Impaired Muscle Performance Research Articles

Doxorubicin causes lesions in the electron transport system of skeletal muscle mitochondria that are associated with a loss of contractile function

Doxorubicin is an anthracycline-based chemotherapeutic that causes myotoxicity with symptoms persisting beyond treatment. Patients experience muscle pain, weakness, fatigue, and atrophy, but the underlying mechanisms are poorly understood. Studies investigating doxorubicin-induced myotoxicity have reported disrupted mitochondrial function. Mitochondria are responsible for regulating both cellular energy status and Ca2+ handling, both of which impact contractile function. Moreover, loss of mitochondrial integrity may initiate muscle atrophy. Skeletal muscle mitochondrial dysregulation may therefore contribute to an overall loss of skeletal muscle quality and performance that may be mitigated by appropriately targeted mitochondrial therapies. We therefore assessed the impact of doxorubicin on muscle performance and applied a multiplexed assay platform to diagnose alterations in mitochondrial respiratory control. Mice received a clinically relevant dose of doxorubicin delivered systemically and were euthanized 72 h later. We measured extensor digitorum longus and soleus muscle forces, fatigue, and contractile kinetics in vitro, along with Ca2+ uptake in isolated sarcoplasmic reticulum. Isolated skeletal muscle mitochondria were used for real-time respirometry or frozen for protein content and activity assays. Doxorubicin impaired muscle performance, which was indicated by reduced force production, fatigue resistance, and sarcoplasmic reticulum-Ca2+ uptake, which were associated with a substrate-independent reduction in respiration and membrane potential but no changes in the NAD(P)H/NAD(P)+ redox state. Protein content and dehydrogenase activity results corroborated these findings, indicating that doxorubicin-induced mitochondrial impairments are located upstream of ATP synthase within the electron transport system. Collectively, doxorubicin-induced lesions likely span mitochondrial complexes I-IV, providing potential targets for alleviating doxorubicin myotoxicity.

N-acetylcysteine Decreases Fibrosis and Increases Force-Generating Capacity of mdx Diaphragm.

Respiratory muscle weakness occurs due to dystrophin deficiency in Duchenne muscular dystrophy (DMD). The mdx mouse model of DMD shows evidence of impaired respiratory muscle performance with attendant inflammation and oxidative stress. We examined the effects of N-acetylcysteine (NAC) supplementation on respiratory system performance in mdx mice. Eight-week-old male wild type (n = 10) and mdx (n = 20) mice were studied; a subset of mdx (n = 10) received 1% NAC in the drinking water for 14 days. We assessed breathing, diaphragm, and external intercostal electromyogram (EMG) activities and inspiratory pressure during ventilatory and non-ventilatory behaviours. Diaphragm muscle structure and function, cytokine concentrations, glutathione status, and mRNA expression were determined. Diaphragm force-generating capacity was impaired in mdx compared with wild type. Diaphragm muscle remodelling was observed in mdx, characterized by increased muscle fibrosis, immune cell infiltration, and central myonucleation. NAC supplementation rescued mdx diaphragm function. Collagen content and immune cell infiltration were decreased in mdx + NAC compared with mdx diaphragms. The cytokines IL-1β, IL-6 and KC/GRO were increased in mdx plasma and diaphragm compared with wild type; NAC decreased systemic IL-1β and KC/GRO concentrations in mdx mice. We reveal that NAC treatment improved mdx diaphragm force-generating capacity associated with beneficial anti-inflammatory and anti-fibrotic effects. These data support the potential use of NAC as an adjunctive therapy in human dystrophinopathies.

Vitamin D Deficiency Is Associated With Impaired Muscle Strength And Physical Performance In Community-Dwelling Older Adults: Findings From The English Longitudinal Study Of Ageing.

PurposeMaintaining skeletal muscle function throughout life is a crucial component of successful ageing. Adequate vitamin D status may be important in preserving muscle function. We aimed to determine the association between impaired muscle function and serum vitamin D status in community-dwelling older adults. Falls were explored as a secondary aim.MethodsData were analyzed from adults aged ≥60 years, from Wave 6 of the English Longitudinal Study of Aging (ELSA). Handgrip strength (HGS) and the short physical performance battery (SPPB) were employed as measures of muscle strength and physical function, respectively. Serum 25-hydroxyvitamin D [25(OH)D] was assessed with concentration <30 nmol/L classed as vitamin D deficient.ResultsThe study comprised 4157 community-dwelling adults with a mean age of 69.8 (SD 6.9). Overall, 30.6% had low HGS and 12.7% had low SPPB (≤6). Participants with the lowest serum 25(OH)D (<30 nmol/L) had the highest prevalence of impaired muscle strength and performance (40.4% and 25.2%) compared with participants with levels ≥50 nmol/L (21.6% and 7.9%). Consistent with this, vitamin D deficiency (<30 nmol/L) was a significant determinant of low HGS (OR 1.44 [1.22, 1.71], p<0.001) and poor physical performance (OR 1.65 [1.31, 2.09], p<0.001) in the logistic regression models. Older adults partaking in regular moderate physical activity had significantly lower odds of impaired muscle strength (OR 0.65 [0.58, 0.79]) and physical function (OR 0.30 [0.24, 0.38]), p <0.001, respectively. Single or multiple falls (15.8% and 10.5% in past year) were not associated with vitamin D status.ConclusionVitamin D deficiency was associated with impaired muscle strength and performance in a large study of community-dwelling older people. It is generally accepted that vitamin D deficiency at the <30 nmol/L cut-off should be reversed to prevent bone disease, a strategy that may also protect skeletal muscle function in ageing.

MAPK, androgen, and glucocorticoid receptor phosphorylation following high-frequency resistance exercise non-functional overreaching.

Stressful training with insufficient recovery can impair muscle performance. Expression of mitogen-activated protein kinases (MAPK) has been reported at rest following overreaching and overtraining. The acute myocellular exercise response to stressful training with insufficient recovery has not been investigated. We investigated MAPK, androgen, and glucocorticoid receptor phosphorylation following a period of stressful training. Sixteen resistance-trained men were matched on barbell squat 1 repetition maximum strength and randomized into a group that performed normal training or stressful training with insufficient recovery. The control group (CON) performed three speed-squat training sessions on non-consecutive days, while the stressful training group (NFOR) performed 15 training sessions over 7.5days. Resting and post-exercise skeletal muscle biopsies were obtained prior to (T1) and after the training period (T2). Samples were analyzed for total and phosphorylated androgen receptor (AR), glucocorticoid receptor (GR), and MAPKs (ERK, JNK, and p38). Total AR were down-regulated post-exercise at T2 in NFOR only. Phospho-AR at ser515 increased in both groups post-exercise at T1; however, ser515 only increased at T2 in NFOR. Phosphorylated ERK, JNK, and p38 increased post-exercise in CON and NFOR at T1 and T2. Post-exercise phospho-p38 was blunted in NFOR at T2 compared to T1. After the training intervention, resting phospho-p38 was higher in NFOR compared to T1. At T2, post-exercise phospho-GR at ser226 was lower compared to T1, and resting levels increased in NFOR. Steroid receptors are phosphorylated after acute resistance exercise, and in addition to MAPKs, are differentially regulated after stressful training with insufficient recovery.

Unilateral hamstrings static stretching can impair the affected and contralateral knee extension force but improve unilateral drop jump height.

Prolonged static stretching (SS) in isolation (no dynamic warm-up) can impair muscle performance. There are conflicting reports whether impairments are present in antagonist and contralateral muscles. The objective of this study was to assess the effect of unilateral hamstrings SS on ipsilateral stretched and contralateral limbs' strength and jump power. The SS (four repetitions of 30-s) and control sessions involved unilateral testing of the stretched leg and contralateral leg for knee extension (KE) maximum voluntary isometric contraction (MVIC) force and electromyography (EMG), drop jump (DJ) height and contact time at 1-min post-stretching. There were significant KE MVIC force impairments for both the SS (p = 0.006, d = 0.3, - 8.1%) and contralateral (p = 0.02, d = 0.20, - 4.2%) leg. With normalized data, there was a near-significant (p = 0.1), small magnitude (d = 0.29), greater force impairment with the ipsilateral (93.0 ± 12.8% of pre-test) versus the contralateral (96.2 ± 9.1% of pre-test) KE MVIC force. DJ height significantly improved for the stretched leg (p = 0.03, d = 0.18, + 9.2%) with near-significant, improvements for the contralateral leg (p = 0.06, d = 0.22, + 12.1%). For the stretched leg, DJ contact time was significantly (p = 0.04, d = 0.18, + 3.4%) prolonged, but there was no significant change with the contralateral leg. Unilateral hamstrings SS induced strength deficits in the ipsilateral and contralateral knee extension MVIC and a prolongation of the stretched leg DJ contact period. In anticipation of maximal force outputs, prolonged SS in isolation (no dynamic warm-up included) can have negative consequences on antagonist and contralateral muscle performance.

Accelerating Recovery from Exercise-Induced Muscle Injuries in Triathletes: Considerations for Olympic Distance Races

The triathlon is one of the fastest developing sports in the world due to expanding participation and media attention. The fundamental change in Olympic triathlon races from a single to a multistart event is highly demanding in terms of recovery from and prevention of exercise-induced muscle injures. In elite and competitive sports, ultrastructural muscle injuries, including delayed onset muscle soreness (DOMS), are responsible for impaired muscle performance capacities. Prevention and treatment of these conditions have become key in regaining muscular performance levels and to guarantee performance and economy of motion in swimming, cycling and running. The aim of this review is to provide an overview of the current findings on the pathophysiology, as well as treatment and prevention of, these conditions in compliance with clinical implications for elite triathletes. In the context of DOMS, the majority of recovery interventions have focused on different protocols of compression, cold or heat therapy, active regeneration, nutritional interventions, or sleep. The authors agree that there is a compelling need for further studies, including high-quality randomized trials, to completely evaluate the effectiveness of existing therapeutic approaches, particularly in triathletes. The given recommendations must be updated and adjusted, as further evidence emerges.

Muscle Performance and Postural Stability Are Reduced in Patients with Newly Diagnosed Graves' Disease.

Background: Reduced muscle strength is an acknowledged symptom of Graves' disease, but the knowledge on severity is sparse. This study aimed to investigate muscle strength, balance, and muscle function in patients with Graves' disease compared to age- and sex-matched healthy controls. Methods: Using a cross-sectional design, 55 patients newly diagnosed with Graves' disease were compared to 55 euthyroid controls, matched on sex, age, and menopausal status. Isometric muscle strength (N) and maximum force production (N/s) were measured across different muscles groups using a dynamometer chair and postural stability (balance) in different positions using a stadiometer. Muscle function was assessed using the Timed-Up-and-Go test and the Repeated Chair Stand test. Results: Patients and controls were well matched. Handgrip maximum muscle strength as well as strength at elbow and knee flexion and extension were significantly impaired in patients compared to controls. Maximum force production was only significantly reduced at elbow flexion. Patients performed the Timed-Up-and-Go and the Repeated Chair Stand test significantly slower than controls, and postural stability was significantly reduced in patients compared to controls in all positions. Free triiodothyronine correlated with reduced muscle strength and postural stability. Conclusions: At the time of diagnosis, Graves' disease is associated with impaired maximum muscle strength, performance, and balance, whereas maximum force production is overall comparable to euthyroid controls.

N‐Acetyl cysteine improves dystrophic (mdx) mouse diaphragm muscle quality and strength

Respiratory muscle weakness occurs as a consequence of dystrophin deficiency in Duchenne muscular dystrophy (DMD), with implications for breathing and airway protective behaviours. The mdx mouse model of DMD shows evidence of impaired respiratory muscle performance with attendant inflammation and oxidative stress. N‐Acetyl cysteine (NAC) is a dietary antioxidant commonly used in the treatment of respiratory disease. We sought to examine the effects of NAC intervention on respiratory system performance in the mdx mouse.Young adult male wild‐type and mdx mice were studied; a subset of mdx received 1% NAC in the drinking water for 14 days. Ventilation was assessed in conscious mice using whole‐body plethysmography. Inspiratory pressure and respiratory muscle (diaphragm and external intercostal) EMG activity were assessed in anaesthetised mice during ventilatory and non‐ventilatory behaviours. Diaphragm ex vivo force‐generating capacity, muscle structure, cytokine concentrations, glutathione status and mRNA expression were determined. Data were statistically compared by unpaired Student's t test.Diaphragm function was severely impaired in mdx, evidenced by reductions in force‐generating capacity (40–160Hz range), total muscle shortening and maximal shortening velocity compared to wild‐type. Extensive diaphragm myofibre remodelling and damage was observed for mdx, characterised by increased muscle fibrosis, immune cell filtration, muscle fibre central nucleation and embryonic myosin expression. The pro‐inflammatory cytokines IL‐1β and IL‐6 were elevated in mdx diaphragm and plasma samples. mRNA studies indicate an increase in gene expression related to muscle atrophy, regeneration and inflammation in mdx diaphragm, and a reduction in anti‐oxidant related gene expression. NAC supplementation increased mdx diaphragm force (60–160Hz), maximal shortening and shortening velocity. Collagen deposition and the infiltration of putative inflammatory cells in mdx diaphragm was decreased following NAC. Mdx diaphragm and plasma IL‐1β and IL‐6 concentrations were decreased following NAC. Glutathione reductase and peroxidase activities were increased in mdx diaphragm; both were unaffected by NAC. mRNA expression of Nrf2 was increased in mdx diaphragm and increased further with NAC supplementation. No adverse effects of NAC intervention were observed on ventilation, inspiratory pressure and EMG, and growth measures.We reveal that NAC treatment improved mdx diaphragm force‐generating capacity by way of beneficial anti‐inflammatory and anti‐fibrotic effects. These data support the potential use of NAC as an adjunctive therapy in the dystrophinopathies.This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.

Yogurt Drink Effectively Rehydrates Athletes After a Strenuous Exercise Session

Abstract Dehydration and electrolyte imbalance as a result of prolonged strenuous exercise leads to poor thermoregulation and impaired muscle performance. Thus, appropriate rehydration during and after exercise with a solution that has a balanced combination of nutrients including electrolytes, carbohydrates and proteins is crucial in preventing the side effects of dehydration. Yogurt drink as a traditional drink with an appropriate nutritious content could be used as an alternative to expensive commercially available drinks for rehydrating athletes after long exercises in warm and humid environments and in developing countries. In this cross-over trial we examined the rehydration potential of yogurt drink in comparison to water and a commercial drink after a strenuous exercise (cycling) session in a hot and humid environment. Blood measurements included blood osmolality, serum glucose, hematocrit and serum electrolytes. Urine measurements included urine volume, osmolality and electrolyte concentrations. The results showed that early after rehydration Yogurt drink compared to water significantly increased urine sodium (mmol/L) (138.8 ± 93.4 vs. 90.0 ± 50.7, P &lt; 0.01), urine potassium (mmol/L) (105.6 ± 55.1 vs. 35.8 ± 22.0, P &lt; 0.05) and urine chloride (mmol/L) (113.2 ± 28.4 vs. 35.8 ± 25.1 P &lt; 0.01). This degree of improvement was the same as with the commercial drink for urine sodium, potassium, and chloride. Yogurt drink prevented dehydration-induced changes in the blood as it stabilized the hematocrit and serum sodium, potassium and osmolality within the normal range after exercise. Finally, our results indicated that yogurt drink, as a natural and affordable rehydration option, can be considered to restore fluid and electrolyte losses after strenuous exercises in hot and humid environments.

Downregulation of EDTP in glial cells suppresses polyglutamine protein aggregates and extends lifespan in Drosophila melanogaster

Drosophila egg-derived tyrosine phosphatase (EDTP) is a lipid phosphatase essential for oogenesis and muscle function. Loss-of-EDTP is lethal at early developmental stages. Hypomorphic mutation of EDTP causes impaired muscle performance and shortened lifespan. Mutation of MTMR14, a mammalian homolog to EDTP, is associated with muscle fatigue in rodents and a rare genetic disease called centronuclear myopathy in humans. Despite the deleterious consequences, downregulation of MTMR14 promotes autophagy. It is proposed that selective downregulation of EDTP/MTMR14 in non-muscle tissues improves the survivorship to cellular wastes and extends lifespan. Here, we show that downregulation of EDTP in glial cells suppressed the expression of polyglutamine (polyQ) protein aggregates and improved survival. Downregulation of EDTP in glial cells also extended lifespan. These effects were not observed by targeting pan-neurons in the nervous system, suggesting the significance of tissue-specificity. Additionally, flies carrying an EDTP mutant had increased survival to prolonged anoxia and altered dynamics of polyQ expression. These data supported the proposal that selective downregulation of EDTP in non-muscle tissues improved survivorship to cellular protein aggregates and extended lifespan. Our findings suggest that EDTP/MTMR14 could be a novel molecular target for the treatment of neurodegeneration.

Effects of aging on hip abductor-adductor neuromuscular and mechanical performance during the weight transfer phase of lateral protective stepping

Aging brings about challenges in the ability to recover balance through protective stepping, especially in the lateral direction. Previous work has suggested that lateral protective stepping during weight transfer may be affected by impaired muscle composition and performance of the hip abductors (AB) in older adults. Hence, this study investigated the influence of hip abductor-adductor (AB-AD) neuromuscular performance on the weight transfer phase of lateral protective stepping in younger and older adults. Healthy younger (n = 15) and older adults (n = 15) performed hip AB-AD isometric maximal voluntary contractions (IMVC). Lateral balance perturbations were applied via motorized waist-pulls. Participants were instructed to recover their balance using a single lateral step. Kinetic, kinematic and electromyographic (EMG) data were analyzed during the weight transfer phase. In the hip IMVC task, older adults showed reduced peak AB-AD torque, AB rate of torque development and AB-AD rate of EMG neuromuscular activation (RActv). During the lateral balance perturbations, older individuals had a lower incidence of lateral steps, reduced hip AB-AD RActv and delayed weight transfer. However, several outcomes were larger in the older group, such as, center of mass momentum at step onset, step-side peak rate of vertical force development, hip AB net joint torque, and power. Although older adults had greater hip muscular output during the weight transfer phase, their lateral balance recovery was still impaired. The reduced maximal hip AB-AD capacity, especially RActv, may have been a greater contributor to this impairment, as it affects the ability to generate rapid force, crucial for balance recovery.

Effect of Compression Garments on the Development of Delayed-Onset Muscle Soreness: A Multimodal Approach Using Contrast-Enhanced Ultrasound and Acoustic Radiation Force Impulse Elastography.

Delayed-onset muscle soreness (DOMS) is one of the most common reasons for impaired muscle performance in sports. However, little consensus exists regarding which treatments may be most effective, and the underlying mechanisms are poorly understood. To investigate the influence of compression garments on the development of DOMS, focusing on changes in muscle perfusion and muscle stiffness. In this controlled laboratory study with repeated measures, muscle perfusion and stiffness, calf circumference, muscle soreness, passive ankle dorsiflexion, and creatine kinase levels were assessed in participants before (baseline) a DOMS-inducing eccentric calf exercise intervention and 60 hours later (follow-up). After DOMS induction, a sports compression garment (18-21 mmHg) was worn on 1 randomly selected calf until follow-up, while the contralateral calf served as an internal control. Muscle perfusion was assessed using contrast-enhanced ultrasound (peak enhancement and wash-in area under the curve), while muscle stiffness was assessed using acoustic radiation force impulse (shear-wave velocities). A magnetic resonance imaging scan of both lower legs was also performed during the follow-up testing session to characterize the extent of exercise-induced muscle damage. Comparisons were made between limbs and over time. Shear-wave velocity values of the medial gastrocnemius showed a significant interaction between time and treatment (P = .006), with the noncompressed muscle demonstrating lower muscle stiffness values at follow-up compared to baseline or to the compressed muscle. No significant differences in soleus muscle stiffness were noted between limbs or over time, as was the case for muscle perfusion metrics (peak enhancement and wash-in area under the curve) for the medial gastrocnemius and soleus muscles. Further, compression had no significant effect on passive ankle dorsiflexion, muscle soreness, calf circumference, or injury severity, per magnetic resonance imaging. Continuous wearing of compression garments during the inflammation phase of DOMS may play an important role in regulating muscle stiffness; however, compression garments have no significant effects on intramuscular perfusion or other common clinical assessments. J Orthop Sports Phys Ther 2018;48(11):887-894. Epub12 Jun 2018. doi:10.2519/jospt.2018.8038.

Impaired Tissue Oxygenation in Metabolic Syndrome Requires Increased Microvascular Perfusion Heterogeneity.

Metabolic syndrome (MS) in obese Zucker rats (OZR) is associated with impaired skeletal muscle performance and blunted hyperemia. Studies suggest that reduced O2 diffusion capacity is required to explain compromised muscle performance and that heterogeneous microvascular perfusion distribution is critical. We modeled tissue oxygenation during muscle contraction in control and OZR skeletal muscle using physiologically realistic relationships. Using a network model of Krogh cylinders with increasing perfusion asymmetry and increased plasma skimming, we predict increased perfusion heterogeneity and decreased muscle oxygenation in OZR, with partial recovery following therapy. Notably, increasing O2 delivery had less impact on VO2 than equivalent decreases in O2 delivery, providing a mechanism for previous empirical work associating perfusion heterogeneity and impaired O2 extraction. We demonstrate that increased skeletal muscle perfusion asymmetry is a defining characteristic of MS and must be considered to effectively model and understand blood-tissue O2 exchange in this model of human disease.

Effects of mechanical disturbance and salinity stress on bioenergetics and burrowing behavior of the soft-shell clam Mya arenaria.

Bioturbation of sediments by burrowing organisms plays a key role in the functioning of coastal ecosystems. Burrowing is considered an energetically expensive activity, yet the energy costs of burrowing and the potential impacts of multiple stressors (such as salinity stress and wave action) on bioenergetics and burrowing performance of marine bioturbators are not well understood. We investigated the effects of mechanical disturbance and salinity stress on the burrowing behavior, aerobic capacity and energy expense of digging in a common marine bioturbator, the soft-shell clam Mya arenaria from the Baltic Sea (control salinity 15). Mya arenaria showed large individual variability in the burrowing efficiency, with an average of ∼7% of the body energy reserves used per burial. Clams with higher mitochondrial capacity and lower energy expenditure per burial showed higher endurance. Acclimation for 3-4 weeks to low (5) or fluctuating (5-15) salinity reduced the burrowing speed and the number of times the clams can rebury but did not affect the mitochondrial capacity of the whole body or the gill. Acclimation to the fluctuating salinity shifted the predominant fuel use for burrowing from proteins to lipids. Our data indicate that the reduced burrowing performance of clams under the salinity stress is not due to the limitations of energy availability or aerobic capacity but must involve other mechanisms (such as impaired muscle performance). The reduction in the burrowing capacity of clams due to salinity stress may have important implications for survival, activity and ecological functions of the clams in shallow coastal ecosystems.

Adaptive shortening of long flexor in patients with claw hand: A short report

Adaptive shortening of long flexors is the common secondary impairment which can occur in patients with long standing claw hand, particularly in those who do not undergo any supervised physiotherapy programme.¹ The main purpose of this short report is to describe the current physiotherapeutic means which are commonly employed for the management of long flexor tightness. This report further gives an insight into the consequences of the delay in corrective surgery and ultimately describes the dire need for further research on this deformity.² Adaptive shortening of the muscles is a phenomenon which can occur for many reasons, like prolonged immobilisation of the of the body segment, postural imbalance, muscle imbalance, impaired muscle performance due to neuromuscular problems or may be due congenital and acquired deformity.Tightness of the muscles leads to limitation of joint range of motion.³ In leprosy the cause of adaptive shortening of the long flexors is muscle imbalance which occurs due to paralysis of the ulnar nerve at the elbow joint. Adaptive shortening of the muscles is a secondary impairment.⁴ Secondary impairments have multidimensional effects on the management of the deformity, including delay in surgery for the correction of deformity which in turn is responsible for the unemployment, social stigma and problems in social integration.⁵ Secondary impairment in some way or other is responsible for the above stated problems, but adaptive shortening of the long flexor (long flexor tightness) is important because sometimes months of therapy are required to attain full muscle length.

Changes in tibialis anterior corticospinal properties after acute prolonged muscle vibration.

Prolonged local vibration is known to impair muscle performance. While involved mechanisms were previously evidenced at the spinal level, changes at the cortical level were also hypothesized. The aims of the present study were to investigate the effects of 30min of 100-Hz tibialis anterior muscle vibration on force production capacities and to further identify the respective changes in spinal loop properties, descending voluntary drive and corticospinal properties. Thirteen subjects were tested before and after a vibration condition, and before and after a resting control condition. Maximal voluntary contraction (MVC) in dorsiflexion was measured. Transcranial magnetic stimulation was superimposed during MVCs to assess cortical voluntary activation (VATMS), motor-evoked potential amplitude (MEP) and cortical silent period length (CSP). MEP and CSP were also measured during 50 and 75% MVC contractions. Spinal excitability was investigated by mean of H-reflex. There were no vibration effects on MVC (p=0.805), maximal EMG activity (p=0.653), VATMS (p=1), and CSP (p=0.877). Vibration tended to decrease MEP amplitude (p=0.117). H-reflex amplitude was depressed following vibration (p=0.008). Dorsiflexion maximal force production capacities were unaffected by 30min of tibialis anterior muscle vibration, despite spinal loop and corticospinal excitabilities being reduced. These findings suggest that acute prolonged vibration has the potential to modulate corticospinal excitability of lower limb muscles without a concomitant functional consequence.

Warm-up effects from concomitant use of vibration and static stretching after cycling.

Static stretch is routinely used in traditional warm-up but impaired muscle performance. Combining vibration with static stretching as a feasible component may be an alternative to static stretching after submaximal aerobic exercise to improve jumping as well as flexibility. Therefore, the purpose of this study was to investigate and compare the effects of aerobic exercise, static stretching, and vibration with static stretching on flexibility and vertical jumping performance. A repeated measures experimental design was used in this study. Twelve participants randomly underwent 5 different warm-ups including cycling alone (C warm-up), static stretching alone (S warm-up), combining vibration with static stretching (VS warm-up), cycling followed by S (C+S warm-up), and cycling followed by VS (C+VS warm-up) on 5 separate days. Sit-and-reach, squat jump (SJ), and counter movement jump (CMJ) were measured for pre- and post- tests. The sit-and-reach scores after the S, VS, C+S and C+VS warm-ups were significantly enhanced (P<0.001), and were significantly greater than that of the C warm-up (P<0.05). The jumping height of SJ and CMJ after the C and C+VS warm-ups were significantly increased (P<0.05), whereas a significant reduction was found after the S warm-up (P<0.05). Vibration combined with stretching after submaximal cycling exercise (C+VS warm-up) could be a feasible warm-up protocol to improve both flexibility and vertical jump performance, compared with the traditional warm-up (C+S warm-up).

Contribution of the Mitochondria to Locomotor Muscle Dysfunction in Patients With COPD.

COPD is a significant public health challenge, notably set to become the third leading cause of death and fifth leading cause of chronic disability worldwide by the next decade. Skeletal muscle impairment is now recognized as a disabling, extrapulmonary consequence of COPD that is associated with reduced quality of life and premature mortality. Because COPD typically manifests in older individuals, these clinical features may overlie normal age-associated declines in muscle function and performance. Although physical inactivity, oxidative stress, inflammation, hypoxia, malnutrition, and medications all likely contribute to this comorbidity, abetter understanding of the underlying mechanism is needed to develop effective therapies. Mitochondrial alterations have been described; these alterations include reductions in density and oxidative enzyme activity, increased mitochondrial reactive oxygen species production, and induction of muscle proteolysis including autophagy. This review focuses on the perspective that mitochondrial alterations contribute to impaired locomotor muscle performance in patients with COPD by reducing oxidative capacity and thus endurance, as well as by triggering proteolysis and thus contributing to atrophy and weakness. We discuss how the potential underlying mechanisms converge on mitochondria by targeting the peroxisome proliferator-activated receptor γ-coactivator-1α signaling pathway (thereby reducing mitochondrial biogenesis and muscle oxidative capacity and potentially increasing fiber atrophy) and how taking advantage of normal muscle plasticity and mitochondrial biogenesis may reverse this pathophysiology. We propose recent therapeutic strategies aimed at increasing peroxisome proliferator-activated receptor γ-coactivator-1α levels, such as endurance training and exercise mimetic drugs, with the strong rationale for increasing mitochondrial biogenesis and function and thus improving the muscle phenotype in COPD.

Some like it hot: Thermal tolerance and oxygen supply capacity in two eurythermal crustaceans.

Thermal sensitivity of the cardiorespiratory oxygen supply capacity has been proposed as the cardinal link underlying the upper boundary of the temperature niche in aquatic ectotherms. Here we examined the evidence for this link in two eurythermal decapods, the Giant tiger shrimp (Penaeus monodon) and the European crayfish (Astacus astacus). We found that both species have a temperature resistant cardiorespiratory system, capable of maintaining oxygen delivery up to their upper critical temperature (Tcrit). In neither species was Tcrit reduced in hypoxia (60% air saturation) and both species showed an exponential increase in heart and gill ventilation rates up to their Tcrit. Further, failure of action potential conduction in preparations of A. astacus motor neurons coincided with Tcrit, indicating that compromised nervous function may provide the underlying determinant for Tcrit rather than oxygen delivery. At high temperatures, absolute aerobic scope was maintained in P. monodon, but reduced in A. astacus. However, A. astacus also displayed reduced exercise intensity indicating that impaired muscle performance with resulting reduced tissue oxygen demand may explain the reduced scope rather than insufficient oxygen supply capacity. This interpretation agrees with early literature on aquatic ectotherms, correlating loss of nervous function with impaired locomotion as temperatures approach Tcrit.

Physical inactivity promotes contractile dysfunction at the whole tissue, cellular and molecular levels in older adults (1102.29)

Age‐related deficits in skeletal muscle function are likely potentiated by corresponding reductions in volitional physical activity. Our objective was to investigate the effects of chronic muscle disuse by comparing structural and functional properties of skeletal muscle between healthy older adults with limited physical mobility secondary to knee osteoarthritis (Disuse; n=16) and healthy, recreationally‐active older adults (Controls; n=15). Knee extensor strength and cellular and molecular contractile characteristics were assessed from vastus lateralis muscle biopsies. Isometric and isokinetic knee extensor strength were reduced (34‐43%; p&lt;0.01 for all) with disuse, as was single fiber force production in MHC I (18%; p 0.1 for all). Myosin‐actin cross‐bridge kinetic parameters were reduced in MHC I with disuse, as evidenced by prolonged actin‐myosin attachment time (+20%; p &lt;0.01), but not in MHC IIA or IIA/X fibers. A strong trend towards more (+23%; p = 0.06) strongly‐bound cross‐bridges was observed in MHC I fibers with disuse. Considering similar MHC I tension between groups, these data suggest intrinsic impairments in molecular level force production/transmission with disuse. In summary, although cellular level deficits in force production are explained by atrophy, molecular level changes, which are independent of fiber size, may contribute to impaired whole muscle performance observed with chronic muscle disuse.Grant Funding Source: Supported by NIH AG033547