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Contains fulltext : 251269.pdf (Publisher’s version ) (Closed access) Behavioral studies have shown that humans account for inertial acceleration in their decisions of hand choice when reaching during body motion. Physiologically, it is unclear at what stage of movement preparation information about body motion is integrated with the process of hand selection. Here, we addressed this question by applying transcranial magnetic stimulation over left motor cortex (M1) of human participants who performed a preferential reach task while they were sinusoidally translated on a linear motion platform. If M1 only represents a read-out of the final hand choice, we expect the body motion not to affect the motor-evoked potential (MEP) amplitude. If body motion biases the hand selection process before target onset, we expect corticospinal excitability to be influenced by the phase of the motion, with larger MEP amplitudes for phases that show a bias to using the right hand. Behavioral results replicate our earlier findings of a sinusoidal modulation of hand choice bias with motion phase. MEP amplitudes also show a sinusoidal modulation with motion phase, suggesting that body motion influences corticospinal excitability, which may ultimately reflect changes of hand preference. The modulation being present before target onset suggests that competition between hands is represented throughout the corticospinal tract. Its phase relationship with the motion profile indicates that other processes after target onset take up time until the hand selection process has been completely resolved, and the reach is initiated.NEW & NOTEWORTHY Full body-motion biases decisions of hand choice. We examined the signatures of this bias in hand preference in corticospinal excitability before a reach target was presented. Our results show that behavior and corticospinal excitability modulate depending on the state of the body in motion. This suggests that information about body motion penetrates deeply within the motor system. 9 p.

Vibration exercise (VE) has been suggested as an effective training for improving muscle strength and coordination. However, the underlying physiological adaptation processes are not yet fully understood, limiting the development of safe and effective exercise protocols. To better understand the neuromuscular responses elicited by VE, we aimed at investigating the acute effects of superimposed vibration on the Hoffmann reflex (H-reflex), measured after fatiguing exercise. Twenty-five volunteers performed four isometric contractions of the right Flexor Carpi Radialis (FCR) with baseline load at 80% of their maximal voluntary contraction (MVC), both with no vibration and with superimposed vibration at 15, 30, and 45 Hz. Fatigue was estimated by MVC test and estimation of electromyographic spectral compression. H-reflex suppression was estimated as the relative decrease after exercise. Our results show that fatiguing exercise determined a decrease in H-reflex amplitude compared to rest condition while vibration determined a lower H-reflex suppression as compared to no vibration. The superimposition of 30-Hz vibration determined the largest acute reduction in force generating capacity (36 N, p < 0.05) and the lowest H-reflex suppression (20%, p < 0.05). These results suggest VE to be particularly suitable in rehabilitation programs for rapid restoration of muscle form and function after immobilization periods.

Hospitalization may induce a decrease of muscle strength and muscle mass in older patients due to physical inactivity, malnutrition and diseases, negatively affecting health outcome. We aimed to examine the literature on change in muscle strength and muscle mass in older patients during hospitalization. A literature search was performed in major electronic databases from inception to March 2016. Studies including hospitalized patients with a mean age ≥ 65 years, describing change of hand grip strength and/or muscle mass were found eligible. Extracted data were divided in hand grip strength or muscle mass and stratified by elective or acute admission. Meta-analysis was conducted using Comprehensive Meta-analysis. Twenty-five studies were included, describing a total of 1789 patients with a mean age range of 65 to 85.8 years and an overall median length of stay of 14.7 days. Pooled hand grip strength and muscle mass were found to significantly decrease in electively admitted older patients during hospitalization (standardized mean difference (95% confidence interval): − 0.42 (− 0.66, − 0.17) and − 0.44 (− 0.61, − 0.27)), but not in acutely admitted older patients (standardized mean difference (95% confidence interval): 0.18 (− 0.02, 0.37) and − 0.25 (− 0.58, 0.09)). In conclusion, decrease in muscle strength and muscle mass in older patients is dependent on the type of admission.

Hospitalization may induce a decrease of muscle strength and muscle mass in older patients due to physical inactivity, malnutrition and diseases, negatively affecting health outcome. We aimed to examine the literature on change in muscle strength and muscle mass in older patients during hospitalization. A literature search was performed in major electronic databases from inception to March 2016. Studies including hospitalized patients with a mean age≥65years, describing change of hand grip strength and/or muscle mass were found eligible. Extracted data were divided in hand grip strength or muscle mass and stratified by elective or acute admission. Meta-analysis was conducted using Comprehensive Meta-analysis. Twenty-five studies were included, describing a total of 1789 patients with a mean age range of 65 to 85.8years and an overall median length of stay of 14.7days. Pooled hand grip strength and muscle mass were found to significantly decrease in electively admitted older patients during hospitalization (standardized mean difference (95% confidence interval): -0.42 (-0.66, -0.17) and -0.44 (-0.61, -0.27)), but not in acutely admitted older patients (standardized mean difference (95% confidence interval): 0.18 (-0.02, 0.37) and -0.25 (-0.58, 0.09)). In conclusion, decrease in muscle strength and muscle mass in older patients is dependent on the type of admission.

Mechanical vibration applied directly to the muscle belly or tendon has been reported to elicit a specific reflex loop named tonic vibration reflex (TVR), which involves motor unit (MU) activation synchronized and un-synchronized within the vibration cycle. Indirect application of vibration to the muscle by vibration exercise (VE) has also been suggested to evoke TVR, as evidenced by the spectral peaks observed at the vibration frequency in the surface electromyography (sEMG). However, other studies interpreted these spectral peaks as the result of motion artifacts (MAs). The aim of the present study is, therefore, to investigate MU activation patterns during VE in order to clarify the nature of those spectral peaks. To this end, low-intensity isometric contractions were executed with and without VE, and high-density sEMG measurements were performed during the contraction tasks. MU action potential (MUAP) trains were extracted by decomposing the recorded high-density sEMG signals. The spectra of the MUAP trains were then calculated and compared between vibration and no-vibration conditions. Clear MU synchronization was observed during VE, confirming the spectral peaks at the vibration frequency to be mainly due to the reflex loop rather than MAs.

Background Due to the post-mitotic nature of myonuclei, postnatal myogenesis is essential for skeletal muscle growth, repair, and regeneration. This process is facilitated by satellite cells through proliferation, differentiation, and subsequent fusion with a pre-existing muscle fiber (i.e., myonuclear accretion). Current knowledge of myogenesis is primarily based on the in vitro formation of syncytia from myoblasts, which represents aspects of developmental myogenesis, but may incompletely portray postnatal myogenesis. Therefore, we aimed to develop an in vitro model that better reflects postnatal myogenesis, to study the cell intrinsic and extrinsic processes and signaling involved in the regulation of postnatal myogenesis. Methods Proliferating C2C12 myoblasts were trypsinized and co-cultured for 3 days with 5 days differentiated C2C12 myotubes. Postnatal myonuclear accretion was visually assessed by live cell time-lapse imaging and cell tracing by cell labeling with Vybrant® DiD and DiO. Furthermore, a Cre/LoxP-based cell system was developed to semi-quantitatively assess in vitro postnatal myonuclear accretion by the conditional expression of luciferase upon myoblast–myotube fusion. Luciferase activity was assessed luminometrically and corrected for total protein content. Results Live cell time-lapse imaging, staining-based cell tracing, and recombination-dependent luciferase activity, showed the occurrence of postnatal myonuclear accretion in vitro. Treatment of co-cultures with the myogenic factor IGF-I (p

BACKGROUND: Muscle mass, strength, and power are known determinants of mobility in older adults but there is limited knowledge on the influence of muscle architecture or tendon properties on mobility. The purpose of this study was to examine the relationship between mobility and plantarflexor muscle-tendon properties in healthy older adults.METHODS: A total of 52 subjects (age 70-81 years) were measured for 6-minute walk test (6MWT), timed "up and go"-test (TUG), isometric plantarflexion strength, Achilles tendon stiffness, triceps surae muscle architecture, lower extremity lean mass, isometric leg extension strength, and leg extension power. Partial correlations and multivariate regression models adjusted for sex, age, body mass, and height were used to examine the relationship between mobility (6MWT and TUG) and lower limb muscle-tendon properties.RESULTS: Multivariate regression models revealed that Achilles tendon stiffness (p = .020), plantarflexion strength (p = .022), and medial gastrocnemius fascicle length (p = .046) were independently associated with 6MWT. Plantarflexion strength (p = .037) and soleus fascicle length (p = .031) were independently associated with TUG.CONCLUSIONS: Plantarflexor muscle-tendon properties were associated with mobility in older adults independent of lower extremity lean mass, leg extension strength, or power. Plantarflexion strength was a stronger predictor of mobility than leg extension strength or power. The novel finding of this study was that muscle architecture and tendon properties explained interindividual differences in mobility. This study highlights the importance of the plantarflexors for mobility in older adults and provides understanding of possible mechanisms of age-related decline in mobility.

International audience; During ageing skeletal muscles undergo a process of structural and functional remodelling that leads to sarcopenia, a syndrome characterized by loss of muscle mass and force and a major cause of physical frailty. To determine the causes of sarcopenia and identify potential targets for interventions aimed at mitigating ageing-dependent muscle wasting, we focussed on the main signalling pathway known to control protein turnover in skeletal muscle, consisting of the insulin-like growth factor 1 (IGF1), the kinase Akt and its downstream effectors, the mammalian target of rapamycin (mTOR) and the transcription factor FoxO. Expression analyses at the transcript and protein level, carried out on well-characterized cohorts of young, old sedentary and old active individuals and on mice aged 200, 500 and 800 days, revealed only modest age-related differences in this pathway. Our findings suggest that during ageing there is no downregulation of IGF1/Akt pathway and that sarcopenia is not due to FoxO activation and upregulation of the proteolytic systems. A potentially interesting result was the increased phosphorylation of the ribosomal protein S6, indicative of increased activation of mTOR complex1 (mTORC1), in aged mice. This result may provide the rationale why rapamycin treatment and caloric restriction promote longevity, since both interventions blunt activation of mTORC1; however, this change was not statistically significant in humans. Finally, genetic perturbation of these pathways in old mice aimed at promoting muscle hypertrophy via Akt overexpression or preventing muscle loss through inactivation of the ubiquitin ligase atrogin1 were found to paradoxically cause muscle pathology and reduce lifespan, suggesting that drastic activation of the IGF1-Akt pathway may be counterproductive, and that sarcopenia is accelerated, not delayed, when protein degradation pathways are impaired.

It is known that adipose tissue mass increases with age, and that a number of hormones, collectively called adipokines, are produced by adipose tissue. For most of them it is not known whether their plasmatic levels change with age. Moreover, it is known that adipose tissue infiltration in skeletal muscle is related to sarcopenia and loss of muscle strength. In this study we investigated the age-related changes of representative adipokines and insulin-like growth factor (IGF)-1 and their effect on muscle strength. We studied the association between circulating levels of adiponectin, leptin, resistin and IGF-1 and muscle strength. This cross-sectional study included 412 subjects of different age (152 subjects aged 18-30 years and 260 subjects aged 69-81 years) recruited within the framework of the European research network project "Myoage". The levels of adiponectin (both in male and female subjects) and leptin (only in males) were significantly higher in old subjects compared to young, while those of IGF-1 were lower in old subjects. In old subjects adiponectin, resistin and the resistin/IGF-1 ratio (but not IGF-1 alone) were inversely associated with quadriceps torque, while only adiponectin was inversely associated with handgrip strength independently from percentage of fat mass, height, age, gender and geographical origin. The ratio of leptin to adiponectin was directly associated with handgrip strength in both young and old subjects. These results suggest that in humans the age-associated loss of strength is associated with the levels of representative adipokines and IGF-1.

The mechanisms controlling skeletal muscle oxygen consumption (V(o)₂) during exercise are not well understood. We determined whether first-order control could explain V(o)₂kinetics at contractions onset (V(o)₂(on)) and cessation (V(o)₂off)) in single skeletal muscle fibres differing in oxdidative capacity, and across stimulation intensities up to V(o)₂(max). Xenopus laevis fibres (n = 21) were suspended in a sealed chamber with a fast response P(o)₂ electrode to measure V(o)₂ every second before, during and after stimulated isometric contractions. A first-order model did not well characterize on-transient V(o)₂ kinetics. Including a time delay (TD) in the model provided a significantly improved characterization than a first-order fit without TD (F-ratio; P < 0.05), and revealed separate 'activation' and 'exponential' phases in 15/21 fibres contracting at V(o)₂(max) (mean ± SD TD: 14 ± 3s). On-transient kinetics (τV(o)₂(on)) was weakly and linearly related to V(o)₂(max) (R² = 0.271, P = 0.015). Off-transient kinetics, however, were first-order, and τV(o)₂(off) was greater in low-oxidative (V(o)₂max < 0.05 nmol mm⁻³s⁻¹ than high-oxidative fibres (V(o)₂(max > 0.10 nmol mm ⁻³ s⁻¹; 170 ± 70 vs. 29 ± 6 s, P < 0.001). 1/ τV(o)₂(off) was proportional to V(o)₂(max) (R² = 0.727, P < 0.001), unlike in the on-transient. The calculated oxygen deficit was larger (P < 0.05) than the post-contraction volume of consumed oxygen at all intensities except V(o)₂(max). These data show a clear dissociation between the kinetic control of V(o)₂at the onset and cessation of contractions and across stimulation intensities. More complex models are therefore required to understand the activation of mitochondrial respiration in skeletal muscle at the start of exercise.

Precise determination of the effect of muscle temperature (Tm) on mitochondrial oxygen consumption kinetics has proven difficult in humans, in part due to the complexities in controlling for Tm-related variations in blood flow, fiber recruitment, muscle metabolism, and contractile properties. To address this issue, intracellular Po2(PiO2) was measured continuously by phosphorescence quenching following the onset of contractions in single Xenopus myofibers ( n = 24) while controlling extracellular temperature. Fibers were subjected to two identical contraction bouts, in random order, at 15°C (cold, C) and 20°C (normal, N; n = 12), or at N and 25°C (hot, H; n = 12). Contractile properties were determined for every contraction. The time delay of the PiO2response was significantly greater in C (59 ± 35 s) compared with N (35 ± 26 s, P = 0.01) and H (27 ± 14 s, P = 0.01). The time constant for the decline in PiO2was significantly greater in C (89 ± 34 s) compared with N (52 ± 15 s; P < 0.01) and H (37 ± 10 s; P < 0.01). There was a linear relationship between the rate constant for PiO2kinetics and Tm( r = 0.322, P = 0.03). Estimated ATP turnover was significantly greater in H than in C ( P < 0.01), but this increased energy requirement alone with increased Tmcould not account for the differences observed in PiO2kinetics among conditions. These results demonstrate that PiO2kinetics in single contracting myofibers are dependent on Tm, likely caused by temperature-induced differences in metabolic demand and by temperature-dependent processes underlying mitochondrial activation at the start of muscle contractions.

OBJECTIVE: Beneficial effects, including improved muscle strength and power performance, have been observed during vibration exercise (VE) and partially ascribed to a specific reflex mechanism referred to as Tonic vibration reflex (TVR). TVR involves motor unit (MU) activation synchronized and un-synchronized with the vibration cycle; this suggests VE to alter the temporal MU recruitment strategy. However, the effects of VE on MU recruitment remain poorly understood. This study aims to elucidate the influence of VE on MU recruitment indirectly, by investigating the effects of low-intensity VE on muscle activation. APPROACH: Twenty volunteers performed isometric contractions on the biceps brachii of the right arm at a baseline (low) force equal to 30% of the maximum voluntary contraction without vibration (control) and with vibration at 20, 30, 40, and 55 Hz. Three vibration amplitudes were employed at 12.5%, 25%, and 50% of the baseline. Mean muscle-fiber conduction velocity (mCV), mean frequency (MF), and root mean square (RMS) value were estimated from surface electromyography as indicators of the alteration in MU recruitment strategies. MAIN RESULTS: The mCV estimates during VE were significantly (p

Contains fulltext : 87888.pdf (Publisher’s version ) (Closed access) Hypoxia may be one of the factors underlying muscle dysfunction during ageing and chronic lung and heart failure. Here we tested the hypothesis that chronic hypoxia per se affects contractile properties of single fibres of the soleus and diaphragm muscle. To do this, the force-velocity relationship, rate of force redevelopment and calcium sensitivity of single skinned fibres from normoxic rats and rats exposed to 4 weeks of hypobaric hypoxia (410 mmHg) were investigated. The reduction in maximal force (P(0)) after hypoxia (p=0.031) was more pronounced in type IIa than type I fibres and was mainly attributable to a reduction in fibre cross-sectional area (p=0.044). In type IIa fibres this was aggravated by a reduction in specific tension (p=0.001). The maximal velocity of shortening (V (max)) and shape of the force velocity relation (a/P(0)), however, did not differ between normoxic and hypoxic muscle fibres and the reduction in maximal power of hypoxic fibres (p=0.012) was mainly due to a reduction in P(0). In conclusion, chronic hypoxia causes muscle fibre dysfunction which is not only due to a loss of muscle mass, but also to a diminished force generating capacity of the remaining contractile material. These effects are similar in the soleus and diaphragm muscle, but more pronounced in type IIa than I fibres. 01 oktober 2010

AIM: To determine whether inhalation of carbon monoxide (CO), resulting in carboxyhaemoglobin (COHb) levels observed in smokers, had an effect on muscle fatigue during electrically evoked and voluntary muscle contractions.METHODS: Young non-smoking males inspired CO from a Douglas bag until their COHb level reached 6%. During the control condition the same participants inspired ambient air from a Douglas bag for 6 min. Fatigue was assessed as the decline in torque in isometric knee extensions, during 2 min of electrically evoked contractions (30 Hz, 1 s on, 1 s off) and during 2 min of maximal isometric voluntary contractions (1 s on, 1 s off). A fatigue index (FI) was calculated as the ratio of final torque : initial torque. Time to peak torque (TPT) and half relaxation time ((1/2)RT) were also determined for the electrically evoked contractions.RESULTS: The FI during both the voluntary fatigue test (control: 0.80 +/- 0.09 vs. CO: 0.70 +/- 0.08; mean +/- SD) and that of the fatigue test with electrically evoked contractions (control: 0.61 +/- 0.09 vs. CO: 0.53 +/- 0.12) was significantly lower after CO inhalation than after inhalation of ambient air (P < 0.05). There was, however, no effect of CO on the changes in TPT or (1/2)RT during the fatigue test.CONCLUSION: Carbon monoxide inhalation resulting in COHb levels found in smokers has an acute impact on the ability of the muscle to resist fatigue.

PURPOSE: This study aimed to determine the effect of passive insulation versus external heating during recovery after a sprint-specific warm-up on thigh muscle temperature and subsequent maximal sprint performance.METHODS: On three separate occasions, 11 male cyclists (age = 24.7 ± 4.2 yr, height = 1.82 ± 0.72 m, body mass = 77.9 ± 9.8 kg; mean ± SD) completed a standardized 15-min intermittent warm-up on a cycle ergometer, followed by a 30-min passive recovery period before completing a 30-s maximal sprint test. Muscle temperature was measured in the vastus lateralis at 1, 2, and 3 cm depth before and after the warm-up and immediately before the sprint test. Absolute and relative peak power output was determined and blood lactate concentration was measured immediately after exercise. During the recovery period, participants wore a tracksuit top and (i) standard tracksuit pants (CONT), (ii) insulated athletic pants (INS), or (iii) insulated athletic pants with integrated electric heating elements (HEAT).RESULTS: Warm-up increased Tm by approximately 2.5 °C at all depths, with no differences between conditions. During recovery, Tm remained elevated in HEAT compared with INS and CONT at all depths (P < 0.001). Both peak and relative power output were elevated by 9.6% and 9.1%, respectively, in HEAT compared with CONT (both P < 0.05). The increase in blood lactate concentration was greater (P < 0.05) after sprint in HEAT (6.3 ± 1.8 mmol·L(-1)) but not INS (4.0 ± 1.8 mmol·L(-1)) versus CONT (4.1 ± 1.9 mmol·L(-1)).CONCLUSIONS: Passive heating of the thighs between warm-up completion and performance execution using pants incorporating electrically heated pads can attenuate the decline in Tm and improve sprint cycling performance.

Within the European multi-centre MyoAge project, one workpackage was designed to investigate the contribution of age-related changes to muscle mass, contractile characteristics and neural control in relation to reductions in mobility in older age. The methodology has been described here. Test centres were located in Manchester, UK; Paris, France; Leiden, The Netherlands; Tartu, Estonia and Jyväskylä, Finland. In total, 182 young (18-30 years old, 52.2 % female) and 322 older adults (69-81 years old, 50 % female) have been examined. The participants were independent living, socially active and free from disease that impaired mobility levels. The older participants were selected based on physical activity levels, such that half exceeded current recommended physical activity levels and the other half had lower physical activity levels than is recommended to maintain health. Measurements consisted of blood pressure; anthropometry and body composition (dual-energy X-ray absorptiometry and magnetic resonance imaging); lung function; standing balance and cognitive function (CANTAB). Mobility was assessed using the Timed Up and Go, a 6 min walk, activity questionnaires and accelerometers to monitor habitual daily activities. Muscle strength, power, fatigue and neural activation were assessed using a combination of voluntary and electrically stimulated contractions. Fasting blood samples and skeletal muscle biopsies were collected for detailed examination of cell and molecular differences between young and older individuals. The results from this study will provide a detailed insight into "normal, healthy" ageing, linking whole-body function to the structure and function of the neuromuscular system and the molecular characteristics of skeletal muscle.

The mechanisms controlling skeletal muscle oxygen consumption (V(o)₂) during exercise are not well understood. We determined whether first-order control could explain V(o)₂kinetics at contractions onset (V(o)₂(on)) and cessation (V(o)₂off)) in single skeletal muscle fibres differing in oxdidative capacity, and across stimulation intensities up to V(o)₂(max). Xenopus laevis fibres (n = 21) were suspended in a sealed chamber with a fast response P(o)₂ electrode to measure V(o)₂ every second before, during and after stimulated isometric contractions. A first-order model did not well characterize on-transient V(o)₂ kinetics. Including a time delay (TD) in the model provided a significantly improved characterization than a first-order fit without TD (F-ratio; P < 0.05), and revealed separate 'activation' and 'exponential' phases in 15/21 fibres contracting at V(o)₂(max) (mean ± SD TD: 14 ± 3s). On-transient kinetics (τV(o)₂(on)) was weakly and linearly related to V(o)₂(max) (R² = 0.271, P = 0.015). Off-transient kinetics, however, were first-order, and τV(o)₂(off) was greater in low-oxidative (V(o)₂max < 0.05 nmol mm⁻³s⁻¹ than high-oxidative fibres (V(o)₂(max > 0.10 nmol mm ⁻³ s⁻¹; 170 ± 70 vs. 29 ± 6 s, P < 0.001). 1/ τV(o)₂(off) was proportional to V(o)₂(max) (R² = 0.727, P < 0.001), unlike in the on-transient. The calculated oxygen deficit was larger (P < 0.05) than the post-contraction volume of consumed oxygen at all intensities except V(o)₂(max). These data show a clear dissociation between the kinetic control of V(o)₂at the onset and cessation of contractions and across stimulation intensities. More complex models are therefore required to understand the activation of mitochondrial respiration in skeletal muscle at the start of exercise.

The aim of this study was to investigate in control subjects the effect of imagery training on the torque of plantar-flexor muscles of the ankle. Twenty-nine subjects were allocated to one of three groups that performed either imagery training, low-intensity strength training, or no training (only measurements). The low-intensity training served as an attention control group. Plantar-flexor torques were measured before, during, directly after, and 4 weeks after the training period. At the end of a 7-week training program, significant differences were observed between the maximal voluntary torque production of the imagery training group (136.3 +/- 21.8% of pretraining torque) vs. the low-intensity training group (112.9 +/- 29.0%; P < 0.02) and the control group (113.6 +/- 19.2%; P < 0.02). The results of this study show that imagery training of lower leg muscles significantly increased voluntary torque production of the ankle plantar-flexor muscles and that the force increase was not due to nonspecific motivational effects. Such muscle strengthening effects might be beneficial in rehabilitation for improving or maintaining muscle torque after immobilization.