Paraspinal muscle function and pain sensitivity following exercise-induced delayed-onset muscle soreness

European Journal of Applied Physiology - The aim of this study was to evaluate the effectiveness of an exercise protocol designed to induce delayed-onset muscle soreness (DOMS) in paraspinal...     

Experimental neck muscle pain impairs standing balance in humans

Impaired postural control has been reported in patients with chronic neck pain of both traumatic and non-traumatic etiologies, but whether painful stimulation of neck muscle per se can affect balance control during quiet standing in humans remains unclear. The purpose of the present experiment was thus to investigate the effect of experimental neck muscle pain on standing balance in young healthy adults. To achieve this goal, 16 male university students were asked to stand upright as still as possible on a force platform with their eyes closed in two conditions of No pain and Pain of the neck muscles elicited by experimental painful electrical stimulation. Postural control and postural performance were assessed by the displacements of the center of foot pressure (CoP) and of the center of mass (CoM), respectively. The results showed increased CoP and CoM displacements variance, range, mean velocity, and mean and median frequencies in the Pain relative to the No pain condition. The present findings emphasize the destabilizing effect of experimental neck muscle pain per se, and more largely stress the importance of intact neck neuromuscular function on standing balance.     

Thermosensitivity of muscle: high-intensity thermal stimulation of muscle tissue induces muscle pain in humans

Small-calibre afferent units responding to thermal stimuli have previously been reported to exist in muscle. The question as to whether these receptors in humans mediate subjective thermal sensations from muscle remains unresolved. The aims of the present study were to determine in humans whether intramuscular injection of warm and cold isotonic saline elicits temperature sensations, muscle pain or any other sensations. In 15 subjects, no thermal sensations assessed on a temperature visual analogue scale (VAS) could be detected with intramuscular injections of isotonic saline (1.5 ml) into the anterior tibial muscle at temperatures ranging from 8 to 48 °C. The same subjects recorded strongly increasing scores on a temperature VAS when thermal stimuli in the same intensity range were applied to the skin overlying the muscle by a contact thermode. However, i.m. isotonic saline of 48 °C induced muscle pain with peak scores of 3.2 ± 0.8 cm on a VAS scale ranging from 0 to 10 cm. Using the the McGill pain questionnaire a subgroup, of subjects qualitatively described the pain using the 'thermal hot' and 'dullness' word groups. Temperature measurements within the muscle during the stimulating injections showed that the time course of the pain sensation elicited by saline at 48 °C paralleled that of the intramuscular temperature and far outlasted the injection time. The present data show that high-intensity thermal stimulation of muscle is associated with muscle pain. High-threshold warm-sensitive receptors may mediate the pain following activation by temperatures of 48 °C or more. Taken together, the data indicate that thermosensation from a given volume of muscle is less potent than nociception.     

Effect of exercise-induced muscle damage on the blood lactate response to incremental exercise in humans

Eccentric muscle actions are known to induce temporary muscle damage, delayed onset muscle soreness (DOMS) and muscle weakness that may persist for several days. The purpose of the present study was to determine whether DOMS-inducing exercise affects blood lactate responses to subsequent incremental dynamic exercise. Physiological and metabolic responses to a standardised incremental exercise task were measured two days after the performance of an eccentric exercise bout or in a control (no prior exercise) condition. Ten healthy recreationally active subjects (9 male, 1 female), aged 20 (SD 1) years performed repeated eccentric muscle actions during 40?min of bench stepping (knee high step; 15 steps?·?min^?1). Two days after the eccentric exercise, while the subjects experienced DOMS, they cycled on a basket loaded cycle ergometer at a starting work rate of 150?W, with increments of 50?W every 2?min until fatigue. The order of the preceding treatments (eccentric exercise or control) was randomised and the treatments were carried out 2 weeks apart. Two days after the eccentric exercise, all subjects reported leg muscle soreness and exhibited elevated levels of plasma creatine kinase activity (P?V˙O₂ during cycling were unaffected by the prior eccentric exercise. Minute volume, respiratory exchange ratio and heart rate responses were similar but venous blood lactate concentration was higher (P?P?相似文献   

Coordinated modulation of locomotor muscle synergies constructs straight-ahead and curvilinear walking in humans

We describe the muscle synergies accompanying steering of walking along curved trajectories, in order to analyze the simultaneous control of progression and balance-threatening emerging forces. For this purpose, we bilaterally recorded in ten subjects the electromyograms (EMGs) of a representative sample of leg and trunk muscles (n=16) during continuous walking along one straight and two curved trajectories at natural speed. Curvilinear locomotion involved a graded, limb-dependent modulation of amplitude and timing of activity of the muscles of the legs and trunk. The turn-related modulation of the motor pattern was highly coordinated amongst muscles and body sides. For all muscles, linear relationships were detected between the spatial and temporal features of muscle EMG activity. The largest modulation of EMG was observed in gastrocnemius medialis and lateralis muscles, which showed opposite changes in timing and amplitude during curve-walking. Moreover, amplitude and timing characteristics of muscle activities were significantly correlated with the spatial and temporal gait adaptations that are associated with curvilinear locomotion. The present results reveal that fine-modulation of the muscle synergies underlying straight-ahead locomotion is enough to generate the adequate propulsive forces to steer walking and maintain balance. These findings suggest that the turn-related command operates by modulation of the phase relationships between the tightly coupled neuronal assemblies that drive motor neuron activity during walking. This would produce the invariant templates for locomotion kinematics that are at the base of human navigation in space.     

Dynamic,but not static,pain sensitivity predicts exercise-induced muscle pain: Covariation of temporal sensory summation and pain intensity

Cross-section studies suggest that measures of pain sensitivity, derived from quantitative sensory testing (QST), are elevated in persons with chronic pain conditions. However, little is known about whether development of chronic pain is preceded by elevated pain sensitivity or pain sensitivity increases as a result of prolonged experience of pain. Here we used QST to test static (single suprathreshold stimuli) and dynamic (temporal sensory summation) pain processing of thermal stimuli. Muscle pain was induced using high-intensity exercise (DOMS). Multi-level modeling approaches determined the daily covariation among static and dynamic QST measures and pain intensity. Variation in responses to static pain sensitivity was not associated with pain intensity from DOMS while, in contrast, variation in dynamic pain sensitivity was positively associated with variation in pain intensity from DOMS. This finding supports the use of TSS as a marker of the central pain state and potentially as an appropriate measure for treatment monitoring.     

Reduction of conditioned pain modulation in humans by naltrexone: an exploratory study of the effects of pain catastrophizing

The current study tested the hypothesis that conditioned pain modulation is mediated by the release of endogenous opioids with a placebo-controlled (sugar pill) study of naltrexone (50 mg) in 33 healthy volunteers over two counter-balanced sessions. Pain modulation consisted of rating of heat pain (palm) during concurrent cold water immersion (foot). Compared to baseline heat pain ratings, concurrent foot immersion lowered pain intensity ratings, which suggests an inhibitory effect, was reduced with naltrexone, suggesting at least partial dependence of inhibition on endogenous opioids. An exploratory analysis revealed that individual differences in catastrophizing moderated the effects of naltrexone; endogenous opioid blockade abolished modulation in subjects lower in catastrophizing while modulation was unaffected by naltrexone among high catastrophizers. The results suggest a role of endogenous opioids in endogenous analgesia, but hint that multiple systems might contribute to conditioned pain modulation, and that these systems might be differentially activated as a function of individual differences in responses to pain.     

聚集体自噬在运动性骨骼肌损伤中的特征

文题释义： 蛋白质质量控制：机体通过分子伴侣系统、泛素-蛋白酶体系统和蛋白聚集体自噬重新折叠或降解未折叠和错误折叠的蛋白质,防止蛋白质聚集产生毒性,避免损害细胞的正常功能。 聚集体自噬：细胞内蛋白聚集体的特异性清除途径是选择性自噬的一种,承担了大部分降解蛋白聚集体的任务,在异常蛋白质量控制系统中起了决定性作用。 组蛋白去乙酰化酶6：是聚集体自噬过程的关键调节因子,它通过泛素连接结构域特异性地连接在泛素化的蛋白聚集物上,另一端连接微管的Dynein蛋白,并通过乙酰化α-tubulin运输蛋白聚集物到微管组织中心,形成蛋白聚集体。 背景：一次大负荷离心运动会诱导骨骼肌损伤、内质网应激、错误折叠蛋白增多,聚集体自噬作为蛋白质质量控制的途径之一,在损伤修复过程中应当发挥一定的作用。 目的：探讨一次大负荷离心运动诱导骨骼肌损伤恢复过程中聚集体自噬的激活程度,分析聚集体自噬在运动诱导骨骼肌损伤中的作用,以完善运动诱导骨骼肌损伤的蛋白降解途径。 方法：将64只成年雄性SD大鼠(购自北京维通利华实验技术有限公司)随机分为安静对照组(n=8)和运动组(n=56),运动组又按运动后时相分为0,3,6,12,24,48,72 h组,每组8只。运动组大鼠进行一次跑台下坡跑运动(-16°,16 m/min,90 min),分别在运动后的相应时刻取比目鱼肌,使用透视电子显微镜观察损伤发生程度,采用 Western Blot方法检测比目鱼肌难溶蛋白聚集体自噬相关蛋白组蛋白去乙酰化酶6和微管相关蛋白1轻链3Ⅱ/Ⅰ的蛋白表达。实验获得北京体育大学运动科学实验伦理委员会批准(2016030A)。 结果与结论：①透射电镜显示一次大负荷离心运动后,大鼠比目鱼肌出现一过性的肌节紊乱、变宽,Z线呈水波状、断裂直至消失,线粒体肿胀、分布不均、结构不清,其中运动后12 h损伤最为严重,于运动后       72 h完全恢复;②Western Blot检测显示,一次性离心运动后即刻组蛋白去乙酰化酶6显著增高,运动后    6 h达到峰值,之后逐渐降低,运动后72 h恢复到对照组水平;一次性离心运动后3 h的微管相关蛋白1轻链3Ⅱ/Ⅰ显著升高,运动后12 h达到峰值,之后显著降低,运动后72 h恢复到对照组水平;③结果表明,一次大负荷离心运动后一过性发生聚集体自噬,在清除错误折叠蛋白、维持细胞环境稳定和骨骼肌损伤恢复中发挥着重要作用。 ORCID: 0000-0002-6365-7822(高扬) 中国组织工程研究杂志出版内容重点：组织构建;骨细胞;软骨细胞;细胞培养;成纤维细胞;血管内皮细胞;骨质疏松;组织工程     

Central and peripheral contributions to muscle fatigue in humans during sustained maximal effort

The purpose of this study was to estimate the relative contributions of central and peripheral factors to the development of human muscle fatigue. Nine healthy subjects [five male, four female; age?=?30 (2) years, mean (SE)] sustained a maximum voluntary isometric contraction (MVC) of the ankle dorsiflexor muscles for 4 min. Fatigue was quantitated as the fall in MVC. Three measures of central activation and one measure of peripheral activation (compound muscle action potential, CMAP) were made using electromyography (EMG) and electrical stimulation. Measures of intramuscular metabolism were made using magnetic resonance spectroscopy. After exercise, MVC and electrically stimulated tetanic contraction (50 Hz, 500 ms) forces were 22.2 (3.7)% and 37.3 (7.1)% of pre-exercise values, respectively. The measures of central activation suggested some central fatigue during exercise: (1) the central activation ratio [MVC/(MVC + superimposed tetanic force)] fell from 0.94 (0.03) to 0.78 (0.09), (2) the MVC/tetanic force ratio fell from 2.3 (0.7) to 1.3 (0.7), and (3) the integral of the EMG (iEMG) signal decreased to 72.6 (9.1)% of the initial value, while the CMAP amplitude was unchanged. Intramuscular pH was associated by regression with the decline in MVC force (and therefore fatigue) and iEMG. The results indicate that central factors, which were not associated with altered peripheral excitability, contributed approximately 20% to the muscle fatigue developed, with the remainder being attributable to intramuscular (i.e., metabolic) factors. The association between pH and iEMG is consistent with proton concentration as a feedback mechanism for central motor drive during maximal effort.     

Etiology of exercise-induced muscle damage.

Muscle damage is caused by strenuous and unaccustomed exercise, especially exercise involving eccentric muscle contractions, where muscles lengthen as they exert force. Damage can be observed both directly at the cellular level and indirectly from changes in various indices of muscle function. Several mechanisms have been offered to explain the etiology of the damage/repair process, including mechanical factors such as tension and strain, disturbances in calcium homeostasis, the inflammatory response, and the synthesis of stress proteins (heat shock proteins). Changes in muscle function following eccentric exercise have been observed at the cellular level as an impairment in the amount and action of transport proteins for glucose and lactate/H+, and at the systems level as an increase in muscle stiffness and a prolonged loss in the muscle's ability to generate force. This paper will briefly review factors involved in the damage/repair process and alterations in muscle function following eccentric exercise.     

Consequences of exercise-induced respiratory muscle work

We briefly review the evidence for a hypothesis, which links the ventilatory response to heavy intensity, sustained exercise-to-exercise performance limitation in health. A key step in this linkage is a respiratory muscle fatigue-induced metaboreflex, which increases sympathetic vasoconstrictor outflow, causing reduced blood flow to locomotor muscles and locomotor muscle fatigue. In turn, the limb fatigue comprises an important dual contribution to both peripheral and central fatigue mechanisms, which contribute to limiting exercise performance. Clinical implications for respiratory limitations to exercise in patients with chronic obstructive lung disease (COPD) and chronic heart failure (CHF) are discussed and key unresolved problems are outlined.     

光生物调节修复运动性肌肉损伤

背景：不习惯强度的运动常导致运动性肌肉损伤,光生物调节治疗运动性肌肉损伤的研究存在不同的结果,且其治疗机制及其量效关系尚不清楚。 目的：总结和分析光生物调节作用的机制以及光生物调节疗法治疗运动性肌肉损伤时的剂量、强度、波长等与效应之间的关系。 方法：通过PubMed数据库(1996-01/2010-04)和中国学术期刊库(2000-01/2010-04)检索了低强度激光或单色光对运动性肌肉损伤的作用及其相关机制的文献,英文检索词为“low-level laser, phototherapy, exercise-induced muscle damage, delayed onset muscle soreness”,中文检索词为“低强度激光,光疗法,运动性肌肉损伤,延迟性肌肉酸痛”。手工补充检索低强度激光疗法的专著。共收集到中、英文文献38篇,排除重复及类似性研究,纳入31篇文献进行综述。 结果与结论：光生物调节作用的机制假说主要包括线粒体机制、一氧化氮机制、氧化还原机制和光生物信息模型理论,光生物调节疗法治疗运动性肌肉损伤的具体机制仍不清楚。光生物调节治疗运动性肌肉损伤只有在剂量和强度达到足够大情况下才有效,而且强度可能比剂量更重要,患部的有效照射剂量和强度受到皮肤厚度和光波波长的影响。由此推论,光生物调节疗法能有效地治疗运动性肌肉损伤,其疗效是剂量和强度依赖性的。     

Effects of experimental pain on jaw muscle activity during goal-directed jaw movements in humans

To study the effects of masseter muscle pain on jaw muscle electromyographic (EMG) activity during goal-directed tasks. Mandibular movement was tracked and EMG activity was recorded from bilateral masseter, and right posterior temporalis, anterior digastric, and inferior head of lateral pterygoid muscles in 22 asymptomatic subjects at postural jaw position, and during three tasks: (a) protrusion, (b) contralateral (left), (c) open jaw movement. Tasks were performed during three conditions: control (no infusion), test 1 [continuous infusion into right masseter of 4.5% hypertonic saline to achieve 30–60 mm pain intensity on 100-mm visual analog scale (VAS)], and test 2 (isotonic saline infusion; in 16 subjects only); the sequence of hypertonic and isotonic saline was randomized. The average EMG root-mean-square values at 0.5 mm increments of mid-incisor-point displacement were analysed using linear mixed effects model statistics (significance: P < 0.05). Right masseter hypertonic saline infusion resulted in significantly (P < 0.0005) more pain (mean ± SD VAS 47.3 ± 14.3 mm) than isotonic infusion (12.2 ± 17.3 mm). Although there was evidence of inter-subject variation, the principal EMG findings were that the significant effects of hypertonic saline-induced pain on EMG activity varied with the task in which the muscle participated irrespective of whether the muscle was an agonist or an antagonist in the tasks. The direction of the hypertonic saline-induced pain effect on EMG activity (i.e., whether the hypertonic saline-induced EMG activity was less than or greater than control EMG activity) could change with the magnitude of jaw displacement. Hypertonic saline infusion had no significant effect on postural EMG activity in any of the recorded jaw muscles. The data suggest that under constrained goal-directed tasks, the pattern of pain-induced changes in jaw muscle EMG activity is not clear cut, but can vary with the task performed, jaw displacement magnitude, and the subject being studied.     

Noradrenergic pain modulation

Norepinephrine is involved in intrinsic control of pain. Main sources of norepinephrine are sympathetic nerves peripherally and noradrenergic brainstem nuclei A1-A7 centrally. Peripheral norepinephrine has little influence on pain in healthy tissues, whereas in injured tissues it has variable effects, including aggravation of pain. Its peripheral pronociceptive effect has been associated with injury-induced expression of novel noradrenergic receptors, sprouting of sympathetic nerve fibers, and pronociceptive changes in the ionic channel properties of primary afferent nociceptors, while an interaction with the immune system may contribute in part to peripheral antinociception induced by norepinephrine. In the spinal cord, norepinephrine released from descending pathways suppresses pain by inhibitory action on alpha-2A-adrenoceptors on central terminals of primary afferent nociceptors (presynaptic inhibition), by direct alpha-2-adrenergic action on pain-relay neurons (postsynaptic inhibition), and by alpha-1-adrenoceptor-mediated activation of inhibitory interneurons. Additionally, alpha-2C-adrenoceptors on axon terminals of excitatory interneurons of the spinal dorsal horn possibly contribute to spinal control of pain. At supraspinal levels, the pain modulatory effect by norepinephrine and noradrenergic receptors has varied depending on many factors such as the supraspinal site, the type of the adrenoceptor, the duration of the pain and pathophysiological condition. While in baseline conditions the noradrenergic system may have little effect, sustained pain induces noradrenergic feedback inhibition of pain. Noradrenergic systems may also contribute to top-down control of pain, such as induced by a change in the behavioral state. Following injury or inflammation, the central as well as peripheral noradrenergic system is subject to various plastic changes that influence its antinociceptive efficacy.     

Glutathione-dependent modulation of exhausting exercise-induced changes in neutrophil function of rats

Reduced glutathione (GSH) plays a central role in maintaining an effective synergism between various physiological and exogenous antioxidants. We tested the effects of GSH andN-acetylcysteine (NAC, a pro-GSH clinical drug), intraperitoneal (i.p.) supplementation and GSH deficiency on exercise-induced leucocyte margination and neutrophil oxidative burst activity. GSH, NAC (1g · kg^–1) or placebo saline was i.p. injected (one or eight times) to male rats (n seven per group). The GSH-deficient rats were prepared by i.p. injections ofl-buthionine-[SR]-sulphoximine (BSO, 6 mmol · 1^–1 · kg^–1) twice daily for 4 days. Exercised animals were subjected to treadmill run to exhaustion. Exhausting treadmill exercise significantly decreased peripheral blood leucocyte count in the controls (P < 0.001). Such exercise-associated leucocyte margination was prevented by GSH supplementation. Peripheral blood neutrophil counts were significantly higher (P < 0.02) in the GSH-supplemented groups compared to the placebo control groups. Exercise-induced increase in peripheral blood neutrophil oxidative burst activity as measured by luminol-enhanced chemiluminescence per volume of blood tended to be higher in the GSH-supplemented group (P < 0.10), and lower in the GSH-deficient rats (P < 0.02). In these experiments, for the first time we have shown that GSH supplementation can induce neutrophil mobilization and decrease exercise-induced leucocyte margination, and that exogenous and endogenous GSH can regulate exercise-induced stimulation of the neutrophil oxidative burst.     

Prefrontal modulation of visual processing in humans

Single neuron, evoked potential and metabolic techniques show that attention influences visual processing in extrastriate cortex. We provide anatomical, electrophysiological and behavioral evidence that prefrontal cortex regulates neuronal activity in extrastriate cortex during visual discrimination. Event-related potentials (ERPs) were recorded during a visual detection task in patients with damage in dorsolateral prefrontal cortex. Prefrontal damage reduced neuronal activity in extrastriate cortex of the lesioned hemisphere. These electrophysiological abnormalities, beginning 125 ms after stimulation and lasting for another 500 ms, were accompanied by behavioral deficits in detection ability in the contralesional hemifield. The results provide evidence for intrahemispheric prefrontal modulation of visual processing.     

Role of adenosine in exercise-induced human skeletal muscle vasodilatation

The role of adenosine in exercise-induced human skeletal muscle vasodilatation remains unknown. We therefore evaluated the effect of theophylline-induced adenosine receptor blockade in six subjects and the vasodilator potency of adenosine infused in the femoral artery of seven subjects. During one-legged, knee-extensor exercise at approximately 48% of peak power output, intravenous (i.v.) theophylline decreased (P < 0.003) femoral artery blood flow (FaBF) by approximately 20%, i.e. from 3.6 +/- 0.5 to 2.9 +/- 0.5 L min(-1), and leg vascular conductance (VC) from 33.4 +/- 9.1 to 27.7 +/- 8.5 mL min-1 mmHg-1, whereas heart rate (HR), mean arterial pressure (MAP), leg oxygen uptake and lactate release remained unaltered (P = n.s.). Bolus injections of adenosine (2.5 mg) at rest rapidly increased (P < 0.05) FaBF from 0.3 +/- 0.03 L min(-1) to a 15-fold peak elevation (P < 0.05) at 4.1 +/- 0.5 L min(-1). Continuous infusion of adenosine at rest and during one-legged exercise at approximately 62% of peak power output increased (P < 0.05) FaBF dose-dependently to level off (P = ns) at 8.3 +/- 1.0 and 8.2 +/- 1.4 L min(-1), respectively. One-legged exercise alone increased (P < 0.05) FaBF to 4.7 +/- 1.7 L min(-1). Leg oxygen uptake was unaltered (P = n.s.) with adenosine infusion during both rest and exercise. The present findings demonstrate that endogenous adenosine controls at least approximately 20% of the hyperaemic response to submaximal exercise in skeletal muscle of humans. The results also clearly show that arterial infusion of exogenous adenosine has the potential to evoke a vasodilator response that mimics the increase in blood flow observed in response to exercise.     

褪黑素在疼痛调节中的作用

褪黑素是松果体合成的一种激素,它的分泌有着明显的昼夜节律和季节规律。褪黑素不仅与睡眠、衰老、免疫关系密切,而且对疼痛的调节也发挥着极其重要的作用。大量研究表明,在急性痛、炎性痛及神经病理性疼痛等多种类型的疼痛中,褪黑素能够预防、减轻乃至逆转伤害性疼痛。关于褪黑素的具体作用机制目前并不是很清楚,但已有的研究认为可能与膜信号通道和核信号途径相关,特别是与中枢神经系统的褪黑素受体和阿片受体关系密切。从而,褪黑素受体可能成为镇痛作用的新靶点,通过褪黑素受体的激活到达有效治疗疼痛的目的。本综述提供了褪黑素作为一种潜在的镇痛药在动物实验和临床研究中的一系列有用的依据。