent muscle repair process.Electronic supplementary materialThe online version of this article (doi:10.1007/s12576-014-0350-7) contains supplementary material, which is available to authorized users.

Histamine blockade reduces femoral blood flow with no apparent change in vascular permeability after muscle damaging exercise (LB523)

Blood flow to previously exercised muscle remains elevated for up to two hrs after exercise and is mediated by activation of histamine receptors. Activation of histamine receptors could lead to increased vascular permeability, an initial stage of inflammation, associated with muscle damage. Therefore, the purpose of this experiment was to determine if histamine receptors contribute to the increased permeability in a model of exercise‐induced muscle damage. Muscle damage was induced in seven volunteers (2F, 5M) by 45‐min of downhill running (‐10% grade) at a heart rate of ~150 BPM. Volunteers were randomly assigned to histamine blockade (540 mg fexofenadine; an H1 blocker and 300 mg ranitidine; an H2 blocker) or control (no drug). Prior to and for 120 min following exercise, femoral blood flow was measured using Doppler ultrasound, while vascular permeability was measured as a change in thigh and calf circumference during four min of supravenous pressure occlusion. The rise in femoral blood flow after exercise was 52 ± 12% (Mean ± SE) lower with histamine blockade vs control (p<0.05). Additionally, thigh and calf vascular permeability tended to be higher with histamine blockade (109 ± 92%; 42 ± 21%) vs control (73 ± 58%; 34 ± 20 %)(p>0.05). Thus, it appears that post‐exercise histamine receptor activation may not contribute to the initial stages of an inflammatory response for muscle damaging exercise.Grant Funding Source: NIH grant HL115027

Protein supplements on delayed onset muscle soreness in active men and women (633.1)

The purpose of this study was to compare the effects of different protein supplements on delayed onset muscle soreness (DOMS) in active men and women. Subjects completed four trials (whey protein isolate, WPI; soy protein isolate, SPI; and hydrolyzed wheat protein, HWP; and water, CON) in a double‐blind randomized fashion. During each trial, subjects consumed one of the treatments, rested for 90 minutes, then ran on a treadmill at 75% HRpeak at ‐9 percent grade for 30 min, DOMS was assessed with a tension gauge post‐run and 24 hr after the downhill run. Diet over the 24 hours was designed to be the same for all conditions based on a self‐selected menu. Repeated Measures ANOVA was used to detect differences between treatments with significance set at p < 0.05. Dietary protein elicited a decreased DOMS compared with water, with no differences observed between WPI, SPI, or HWP. These data indicate that dietary protein decreased DOMS when ingested prior to muscle damaging exercise in active men and women.Grant Funding Source: Supported by USDA/AES Hatch funds (KS‐475)

Effects of β-hydroxy-β-methylbutyrate free acid and cold water immersion on expression of CR3 and MIP-1β following resistance exercise

The inflammatory response to muscle-damaging exercise requires monocyte mobilization and adhesion. Complement receptor type 3 (CR3) and macrophage inflammatory protein (MIP)-1β enables monocyte recruitment, adhesion, and subsequent infiltration into damaged muscle tissue. The purpose of this study was to examine the effects of cold water immersion (CWI) and/or β-hydroxy-β-methylbutyrate free acid (HMB-FA) on CR3 expression and MIP-1β concentration after four sets of up to 10 repetitions of squat, dead lift, and split squat exercises at 70-80% 1-repetition maximum. Thirty-nine resistance-trained men (22.2 ± 2.5 yr) were randomly divided into four groups: 1) placebo (PL), 2) HMB-FA, 3) HMB-FA-CWI, and 4) PL-CWI. The HMB-FA groups ingested 3 g/day, and CWI groups were submersed into 10-12°C water for 10 min after exercise. Blood was sampled at baseline (PRE), immediately post- (IP), 30 min post- (30P), 24 h post- (24P), and 48 h post (48P)-exercise. Circulating MIP-1β was assayed and CR3 expression on CD14+ monocytes was measured by flow cytometry. Without treatment, CR3 expression significantly elevated at 30P compared with other time points (P = 0.030-0.047). HMB-FA significantly elevated the percentage of monocytes expressing CR3 between IP and 24P (P = 0.046) and between IP and 48P (P = 0.046). No time effect was observed for MIP-1β concentration. The recovery modalities showed to attenuate the rise in CR3 following exercise. Additionally, supplementation with HMB-FA significantly elevated the percentage of monocytes expressing CR3 during recovery. Although the time course that inflammatory responses are most beneficial remains to be determined, recovery modalities may alter immune cell mobilization and adhesion mechanisms during tissue recovery.

The Effects of Low Intensity Endurance Activity on Various Physiological Parameters and Exercise Induced Oxidative Stress in Dogs

The study of canine athlete physiology has focused on endurance sled dog racing and high intensity short duration Greyhound racing, yet the number of dogs competing in low intensity endurance activities is rising due to the increased numbers of hunting and companion dog activities. There is little information on the physiological effect of longer duration low intensity endurance activities. We set out to evaluate the serum biochemistry, oxidative stress, and cortisol response before and after two consecutive days of exercise in ten healthy unconditioned male dogs. Exercise sessions consisted of 120 minutes on an exercise wheel at 11 km/hour on 2 consecutive days. Blood was collected at four time points: 24 hours pre-exercise (sample 1, Day 0, resting); 2 min post-exercise on days 1 and 2, (samples 2 and 3, respectively); and 20 hours post-exercise, collected on day 3(sample 4). Hematocrit, blood gases, serum chemistry, uric acid, cortisol, and F2-isoprostanes were determined. Serum biochemistry and hematocrit suggested hemoconcentration, mild muscle damage and respiratory alkalosis during exercise, which was expected in the unconditioned canine athlete. In addition, plasma indices of oxidative damage (F2-isoprostanes) increased, as did plasma uric acid (an endogenous antioxidant). Importantly, similar to human studies, plasma F2-isoprostanes decreased 24 hours after exercise suggesting a protective effect of exercise. Serum cortisol concentrations were also markedly elevated at the end of exercise on both days suggesting that timing of sampling may play a role in interpreting cortisol results when looking at previous field studies.

Muscle-Damaging Exercise Increases Heat Strain during Subsequent Exercise Heat Stress

It remains unclear whether exercise-induced muscle damage (EIMD) increases heat strain during subsequent exercise heat stress, which in turn may increase the risk of exertional heat illness. We examined heat strain during exercise heat stress 30 min after EIMD to coincide with increases in circulating pyrogens (e.g., interleukin-6 [IL-6]) and 24 h after EIMD to coincide with the delayed muscle inflammatory response when a higher rate of metabolic energy expenditure (M˙) and thus decreased economy might also increase heat strain. Thirteen non-heat-acclimated males (mean ± SD, age = 20 ± 2 yr) performed exercise heat stress tests (running for 40 min at 65% V˙O2max in 33°C, 50% humidity) 30 min (HS1) and 24 h (HS2) after treatment, involving running for 60 min at 65% V˙O2max on either -10% gradient (EIMD) or +1% gradient (CON) in a crossover design. Rectal (Tre) and skin (Tsk) temperature, local sweating rate, and M˙ were measured throughout HS tests. Compared with CON, EIMD evoked higher circulating IL-6 pre-HS1 (P < 0.01) and greater plasma creatine kinase and muscle soreness pre-HS2 (P < 0.01). The ΔTre was greater after EIMD than CON during HS1 (0.35°C, 95% confidence interval = 0.11°C-0.58°C, P < 0.01) and HS2 (0.17°C, 95% confidence interval = 0.07°C-0.28°C, P < 0.01). M˙ was higher on EIMD throughout HS1 and HS2 (P < 0.001). Thermoeffector responses (Tsk, sweating rate) were not altered by EIMD. Thermal sensation and RPE were higher on EIMD after 25 min during HS1 (P < 0.05). The final Tre during HS1 correlated with the pre-HS1 circulating IL-6 concentration (r = 0.67). Heat strain was increased during endurance exercise in the heat conducted 30 min after and, to a much lesser extent, 24 h after muscle-damaging exercise. These data indicate that EIMD is a likely risk factor for exertional heat illness particularly during exercise heat stress when behavioral thermoregulation cues are ignored.

Effect of Milk on Team Sport Performance after Exercise-Induced Muscle Damage

Exercise-induced muscle damage (EIMD) leads to increases in intramuscular proteins observed in the blood stream and delayed onset of muscle soreness, but crucial for athletes are the decrements in muscle performance observed. Previous research has demonstrated that carbohydrate-protein supplements limit these decrements; however, they have primarily used isokinetic dynamometry, which has limited applicability to dynamic sport settings. Therefore, the aim of this study was to investigate the effects of a carbohydrate-protein milk supplement consumed after muscle-damaging exercise on performance tests specific to field-based team sports. Two independent groups of seven males consumed either 500 mL of milk or a control immediately after muscle-damaging exercise. Passive and active delayed onset of muscle soreness, creatine kinase, myoglobin, countermovement jump height, reactive strength index, 15-m sprint, and agility time were assessed before and 24, 48, and 72 h after EIMD. The Loughborough Intermittent Shuttle Test was also performed before and 48 h after EIMD. At 48 h, milk had a possible benefit for limiting increases in 10-m sprint time and a likely benefit of attenuating increases in mean 15-m sprint time during the Loughborough Intermittent Shuttle Test. At 72 h, milk had a possible benefit for limiting increases in 15-m sprint time and a likely benefit for the attenuation of increases in agility time. All other effects for measured variables were unclear. The consumption of milk limits decrements in one-off sprinting and agility performance and the ability to perform repeated sprints during the physiological simulation of field-based team sports.

Effect of cryotherapy on muscle recovery and inflammation following a bout of damaging exercise

The purpose of this study was to determine the effect of cryotherapy on the inflammatory response to muscle-damaging exercise using a randomized trial. Twenty recreationally active males completed a 40-min run at a -10% grade to induce muscle damage. Ten of the subjects were immersed in a 5°C ice bath for 20min and the other ten served as controls. Knee extensor peak torque, soreness rating, and thigh circumference were obtained pre- and post-run, and 1, 6, 24, 48, and 72h post-run. Blood samples were obtained pre- and post-run, and 1, 6 and 24h post-run for assay of plasma chemokine ligand 2 (CCL2). Peak torque decreased from 270±57 Nm at baseline to 253±65 Nm post-run and increased to 295±68Nm by 72h post-run with no differences between groups (p=0.491). Soreness rating increased from 3.6±6.0mm out of 100mm at baseline to 47.4±28.2mm post-run and remained elevated at all time points with no differences between groups (p=0.696). CCL2 concentrations increased from 116±31pgmL(-1) at baseline to 293±109pgmL(-1) at 6h post-run (control) and from 100±27pgmL(-1) at baseline to 208±71pgmL(-1) at 6h post-run (cryotherapy). The difference between groups was not significant (p=0.116), but there was a trend for lower CCL2 in the cryotherapy group at 6h (p=0.102), though this measure was highly variable. In conclusion, 20min of cryotherapy was ineffective in attenuating the strength decrement and soreness seen after muscle-damaging exercise, but may have mitigated the rise in plasma CCL2 concentration. These results do not support the use of cryotherapy during recovery.

Exercising in a hot environment with muscle damage: effects on acute kidney injury biomarkers and kidney function

Unaccustomed strenuous physical exertion in hot environments can result in heat stroke and acute kidney injury (AKI). Both exercise-induced muscle damage and AKI are associated with the release of interleukin-6, but whether muscle damage causes AKI in the heat is unknown. We hypothesized that muscle-damaging exercise, before exercise in the heat, would increase kidney stress. Ten healthy euhydrated men underwent a randomized, crossover trial involving both a 60-min downhill muscle-damaging run (exercise-induced muscle damage; EIMD), and an exercise intensity-matched non-muscle-damaging flat run (CON), in random order separated by 2 wk. Both treatments were followed by heat stress elicited by a 40-min run at 33°C. Urine and blood were sampled at baseline, after treatment, and after subjects ran in the heat. By design, EIMD induced higher plasma creatine kinase and interleukin-6 than CON. EIMD elevated kidney injury biomarkers (e.g., urinary neutrophil gelatinase-associated lipocalin (NGAL) after a run in the heat: EIMD-CON, mean difference [95% CI]: 12 [5, 19] ng/ml) and reduced kidney function (e.g., plasma creatinine after a run in the heat: EIMD-CON, mean difference [95% CI]: 0.2 [0.1, 0.3] mg/dl), where CI is the confidence interval. Plasma interleukin-6 was positively correlated with plasma NGAL (r = 0.9, P = 0.001). Moreover, following EIMD, 5 of 10 participants met AKIN criteria for AKI. Thus for the first time we demonstrate that muscle-damaging exercise before running in the heat results in a greater inflammatory state and kidney stress compared with non-muscle-damaging exercise. Muscle damage should therefore be considered a risk factor for AKI when performing exercise in hot environments.

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

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. The objective was to examine how thiol-based antioxidant supplementation affects skeletal muscle's performance and redox-sensitive signaling during the inflammatory and repair phases associated with exercise-induced microtrauma. 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. 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. 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.

Walking kinematics and kinetics following eccentric exercise-induced muscle damage

The goal of this investigation was to investigate how walking patterns are affected following muscle-damaging exercise by quantifying both lower limb kinematics and kinetics. Fifteen young women conducted a maximal isokinetic eccentric exercise (EE) muscle damage protocol (5×15) of the knee extensors and flexors of both legs at 60°/s. Three-dimensional motion data and ground reaction forces (GRFs) were collected 24h pre-EE while the participants walked at their preferred self-selected walking speed (SWS). Participants were asked to perform two gait conditions 48h post-EE. The first condition (COND1) was to walk at their own speed and the second condition (COND2) to maintain the SWS (±5%) they had 24h pre-EE. Walking speed during COND1 was significantly lower compared to pre-exercise values. When walking speed was controlled during COND2, significant effects of muscle damage were noticed, among other variables, for stride frequency, loading rate, lateral and vertical GRFs, as well as for specific knee kinematics and kinetics. These findings provide new insights into how walking patterns are adapted to compensate for the impaired function of the knee musculature following muscle damage. The importance to distinguish the findings caused by muscle damage from those exhibited in response to changes in stride frequency is highlighted.

Intramuscular responses with muscle damaging exercise and the interplay between multiple intracellular networks: A human perspective

Damaging exercise invokes a series of widespread changes that impact many aspects of skeletal muscle physiology. When examining candidate intramuscular mechanisms, those associated with oxidative stress, inflammation, proteolysis and apoptosis appear to have garnered the most interest in the literature, but many aspects of these pathways remain in question. Due to the vast integrated network of signaling activities as well as the many known areas (and likely many unknown areas) of crosstalk throughout these mechanisms, in vivo research can be challenging. Currently, a relatively small number of studies have examined time-course related changes to blood-based markers of oxidative stress and even fewer have examined intramuscular changes using in vivo models. An equally small number of studies have examined intramuscular changes in apoptotic activity. While changes in other tissues hold importance, intramuscular adaptations and the mechanisms involved are of the highest importance for determining how skeletal muscle adapts and respond to stressful, damaging stimuli.

Intra- and interday reliability of voluntary and electrically stimulated isometric contractions of the quadriceps femoris

The reliability of voluntary and electrically stimulated isometric contractions of m. quadriceps femoris of male participants (n=10; age 30±8years; height 1.79±0.05m; body mass 79.4±8.3kg) was investigated using ratio limits of agreement (LoA) on a time scale common to examine recovery from muscle damaging exercise. No systematic changes in reliability occurred over time (baseline versus 2, 24, 48, and 72h). Maximal voluntary contraction (MVC) and interpolated twitch technique (ITT) showed no mean bias (P>0.05) with 95% LoA of ±12.7 and ±5.4, respectively. Resting twitch and potentiated doublet peak force showed no mean bias (P>0.05). However, 95% LoA were smaller for the doublet (±13.9) than the twitch (±32.0). Twitch and doublet rates showed similar trends. Ratio of low (20Hz) to high (50Hz) frequency forces showed no mean bias (P>0.05) and 95% LoA of (±9.2). However, there was significant mean bias (P<0.05) and wider 95% LoA for peak force, contraction and relaxation parameters of the low and high frequency forces. In conclusion, MVC, ITT, potentiated doublet and the ratio of low to high frequency forces are recommended to most reliably examine functional muscle recovery between 2 and 72h after damaging exercise.

Muscle fascicle strains in human gastrocnemius during backward downhill walking

Extensive muscle damage can be induced in isolated muscle preparations by performing a small number of stretches during muscle activation. While typically these fiber strains are large and occur over long lengths, the extent of exercise-induced muscle damage (EIMD) observed in humans is normally less even when multiple high-force lengthening actions are performed. This apparent discrepancy may be due to differences in muscle fiber and tendon dynamics in vivo; however, muscle and tendon strains have not been quantified during muscle-damaging exercise in humans. Ultrasound and an infrared motion analysis system were used to measure medial gastrocnemius fascicle length and lower limb kinematics while humans walked backward, downhill for 1 h (inducing muscle damage), and while they walked briefly forward on the flat (inducing no damage). Supramaximal tibial nerve stimulation, ultrasound, and an isokinetic dynamometer were used to quantify the fascicle length-torque relationship pre- and 2 h postexercise. Torque decreased ~23%, and optimal fascicle length shifted rightward ~10%, indicating that EIMD occurred during the damage protocol even though medial gastrocnemius fascicle stretch amplitude was relatively small (~18% of optimal fascicle length) and occurred predominantly within the ascending limb and plateau region of the length-torque curve. Furthermore, tendon contribution to overall muscle-tendon unit stretch was ~91%. The data suggest the compliant tendon plays a role in attenuating muscle fascicle strain during backward walking in humans, thus minimizing the extent of EIMD. As such, in situ or in vitro mechanisms of muscle damage may not be applicable to EIMD of the human gastrocnemius muscle.

Effects of muscle-damaging exercise on physiological, metabolic, and perceptual responses during two modes of endurance exercise

Research on submaximal endurance exercise after exercise-induced muscle damage (EIMD) has produced equivocal findings. One possible explanation for this is that the responses are likely to be sensitive to the mode of endurance exercise adopted. Therefore, this study examined the influence of exercise mode (cycling vs. running) after EIMD. Twenty-four and 48 hours after EIMD, 10 male participants were measured for perceived muscle soreness, creatine kinase (CK) activity, knee extensor strength, and physiological (V˙O2, ventilation), metabolic (blood lactate), and perceptual [rating of perceived exertion (RPE)] responses during two counterbalanced 10-minute cycling and running bouts at lactate threshold. The muscle-damaging exercise was effective (p < 0.05) in increasing muscle soreness, elevating CK activity, and decreasing knee extensor strength at 24 and 48 hours. Similarly, increases in V˙O2, ventilation, and RPE were observed during both cycling and running after EIMD (p < 0.05), while blood lactate responses remained unchanged (p > 0.05). There was an interaction of time × mode for ventilation (p < 0.05), reflecting a higher relative increase for running at 24 hours post EIMD than cycling, but not for V˙O2, RPE, or blood lactate responses. The increased V˙O2 response during running could be attributed to changes in lower limb kinematics (stride length and stride frequency) and a decreased ability to utilize the stretch-shortening cycle, while the unexpectedly increased V˙O2 cycling response might be due to the recruitment of auxiliary muscles after EIMD. It is postulated that the differences in ventilation between exercise modes are due to different stimuli activating afferent fibers post-EIMD.

Milk ingestion in athletes and physically active individuals

SummaryMilk is a cheap drink that naturally contains nutrients in similar amounts as found in typical carbohydrate‐electrolyte sports drinks, as well as providing some protein (36 g/l). While there is little information about the ingestion of milk during exercise, the available evidence suggests that milk might enhance certain aspects of recovery when ingested after resistance and endurance exercise. The protein content of milk means that ingestion of milk immediately after resistance exercise acutely increases muscle protein synthesis, and if used chronically during a resistance training programme, milk ingestion enhances lean mass gains and fat mass losses compared with other protein sources (e.g. soy protein) or ingestion of carbohydrate. Ingesting milk after muscle damaging exercise also appears to alleviate some of the symptoms of exercise‐induced muscle damage, while the electrolytes naturally occurring in milk, as well as the milk protein, appear to enhance rehydration after endurance exercise. In summary, milk appears to be an appropriate post‐exercise drink for athletes and physically active individuals that are not intolerant to lactose and/or dairy. Milk might enhance some aspects of recovery after exercise and it appears that the proteins contained in milk are responsible for most of these enhancements.

Effects of repeated bouts of squatting exercise on sub-maximal endurance running performance

It is well established that exercise-induced muscle damage (EIMD) has a detrimental effect on endurance exercise performed in the days that follow. However, it is unknown whether such effects remain after a repeated bout of EIMD. Therefore, the purpose of this study was to examine the effects of repeated bouts of muscle-damaging exercise on sub-maximal running exercise. Nine male participants completed baseline measurements associated with a sub-maximal running bout at lactate turn point. These measurements were repeated 24-48 h after EIMD, comprising 100 squats (10 sets of 10 at 80 % body mass). Two weeks later, when symptoms from the first bout of EIMD had dissipated, all procedures performed at baseline were repeated. Results revealed significant increases in muscle soreness and creatine kinase activity and decreases in peak knee extensor torque and vertical jump performance at 24-48 h after the initial bout of EIMD. However, after the repeated bout, symptoms of EIMD were reduced from baseline at 24-48 h. Significant increases in oxygen uptake (.VO2), minute ventilation (.VE), blood lactate ([BLa]), rating of perceived exertion (RPE), stride frequency and decreases in stride length were observed during sub-maximal running at 24-48 h following the initial bout of EIMD. However, following the repeated bout of EIMD, .VO2, .VE, [BLa], RPE and stride pattern responses during sub-maximal running remained unchanged from baseline at all time points. These findings confirm that a single resistance session protects skeletal muscle against the detrimental effects of EIMD on sub-maximal running endurance exercise.

Knee joint neuromuscular activation performance during muscle damage and superimposed fatigue

This study examined the concurrent effects of exercise-induced muscle damage and superimposed acute fatigue on the neuromuscular activation performance of the knee flexors of nine males (age: 26.7±6.1 years; height 1.81±0.05 m; body mass 81.2±11.7 kg [mean±s]). Measures were obtained during three experimental conditions: (i) ‘fatigue-muscle damage’, involving acute fatiguing exercise performed on each assessment occasion plus a single episode of eccentric exercise performed on the first occasion and after the fatigue trial; (ii) ‘fatigue’, involving the fatiguing exercise only; and (iii) ‘control’ consisting of no exercise. Assessments were performed prior to (pre) and at 1 h, 24 h, 48 h, 72 h, and 168 h relative to the muscle damaging eccentric exercise. Repeated-measures analyses of variance (ANOVAs) showed that muscle damage elicited reductions of up to 38%, 24% and 65% in volitional peak force, electromechanical delay and rate of force development compared to baseline and controls, respectively (F [10, 80] = 2.3 to 4.6; P < 0.05) with further impairments (6.2% to 30.7%) following acute fatigue (F [2, 16] = 4.3 to 9.1; P < 0.05). By contrast, magnetically-evoked electromechanical delay was not influenced by muscle damage and was improved during the superimposed acute fatigue (∼14%; F [2, 16] = 3.9; P < 0.05). The safeguarding of evoked muscle activation capability despite compromised volitional performance might reveal aspects of capabilities for emergency and protective responses during episodes of fatigue and antecedent muscle damaging exercise.

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

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