Sensitivity of maximum sprinting speed to characteristic parameters of the muscle force-velocity relationship

An accumulation of evidence suggests that the force–velocity relationship (FVR) of skeletal muscle plays a major role in limiting maximum human sprinting speed. However, most of the theories on this limiting role have been non-specific as to how the FVR limits speed. The FVR is characterized by three parameters that each have a different effect on its shape, and could thus limit sprinting speed in different ways: the maximum shortening velocity V_max, the shape parameter A_R, and the eccentric plateau C_ecc. In this study, we sought to determine how specifically the FVR limits sprinting speed using forward dynamics simulations of human locomotion to examine the sensitivity of maximum speed to these three FVR parameters. Simulations were generated by optimizing the model's muscle excitations to maximize the average horizontal speed. The simulation's speed, temporal stride parameters, joint angles, GRF, and muscle activity in general compared well to data from human subjects sprinting at maximum effort. Simulations were then repeated with incremental and isolated adjustments in V_max, A_R, and C_ecc across a physiological range. The range of speeds (5.22–6.91 m s^?1) was most sensitive when V_max was varied, but the fastest speed of 7.17 m s^?1 was attained when A_R was set to its maximum value, which corresponded to all muscles having entirely fast-twitch fibers. This result was explained by the muscle shortening velocities, which tended to be moderate and within the range where A_R had its greatest effect on the shape of the FVR. Speed was less sensitive to adjustments in C_ecc, with a range of 6.23–6.70 m s^?1. Increases in speed with parameter changes were due to increases in stride length more so than stride frequency. The results suggest that the shape parameter A_R, which primarily determines the amount of muscle force that can be produced at moderate shortening velocities, plays a major role in limiting the maximum sprinting speed. Analysis of muscle force sensitivity indicated support for previous theories on the time to generate support forces in stance (Weyand et al., 2000, Journal of Applied Physiology, 89, 1991–1999) and energy management of the leg in swing (Chapman &; Caldwell, 1983, Journal of Biomechanics 16, 79–83) as important factors in limiting maximum speed. However, the ability of the knee flexors to slow the rotational velocity of the leg in preparation for footstrike did not appear to play a major role in limiting speed.     

Limitations imposed by wearing armour on Medieval soldiers' locomotor performance

In Medieval Europe, soldiers wore steel plate armour for protection during warfare. Armour design reflected a trade-off between protection and mobility it offered the wearer. By the fifteenth century, a typical suit of field armour weighed between 30 and 50 kg and was distributed over the entire body. How much wearing armour affected Medieval soldiers' locomotor energetics and biomechanics is unknown. We investigated the mechanics and the energetic cost of locomotion in armour, and determined the effects on physical performance. We found that the net cost of locomotion (C(met)) during armoured walking and running is much more energetically expensive than unloaded locomotion. C(met) for locomotion in armour was 2.1-2.3 times higher for walking, and 1.9 times higher for running when compared with C(met) for unloaded locomotion at the same speed. An important component of the increased energy use results from the extra force that must be generated to support the additional mass. However, the energetic cost of locomotion in armour was also much higher than equivalent trunk loading. This additional cost is mostly explained by the increased energy required to swing the limbs and impaired breathing. Our findings can predict age-associated decline in Medieval soldiers' physical performance, and have potential implications in understanding the outcomes of past European military battles.     

Terror birds on the run: a mechanical model to estimate its maximum running speed

'Terror bird' is a common name for the family Phorusrhacidae. These large terrestrial birds were probably the dominant carnivores on the South American continent from the Middle Palaeocene to the Pliocene-Pleistocene limit. Here we use a mechanical model based on tibiotarsal strength to estimate maximum running speeds of three species of terror birds: Mesembriornis milneedwardsi, Patagornis marshi and a specimen of Phorusrhacinae gen. The model is proved on three living large terrestrial bird species. On the basis of the tibiotarsal strength we propose that Mesembriornis could have used its legs to break long bones and access their marrow.     

Modelling the mechanical properties of cardiac muscle

A model of passive and active cardiac muscle mechanics is presented, suitable for use in continuum mechanics models of the whole heart. The model is based on an extensive review of experimental data from a variety of preparations (intact trabeculae, skinned fibres and myofibrils) and species (mainly rat and ferret) at temperatures from 20 to 27°C. Experimental tests include isometric tension development, isotonic loading, quick-release/restretch, length step and sinusoidal perturbations. We show that all of these experiments can be interpreted with a four state variable model which includes (i) the passive elasticity of myocardial tissue, (ii) the rapid binding of Ca²⁺ to troponin C and its slower tension-dependent release, (iii) the kinetics of tropomyosin movement and availability of crossbridge binding sites and the length dependence of this process and (iv) the kinetics of crossbridge tension development under perturbations of myofilament length.     

The effect of 40-m repeated sprint training on maximum sprinting speed, repeated sprint speed endurance, vertical jump, and aerobic capacity in young elite male soccer players

The purpose of this study was to examine the effect of 10 weeks' 40-m repeated sprint training program that does not involve strength training on sprinting speed and repeated sprint speed on young elite soccer players. Twenty young well-trained elite male soccer players of age (±SD) 16.4 (±0.9) years, body mass 67.2 (±9.1) kg, and stature 176.3 (±7.4) cm volunteered to participate in this study. All participants were tested on 40-m running speed, 10 × 40-m repeated sprint speed, 20-m acceleration speed, 20-m top speed, countermovement jump (CMJ), and aerobic endurance (beep test). Participants were divided into training group (TG) (n = 10) and control group (CG) (n = 10). The study was conducted in the precompetition phase of the training program for the participants and ended 13 weeks before the start of the season; the duration of the precompetition period was 26 weeks. The TG followed a Periodized repeated sprint training program once a week. The training program consisted of running 40 m with different intensities and duration from week to week. Within-group results indicate that TG had a statistically marked improvement in their performance from pre to posttest in 40-m maximum sprint (-0.06 seconds), 10 × 40-m repeated sprint speed (-0.12 seconds), 20- to 40-m top speed (-0.05 seconds), and CMJ (2.7 cm). The CG showed only a statistically notable improvement from pre to posttest in 10 × 40-m repeated sprint speed (-0.06 seconds). Between-group differences showed a statistically marked improvement for the TG over the CG in 10 × 40-m repeated sprint speed (-0.07 seconds) and 20- to 40-m top speed (-0.05 seconds), but the effect of the improvement was moderate. The results further indicate that a weekly training with repeated sprint gave a moderate but not statistically marked improvement in 40-m sprinting, CMJ, and beep test. The results of this study indicate that the repeated sprint program had a positive effect on several of the parameters tested. However, because the sample size in this study is 20 participants, the results are valid only for those who took part in this study. Therefore, we advice to use repeated sprint training similar to the one in this study only in periods where the players have no speed training included in their program. Furthermore, the participants in this study should probably trained strength, however, benefits were observed even without strength training is most likely to be caused by the training specificity.     

Limitations imposed by testicular blood flow on the function of Leydig cells in rats in vivo

Testis blood flow per testis closely follows testis weight in rats made aspermatogenic by a single exposure of the testis to 43 degrees C for 30 min or 500 rad (5 Gy) of irradiation from a caesium source, or following ligation of the efferent ducts. Aspermatogenesis following these treatments was associated with only minor changes in the concentrations of testosterone in peripheral blood before stimulation with human chorionic gonadotrophin (hCG), and a reduced responsiveness to hCG when testis weight had fallen after heating. The concentrations of testosterone in testicular venous blood was normal or above normal during aspermatogenesis resulting from heat or irradiation, and only slightly reduced following efferent duct ligation. Consequently testosterone production (defined as the product of plasma flow and the veno-arterial concentration difference for testosterone) was markedly reduced during aspermatogenesis, both before and after stimulation with hCG. It appears that the reduced blood flow limits the amount of testosterone leaving the testis, and while the Leydig cells are capable under some circumstances of compensating partially for this fall by increasing the concentration of testosterone in the testicular venous blood, this compensation is not complete when there are severe reductions in blood flow. Therefore one can conclude that the mass of the tubules is the main determinant of testis blood flow and the Leydig cells must manage with what the tubules require.     

Unravelling the response of poplar (Populus nigra) roots to mechanical stress imposed by bending

Abstract

Mechanical stress is a widespread environmental condition that can be caused by several factors (i.e. gravity, touch, wind, soil density, soil compaction and grazing, slope) and that can severely affect plant stability. In response to mechanical stress and to improve their anchorage, plants have developed complex mechanisms to detect mechanical perturbation and to induce a suite of modifications at anatomical, physiological, biochemical, biophysical and molecular level. Although it is well recognized that one of the primary functions of root systems is to anchor the plant to the soil, root response to mechanical stresses have been investigated mainly at morphological and biomechanical level, whereas investigations about the molecular mechanisms underlying these important alterations are still in an initial stage. We have used an experimental system in which the taproot poplar seedlings are bent to simulate mechanical perturbation to begin investigate the mechanisms involved in root response to mechanical stress. The results reported herein show that, in response to bending, the poplar root changes its morphology by emitting new lateral roots, and its biomechanical properties by increasing the root biomass and lignin synthesis. In addition, using a proteomic approach, we found that several proteins involved in the signal transduction pathway, detoxification and metabolism are up-regulated and/or down-regulated in the bent root. These results provide new insight into the obscure field of woody root response to mechanical stress, and can serve as a basis for future investigations aimed at unravelling the complex mechanism involved in the reaction of root biology to environmental stress.     

Limitations on geminivirus genome size imposed by plasmodesmata and virus-encoded movement protein: insights into DNA trafficking

Animals and plants evolved systems to permit non-cell-autonomous trafficking of RNA, whereas DNA plays a cell-autonomous role. In plants, plasmodesmata serve as the conduit for this phenomenon, and viruses have evolved to use this pathway for the spread of infectious nucleic acids. In this study, a plant DNA virus was used to explore the constraints imposed on the movement of DNA through this endogenous RNA trafficking pathway. The combined properties of the geminivirus-encoded movement protein and plasmodesmata were shown to impose a strict limitation on the size of the viral genome at the level of cell-to-cell movement. Size-increased viral genome components underwent homologous and nonhomologous recombination to overcome this strict limitation. Our results provide insights into the genetic mechanisms that underlie viral evolution and provide a likely explanation for why relatively few types of plant DNA viruses have evolved: they would have had to overcome the constraints imposed by an endogenous system operating to ensure that DNA acts in a cell-autonomous manner.     

Limitations to exercise- and maximal insulin-stimulated muscle glucose uptake

The hypothesisof this investigation was that insulin and muscle contraction, byincreasing the rate of skeletal muscle glucose transport, would biascontrol so that glucose delivery to the sarcolemma (and t tubule) andphosphorylation of glucose intracellularly would exert more influenceover glucose uptake. Because of the substantial increases in blood flow(and hence glucose delivery) that accompany exercise, we predicted thatglucose phosphorylation would become more rate determining duringexercise. The transsarcolemmal glucose gradient (TSGG; the glucoseconcentration difference across the membrane) is inversely related tothe degree to which glucose transport determines the rate of glucoseuptake. The TSGG was determined by using isotopic methods in consciousrats during euglycemic hyperinsulinemia [Ins; 20 mU/(kg · min); n = 7], during treadmill exercise (Ex,n = 6), and in sedentary,saline-infused rats (Bas, n = 13).Rats received primed, constant intravenous infusions of trace3-O-[³H]methyl-D-glucoseand [U-¹⁴C]mannitol.Then2-deoxy-[³H]glucosewas infused for the calculation of a glucose metabolic index(R_g). At the end of experiments,rats were anesthetized, and soleus muscles were excised. Total soleusglucose concentration and the steady-state ratio of intracellular toextracellular3-O-[³H]methyl-D-glucose(which distributes on the basis of the TSGG) were used to calculateranges of possible glucose concentrations ([G]) at theinner and outer sarcolemmal surfaces([G]_im and[G]_om, respectively).Soleus R_g was increased in Ins andfurther increased in Ex. In Ins, total soleus glucose,[G]_om, and the TSGGwere decreased compared with Bas, while[G]_im remained near 0. In Ex, total soleus glucose and[G]_im were increasedcompared with Bas, and there was not a decrease in[G]_om as was observedin Ins. In addition, accumulation of intracellular free2-deoxy-[³H]glucoseoccurred in soleus in both Ex and Ins. Taken together, these dataindicate that, in Ex, glucose phosphorylation becomes an importantlimitation to soleus glucose uptake. In Ins, both glucose delivery andglucose phosphorylation influence the rate of soleus glucose uptakemore than under basal conditions.

     

Pre-power-stroke cross-bridges contribute to force transients during imposed shortening in isolated muscle fibers

When skeletal muscles are activated and mechanically shortened, the force that is produced by the muscle fibers decreases in two phases, marked by two changes in slope (P₁ and P₂) that happen at specific lengths (L₁ and L₂). We tested the hypothesis that these force transients are determined by the amount of myosin cross-bridges attached to actin and by changes in cross-bridge strain due to a changing fraction of cross-bridges in the pre-power-stroke state. Three separate experiments were performed, using skinned muscle fibers that were isolated and subsequently (i) activated at different Ca²⁺ concentrations (pCa²⁺ 4.5, 5.0, 5.5, 6.0) (n = 13), (ii) activated in the presence of blebbistatin (n = 16), and (iii) activated in the presence of blebbistatin at varying velocities (n = 5). In all experiments, a ramp shortening was imposed (amplitude 10%L_o, velocity 1 L_o•sarcomere length (SL)•s⁻¹), from an initial SL of 2.5 µm (except by the third group, in which velocities ranged from 0.125 to 2.0 L_o•s⁻¹). The values of P₁, P₂, L₁, and L₂ did not change with Ca²⁺ concentrations. Blebbistatin decreased P₁, and it did not alter P₂, L₁, and L₂. We developed a mathematical cross-bridge model comprising a load-dependent power-stroke transition and a pre-power-stroke cross-bridge state. The P₁ and P₂ critical points as well as the critical lengths L₁ and L₂ were explained qualitatively by the model, and the effects of blebbistatin inhibition on P₁ were also predicted. Furthermore, the results of the model suggest that the mechanism by which blebbistatin inhibits force is by interfering with the closing of the myosin upper binding cleft, biasing cross-bridges into a pre-power-stroke state.     

The muscle twitch and the maximum swimming speed of giant bluefin tuna, Thunnus thynnus L.

Sustained swimming of bluefin tuna was analysed from video recordings made of a captive patrolling fish school [lengths (L) 1.7–3.3 m, body mass (M) 54–433 kg]. Speeds ranged from 0.6 to 1.2 L s⁻¹ (86–260 km day⁻¹) while stride length during steady speed swimming varied between 0.54 and 0.93 L. Maximum swimming speed was estimated by measuring twitch contraction of the anaerobic swimming muscle in pithed fish 5 min after death. Muscle contraction time increased from the shortest just behind the head (30–50 ms at 20% L) to the longest at the tail peduncle (80–90 ms at 80% L) (all at 28°C). A fish (L = 2.26 m) with a muscle contraction time of 50 ms at 25% L can have a maximum tail beat frequency of 10 Hz and maximum swimming speed of 15m s⁻¹ (54km h⁻¹) with a stride length of 0.65L. With a stride length of 1 L a speed of 22.6 m s⁻¹ (81.4 km h⁻¹) is possible. Power used at maximum speed was estimated for this fish at between 10 and 40 kW, with corresponding values for the drag coefficient at a Reynolds number of 4.43 × 10⁷ of 0.0007 and 0.0027.     

History-dependent mechanical properties of permeabilized rat soleus muscle fibers.

Permeabilized rat soleus muscle fibers were subjected to repeated triangular length changes (paired ramp stretches/releases, 0.03 l(0), +/- 0.1 l(0) s(-1) imposed under sarcomere length control) to investigate whether the rate of stiffness recovery after movement increased with the level of Ca(2+) activation. Actively contracting fibers exhibited a characteristic tension response to stretch: tension rose sharply during the initial phase of the movement before dropping slightly to a plateau, which was maintained during the remainder of the stretch. When the fibers were stretched twice, the initial phase of the response was reduced by an amount that depended on both the level of Ca(2+) activation and the elapsed time since the first movement. Detailed analysis revealed three new and important findings. 1) The rates of stiffness and tension recovery and 2) the relative height of the tension plateau each increased with the level of Ca(2+) activation. 3) The tension plateau developed more quickly during the second stretch at high free Ca(2+) concentrations than at low. These findings are consistent with a cross-bridge mechanism but suggest that the rate of the force-generating power-stroke increases with the intracellular Ca(2+) concentration and cross-bridge strain.     

Stretch-induced nitric oxide modulates mechanical properties of skeletal muscle cells

In this study, we examined the hypothesis that stretch-induced (nitric oxide) NO modulates the mechanical properties of skeletal muscles by increasing accumulation of protein levels of talin and vinculin and by inhibiting calpain-induced proteolysis, thereby stabilizing the focal contacts and the cytoskeleton. Differentiating C₂C₁₂ myotubes were subjected to a single 10% step stretch for 0–4 days. The apparent elastic modulus of the cells, E_app, was subsequently determined by atomic force microscopy. Static stretch led to significant increases (P < 0.01) in E_app beginning at 2 days. These increases were correlated with increases in NO activity and neuronal NO synthase (nNOS) protein expression. Expression of talin was upregulated throughout, whereas expression of vinculin was significantly increased only on days 3 and 4. Addition of the NO donor L-arginine onto stretched cells further enhanced E_app, NOS activity, and nNOS expression, whereas the presence of the NO inhibitor N-nitro-L-arginine methyl ester (L-NAME) reversed the effects of mechanical stimulation and of L-arginine. Overall, viscous dissipation, as determined by the value of hysteresis, was not significantly altered. For assessment of the role of vinculin and talin stability, cells treated with L-NAME showed a significant decrease in E_app, whereas addition of a calpain inhibitor abolished the effect. Thus our results show that NO inhibition of calpain-initiated cleavage of cytoskeleton proteins was correlated with the changes in E_app. Together, our data suggest that NO modulates the mechanical behavior of skeletal muscle cells through the combined action of increased talin and vinculin levels and a decrease in calpain-mediated talin proteolysis. mechanical stimulation; apparent elastic modulus; skeletal muscle cells; nitric oxide; stretch     

The redox properties of cytochromes b imposed by the membrane electrostatic environment.

The effect of the dipole potential field of extended membrane spanning alpha-helices on the redox potentials of b cytochromes in energy transducing membranes has been calculated in the context of a three phase model for the membrane. In this model, the membrane contains three dielectric layers; (i) a 40-A hydrophobic membrane bilayer, with dielectric constant em = 3-4, (ii) 10-20-A interfacial layers of intermediate polarity, ein = 12-20, that consist of lipid polar head groups and peripheral protein segments, and (iii) an external infinite water medium, ew = 80. The unusually positive midpoint potential, Em = +0.4 V, of the "high potential" cytochrome b-559 of oxygenic photosynthetic membranes, a previously enigmatic property of this cytochrome, can be explained by (i) the position of the heme in the positive dipole potential region near the NH2 termini of the two parallel helices that provide its histidine ligands, and (ii) the loss of solvation energy of the heme ion due to the low dielectric constant of its surroundings, leading to an estimate of +0.31 to +0.37 V for the cytochrome Em. The known tendency of this cytochrome to undergo a large -delta Em shift upon exposure of thylakoid membranes to proteases or damaging treatments is explained by disruption of the intermediate polarity (ein) surface dielectric layer and the resulting contact of the heme with the external water medium. Application of this model to the two hemes (bn and bp) of cytochrome b of the cytochrome bc1 complex, with the two hemes placed symmetrically in the low dielectric (em) membrane bilayer, results in Em values of hemes bn and bp that are, respectively, somewhat too negative (approximately -0.1 V), and much too positive (approximately +0.3 V), leading to a potential difference, Em(bp) - Em(bn), with the wrong sign and magnitude, +0.25 V instead of -0.10 to -0.15 V. The heme potentials can only be approximately reconciled with experiment, if it is assumed that the two hemes are in different dielectric environments, with that of heme bp being more polar.     

Macroscopic-microscopic characterization of the passive mechanical properties in rat soleus muscle

The purpose of the study was to investigate changes in passive mechanical properties of the soleus muscle of the rat during the first year of life. These mechanical changes were quantified at a macroscopic (whole muscle) and a microscopic level (fiber) and were correlated with biochemical and morphological properties. Three passive mechanical tests (a relaxation test, a ramp stretch test and a stretch release cycle test) with different amplitudes and velocities were performed on isolated soleus muscles and fibers in rats at ages 1 (R1), 4 (R4) and 12 (R12) months. Mechanical parameters (dynamic and static forces, stresses and normalized stiffness) were recorded and measured. The morphological properties (size of fibers and muscles) for the three groups of rats were assessed by light microscopy which allowed us to observe the evolution of the fiber type (I, IIc and IIa) in the belly region and along the longitudinal axis of the muscle. In addition, biochemical analyses were performed at the level of the whole muscle in order to determine the collagen content. The results of the passive mechanical properties between the macroscopic (muscle) and microscopic (fiber) levels showed a similar evolution. Thus, an increase of the dynamic and static forces appeared between 1 and 4 months while a decrease of the passive tension occurred between 4 and 12 months. These mechanical changes were correlated to the morphological properties. In addition, the size of the three fibers type which grew with age could explain the increase of forces between 1 and 4 months. Furthermore, the biochemical analysis showed an increase of the collagen content during the same period which could also be associated with the increase of the passive forces. After 4 months, the passive tension decreased while the size of the fiber continued to increase. The biochemical analysis showed a decrease of the collagen content after 4 months, which could explain the loss of passive tension in the whole muscle. Concerning the similar loss at the fiber level, other assumptions are required such as a myofibril loss process and an increase of intermyofibrillar spaces. The originality of this present study was to compare the passive mechanical properties between two different levels of anatomical organization within the soleus muscle of the rat and to explain these mechanical changes in terms of biochemical and morphological properties.