988 resultados para Muscle force


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Background and Objectives: There are some indications that low-level laser therapy (LLLT) may delay the development of skeletal muscle fatigue during high-intensity exercise. There have also been claims that LED cluster probes may be effective for this application however there are differences between LED and laser sources like spot size, spectral width, power output, etc. In this study we wanted to test if light emitting diode therapy (LEDT) can alter muscle performance, fatigue development and biochemical markers for skeletal muscle recovery in an experimental model of biceps humeri muscle contractions. Study Design/Materials and Methods: Ten male professional volleyball players (23.6 [SD +/- 5.6] years old) entered a randomized double-blinded placebo-controlled crossover trial. Active cluster LEDT (69 LEDs with wavelengths 660/850 nm, 10/30 mW, 30 seconds total irradiation time, 41.7J of total energy irradiated) or an identical placebo LEDT was delivered under double-blinded conditions to the middle of biceps humeri muscle immediately before exercise. All subjects performed voluntary biceps humeri contractions with a workload of 75% of their maximal voluntary contraction force (MVC) until exhaustion. Results: Active LEDT increased the number of biceps humeri contractions by 12.9% (38.60 [SD +/- 9.03] vs. 34.20 [SD +/- 8.68], P = 0.021) and extended the elapsed time to perform contractions by 11.6% (P = 0.036) versus placebo. In addition, post-exercise levels of biochemical markers decreased significantly with active LEDT: Blood Lactate (P = 0.042), Creatine Kinase (P = 0.035), and C-Reative Protein levels (P = 0.030), when compared to placebo LEDT. Conclusion: We conclude that this particular procedure and dose of LEDT immediately before exhaustive biceps humeri contractions, causes a slight delay in the development of skeletal muscle fatigue, decreases post-exercise blood lactate levels and inhibits the release of Creatine Kinase and C-Reative Protein. Lasers Surg. Med. 41:572-577, 2009. (C) 2009 Wiley-Liss, Inc.

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This study aimed to investigate the effect of 830 nm low-level laser therapy (LLLT) on skeletal muscle fatigue. Ten healthy male professional volleyball players entered a crossover randomized double-blinded placebo-controlled trial. Active LLLT (830 nm wavelength, 100 mW output, spot size 0.0028 cm(2), 200 s total irradiation time) or an identical placebo LLLT was delivered to four points on the biceps humeri muscle immediately before exercises. All subjects performed voluntary biceps humeri contractions with a load of 75% of the maximum voluntary contraction (MVC) force until exhaustion. After active LLLT the mean number of repetitions was significantly higher than after placebo irradiation [mean difference 4.5, standard deviation (SD) +/- 6.0, P = 0.042], the blood lactate levels increased after exercises, but there was no significant difference between the treatments. We concluded that 830 nm LLLT can delay the onset of skeletal muscle fatigue in high-intensity exercises, in spite of increased blood lactate levels.

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Background. Impaired hand function is common in patients with arthritis and it affects performance of daily activities; thus, hand exercises are recommended. There is little information on the extent to which the disease affects activation of the flexor and extensor muscles during these hand-dexterity tasks. The purpose of this study was to compare muscle activation during such tasks in subjects with arthritis and in a healthy reference group. Methods. Muscle activation was measured in m. extensor digitorium communis (EDC) and in m. flexor carpi radialis (FCR) with surface electromyography (EMG) in women with rheumatoid arthritis (RA, n = 20), hand osteoarthritis (HOA, n = 16) and in a healthy reference group (n = 20) during the performance of four daily activity tasks and four hand exercises. Maximal voluntary isometric contraction (MVIC) was measured to enable intermuscular comparisons, and muscle activation is presented as %MVIC. Results. The arthritis group used a higher %MVIC than the reference group in both FCR and EDC when cutting with a pair of scissors, pulling up a zipper and—for the EDC—also when writing with a pen and using a key (p < 0.02). The exercise “rolling dough with flat hands” required the lowest %MVIC and may be less effective in improving muscle strength. Conclusions. Women with arthritis tend to use higher levels of muscle activation in daily tasks than healthy women, and wrist extensors and flexors appear to be equally affected. It is important that hand training programs reflect real-life situations and focus also on extensor strength.

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This study investigated whether there was a worsening of the neuromuscular capacity of older adults after the seventh decade of life. The results suggest that the age-related deterioration in maximal strength measures and rapid force production characteristics in older adults could be related to a reduction in the mass and neural activation of the thigh muscles.

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The purpose of the study was to quantify the strength of motor unit synchronization and coherence from pairs of concurrently active motor units before and after short-term (4–8 weeks) strength training of the left first dorsal interosseous (FDI) muscle. Five subjects (age 24.8 ± 4.3 years) performed a training protocol three times/week that consisted of six sets of ten maximal isometric index finger abductions, whereas three subjects (age 27.3 ± 6.7 years) acted as controls. Motor unit activity was recorded from pairs of intramuscular electrodes in the FDI muscle with two separate motor unit recording sessions obtained before and after strength training (trained group) or after 4 weeks of normal daily activities that did not involve training (control group). The training intervention resulted in a 54% (45.2 ± 8.3 to 69.5 ± 13.8 N, P = 0.001) increase in maximal index finger abduction force, whereas there was no change in strength in the control group. A total of 163 motor unit pairs (198 single motor units) were examined in both subject groups, with 52 motor unit pairs obtained from 10 recording sessions before training and 51 motor unit pairs from 10 recording sessions after training. Using the cross-correlation procedure, there was no change in the strength of motor unit synchronization following strength training (common input strength index; 0.71 ± 0.41 to 0.67 ± 0.43 pulses/s). Furthermore, motor unit coherence z scores at low (0–10 Hz; 3.9 ± 0.3 before to 4.4 ± 0.4 after) or high (10–30 Hz; 1.7 ± 0.1 before to 1.9 ± 0.1 after) frequencies were not influenced by strength training. These motor unit data indicate that increases in strength following several weeks of training a hand muscle are not accompanied by changes in motor unit synchronization or coherence, suggesting that these features of correlated motor unit activity are not important in the expression of muscle strength.

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The effects of two amino acids, arginine which has a positively charged side-chain and glutamate which has a negatively charged side-chain on the Ca2+-activation properties of the contractile apparatus were examined in four structurally and functionally different types of skeletal muscle; long- and short-sarcomere fibres from the claw muscle of the yabby (a freshwater decapod crustacean), and fast- and slow-twitch fibres from limb muscles of the rat. Single skinned fibres were activated in carefully balanced solutions of different pCa (-log10[Ca2+]) that either contained the test solute (“test”) or not (“control”). The effect of phosphoarginine, a phosphagen that bears a nett negative charge, was also compared to the effects of arginine. Results show that (i) arginine (33-36 mmol l-1) significantly shifted the force–pCa curve by 0.08–0.13 pCa units in the direction of increased sensitivity to Ca2+-activated contraction in all fibre types; (ii) phosphoarginine (9–10 mmol l-1) induced a significant shift of the force–pCa curve by 0.18–0.24 pCa units in the direction of increased sensitivity to Ca2+ in mammalian fast- and slow-twitch fibres, but had no significant effects on the force–pCa relation in either long- or short-sarcomere crustacean fibres; (iii) glutamate (36–40 mmol l-1), like arginine affected the force–pCa relation of all fibre types investigated, but in the opposite direction, causing a significant decrease in the sensitivity to Ca2+-activated contraction by 0.08–0.19 pCa units; (iv) arginine, phosphoarginine and glutamate had little or no effect on the maximum Ca2+-activated force of crustacean and mammalian fibres. The results suggest that the opposing effects of glutamate and arginine are not related to simply their charge structure, but must involve complex interactions between these molecules, Ca2+ and the regulatory and other myofibrillar proteins.

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This investigation was undertaken to determine if there are altered histological, pathological and contractile properties in presymptomatic or endstage diseased muscle fibres from representative slow-twitch and fast-twitch muscles of SOD1 G93A mice in comparison to wildtype mice. In presymptomatic SOD1 G93A mice, there was no detectable peripheral dysfunction, providing evidence that muscle pathology is secondary to motor neuronal dysfunction. At disease endstage however, single muscle fibre contractile analysis demonstrated that fast-twitch muscle fibres and neuromuscular junctions are preferentially affected by amyotrophic lateral sclerosis-induced denervation, being unable to produce the same levels of force when activated by calcium as muscle fibres from their age-matched controls. The levels of transgenic SOD1 expression, aggregation state and activity were also examined in these muscles but there no was no preference for muscle fibre type. Hence, there is no simple correlation between SOD1 protein expression/activity, and muscle fibre type vulnerability in SOD1 G93A mice.

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During gait termination at normal walking speed, older adults more frequently employ two-step responses, increasing their stopping distance and stopping time more than younger controls. This study investigated ageing effects on lower limb muscle recruitment patterns during stopping at three walking speeds. Twelve young male (26±3.7 years, range 19–30) and 12 gender-matched older participants (72±4.3 years, range 65–82) terminated walking at normal, medium and maximum speed. A visual stopping stimulus was presented 10 ms following either left or right heel-contact with no stimulus (catch) on 30% of trials. Electromyographic (EMG) activity was recorded from the tibialis anterior (TA), soleus (SOL), biceps femoris (BF), vastus lateralis (VL) and gluteus medius (GM). Older males more frequently (46% of trials) took two-steps to stop than young males (20%). The stance leg muscles responded significantly faster than the swing leg, and with increased speed, fewer swing limb muscles contributed to stopping. Older males were slower to respond with the stance leg, at 215 ms following the stimulus compared with 176 ms for the younger group. They also recruited fewer swing leg muscles with less frequent activation of the soleus and gluteus medius. Failure to activate muscles would provide less extensor torque to maintain the centre of gravity anterior to the forward base of support. This would decrease the total force opposing horizontal velocity in order to bring the body to rest and, as a consequence, encourage an additional step prior to stopping.

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Isonitrogenous amounts of two protein sources differing in rumen degradation rate and in lipid composition were fed to sheep with or without a rapidly fermentable cereal grain. The effects on intake, carcass leanness, and muscle fatty acid (FA) composition were examined. Thirty-eight crossbred wether lambs (9 mo, 35 to 48 kg) were allocated by stratified randomization to six treatment groups: 1) basal diet of alfalfa hay:oat hay (20:80) ad libitum = basal; 2) basal + lupin (358 g DM/d) = lupin; 3) basal + fish meal (168 g DM/d) = fish meal; 4) basal + barley (358 g DM/d) = barley; 5) basal + barley + lupin (179 + 179 g DM/d) = barley/lupin; or 6) basal + barley + fish meal (179 + 84 g DM/d) = barley/ fish meal. Lambs were fed individually. Dietary treatments were imposed for 8 wk, and the supplements were offered at 2-d intervals. Daily feed intake and weekly BW of lambs were recorded. At the end of the feeding period lambs were slaughtered after an overnight fast. Hot carcass weight (HCW) and fat depth (GR; total fat and muscle tissue depth at 12th rib, 110 mm from midline) were recorded. At 24 h postmortem samples of longissimus thoracis (LT) and longissimus lumborum (LL) muscles were taken from chilled (4 deg C) carcasses for the assessment of FA composition and meat tenderness, respectively. Lambs fed lupin or fish meal with or without barley had heavier slaughter weights (P < 0.004) and HCW (P < 0.001) than lambs fed basal or barley when initial BW was included as a covariate. The lupin diet also resulted in heavier carcasses (P < 0.05) than the fish meal or barley/fish meal diets. With GR as an indicator, fish meal and barley/ fish meal diets produced leaner carcasses (P < 0.01) than lupin and barley/lupin lambs. Long-chain n-3 FA content [20:5n-3 (P < 0.001), 22:5n-3 (P < 0.003), and 22:6n-3 (P < 0.001)] in the LT muscle were substantially higher with the fish meal and barley/fish meal diets, whereas muscle total n-6 FA was increased (P < 0.003) by lupin and barley/lupin compared with all other diets. Thus, increased muscle long-chain n-3 FA content occurred without an increase in fatness measured as GR, whereas increased muscle n-6 FA content was associated with an increase in carcass fatness. Under these circumstances, a reduction in carcass fatness had no effect on meat tenderness measured as Warner-Bratzler shear force.

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OBJECTIVE: We have previously shown in humans that local infusion of a nitric oxide synthase (NOS) inhibitor into the femoral artery attenuates the increase in leg glucose uptake during exercise without influencing total leg blood flow. However, rodent studies examining the effect of NOS inhibition on contraction-stimulated skeletal muscle glucose uptake have yielded contradictory results. This study examined the effect of local infusion of an NOS inhibitor on skeletal muscle glucose uptake (2-deoxyglucose) and capillary blood flow (contrast-enhanced ultrasound) during in situ contractions in rats.

RESEARCH DESIGN AND METHODS: Male hooded Wistar rats were anesthetized and one hindleg electrically stimulated to contract (2 Hz, 0.1 ms) for 30 min while the other leg rested. After 10 min, the NOS inhibitor NG-nitro-L-arginine methyl ester (L-NAME) (arterial concentration of 5 µmol/l) or saline was infused into the epigastric artery of the contracting leg.

RESULTS: Local NOS inhibition had no effect on blood pressure, heart rate, or muscle contraction force. Contractions increased (P < 0.05) skeletal muscle NOS activity, and this was prevented by L-NAME infusion. NOS inhibition caused a modest significant (P < 0.05) attenuation of the increase in femoral blood flow during contractions, but importantly there was no effect on capillary recruitment. NOS inhibition attenuated (P < 0.05) the increase in contraction-stimulated skeletal muscle glucose uptake by ~35%, without affecting AMP-activated protein kinase (AMPK) activation.

CONCLUSIONS: NOS inhibition attenuated increases in skeletal muscle glucose uptake during contraction without influencing capillary recruitment, suggesting that NO is critical for part of the normal increase in skeletal muscle fiber glucose uptake during contraction.

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Cerebral amyloid angiopathy (CAA) is a major feature of Alzheimer's disease pathology. In CAA, degeneration of vascular smooth muscle cells (VSMCs) occurs close to regions of the basement membrane where the amyloid protein (Aβ) builds up. In this study, the possibility that Aβ disrupts adhesive interactions between VSMCs and the basement membrane was examined. VSMCs were cultured on a commercial basement membrane substrate (Matrigel). The presence of Aβ in the Matrigel decreased cell-substrate adhesion and cell viability. Full-length oligomeric Aβ was required for the effect, as N- and C-terminally truncated peptide analogues did not inhibit adhesion. Aβ that was fluorescently labelled at the N-terminus (fluo-Aβ) bound to Matrigel as well as to the basement membrane heparan sulfate proteoglycan (HSPG) perlecan and laminin. Adhesion of VSMCs to perlecan or laminin was decreased by Aβ. As perlecan influences VSMC viability through the extracellular signal-regulated kinase (ERK)1/2 signalling pathway, the effect of Aβ1–40 on ERK1/2 phosphorylation was examined. The level of phospho-ERK1/2 was decreased in cells following Aβ treatment. An inhibitor of ERK1/2 phosphorylation enhanced the effect of Aβ on cell adhesion. The studies suggest that Aβ can decrease VSMC viability by disrupting VSMC–extracellular matrix (ECM) adhesion.

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Calcineurin activation ameliorates the dystrophic pathology of hindlimb muscles in mdx mice and decreases their susceptibility to contraction damage. In mdx mice, the diaphragm is more severely affected than hindlimb muscles and more representative of Duchenne muscular dystrophy. The constitutively active calcineurin A transgene (CnA) was overexpressed in skeletal muscles of mdx (mdx CnA*) mice to test whether muscle morphology and function would be improved. Contractile function of diaphragm strips and extensor digitorum longus and soleus muscles from adult mdx CnA* and mdx mice was examined in vitro. Hindlimb muscles from mdx CnA* mice had a prolonged twitch time course and were more resistant to fatigue. Because of a slower phenotype and a decrease in fiber cross-sectional area, normalized force was lower in fast- and slow-twitch muscles of mdx CnA* than mdx mice. In the diaphragm, despite a slower phenotype and a 35% reduction in fiber size, normalized force was preserved. This was likely mediated by the reduction in the area of the diaphragm undergoing degeneration (i.e., mononuclear cell and connective and adipose tissue infiltration). The proportion of centrally nucleated fibers was reduced in mdx CnA* compared with mdx mice, indicative of improved myofiber viability. In hindlimb muscles of mdx mice, calcineurin activation increased expression of markers of regeneration, particularly developmental myosin heavy chain isoform and myocyte enhancer factor 2A. Thus activation of the calcineurin signal transduction pathway has potential to ameliorate the mdx pathophysiology, especially in the diaphragm, through its effects on muscle degeneration and regeneration and endurance capacity.

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Damaged skeletal muscle fibres are replaced with new contractile units via muscle regeneration. Regenerating muscle fibres synthesize functionally distinct isoforms of contractile and regulatory proteins but little is known of their functional properties during the regeneration process. An advantage of utilizing single muscle fibre preparations is that assessment of their function is based on the overall characteristics of the contractile apparatus and regulatory system and as such, these preparations are sensitive in revealing not only coarse, but also subtle functional differences between muscle fibres. We examined the Ca2+- and Sr2+-activated contractile characteristics of permeabilized fibres from rat fast-twitch (extensor digitorum longus) and slow-twitch (soleus) muscles at 7, 14 and 21 days following myotoxic injury, to test the hypothesis that fibres from regenerating fast and slow muscles have different functional characteristics to fibres from uninjured muscles. Regenerating muscle fibres had ∼10% of the maximal force producing capacity (Po) of control (uninjured) fibres, and an altered sensitivity to Ca2+ and Sr2+ at 7 days post-injury. Increased force production and a shift in Ca2+ sensitivity consistent with fibre maturation were observed during regeneration such that Po was restored to 36–45% of that in control fibres by 21 days, and sensitivity to Ca2+ and Sr2+ was similar to that of control (uninjured) fibres. The findings support the hypothesis that regenerating muscle fibres have different contractile activation characteristics compared with mature fibres, and that they adopt properties of mature fast- or slow-twitch muscle fibres in a progressive manner as the regeneration process is completed.

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Although mdx mice share the same genetic defect and lack dystrophin expression as in Duchenne muscular dystrophy (DMD), their limb muscles have a high regenerative capacity that ensures a more benign phenotype and essentially normal function. The cellular pathways responsible for this enhanced regenerative capacity are unknown. We tested the hypothesis that the calcineurin signal transduction pathway is essential for the successful regeneration following severe degeneration observed in the limb muscles of young mdx mice (2–4 weeks old) and that inhibition of this pathway using cyclosporine A (CsA) would exacerbate the dystrophic pathology. Eighteen-day-old mdx and C57BL/10 mice were treated with CsA for 16 days. CsA administration severely disrupted muscle regeneration in mdx mice, but had minimal effect in C57BL/10 mice. Muscles from CsA-treated mdx mice had fewer centrally nucleated fibers and extensive collagen, connective tissue, and mononuclear cell infiltration than muscles from vehicle-treated littermates. The deleterious effects of CsA on muscle morphology were accompanied by a 30–35% decrease in maximal force producing capacity. Taken together, these observations indicate that the calcineurin signal transduction pathway is a significant determinant of successful skeletal muscle regeneration in young mdx mice. Up-regulating this pathway may have clinical significance for DMD.

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Eccentrically biased exercise results in skeletal muscle damage and stimulates adaptations in muscle, whereby indexes of damage are attenuated when the exercise is repeated. We hypothesized that changes in ultrastructural damage, inflammatory cell infiltration, and markers of proteolysis in skeletal muscle would come about as a result of repeated eccentric exercise and that gender may affect this adaptive response. Untrained male (n = 8) and female (n = 8) subjects performed two bouts (bout 1 and bout 2), separated by 5.5 wk, of 36 repetitions of unilateral, eccentric leg press and 100 repetitions of unilateral, eccentric knee extension exercises (at 120% of their concentric single repetition maximum), the subjects' contralateral nonexercised leg served as a control (rest). Biopsies were taken from the vastus lateralis from each leg 24 h postexercise. After bout 2, the postexercise force deficit and the rise in serum creatine kinase (CK) activity were attenuated. Women had lower serum CK activity compared with men at all times (P < 0.05), but there were no gender differences in the relative magnitude of the force deficit. Muscle Z-disk streaming, quantified by using light microscopy, was elevated vs. rest only after bout 1 (P < 0.05), with no gender difference. Muscle neutrophil counts were significantly greater in women 24 h after bout 2 vs. rest and bout 1 (P < 0.05) but were unchanged in men. Muscle macrophages were elevated in men and women after bout 1 andbout 2 (P < 0.05). Muscle protein content of the regulatory calpain subunit remained unchanged whereas ubiquitin-conjugated protein content was increased after both bouts (P < 0.05), with a greater increase after bout 2. We conclude that adaptations to eccentric exercise are associated with attenuated serum CK activity and, potentially, an increase in the activity of the ubiquitin proteosome proteolytic pathway.