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Maximal Force (maximal + force)
Selected AbstractsResistance training increases in vivo quadriceps femoris muscle specific tension in young menACTA PHYSIOLOGICA, Issue 1 2010R. M. Erskine Abstract Aim:, The present study investigated whether in vivo human quadriceps femoris (QF) muscle specific tension changed following strength training by systematically determining QF maximal force and physiological cross-sectional area (PCSA). Methods:, Seventeen untrained men (20 ± 2 years) performed high-intensity leg-extension training three times a week for 9 weeks. Maximum tendon force (Ft) was calculated from maximum voluntary contraction (MVC) torque, corrected for agonist and antagonist muscle activation, and moment arm length (dPT) before and after training. QF PCSA was calculated as the sum of the four component muscle volumes, each divided by its fascicle length. Dividing Ft by the sum of the component muscle PCSAs, each multiplied by the cosine of the respective fascicle pennation angle, provided QF specific tension. Results:, MVC torque and QF activation increased by 31% (P < 0.01) and 3% (P < 0.05), respectively, but there was no change in antagonist co-activation or dPT. Subsequently, Ft increased by 27% (P < 0.01). QF volume increased by 6% but fascicle length did not change in any of the component muscles, leading to a 6% increase in QF PCSA (P < 0.05). Fascicle pennation angle increased by 5% (P < 0.01) but only in the vastus lateralis muscle. Consequently, QF specific tension increased by 20% (P < 0.01). Conclusion:, An increase in human muscle specific tension appears to be a real consequence of resistance training rather than being an artefact of measuring errors but the underlying cause of this phenomenon remains to be determined. [source] Using scissors to quantify hardness of insects: do bats select for size or hardness?JOURNAL OF ZOOLOGY, Issue 4 2007P. W. Freeman Abstract Scissors are used to determine the hardness of fresh insects of different size and taxa. Our results indicate a strong relationship between the size of an insect and its hardness, which can be expressed as log(Fmax)=0.65 × log(V)+,. Fmax is the maximal force needed to cut the insect and is our measure of insect hardness. V is the volume of the insect and , is a constant that can be derived for different insect taxa. The value of 0.65 was found as an average of beetle and moth samples, and this number appears consistent across insect taxa. We found that beetles averaged about 3.2 times harder than moths of the same size. Beetles were also more variable in hardness than moths, with the softest beetles about equal in hardness to an average moth of the same size. Using our data on insect hardness coupled with data on the diets of bats and their bite forces from the literature, we attempt to determine whether the upper size limit of insects taken by a bat is limited by the insect's dimensions or its hardness. Our results indicate that both these factors may be important. [source] Single muscle fiber size and contractility after spinal cord injury in ratsMUSCLE AND NERVE, Issue 1 2006Walter R. Frontera MD Abstract Spinal cord injury (SCI) results in muscle weakness but the degree of impairment at the level of single fibers is not known. The purpose of this study was to examine the effects of T9,level SCI on single muscle fibers from the tibialis anterior of rats. Significant decreases in cross-sectional area (CSA), maximal force (Po), and specific force (SF = Po/CSA) were noted at 2 weeks. Atrophy and force-generating capacity were reversed at 4 weeks, but SF remained impaired. Maximum shortening velocity (Vo) did not change after injury. SCI thus appears to affect various contractile properties of single muscle fibers differently. Normal cage activity may partially restore function but new interventions are needed to restore muscle fiber quality. Muscle Nerve, 2006 [source] Fluctuations in isometric muscle force can be described by one linear projection of low-frequency components of motor unit discharge ratesTHE JOURNAL OF PHYSIOLOGY, Issue 24 2009Francesco Negro The aim of the study was to investigate the relation between linear transformations of motor unit discharge rates and muscle force. Intramuscular (wire electrodes) and high-density surface EMG (13 × 5 electrode grid) were recorded from the abductor digiti minimi muscle of eight healthy men during 60 s contractions at 5%, 7.5% and 10% of the maximal force. Spike trains of a total of 222 motor units were identified from the EMG recordings with decomposition algorithms. Principal component analysis of the smoothed motor unit discharge rates indicated that one component (first common component, FCC) described 44.2 ± 7.5% of the total variability of the smoothed discharge rates when computed over the entire contraction interval and 64.3 ± 10.2% of the variability when computed over 5 s intervals. When the FCC was computed from four or more motor units per contraction, it correlated with the force produced by the muscle (62.7 ± 10.1%) by a greater degree (P < 0.001) than the smoothed discharge rates of individual motor units (41.4 ± 7.8%). The correlation between FCC and the force signal increased up to 71.8 ± 13.1% when the duration and the shape of the smoothing window for discharge rates were similar to the average motor unit twitch force. Moreover, the coefficients of variation (CoV) for the force and for the FCC signal were correlated in all subjects (R2 range = 0.14,0.56; P < 0.05) whereas the CoV for force was correlated to the interspike interval variability in only one subject (R2= 0.12; P < 0.05). Similar results were further obtained from measures on the tibialis anterior muscle of an additional eight subjects during contractions at forces up to 20% of the maximal force (e.g. FCC explained 59.8 ± 11.0% of variability of the smoothed discharge rates). In conclusion, one signal captures most of the underlying variability of the low-frequency components of motor unit discharge rates and explains large part of the fluctuations in the motor output during isometric contractions. [source] Acute heavy-resistance exercise,induced pain and neuromuscular fatigue in elderly women with fibromyalgia and in healthy controls: Effects of strength trainingARTHRITIS & RHEUMATISM, Issue 4 2006Heli Valkeinen Objective To examine heavy-resistance exercise,induced acute neuromuscular fatigue, blood lactate concentration, and muscle pain in elderly women with fibromyalgia (FM) and in healthy controls before and after a period of strength training. Methods Thirteen elderly women with FM (mean ± SD age 60 ± 2 years) and 10 healthy women (mean ± SD age 64 ± 3 years) performed a heavy-resistance fatiguing protocol (5 sets of leg presses with 10 repetitions maximum) before and after a 21-week strength training period. Maximal isometric force and electromyography (EMG) activity of leg extensors and blood lactate concentration were measured during the loading. Pain was assessed by visual analog scale. Results The strength training led to large increases in maximal force and EMG activity of the muscles and contributed to the improvement in loading performance (average load/set) at week 21. The fatiguing loading sessions typically applied in strength training before and after the experimental period caused remarkable and comparable acute decreases in maximal force and increases in blood lactate concentration in both groups. Acute exercise-induced muscle pain increased similarly in both groups, and the pain level in women with FM was lowered after the 21-week training period. Conclusion The increased strength in women with FM improved high-load performance and also seemed to attenuate perceived pain. Acute exercise-induced neuromuscular changes and the time course of muscle pain in women with FM were comparable with findings in healthy controls, which suggests a typical fatiguing process and a similar trainability of the muscles in elderly women with FM. [source] Intracellular distribution of peroxynitrite during doxorubicin cardiomyopathy: evidence for selective impairment of myofibrillar creatine kinaseBRITISH JOURNAL OF PHARMACOLOGY, Issue 3 2002Michael J Mihm Cardiac peroxynitrite and protein nitration are increased during doxorubicin cardiotoxicity, but the intracellular targets and functional consequences have not been defined. We investigated the intracellular distribution of protein nitration during doxorubicin cardiotoxicity in mice. Following in vivo cardiac function assessments by echocardiography, cardiac tissues were prepared for immunohistochemistry and electron microscopy 5 days after doxorubicin (20 mg kg,1) or vehicle control. Increased cardiac 3-nitrotyrosine was observed using light microscopy in doxorubicin treated animals. Immunogold electron microscopy (55,000×) revealed increased myofibrillar and mitochondrial 3-nitrotyrosine levels following doxorubicin, but cellular 3-nitrotyrosine density was 2 fold higher in myofibrils. We therefore investigated the actions of peroxynitrite on intact cardiac contractile apparatus. Skinned ventricular trabeculae were exposed to physiologically relevant peroxynitrite concentrations (50 or 300 nM) for 1 h, then Ca2+ induced contractile responses were measured in the presence of ATP (4 mM) or phosphocreatine (12 mM) as high energy phosphate supplier. ATP maximal force generation was unaltered after 50 nM peroxynitrite, but phosphocreatine/ATP response was reduced (0.99±0.63 vs 1.59±0.11), suggesting selective inactivation of myofibrillar creatine kinase (MM-CK). Reduction of ATP maximal force was observed at 300 nM peroxynitrite and phosphocreatine/ATP response was further reduced (0.64±0.30). Western blotting showed concentration dependent nitration of MM-CK in treated trabeculae. Similarly, cardiac tissues from doxorubicin treated mice demonstrated increased nitration and inactivation of MM-CK compared to controls. These results demonstrate that peroxynitrite-related protein nitration are mechanistic events in doxorubicin cardiomyopathy and that the cardiac myofibril is an important oxidative target in this setting. Furthermore, MM-CK may be a uniquely vulnerable target to peroxynitrite in vivo. British Journal of Pharmacology (2002) 135, 581,588; doi:10.1038/sj.bjp.0704495 [source] | |||||||||||||