Role of brain IL-1beta on fatigue after exercise-induced muscle damage

Brain cytokines, induced by various inflammatory challenges, have been linked to sickness behaviors, including fatigue. However, the relationship between brain cytokines and fatigue after exercise is not well understood. Delayed recovery of running performance after muscle-damaging downhill running is associated with increased brain IL-1beta concentration compared with uphill running. However, there has been no systematic evaluation of the direct effect of brain IL-1beta on running performance after exercise-induced muscle damage. This study examined the specific role of brain IL-1beta on running performance (either treadmill or wheel running) after uphill and downhill running by manipulating brain IL-1beta activity via intracerebroventricular injection of either IL-1 receptor antagonist (ra; downhill runners) or IL-1beta (uphill runners). Male C57BL/6 mice were assigned to the following groups: uphill-saline, uphill-IL-1beta, downhill-saline, or downhill-IL-1ra. Mice initially ran on a motor-driven treadmill at 22 m/min and -14% or +14% grade for 150 min. After the run, at 8 h (wheel cage) or 22 h (treadmill), uphill mice received intracerebroventricular injections of IL-1beta (900 pg in 2 microl saline) or saline (2 microl), whereas downhill runners received IL-1ra (1.8 microg in 2 microl saline) or saline (2 microl). Later (2 h), running performance was measured (wheel running activity and treadmill run to fatigue). Injection of IL-1beta significantly decreased wheel running activity in uphill runners (P<0.01), whereas IL-1ra improved wheel running in downhill runners (P<0.05). Similarly, IL-1beta decreased and Il-1ra increased run time to fatigue in the uphill and downhill runners, respectively (P<0.01). These results support the hypothesis that increased brain IL-1beta plays an important role in fatigue after muscle-damaging exercise.     

Role of mitochondrial ATP-sensitive potassium channels on fatigue in mouse muscle fibers

The role of mitochondrial K_ATP (mitoK_ATP) channels on muscle fatigue was assessed in adult mouse skeletal muscle bundles. Muscle fatigue was produced by eliciting short repetitive tetani. Isometric tension and the rate of production of reactive oxygen species (ROS) were measured at room temperature (20-22 °C) using a force transducer and the fluorescent indicator CM-H₂DCFDA. We found that opening mitoK_ATP channels with diazoxide (100 μM) significantly reduced muscle fatigue. Fatigue tension was 34% higher in diazoxide-treated fibers relative to controls. This effect was blocked by the mitoK_ATP channel blocker 5-hydroxydecanoate (5-HD), by the protein kinase C (PKC) inhibitor chelerythrine, and by the nitric oxide (NO) synthase inhibitor N^G-nitro-l-arginine methyl ester hydrochloride (l-NAME) but was not accompanied by a change in the rate of ROS production during fatigue. A physiological role of mitoK_ATP channels on muscle fatigue is proposed.     

Methane production and methane consumption: a review of processes underlying wetland methane fluxes

Potential rates of both methane production and methane consumptionvary over three orders of magnitude and their distribution is skew.These rates are weakly correlated with ecosystem type, incubationtemperature, in situ aeration, latitude, depth and distanceto oxic/anoxic interface. Anaerobic carbon mineralisation is amajor control of methane production. The large range in anaerobicCH₄:CO₂ production rates indicate that a largepart of the anaerobically mineralised carbon is used for reduction ofelectron acceptors, and, hence, is not available for methanogenesis.Consequently, cycling of electron acceptors needs to be studied tounderstand methane production. Methane and oxygen half saturationconstants for methane oxidation vary about one order of magnitude.Potential methane oxidation seems to be correlated withmethanotrophic biomass. Therefore, variation in potential methaneoxidation could be related to site characteristics with a model ofmethanotrophic biomass.     

Effects of respiratory muscle unloading on exercise-induced diaphragm fatigue.

We previously compared the effects of increased respiratory muscle work during whole body exercise and at rest on diaphragmatic fatigue and showed that the amount of diaphragmatic force output required to cause fatigue was reduced significantly during exercise (Babcock et al., J Appl Physiol 78: 1710, 1995). In this study, we use positive-pressure proportional assist ventilation (PAV) to unload the respiratory muscles during exercise to determine the effects of respiratory muscle work, per se, on exercise-induced diaphragmatic fatigue. After 8-13 min of exercise to exhaustion under control conditions at 80-85% maximal oxygen consumption, bilateral phrenic nerve stimulation using single-twitch stimuli (1 Hz) and paired stimuli (10-100 Hz) showed that diaphragmatic pressure was reduced by 20-30% for up to 60 min after exercise. Usage of PAV during heavy exercise reduced the work of breathing by 40-50% and oxygen consumption by 10-15% below control. PAV prevented exercise-induced diaphragmatic fatigue as determined by bilateral phrenic nerve stimulation at all frequencies and times postexercise. Our study has confirmed that high- and low-frequency diaphragmatic fatigue result from heavy-intensity whole body exercise to exhaustion; furthermore, the data show that the workload endured by the respiratory muscles is a critical determinant of this exercise-induced diaphragmatic fatigue.     

The roles of ion fluxes in skeletal muscle fatigue

Intense muscle contractions result in large changes in the intracellular concentrations of electrolytes. The purpose of this study was to examine the contributions of changes in intracellular strong ions to calculated changes in steady-state membrane potential (Em) and muscle intracellular H+ concentration ([H+]i). A physicochemical model is used to examine the origin of the changes in [H+]i during intense muscle contraction. The study used the isolated perfused rat hindlimb intermittently stimulated to contract at high intensity for 5 min. This resulted in significant K+ depletion of both slow (soleus) and fast (white gastrocnemius, WG) muscle fibers and a release of K+ and lactate (Lac-) into venous perfusate. The major contributor to a 12- to 14-mV depolarization of Em in soleus and WG was the decrease in intracellular K+ concentration ([K+]i). The major independent contributors to [H+]i are changes in the concentrations of strong and weak ions and in CO2. Significant decreases in the strong ion difference [( SID]i) in both soleus and WG contributed substantially to the increase in [H+]i during stimulation. In WG the model showed that the decrease in [SID]i accounted for 35% of the increase in [H+]i (133-312 nequiv/L; pHi = 6.88-6.51) at the end of stimulation. Of the main contributors to decreased [SID]i, increased [Lac-]i and decreased [K+]i contributed 40 and 60%, respectively, to increased [H+]i, whereas a decrease in [PCr2-]i contributed to reduced [H+]i. It is concluded that decreased muscle [K+]i during intense contractions is the single most important contributor to reduced Em and increased [H+]i. Depletion of PCr2- simultaneous to the changes in [Lac-]i and [K+]i prevents larger increases in [H+]i and helps maintain the intracellular acid-base state.     

Sodium and potassium fluxes in isolated barnacle muscle fibers

Sodium and potassium influxes and outfluxes have been studied in single isolated muscle fibers from the giant barnacle both by microinjection and by external loading. The sodium influxes and outfluxes were 49 and 39 pmoles /cm²-sec (temperature = 15–16°C) respectively. The potassium influxes and outfluxes were 28 and 60 pmoles/cm²-sec (temperature = 13–16°C) respectively. Replacement of external sodium by lithium reduced sodium outflux by 67% but had no effect on potassium outflux. Removal of external potassum reduced the sodium outflux by 51% but had no effect on potassium outflux. External strophanthidin (10–30 µM) reduced sodium outflux by 80–90% and increased potassium outflux by 40% in normal fibers. The time constant for sodium exchange increased linearly with internal sodium concentration, as did the fraction of sodium outflux insensitive to a maximally inhibitory concentration of external strophanthidin in the range of 10 tO 80 mM internal sodium. The strophanthidin-sensitive component of sodium outflux could be related to the internal sodium concentration by the following empirical formula: See PDF for Equation     

Recovery from training: a brief review: brief review

Athletes spend a much greater proportion of their time recovering than they do in training. Yet, much attention has been given to training with very little investigation of recovery. The purpose of this review is to stimulate further research into this vital area of training. Recovery can be categorized in three terms: i) immediate recovery between exertions; ii) short-term recovery between repeats (e.g., between resistance sets or interval bouts); and iii) training recovery between workouts. The focus of this review is training recovery. Full training recovery is essential to optimal performance and improvement. This review includes an examination of extant research on recovery and a very brief review of some potential modalities and techniques for hastening recovery and the time course of recovery and responses to some treatments. Measures of recovery and practical considerations are discussed briefly. Much research is needed in this area, but there are obstacles to high quality research. Attention must be given to key issues in research on recovery, especially the individual response to recovery treatments.     

Biochemical correlates of fatigue. A brief review

Muscle fatigue, defined as a decreased force generating capacity, develops gradually during exercise and is distinct from exhaustion, which occurs when the required force or exercise intensity can no longer be maintained. We have reviewed several biochemical and ionic changes reported to occur in exercising muscle, and analysed the possible effects these changes may have on the electrical and contractile properties of the muscle. There is no evidence that substrate depletion can account for the decreased force generating capacity, but this factor may be important for the rate of energy turnover and be a major determinant for endurance. Increased concentration of inorganic phosphate and hydrogen ions will depress the force generating capacity, but since fatigue can develop gradually without accumulation of these ions they can only be important when aerobic ATP production is insufficient to support the contractions. Evidence is presented showing that a disturbed balance of K+ alone might cause depolarisation block at high stimulation frequencies, but extracellular K+ accumulation does not increase gradually during prolonged dynamic or static exercise, and is therefore not closely related to fatigue. The repeated release of Ca2+ from the sarcoplasmic reticulum (SR) during muscular activity is suggested of Ca2+ by the mitochondria, increasing with stimulation frequency and duration and possibly also deteriorating mitochondrial function. We therefore speculate that decreased Ca2+ availability for release from SR might contribute to a gradual decline in force generating capacity during all types of exercise.     

Proteomic investigation of changes in rat skeletal muscle after exercise-induced fatigue

The mechanisms of exercise-induced fatigue have not been investigated using proteomic techniques, an approach that could improve our understanding and generate novel information regarding the effects of exercise. In this study, the proteom alterations of rat skeletal muscle were investigated during exercise-induced fatigue. The proteins were extracted from the skeletal muscle of SD rat thigh, and then analyzed by two-dimensional electrophoresis and PDQuest software. Compared to control samples, 10 significantly altered proteins were found in exercise samples, two of them were upregulated and eight of them were downregulated. These proteins were identified by MALDI TOF-MS. The two upregulated proteins were identified as MLC1 and myosin L2 (DTNB) regulatory light-chain precursors. The eight decreased proteins are Glyceraldehyde-3-phosphate Dehydrogenas (GAPDH); Beta enolase; Creatine kinase M chain (M-CK); ATP-AMP Transphosphorylase (AK1); myosin heavy chain (MHC); actin; Troponin I, fast-skeletal muscle (Troponin I fast-twitch isoform), fsTnI; Troponin T, fast-skeletal muscle isoforms (TnTF). In these proteins, four of the eight decreased proteins are related directly or indirectly to exercise induced fatigue. The other proteins represent diverse sets of proteins including enzymyes related to energy metabolism, skeletal muscle fabric protein and protein with unknown functions. They did not exhibit evident relationship with exercise-induced fatigue. Whereas the two identified increased proteins exhibit evident relationship with fatigue. These findings will help in understanding the mechanisms involved in exercise-induced fatigue.     

Effect of exercise-induced arterial hypoxemia on quadriceps muscle fatigue in healthy humans

The effect of exercise-induced arterial hypoxemia (EIAH) on quadriceps muscle fatigue was assessed in 11 male endurance-trained subjects [peak O2 uptake (VO2 peak) = 56.4 +/- 2.8 ml x kg(-1) x min(-1); mean +/- SE]. Subjects exercised on a cycle ergometer at >or=90% VO2 peak) to exhaustion (13.2 +/- 0.8 min), during which time arterial O2 saturation (Sa(O2)) fell from 97.7 +/- 0.1% at rest to 91.9 +/- 0.9% (range 84-94%) at end exercise, primarily because of changes in blood pH (7.183 +/- 0.017) and body temperature (38.9 +/- 0.2 degrees C). On a separate occasion, subjects repeated the exercise, for the same duration and at the same power output as before, but breathed gas mixtures [inspired O2 fraction (Fi(O2)) = 0.25-0.31] that prevented EIAH (Sa(O2) = 97-99%). Quadriceps muscle fatigue was assessed via supramaximal paired magnetic stimuli of the femoral nerve (1-100 Hz). Immediately after exercise at Fi(O2) 0.21, the mean force response across 1-100 Hz decreased 33 +/- 5% compared with only 15 +/- 5% when EIAH was prevented (P < 0.05). In a subgroup of four less fit subjects, who showed minimal EIAH at Fi(O2) 0.21 (Sa(O2) = 95.3 +/- 0.7%), the decrease in evoked force was exacerbated by 35% (P < 0.05) in response to further desaturation induced via Fi(O2) 0.17 (Sa(O2) = 87.8 +/- 0.5%) for the same duration and intensity of exercise. We conclude that the arterial O2 desaturation that occurs in fit subjects during high-intensity exercise in normoxia (-6 +/- 1% DeltaSa(O2) from rest) contributes significantly toward quadriceps muscle fatigue via a peripheral mechanism.     

Mechanisms underlying fatigue: a voxel-based morphometric study of chronic fatigue syndrome

Background  

Fatigue is a crucial sensation that triggers rest, yet its underlying neuronal mechanisms remain unclear. Intense long-term fatigue is a symptom of chronic fatigue syndrome, which is used as a model to study the mechanisms underlying fatigue.     

Role of intracellular pH in muscle fatigue

Intracellular pH of in vitro diaphragm preparations was determined following low- (5 Hz, 1.5 min) and high- (75 Hz, 1 min) frequency stimulation, using glass microelectrodes of the liquid membrane type (pHm). Results were compared with values obtained by the standard homogenate technique (pHh). High- and low-frequency stimulation reduced peak tetanic tension to 21 +/- 1 (SE) and 71 +/- 2% of initial values, respectively. Peak tetanic tension returned to resting values after 10- to 15-min recovery from high- or low-frequency stimulation. Resting pHm was 7.063 +/- 0.011 (n = 72), and after fatiguing stimulation declined to values as low as 6.33. During recovery pHm significantly increased and by 10 min had returned to prefatigue values. No difference was observed in the recovery of pHm between the low- and high-frequency stimulation groups (analysis of variance test, ANOVA), and in both groups pHm recovery was highly correlated to the recovery of peak tetanic tension (r = 0.94, P less than 0.001). Resting pHh was 7.219 +/- 0.023 (n = 13), which was significantly higher than the pHm value. In contrast to pHm, intracellular pHh was significantly higher during recovery from 75- vs. 5-Hz stimulation (P less than 0.05). For both groups pHh increased significantly with time and by 10 min returned to prestimulation values. The ANOVA test demonstrated that pHh values were significantly higher than pHm values during recovery from fatigue. The results from this study support our hypothesis that fatigue from both high- and low-frequency stimulation is at least partially due to the deleterious effects of intracellular acidosis on excitation-contraction coupling.     

Tart cherry and pomegranate supplementations enhance recovery from exercise-induced muscle damage: a systematic review

Phenolic compounds have antioxidant and anti-inflammatory properties and may prevent inflammation and oxidative stress as well as help the athletes to recover from exercise-induced muscle damage (EIMD). Tart cherry (TC) and pomegranate (PG) are two fruits with high content of polyphenols. Their antioxidant and anti-inflammatory properties have recently attracted substantial interest for their potential to reduce strength loss and promote recovery from EIMD. The aims of this review are (1) to summarise the effects of tart cherry and pomegranate supplementation on oxidative stress, inflammation and recovery, and (2) to outline the differences found in supplementation with tart cherries or pomegranates. SPORTDiscus, PubMed, Web of Science and Scopus were searched according to Preferred Reporting Items for Systematic Reviews and Meta-Analysis and 25 studies were included. The existing evidence suggests that both types of supplementation are good strategies to accelerate recovery of functional performance variables, perceptual variables and inflammation but PG supplementation shows better recovery of oxidative stress. However, positive effects are more likely: 1) when supplementation starts some days before muscle damage is induced and finishes some days after, for a total period of at least 8/10 days, 2) with pronounced muscle damage of the muscles involved, and 3) when total phenolic content is at least 1000 mg/day. This review may help to optimise TC or PG supplementation practice to improve post-exercise recovery.     

运动性疲劳对血液流变学的影响

运动性疲劳是运动生理学和运动医学的核心问题。如何彻底消除疲劳,关键在于确定运动性疲劳的发生机制。综述了当前国内外在大强度运动所致运动性疲劳对血液流变学影响的研究成果。为进一步探讨运动性疲劳的发生机制,从而寻找迅速和彻底消除运动疲劳的措施提供理论依据。     

Role of passive potassium fluxes in cell volume regulation in cultured HeLa cells

Summary Cultured HeLa cells behave as ideal osmometers when subjected to hyperosmolar media, and show no volume regulatory behavior. In hypoosmolar solutions, cell swelling is not as great as predicted, and this is due largely to a loss of intracellular KCl. In hyperosmolar solutions there is a stimulation of the ouabain-insensitive but loop diuretic-sensitive⁸⁶Rb⁺ (K⁺) pathway. Analysis of the K⁺, Na⁺ and Cl^– dependency of this K⁺ flux pathway demonstrates that the increase is principally due to an increase in its maximal velocity (V _max). The sensitivity of this pathway to diuretic inhibition is unchanged in hyperosmolar media. Diuretic-sensitive⁸⁶Rb⁺ (K⁺) efflux stimulated by hypertonicity shows no marked dependence on external K⁺. The K⁺ loss observed in hypoosmolar media is distinct from the K⁺ transport pathway stimulated by hyperosmolar media on the basis of its sensitivity to furosemide and anion dependence.     

Membrane proteins involved in potassium shifts during muscle activity and fatigue

Muscle activity is associated with potassium displacements, which may cause fatigue. It was reported previously that the density of the large-conductance Ca2+-dependent K+ (BK(Ca)) channel is higher in the T tubule membrane than in the sarcolemmal membrane and that the opposite is the case for the ATP-sensitive K+ (K(ATP)) channel. In the present experiments, we investigated the subcellular localizations of the strong inward rectifier 2.1 K+ (Kir2.1) channel and the Na+-K+-2Cl- (NKCC)1 cotransporter with Western blot analysis of different muscle fractions. Furthermore, muscle function was studied while trying to manipulate the opening probability or transport capacity of these proteins during electrical stimulation of isolated soleus muscles. All experiments were made with excised muscle from male Wistar rats. Kir2.1 channels were almost undetectable in the sarcolemmal membrane but present in the T tubule membrane, whereas NKCC1 cotransporters were present in the sarcolemmal membrane. For muscles incubated in a buffer containing pinacidil, NS1619, Ba2+, or bumetanide, there was a faster reduction in peak force (P < 0.05). Furthermore, bumetanide incubation reduced the peak force at the onset of electrical stimulation (P < 0.05). Thus the effects on muscle force indicate that these drugs can affect K+-transporting proteins and thereby influence K+ accumulation, especially in the T tubules, suggesting that K(ATP) and BK(Ca) channels are responsible for K+ release and decrease in force during repeated muscle contractions, whereas Kir2.1 and NKCC1 may have a role in K+ reuptake.