Skeletal Muscle Fatigue Research Articles

Infrared Thermography Protocol on Reducing the Incidence of Soccer Injuries.

Infrared thermography has been used to detect skeletal muscle overload and fatigue in athletes, but its use in injury prevention in professional soccer has not been studied to date. To establish a novel injury prevention program based on infrared thermography and to determine its influence on the injury incidence in professional soccer players in the preseason. A cross-sectional, prospective study design was used to compare a conventional injury prevention program (CPP) applied over the first preseason and an infrared thermography injury prevention program (IRTPP) carried out in the following preseason. Soccer training ground. Twenty-four players belonging to a first division soccer team from Spain. Injury incidences of each player were recorded according to the Orchard Sports Injury Classification System (version 10.0) convention to determine the injury classification, location, and type. The incidence of injuries decreased from 15 injuries in the CPP preseason (0.63 [0.77] injuries per player) to 6 injuries in the second preseason when the IRTPP was applied (0.25 [0.53] injuries per player). The days of absence due to injuries also decreased from the CPP preseason (156d, 10.4 [11.0]d per injury) to the IRTPP preseason (14 d, 2.3 [2.8]d per injury). The injury severity also decreased from the first preseason to the second preseason, and fewer musculoskeletal injuries in the thigh, hip, and groin were reported. The implementation of an IRTPP can reduce the presence of injuries by identifying players potentially at risk and as a result, reducing the injury severity and days lost as a consequence.

The Popeye mythology may be true: eating spinach can make you fatigue resistant!

The Popeye mythology may be true: eating spinach can make you fatigue resistant!

The Effects of Skeletal Muscle Mass and Muscle Fatigue on the Proprioceptive Position Sense of the Knee Joint

The Effects of Skeletal Muscle Mass and Muscle Fatigue on the Proprioceptive Position Sense of the Knee Joint

Exploring the role of fatigue-related metabolite activity during high-intensity exercise using a simplified whole-body mathematical model

Intense exercise leads to muscle fatigue, a contractile and metabolic failure of contracting muscle to sustain desired work. It is widely accepted that the close relationship between intense exercise and the accumulation of metabolic by-products is the major cause of skeletal muscle fatigue. High-intensity exercise activates ATPase activity and strongly promotes ATP production, leading to an alteration of metabolic by-products. However, the complex mechanisms underlying the development of muscle fatigue are not fully understood. In this study, we developed a novel mathematical model for whole-body mechanisms that can reproduce the key biological processes of metabolic fatigue during high-intensity exercise. Five vital compartments are represented: skeletal muscle, liver, lungs, blood vessels and other organs. These compartments capture the key mechanisms involved, including the buffering role of creatine kinase, the bicarbonate buffer system in the regulation of blood pH, and the accumulation of metabolic by-products. The simulation results provide the essential evidence for a better understanding of muscle fatigue such as increases in blood lactate and muscle inorganic phosphate, and drop in blood pH level. Moreover, we revised our previous contraction model by introducing the inhibitory effect of metabolic by-products based on structural and experimental data. The accumulation of metabolic by-products reduces the number of strongly bound cross-bridges, leading to a reduction in maximal contraction. In conclusion, our simplified model reliably reflects metabolic fluxes and concentrations that are in good agreement with experimental findings, yielding a better understanding of metabolic fatigue during high-intensity exercise. • Whole-body mathematical model quantitatively estimates the key metabolic fluxes and concentrations during intense exercise. • The constant workload expressed as percentage of maximum oxygen uptake is used as an input parameter for this novel model. • The model has several parameters that can be modified to analyze the effect of individual differences.

Lower-limb Dynamics of Muscle Oxygen Saturation During the Back-squat Exercise: Effects of Training Load and Effort Level.

Gómez-Carmona, CD, Bastida-Castillo, A, Rojas-Valverde, D, de la Cruz Sánchez, E, García-Rubio, J, Ibáñez, SJ, and Pino-Ortega, J. Lower-limb dynamics of muscle oxygen saturation during the back-squat exercise: effects of training load and effort level. J Strength Cond Res 34(5): 1227-1236, 2020-The aim of this study was to analyze the effect of strength training on lower limb muscle oxygenation. The sample consisted of 12 male subjects (22.4 ± 1.73 years; 1.81 ± 0.08 cm height and 77.76 ± 8.77 kg body mass). Six different strength training stimuli were analyzed, based on the training variables: load (60-75% 1 repetition maximum [1RM]) and level of effort (LE) (E1: 4 × 8 [20RM], E2: 4 × 12 [20RM], E3: 4 × 16 [20RM], E4: 4 × 4 [10RM], E5: 4 × 6 [10RM], and E6: 4 × 8 [10RM]) in the squat exercise up to 90° with a 2-second stop between repetitions to avoid the myotatic reflex. Oxygen saturation at the beginning of the series (SmO2start), oxygen saturation at the end of the series (SmO2stop), percentage of oxygen saturation loss (▽%SmO2), and reoxygenation time (SmO2recT) were assessed using a near-infrared spectroscopy device. In addition, the percentage of mean propulsive velocity loss (%MPVL) was recorded using a linear transducer. The results suggested an influence of LE and training load on muscle oxygenation. A greater LE was directly associated with SmO2recT (r = 0.864), ▽%SmO2 (r = 0.873), and %MPVL (r = 0.883) and inversely with SmO2stop (r = -0.871). When the same LE was used (E1 vs. E4, E2 vs. E5, and E3 vs. E6), it was found that the stimuli with a higher load had a lower SmO2recT, ▽%SmO2, and %MPVL and a higher SmO2stop. Muscle oxygen saturation was found to be minimal (%SmO2 = 0) in stimuli with a LE greater than 60% (E3 and E6). The SmO2 variables studied in the present research could be considered as an easier and more useful method for understanding skeletal muscle fatigue during resistance training.

Circulating levels of GDF15 in patients with myalgic encephalomyelitis/chronic fatigue syndrome

BackgroundMyalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) is a debilitating condition characterised by fatigue and post-exertional malaise. Its pathogenesis is poorly understood. GDF15 is a circulating protein secreted by cells in response to a variety of stressors. The receptor for GDF15 is expressed in the brain, where its activation results in a range of responses. Among the conditions in which circulating GDF15 levels are highly elevated are mitochondrial disorders, where early skeletal muscle fatigue is a key symptom. We hypothesised that GDF15 may represent a marker of cellular stress in ME/CFS.MethodsGDF15 was measured in serum from patients with ME/CFS (n = 150; 100 with mild/moderate and 50 with severe symptoms), “healthy volunteers” (n = 150) and a cohort of patients with multiple sclerosis (n = 50).ResultsCirculating GDF15 remained stable in a subset of ME/CFS patients when sampled on two occasions ~ 7 months (IQR 6.7–8.8) apart, 720 pg/ml (95% CI 625–816) vs 670 pg/ml (95% CI 598–796), P = 0.5. GDF15 levels were 491 pg/ml in controls (95% CI 429–553), 546 pg/ml (95% CI 478–614) in MS patients, 560 pg/ml (95% CI 502–617) in mild/moderate ME/CFS patients and 602 pg/ml (95% CI 531–674) in severely affected ME/CFS patients. Accounting for potential confounders, severely affected ME/CFS patients had GDF15 concentrations that were significantly increased compared to healthy controls (P = 0.01). GDF15 levels were positively correlated (P = 0.026) with fatigue scores in ME/CFS.ConclusionsSevere ME/CFS is associated with increased levels of GDF15, a circulating biomarker of cellular stress that appears which stable over several months.

Skeletal muscle fatigue does not affect shooting accuracy of handball players

Skeletal muscle fatigue does not affect shooting accuracy of handball players

Decrease in physical performance during the hospitalisation phase of haematopoietic stem cell transplantation

Background/Aims The negative impact caused by haematopoietic stem cell transplantation still requires further investigation. This study aims to investigate the effects of this procedure on skeletal muscle strength, functional performance and fatigue sensation in the hospitalisation phase. Methods This prospective cohort study aimed to assess physical performance by measuring ventilatory muscle strength, peripheral muscle strength and fatigue in patients who underwent haematopoietic stem cell transplantation. Results The sample consisted of 30 patients of both sexes (63% men) with a mean age of 48.6 ± 13.2 years. Maximal inspiratory pressure and expiratory pressure decreased by 19% and 16%, respectively (P<0.001). There was a 16% reduction in handgrip strength in the second assessment (P<0.001), as well as a reduction of 30.6% in the 30-Second Chair Stand Test (P<0.001). The fatigue test score increased exponentially (60%) (P<0.001). Individuals with worse results in the 30-Second Chair Stand Test remained hospitalised for a longer period than those with better results (P=0.024). Conclusions This study concluded that after the transplantation of haematopoietic stem cells there was a relevant reduction in the results of the applied tests, as well as an increase in fatigue.

Incubation with sodium nitrite attenuates fatigue development in intact single mouse fibres at physiological .

Dietary nitrate supplementation increases plasma nitrite concentration, which provides an oxygen-independent source of nitric oxide and can delay skeletal muscle fatigue. Nitrate supplementation has been shown to increase myofibre calcium release and force production in mouse skeletal muscle during contractions at a supra-physiological oxygen tension, but it is unclear whether nitrite exposure can delay fatigue development and improve myofibre calcium handling at a near-physiological oxygen tension. Single mouse muscle fibres acutely treated with nitrite had a lower force and cytosolic calcium concentration during single non-fatiguing contractions at a near-physiological oxygen tension. Nitrite treatment delayed fatigue development during repeated fatiguing isometric contractions at near-physiological, but not at supra-physiological, oxygen tension in combination with better maintenance of myofilament calcium sensitivity and sarcoplasmic reticulum calcium pumping. These findings improve understanding of the mechanisms by which increased skeletal muscle nitrite exposure might be ergogenic and imply that this is related to improved calcium handling. Dietary nitrate (NO3- ) supplementation, which increases plasma nitrite (NO2- ) concentration, has been reported to attenuate skeletal muscle fatigue development. Sarcoplasmic reticulum (SR) calcium (Ca2+ ) release is enhanced in isolated single skeletal muscle fibres following NO3- supplementation or NO2- incubation at a supra-physiological but it is unclear whether NO2- incubation can alter Ca2+ handling and fatigue development at a near-physiological . We hypothesised that NO2- treatment would improve Ca2+ handling and delay fatigue at a physiological in intact single mouse skeletal muscle fibres. Each muscle fibre was perfused with Tyrode solution pre-equilibrated with either 20% ( ∼150Torr) or 2% O2 ( =15.6Torr) in the absence and presence of 100µM NaNO2 . At supra-physiological (i.e. 20% O2 ), time to fatigue was lowered by 34% with NaNO2 (control: 257±94 vs. NaNO2 : 159±46s, Cohen's d=1.63, P<0.05), but extended by 21% with NaNO2 at 2% O2 (control: 308±217 vs. NaNO2 : 368±242s, d=1.14, P<0.01). During the fatiguing contraction protocol completed with NaNO2 at 2% O2 , peak cytosolic Ca2+ concentration ([Ca2+ ]c ) was not different (P>0.05) but [Ca2+ ]c accumulation between contractions was lower, concomitant with a greater SR Ca2+ pumping rate (P<0.05) compared to the control condition. These results demonstrate that increased exposure to NO2- blunts fatigue development at near-physiological, but not at supra-physiological, through enhancing SR Ca2+ pumping rate in single skeletal muscle fibres. These findings extend our understanding of the mechanisms by which increased NO2- exposure can mitigate skeletal muscle fatigue development.

Associations of BAFF rs2893321 polymorphisms with myasthenia gravis susceptibility

BackgroundMyasthenia gravis (MG) is an autoimmune diseases characterized by fatigue and weakness of skeletal muscles. B-lymphocyte-activating factor (BAFF), an essential factor for B cell differentiation and development, is important in the progression of MG. The current study aimed to investigate the association between single nucleotide polymorphism rs2893321 in BAFF with MG susceptibility in Chinese Han population.MethodsOne hundred forty-nine patients with MG and 148 healthy controls were recruited. Using improved multiple ligase detection reaction technology, the polymorphisms of rs2893321 between groups and among MG subgroups have been compared.ResultsA significant differences between the MG group and the healthy control group was observed. Additionally, rs2893321 was found to be associated with gender and age in patients with MG.ConclusionGenetic variations of rs2893321 in BAFF might be associated with susceptibility to MG in the Chinese Han population.

CHALLENGES TO ANIMAL WELFARE ASSOCIATED WITH CAPTURE AND LONG ROAD TRANSPORT IN BOMA-ADAPTED BLACK (DICEROS BICORNIS) AND SEMI-CAPTIVE WHITE (CERATOTHERIUM SIMUM) RHINOCEROSES

Capture and transport are part of translocation and expose animals to a variety of stressors that can lead to morbidity and mortality. We aimed to establish a better understanding of the physiologic responses to capture and transport in black (Diceros bicornis) and white (Ceratotherium simum) rhinoceroses in Southern Africa. Fourteen adult black rhinoceroses were transported 600 km by vehicle and 32 white rhinoceroses (24 adults and 8 juveniles) were transported 1,300 km by vehicle. The black rhinoceroses had been wild-caught and boma-adapted over 6 wk prior to the translocation and were only sedated to allow for loading into the transport crates. The white rhinoceroses originated from a game farm and were chemically immobilized from a helicopter and then loaded. Paired blood samples were collected from animals at loading (capture) and after transport and evaluated for changes in clinical chemistry analytes, acute phase reactants, and oxidative stress biomarkers. The Wilcoxon rank sum test was used to compare changes in measured analytes from capture and after transport. All rhinoceroses survived capture and transport. Rhinoceroses experienced total body water loss, mobilization of energy reserves, and muscular damage. Alterations in acute phase reactants suggested that animals mounted a stress response. Oxidative stress was observed in black rhinoceroses. We identified the following challenges to animal welfare during transport: hydration status, energy balance, skeletal muscle fatigue, and stress-induced immunomodulation. Measures to mitigate these challenges, such as administration of fluids, need to be included in the planning of future translocations.

Вплив N-ацетилцистеїну на рухову активність геміпаркінсо-нічних щурів, викликану ін’єкцією агоніста дофамінових рецепторів

Мета роботи – виявити профілактичний ефект попередньої ін’єкції N-АЦ на розвиток м’язової втоми в неанестезованої тварини з експериментальним геміпаркінсонізмом під час тривалих циркуляторних рухів, викликаних ін’єкцією апоморфіну (АМ).Дослідження проводили на щурах лінії Вістар-Кіото, у яких викликали однобічне руйнування дофамінергічної (ДА) висхідної системи мозку за допомогою ін’єкції 8 мкг 6-гідроксидофаміну, розчиненого в 4 мкл фізіологічного розчину з додатком 0,1 % аскорбінової кислоти, яка гальмує окислення нейротоксину. Поведінкові реакції тварин на ін’єкцію дофаміноміметика апоморфіну були непрямим тестом на ступінь дегенерації ДА-нейронів середнього мозку. Через сім днів після введення 6-гідроксидофаміну тварин розділили на такі групи: 1 – контрольні тварини, у яких викликали інтенсивні циркуляторні рухи за допомогою ін’єкції апоморфіну (0,5 мг/кг) (n = 6); 2 – щури, яким за годину до ін’єкції АМ вводили 0,5 мл фізіологічного розчину (n = 6); 3 – тварини, яким за годину до ін’єкції АМ вводили розчин N-ацетилцистеїну (150 мг/кг) (n = 6).Порівнюючи поведінкові тести на щурах у трьох групах, можемо припустити, що зменшення числа обертів щурів контрольної групи й тварин із попередньою ін’єкцією фізіологічного розчину відбувалося не через припинення дії апоморфіну, а через розвиток м’язової втоми під час тривалих циркуляторних рухів. Водночас у щурів третьої групи після застосування N-АЦ зниження середньої кількості обертів не спостерігали. Це може вказувати на активацію захисної дії антиоксидантної системи у відповідь на тривалу м’язову активність, а N-АЦ можна розглядати як потужний активатор захисних механізмів, спрямованих на зниження втоми скелетних м’язів.

Geranylgeraniol prevents statin-induced skeletal muscle fatigue without causing adverse effects in cardiac or vascular smooth muscle performance

The administration of geranylgeranyl pyrophosphate (GGPP) (or its precursor, geranylgeraniol [GGOH]) has been shown by several in vitro studies to be capable of abrogating statin-induced myotoxicity. Nonetheless, the potential of GGPP repletion to prevent statin-associated muscle symptoms (SAMS) in vivo is yet to be investigated. Therefore, this study aimed to evaluate the ability of GGOH to prevent SAMS in rodents. Female Wistar rats (12 weeks of age) were randomised to 1 of 4 treatment groups: control, control with GGOH, simvastatin or simvastatin with GGOH. Ex vivo assessment of force production was conducted in skeletal muscles of varying fiber composition. Ex vivo left ventricular performance and blood vessel function was also assessed to determine if the administration of GGOH caused adverse changes in these parameters. Statin administration was associated with reduced force production in fast-twitch glycolytic muscle, but coadministration with GGOH completely abrogated this effect. Additionally, GGOH improved the performance of muscles not adversely affected by simvastatin (ie, those with a greater proportion of slow-twitch oxidative fibers), and increased force production in the control animals. Neither control nor statin-treated rodents given GGOH exhibited adverse changes in cardiac function. Vascular relaxation was also maintained following treatment with GGOH. The findings of this study demonstrate that GGOH can prevent statin-induced skeletal muscle fatigue in rodents without causing adverse changes in cardiovascular function. Further studies to elucidate the exact mechanisms underlying the effects observed in this investigation are warranted.

Phosphoproteomics reveals conserved exercise-stimulated signaling and AMPK regulation of store-operated calcium entry.

Exercise stimulates cellular and physiological adaptations that are associated with widespread health benefits. To uncover conserved protein phosphorylation events underlying this adaptive response, we performed mass spectrometry-based phosphoproteomic analyses of skeletal muscle from two widely used rodent models: treadmill running in mice and insitu muscle contraction in rats. We overlaid these phosphoproteomic signatures with cycling in humans to identify common cross-species phosphosite responses, as well as unique model-specific regulation. We identified >22,000 phosphosites, revealing orthologous protein phosphorylation and overlapping signaling pathways regulated by exercise. This included two conserved phosphosites on stromal interaction molecule 1 (STIM1), which we validate as AMPK substrates. Furthermore, we demonstrate that AMPK-mediated phosphorylation of STIM1 negatively regulates store-operated calcium entry, and this is beneficial for exercise in Drosophila. This integrated cross-species resource of exercise-regulated signaling in human, mouse, and rat skeletal muscle has uncovered conserved networks and unraveled crosstalk between AMPK and intracellular calcium flux.

Acidosis decreases the Ca2+ sensitivity of thin filaments by preventing the first actomyosin interaction.

Intracellular acidosis is a putative agent of skeletal muscle fatigue, in part, because it depresses the calcium (Ca2+) sensitivity of the myofilaments. However, the molecular mechanism behind this depression in Ca2+ sensitivity is unknown, providing a significant challenge to a complete understanding of the fatigue process. To elucidate this mechanism, we directly determined the effect of acidosis on the ability of a single myosin molecule to bind to a regulated actin filament in a laser trap assay. Decreasing pH from 7.4 to 6.5 significantly (P < 0.05) reduced the frequency of single actomyosin-binding events at submaximal (pCa 8-pCa 6) but not at maximal Ca2+ concentration (pCa 5-pCa 4). To delineate whether this was due to a direct effect on myosin versus an indirect effect on the regulatory proteins troponin (Tn) and tropomyosin (Tm), binding frequency was also quantified in the absence of Tn and Tm. This revealed that acidosis did not significantly alter the frequency of actomyosin binding events in the absence of regulatory proteins (1.4 ± 0.15 vs. 1.4 ± 0.15 events/s for pH 7.4 and 6.5, respectively). Acidosis also did not significantly affect the size of myosin's powerstroke or the duration of binding events in the presence of regulatory proteins, at every [Ca2+]. These data suggest acidosis impedes activation of the thin filament by competitively inhibiting Ca2+ binding to TnC. This slows the rate at which myosin initially attaches to actin; therefore, less cross bridges will be bound and generating force at any given submaximal [Ca2+]. These data provide a molecular explanation for the acidosis-induced decrease in force observed at the submaximal Ca2+ concentrations that might contribute to the loss of force during muscle fatigue.

Fast skeletal muscle troponin activator CK-2066260 increases fatigue resistance by reducing the energetic cost of muscle contraction.

Key points Skeletal muscle fatigue limits performance in various physical activities, with exercise intolerance being a key symptom in a broad spectrum of diseases.We investigated whether a small molecule fast skeletal troponin activator (FSTA), CK‐2066260, can mitigate muscle fatigue by reducing the cytosolic free [Ca2+] required to produce a given submaximal force and hence decreasing the energy requirement.Isolated intact single mouse muscle fibres and rat muscles in‐situ treated with CK‐2066260 showed improved muscle endurance., which was accompanied by decreased ATP demand and reduced glycogen usage.CK‐2066260 treatment improved in‐vivo exercise capacity in healthy rats and in a rat model of peripheral artery insufficiency.In conclusion, we show that the FSTA CK‐2066260 effectively counteracts muscle fatigue in rodent skeletal muscle in vitro, in situ, and in vivo. This may translate to humans and provide a promising pharmacological treatment to patients suffering from severe muscle weakness and exercise intolerance. Skeletal muscle fatigue limits performance during physical exercise and exacerbated muscle fatigue is a prominent symptom among a broad spectrum of diseases. The present study investigated whether skeletal muscle fatigue is affected by the fast skeletal muscle troponin activator (FSTA) CK‐2066260, which increases myofibrillar Ca2+ sensitivity and amplifies the submaximal force response. Because more force is produced for a given Ca2+, we hypothesized that CK‐2066260 could mitigate muscle fatigue by reducing the energetic cost of muscle activation. Isolated single mouse muscle fibres were fatigued by 100 repeated 350 ms contractions while measuring force and the cytosolic free [Ca2+] or [Mg2+] ([Mg2+]i). When starting fatiguing stimulation at matching forces (i.e. lower stimulation frequency with CK‐2066260): force was decreased by ∼50% with and by ∼75% without CK‐2066260; [Mg2+]i was increased by ∼10% with and ∼32% without CK‐2066260, reflecting a larger decrease in [ATP] in the latter. The glycogen content in in situ stimulated rat muscles fatigued by repeated contractions at matching forces was about two times higher with than without CK‐2066260. Voluntary exercise capacity, assessed by rats performing rotarod exercise and treadmill running, was improved in the presence of CK‐2066260. CK‐2066260 treatment also increased skeletal muscle fatigue resistance and exercise performance in a rat model of peripheral artery insufficiency. In conclusion, we demonstrate that the FSTA CK‐2066260 mitigates skeletal muscle fatigue by reducing the metabolic cost of force generation.

Uremic metabolites impair skeletal muscle mitochondrial energetics through disruption of the electron transport system and matrix dehydrogenase activity.

Chronic kidney disease (CKD) leads to increased skeletal muscle fatigue, weakness, and atrophy. Previous work has implicated mitochondria within the skeletal muscle as a mediator of muscle dysfunction in CKD; however, the mechanisms underlying mitochondrial dysfunction in CKD are not entirely known. The purpose of this study was to define the impact of uremic metabolites on mitochondrial energetics. Skeletal muscle mitochondria were isolated from C57BL/6N mice and exposed to vehicle (DMSO) or varying concentrations of uremic metabolites: indoxyl sulfate, indole-3-acetic-acid, l-kynurenine, and kynurenic acid. A comprehensive mitochondrial phenotyping platform that included assessments of mitochondrial oxidative phosphorylation (OXPHOS) conductance and respiratory capacity, hydrogen peroxide production (JH2O2), matrix dehydrogenase activity, electron transport system enzyme activity, and ATP synthase activity was employed. Uremic metabolite exposure resulted in a ~25-40% decrease in OXPHOS conductance across multiple substrate conditions (P < 0.05, n = 5-6/condition), as well as decreased ADP-stimulated and uncoupled respiratory capacity. ATP synthase activity was not impacted by uremic metabolites; however, a screen of matrix dehydrogenases indicated that malate and glutamate dehydrogenases were impaired by some, but not all, uremic metabolites. Assessments of electron transport system enzymes indicated that uremic metabolites significantly impair complex III and IV. Uremic metabolites resulted in increased JH2O2 under glutamate/malate, pyruvate/malate, and succinate conditions across multiple levels of energy demand (all P < 0.05, n = 4/group). Disruption of mitochondrial OXPHOS was confirmed by decreased respiratory capacity and elevated superoxide production in cultured myotubes. These findings provide direct evidence that uremic metabolites negatively impact skeletal muscle mitochondrial energetics, resulting in decreased energy transfer, impaired complex III and IV enzyme activity, and elevated oxidant production.

Independent and Combined Effects of All-Out Sprint and Low-Intensity Continuous Exercise on Plasma Oxidative Stress Biomarkers in Trained Judokas

The purpose of this study was to assess oxidative stress biomarkers prior to and following different forms of exercise. Ten elite male judokas (age: 18.1 ± 1.7 years, athletic experience: 6 years with a training frequency of 6 Judo-sessions/week) performed three cycle ergometry sessions comprising a 30 s Wingate test (MAX), 30 min at 60% maximal-aerobic-power-output (LOW) or these two exercise protocols combined (COMBINED) in a repeated-measures design. Venous blood-samples were collected before, and 0(P0), 5(P5), 10(P10) and 20(P20) min after each exercise protocol and assessed for malondialdehyde concentration ([MDA]), glutathione peroxidase (GPX), superoxide dismutase (SOD) and glutathione reductase (GR) content, and total-antioxidant-status (TAS). Plasma [MDA] was found to be increased above baseline at P0 and P5 in the MAX, LOW and COMBINED conditions (p < 0.05), but was greater at P10 and P20 in the LOW condition compared to MAX and COMBINED conditions (p < 0.05). Blood GPX and SOD content increased above baseline at P0 in MAX and COMBINED and at P5 in LOW (p < 0.05), with GR content being similar between groups at P0 and P5 (p > 0.05). 20 min post-exercise, GPX, SOD, GR content and TAS were lower in the MAX compared to the LOW and COMBINED conditions (p < 0.05). In conclusion, the findings from this study reveal that redox-related biomarkers exhibited divergent response dynamics following different forms of exercise, which might have implications for understanding the mechanisms of exercise-induced skeletal muscle fatigue and adaptive remodeling.

A Novel Blue-Red Photobiomodulation Therapy Patch Effects on a Repetitive Elbow-Flexion Fatigue Task.

Photobiomodulation (laser/light) therapy has reduced skeletal muscle fatigue and improved performance in previous research. To determine if the application of a novel blue (450nm) and red (645nm) light-emitting diode photobiomodulation therapy patch improves muscle function and decreases perceived exertion after an elbow-flexion fatigue protocol. Thirty-four strength-trained individuals (male = 32 and female = 2, age = 22.5 [2.7]y). Participants were randomly assigned to an active or placebo treatment. On visit 1, participants' 1-repetition maximal biceps curl was determined, and an orientation session of the fatigue task occurred to ensure no learning effects. Fifty percent of the participants' 1-repetition maximum was used during the fatigue protocol. On visit 2, participants performed biceps curl repetitions at a speed of 25 repetitions per minute until they could not physically move the weight past 90° of elbow flexion or stay with the set pace. After the fatigue protocol, a 30-minute blue/red light (wavelength = 450 and 645nm, peak irradiance = 9mW/cm2, duty cycle = pulsed 33%, and fluence = 5.4J/cm2) or sham treatment was administered based on the randomized group assignment. Immediately following, the participants repeated the fatigue protocol. The number of complete repetitions was counted, and the participants rated their perceived level of exertion on the Borg scale immediately after each fatigue bout. Overall, fatigue occurred between the 2 exercise bouts (pretreatment = 44.1 [12.3] and posttreatment = 37.4 [9.6] repetitions, P = .02). However, less fatigue was noted in the number of participants of the active treatment group than the sham treatment group. During the posttreatment fatigue task, 29.4% of participants in the active treatment group improved compared to 0% in the sham treatment (P = .045). Nearly 30% of participants had an increase benefit during a repeated-bout fatigue task due to the blue/red light-emitting diode photobiomodulation light patch.

Skeletal Muscle Fatigue: Mechanisms And Mitigation At The Cellular And Molecular Levels In Older Adults

Skeletal muscle fatigue, or the contraction-induced decline in whole muscle force or power, decreases physical function in older adults. Fatigue primarily results from elevated hydrogen (H+) and phosphate (Pi) altering myosin-actin interactions; however, which steps of the myosin-actin cross-bridge cycle are altered and whether these changes are reversible at the molecular and cellular levels are unclear. PURPOSE: The study objectives were to: 1) Examine the effects of simulated fatigue on molecular and cellular function, and 2) Test the ability of deoxyadenosine triphosphate (dATP), an alternative energy to adenosine triphosphate (ATP), to reverse fatigue-induced changes. METHODS: Maximal force production, myofilament mechanics and cross-bridge kinetics were measured in single fibers (20 per person) from the vastus lateralis of 8 (4 men) healthy, sedentary older adults (65-75 years) under normal (5 mM Pi, pH 7.0), fatigue (30 mM Pi, pH 6.2) and fatigue with dATP conditions. ANOVAs with post-hoc tests were used to evaluate differences between means by fiber-type and results were considered significant at P ≤ 0.05. RESULTS: Force declined with fatigue in slow- (myosin heavy chain (MHC) I, 22%) and fast-contracting (MHC II, 30%) fibers due to a reduced number or stiffness of strongly bound myosin heads (30-36%) and slower cross-bridge kinetics (longer myosin attachment times (18-31%) and reduced rates of force production (17-37%)). MHC I myofilaments became stiffer with fatigue (59%), suggesting a fiber-type specific mechanism to partially mitigate fatigue-induced force reduction. Fatigue with dATP moderately improved force production similarly in both fiber types (10-12%) compared to fatigue with ATP. In MHC I fibers, fatigue with dATP returned the number or stiffness of myosin heads and cross-bridge kinetics to normal values. In MHC II fibers, fatigue with dATP left the number or stiffness of myosin heads similar to fatigue conditions, while the cross-bridge kinetics were 19-22% faster than normal. CONCLUSION: These results identify novel fiber-type specific changes in myosin-actin interactions and myofilament stiffness that help explain fatigue-related force reduction in older adults as well as an alternative energy source that partially reverses the effects of fatigue. Supported by: NIH AG047245