2,888 research outputs found

    Rates of Performance Loss and Neuromuscular Activity in Men and Women During Cycling: Evidence for A Common Metabolic Basis of Muscle Fatigue

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    The durations that muscular force and power outputs can be sustained until failure fall predictably on an exponential decline between an individual’s 3-s burst maximum to the maximum performance they can sustain aerobically. The exponential time constants describing these rates of performance loss are similar across individuals, suggesting that a common metabolically based mechanism governs muscle fatigue; however, these conclusions come from studies mainly on men. To test whether the same physiological understanding can be applied to women, we compared the performance-duration relationships and neuromuscular activity between seven men [23.3 ± 1.9 (SD) yr] and seven women (21.7 ± 1.8 yr) from multiple exhaustive bouts of cycle ergometry. Each subject performed trials to obtain the peak 3-s power output (Pmax), the mechanical power at the aerobic maximum (Paer), and 11–14 constant-load bouts eliciting failure between 3 and 300 s. Collectively, men and women performed 180 exhaustive bouts spanning an ~6-fold range of power outputs (118–1116 W) and an ~35-fold range of trial durations (8–283 s). Men generated 66% greater Pmax (956 ± 109 W vs. 632 ± 74 W) and 68% greater Paer (310 ± 47 W vs. 212 ± 15 W) than women. However, the metabolically based time constants describing the time course of performance loss were similar between men (0.020 ± 0.003/s) and women (0.021 ± 0.003/s). Additionally, the fatigue-induced increases in neuromuscular activity did not differ between the sexes when compared relative to the pedal forces at Paer. These data suggest that muscle fatigue during short-duration dynamic exercise has a common metabolically based mechanism determined by the extent that ATP is resynthesized by anaerobic metabolism

    Mechanisms for the Age-related Increase in Fatigability of the Knee Extensors in Old and Very Old Adults

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    The mechanisms for the age-related increase in fatigability during high-velocity contractions in old and very old adults ({greater than or equal to}80 yrs) are unresolved. Moreover, whether the increased fatigability with advancing age and the underlying mechanisms differ between men and women are not known. The purpose of this study was to quantify the fatigability of knee extensor muscles and identify the mechanisms of fatigue in 30 young (22.6 {plus minus} 0.4 yrs; 15 men), 62 old (70.5 {plus minus} 0.7 yrs; 33 men), and 12 very old (86.0 {plus minus} 1.3 yrs; 6 men) men and women elicited by high-velocity concentric contractions. Participants performed 80 maximal velocity contractions (1 contraction per 3 s) with a load equivalent to 20% of the maximum voluntary isometric contraction. Voluntary activation and contractile properties were quantified before and immediately following exercise (\u3c10 \u3es) using transcranial magnetic stimulation and electrical stimulation. Absolute mechanical power output was 97% and 217% higher in the young compared to old and very old adults, respectively. Fatigability (reductions in power) progressively increased across age groups, with a power loss of 17% in young, 31% in old, and 44% in very old adults. There were no sex differences in fatigability among any of the age groups. The age-related increase in power loss was strongly associated with changes in the involuntary twitch amplitude (r=0.75,

    Effects of Elevated H\u3csup\u3e+\u3c/sup\u3e And P\u3csub\u3ei\u3c/sub\u3e on The Contractile Mechanics of Skeletal Muscle Fibres From Young and Old Men: Implications for Muscle Fatigue in Humans

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    The present study aimed to identify the mechanisms responsible for the loss in muscle power and increased fatigability with ageing by integrating measures of whole‐muscle function with single fibre contractile mechanics. After adjusting for the 22% smaller muscle mass in old (73–89 years, n = 6) compared to young men (20–29 years, n = 6), isometric torque and power output of the knee extensors were, respectively, 38% and 53% lower with age. Fatigability was ∼2.7‐fold greater with age and strongly associated with reductions in the electrically‐evoked contractile properties. To test whether cross‐bridge mechanisms could explain age‐related decrements in knee extensor function, we exposed myofibres (n = 254) from the vastus lateralis to conditions mimicking quiescent muscle and fatiguing levels of acidosis (H+) (pH 6.2) and inorganic phosphate (Pi) (30 mm). The fatigue‐mimicking condition caused marked reductions in force, shortening velocity and power and inhibited the low‐ to high‐force state of the cross‐bridge cycle, confirming findings from non‐human studies that these ions act synergistically to impair cross‐bridge function. Other than severe age‐related atrophy of fast fibres (−55%), contractile function and the depressive effects of the fatigue‐mimicking condition did not differ in fibres from young and old men. The selective loss of fast myosin heavy chain II muscle was strongly associated with the age‐related decrease in isometric torque (r = 0.785) and power (r = 0.861). These data suggest that the age‐related loss in muscle strength and power are primarily determined by the atrophy of fast fibres, but the age‐related increased fatigability cannot be explained by an increased sensitivity of the cross‐bridge to H+ and Pi

    Caustic formation in a non-Gaussian model for turbulent aerosols

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    Caustics in the dynamics of heavy particles in turbulence accelerate particle collisions. The rate J\mathscr{J} at which these singularities form depends sensitively on the Stokes number St, the non-dimensional inertia parameter. Exact results for this sensitive dependence have been obtained using Gaussian statistical models for turbulent aerosols. However, direct numerical simulations of heavy particles in turbulence yield much larger caustic-formation rates than predicted by the Gaussian theory. In order to understand possible mechanisms explaining this difference, we analyse a non-Gaussian statistical model for caustic formation in the limit of small St. We show that at small St, J\mathscr{J} depends sensitively on the tails of the distribution of Lagrangian fluid-velocity gradients. This explains why different authors obtained different St-dependencies of J\mathscr{J} in numerical-simulation studies. The most-likely gradient fluctuation that induces caustics at small St, by contrast, is the same in the non-Gaussian and Gaussian models. Direct-numerical simulation results for particles in turbulence show that the optimal fluctuation is similar, but not identical, to that obtained by the model calculations.Comment: 12 pages, 3 figures, 1 tabl

    Age-related Deficits in Voluntary Activation: A Systematic Review and Meta-analysis

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    Whether there are age-related differences in neural drive during maximal effort contractions is not clear. This review determined the effect of age on voluntary activation during maximal voluntary isometric contractions. The literature was systematically reviewed for studies reporting voluntary activation quantified with the interpolated twitch technique (ITT) or central activation ratio (CAR) during isometric contractions in young (18–35 yr) and old adults (\u3e60 yr; mean, ≥65 yr). Of the 2697 articles identified, 54 were eligible for inclusion in the meta-analysis. Voluntary activation was assessed with electrical stimulation and transcranial magnetic stimulation on five different muscle groups. Random-effects meta-analysis revealed lower activation in old compared with young adults (d = −0.45; 95% confidence interval, −0.62 to −0.29; P \u3c 0.001), with moderate heterogeneity (52.4%). To uncover the sources of heterogeneity, subgroup analyses were conducted for muscle group, calculation method (ITT or CAR), and stimulation type (electrical stimulation or transcranial magnetic stimulation) and number (single, paired, or train stimulations). The age-related reduction in voluntary activation occurred for all muscle groups investigated except the ankle dorsiflexors. Both ITT and CAR demonstrated an age-related reduction in voluntary activation of the elbow flexors, knee extensors, and plantar flexors. ITT performed with paired and train stimulations showed lower activation for old than young adults, with no age difference for the single electrical stimulation. Together, the meta-analysis revealed that healthy older adults have a reduced capacity to activate some upper and lower limb muscles during maximal voluntary isometric contractions; however, the effect was modest and best assessed with at least paired stimulations to detect the difference

    Hyaline Arteriolosclerosis in 30 Strains of Aged Inbred Mice.

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    During a screen for vascular phenotypes in aged laboratory mice, a unique discrete phenotype of hyaline arteriolosclerosis of the intertubular arteries and arterioles of the testes was identified in several inbred strains. Lesions were limited to the testes and did not occur as part of any renal, systemic, or pulmonary arteriopathy or vasculitis phenotype. There was no evidence of systemic or pulmonary hypertension, and lesions did not occur in ovaries of females. Frequency was highest in males of the SM/J (27/30, 90%) and WSB/EiJ (19/26, 73%) strains, aged 383 to 847 days. Lesions were sporadically present in males from several other inbred strains at a much lower (<20%) frequency. The risk of testicular hyaline arteriolosclerosis is at least partially underpinned by a genetic predisposition that is not associated with other vascular lesions (including vasculitis), separating out the etiology of this form and site of arteriolosclerosis from other related conditions that often co-occur in other strains of mice and in humans. Because of their genetic uniformity and controlled dietary and environmental conditions, mice are an excellent model to dissect the pathogenesis of human disease conditions. In this study, a discrete genetically driven phenotype of testicular hyaline arteriolosclerosis in aging mice was identified. These observations open the possibility of identifying the underlying genetic variant(s) associated with the predisposition and therefore allowing future interrogation of the pathogenesis of this condition

    Zeeman Anisotropy Fluorescence Spectroscopy, Characteristic Radiative Lifetimes, and Novel Site Symmetries in KCl: Sm 2+

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    By means of Zeeman anisotropy fluorescence (ZAF) and its field dependence (up to 55.8 kG), the authors have investigated the 4.2 K narrow-line fluorescence of KCl:Sm2+ and identified some hitherto unreported Sm2+ sites. The strong no-field line at 7693.5 Å (5D0→7F3) and a very weak no-field line at 8742.8 Å (5D0→7F5) are shown to be of C3v symmetry origin. The 24.5-kG ZAF pattern observed in the 7696-7700-Å (5D0→7F3) region has been identified to originate from a type-II Cs site. The 26.5-kG ZAF patterns of the C3v no-field line at 7693.5 Å and the type-I Cs no-field line at 7694.5 Å overlap in the 7693-7695.3-Å region, and are elucidated through the field dependence of their Zeeman components. Characteristic radiative lifetimes of the 5D0 level in several Sm2+ symmetry types have been determined from dominant transitions to the 7FJ (J\u3c~4) levels. There are two distinct C4v sites: one with a lifetime of 9.5 msec, and the other 11.2 msec. C2v and type-I Cs sites have lifetimes of 10.5 and 10.8 msec, respectively, which are indistinguishable within the experimental error. The role of O2− compensation of Sm2+ in addition to K+ vacancy compensation in KCl is discussed in terms of these findings

    Biomechanical determination of distal level for fusions across the cervicothoracic junction

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    Study Design In vitro testing. Objective To determine whether long cervical and cervicothoracic fusions increase the intradiscal pressure at the adjacent caudal disk and to determine which thoracic end vertebra causes the least increase in the adjacent-level intradiscal pressure. Methods A bending moment was applied to six cadaveric cervicothoracic spine specimens with intact rib cages. Intradiscal pressures were recorded from C7–T1 to T9–10 before and after simulated fusion by anterior cervical plating and posterior thoracic pedicle screw constructs. The changes in the intradiscal pressure from baseline were calculated and compared. Results No significant differences where found when the changes of the juxtafusion intradiscal pressure at each level were compared for the flexion, extension, and left and right bending simulations. However, combining the pressures for all directions of bending at each level demonstrated a decrease in the pressures at the T2–T3 level. Exploratory analysis comparing changes in the pressure at T2–T3 to other levels showed a significant decrease in the pressures at this level (p = 0.005). Conclusions Based on the combined intradiscal pressures alone it may be advantageous to end long constructs spanning the cervicothoracic junction at the T2 level if there are no other mitigating factors
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