Pliometric contraction-induced injury of mouse skeletal muscle: effect of initial length

Hunter, Kam D., and John A. Faulkner. Pliometriccontraction-induced injury of mouse skeletal muscle: effect of initial length. J. Appl. Physiol. 82(1):278-283, 1997.For single pliometric (lengthening) contractionsinitiated from optimal fiber length (L_f), the mostimportant factor determining the subsequent force deficit is the workinput during the stretch. We tested the hypothesis that regardless ofthe initial length, the force deficit is primarily a function of thework input. Extensor digitorum longus muscles of mice were maximallyactivated in situ and lengthened at 2 L_f /s from oneof three initial fiber lengths (90, 100, or 120% of L_f) to one ofthree final fiber lengths (150, 160, or 170% of L_f). Maximalisometric force production was assessed before and after the pliometriccontraction. No single mechanical factor, including thework input(r² = 0.34), was sufficient to explain the differences in force deficits observed among groups. Therefore, the force deficit appears to arisefrom a complex interaction of mechanicalevents. With the data grouped by initial fiber length,the correlation between the average work and the average force deficitwas high(r² = 0.97-0.99). Consequently, differences in force deficits among groups were best explained on the basis of the initial fiber length andthe work input during the stretch.

     

Alignment of microvascular units along skeletal muscle fibers of hamster retractor

Emerson, Geoffrey G., and Steven S. Segal. Alignment ofmicrovascular units along skeletal muscle fibers of hamster retractor.J. Appl. Physiol. 82(1): 42-48, 1997.When muscle fibers contract, blood flow requirements increasealong their entire length. However, the organization of capillaryperfusion along muscle fibers is unclear. The microvascular unit (MVU)is defined as a terminal arteriole and the group of capillaries itsupplies. We investigated whether neighboring MVUs along the fiber axis perfused the same group of muscle fibers by using the parallel-fibered retractor muscle. Hamsters were anesthetized and perfused with Microfilto visualize MVUs relative to muscle fibers. Fields of study, whichencompassed five to seven neighboring MVUs along a muscle fiber, werechosen from the interior of muscles and along muscle edges. On average,MVUs were 1 mm in length, 0.50 mm in width, and 0.1 mm deep; segmentsof ~30 fibers were contained in this tissue volume of 0.05 mm³ (20 MVUs/mg muscle). The totaldistance across muscle fibers encompassed by a pair of MVUs isdesignated "union" (U); the fraction of this distance common toboth MVUs is designated "intersection" (I). The ratio of I to Ufor the widths of neighboring MVUs provides an index of MVU alignmentalong muscle fibers (e.g., I/U = 1.0 indicates complete alignment,where the fibers perfused by one MVU are the same as those perfused bythe neighboring MVU). We found that I/U along muscle edges (0.71 ± 0.02) was greater (P < 0.05) thanthe ratio measured within muscles (0.66 ± 0.02). A model predicteda maximum I/U of 0.58 with random MVU alignment. Thus measured valueswere closer to random than to complete alignment. These findingsindicate that an increase in blood flow along muscle fibers requiresthe perfusion of many MVUs and imply that vasodilation is coordinatedamong the parent arterioles from which corresponding MVUsarise.

     

Induction of neuronal type nitric oxide synthase in skeletal muscle by chronic electrical stimulation in vivo

Reiser, Peter J., William O. Kline, and Pal L. Vaghy.Induction of neuronal type nitric oxide synthase in skeletal muscle by chronic electrical stimulation in vivo. J. Appl. Physiol. 82(4): 1250-1255, 1997.Fast-twitch skeletal muscles contain more neuronal-type nitricoxide synthase (nNOS) than slow-twitch muscles because nNOS is presentonly in fast (type II) muscle fibers. Chronic in vivo electricalstimulation of tibialis anterior and extensor digitorum longus musclesof rabbits was used as a method of inducing fast-to-slow fiber typetransformation. We have studied whether an increase in musclecontractile activity induced by electrical stimulation alters nNOSexpression, and if so, whether the nNOS expression decreases to thelevels present in slow muscles. Changes in the expression of myosinheavy chain isoforms and maximum velocity of shortening of skinnedfibers indicated characteristic fast-to-slow fiber type transformationafter 3 wk of stimulation. At the same time, activity of NOS doubled inthe stimulated muscles, and this correlated with an increase in theexpression of nNOS shown by immunoblot analysis. These data suggestthat nNOS expression in skeletal muscle is regulated by muscle activityand that this regulation does not necessarily follow the fast-twitchand slow-twitch pattern during the dynamic phase of phenotypetransformation.

     

Contraction-induced injury to single muscle fibers: velocity of stretch does not influence the force deficit

We tested the null hypothesis that theseverity of injury to single muscle fibers following a singlepliometric (lengthening) contraction is not dependent on the velocityof stretch. Each single permeabilized fiber obtained from extensordigitorum longus muscles of rats was maximally activated and thenexposed to a single stretch of either 5, 10, or 20% strain [%of fiber length (L_f)] ata velocity of 0.5, 1.0, or 2.0 L_f /s. Theforce deficit, the difference between maximum tetanic isometric force(P_o) before and after the stretch expressed as apercentage of the control value forP_o before the stretch, provided anestimate of the magnitude of muscle injury. Despite a fourfold rangefrom the lowest to the highest velocities, force deficits were notdifferent among stretches of the same strain. At stretches of 20%strain, even an eightfold range of velocities produced no difference inthe force deficit, although 40% of the fibers were torn apart at a velocity of 4 L_f /s. We conclude that, withinthe range of velocities tolerated by single permeabilized fibers, theseverity of contraction-induced injury is not related to the velocityof stretch.

     

Critical sarcomere extension required to recruit a decaying component of extra force during stretch in tetanic contractions of frog skeletal muscle fibers

29 single frog skeletal muscle fibers were stretched during fused tetanic contractions. The force increase during stretch exhibited a breakpoint at a critical length change (average: 16.6 nm per one-half sarcomere) that was independent of velocity of stretch and of sarcomere length between 1.8 and 2.8 microns. After stretch there was an early decaying force component with a force-extension curve similar to that during stretch, which disappeared over approximately 2 s. This component was removed by a small, quick release, leaving a longer- lasting component. The critical amplitude of release required to produce this result was found by clamping the fiber to a load at which there was zero velocity of shortening. This amplitude increased with time up to the angle in the force record during stretch, was constant for the remainder of the stretch, and decreased with time after the end of stretch; it was consistently less than the critical amplitude of stretch required to reach the breakpoint of force enhancement during stretch but was also independent of sarcomere length. The force drop accompanying the critical release showed a small increase up to an optimum magnitude at 2.4--2.7 microns sarcomere length, with a decrease at longer lengths.     

Stretch-induced,steady-state force enhancement in single skeletal muscle fibers exceeds the isometric force at optimum fiber length

Stretch-induced force enhancement has been observed in a variety of muscle preparations and on structural levels ranging from single fibers to in vivo human muscles. It is a well-accepted property of skeletal muscle. However, the mechanism causing force enhancement has not been elucidated, although the sarcomere-length non-uniformity theory has received wide support. The purpose of this paper was to re-investigate stretch-induced force enhancement in frog single fibers by testing specific hypotheses arising from the sarcomere-length non-uniformity theory. Single fibers dissected from frog tibialis anterior (TA) and lumbricals (n=12 and 22, respectively) were mounted in an experimental chamber with physiological Ringer's solution (pH=7.5) between a force transducer and a servomotor length controller. The tetantic force-length relationship was determined. Isometric reference forces were determined at optimum length (corresponding to the maximal, active, isometric force), and at the initial and final lengths of the stretch experiments. Stretch experiments were performed on the descending limb of the force-length relationship after maximal tetanic force was reached. Stretches of 2.5-10% (TA) and 5-15% lumbricals of fiber length were performed at 0.1-1.5 fiber lengths/s. The stretch-induced, steady-state, active isometric force was always equal or greater than the purely isometric force at the muscle length from which the stretch was initiated. Moreover, for stretches of 5% fiber length or greater, and initiated near the optimum length of the fiber, the stretch-enhanced active force always exceeded the maximal active isometric force at optimum length. Finally, we observed a stretch-induced enhancement of passive force. We conclude from these results that the sarcomere length non-uniformity theory alone cannot explain the observed force enhancement, and that part of the force enhancement is associated with a passive force that is substantially greater after active compared to passive muscle stretch.     

Effects of shortening on stretch-induced force enhancement in single skeletal muscle fibers

The main purpose of this study was to evaluate the effects of shortening on the stretch-induced force enhancement in single muscle fibers, and indirectly test the hypothesis that force enhancement may be associated with the engagement of a passive element upon activation. Fibers were placed on the descending limb of the force-length relationship, and stretch and shortening contractions were performed. Fibers underwent two sets of shortening-stretch cycles. First, fibers were shortened by a fixed amplitude and speed (10% fiber length, and at 40% fiber length/s), and then were stretched (10% fiber length, and at 40% fiber length/s) immediately following shortening, or 500 or 1000 ms following the shortening. Second, fibers were shortened by varying amounts (5%, 10% and 15% fiber length) and at a constant speed (40% fiber length/s) immediately preceding a given fiber stretch (10% fiber length, and at 40% fiber length/s). When stretching was immediately preceded by shortening, force enhancement was decreased proportionally with the shortening magnitude. When intervals were introduced between shortening and stretch, the effects of shortening on the stretch-induced force enhancement became less prominent. We concluded that, in contrast to published suggestions, shortening affects the stretch-induced force enhancement in an amplitude-dependent manner in single fibers, as it does in whole muscles, but this effect is diminished by increasing the time period between the shortening and stretch phases.     

Potentiation of in vitro concentric work in mouse fast muscle

Grange, R. W., R. Vandenboom, J. Xeni, and M. E. Houston.Potentiation of in vitro concentric work in mouse fast muscle. J. Appl. Physiol. 84(1): 236-243, 1998.Phosphorylation of myosin regulatory light chain (R-LC) isassociated with potentiated work and power during twitch afterloadedcontractions in mouse extensor digitorum longus muscle [R. W. Grange, C. R. Cory, R. Vandenboom, and M. E. Houston.Am. J. Physiol. 269 (Cell Physiol. 38): C713-C724, 1995]. We now describe the association between R-LCphosphorylation and potentiated concentric work when the extensordigitorum longus muscle is rhythmically shortened and lengthened tosimulate contractions in vivo. Work output (at 25°C) wascharacterized at sine frequencies of 3, 5, 7, 10, and 15 Hz atexcursions of 0.6, 1.2, and 1.6 mm (~5, 9, and 13% optimal musclelength) at a low level of R-LC phosphorylation. Muscles stimulatedduring the sine function with a single twitch at specific times beforeor after the longest muscle length yielded maximal concentric work nearthe longest muscle length at a sine frequency of 7 Hz (e.g., excursion~9% optimal muscle length = 1.6 J/kg). Power increased linearlybetween sine frequencies of 3 and 15 Hz at all excursions (maximum~29 W). After a 5-Hz 20-s conditioning stimulus and coincident with a3.7-fold increase in R-LC phosphate content (e.g., from 0.19 to 0.70 mol phosphate/mol R-LC), work at the three excursions and a sinefrequency of 7 Hz was potentiated a mean of 25, 44, and 50%(P < 0.05), respectively. Thepotentiated work during rhythmic contractions is consistent withenhanced interaction between actin and myosin in the force-generatingstates. On the basis of observations in skinned skeletal muscle fibers(H. L. Sweeney and J. T. Stull. Proc. Natl. Acad. Sci.USA 87: 414-418, 1990), this enhancement couldresult from increased phosphate incorporation by the myosin R-LC. Underthe assumption that the predominant effect of the conditioning stimuluswas to increase R-LC phosphate content, our data suggest that a similarmechanism may be evident in intact muscle.

     

Changes in skeletal muscle biochemistry and histology relative to fiber type in rats with heart failure

Delp, Michael D., Changping Duan, John P. Mattson, andTimothy I. Musch. Changes in skeletal muscle biochemistry and histology relative to fiber type in rats with heart failure.J. Appl. Physiol. 83(4):1291-1299, 1997.One of the primary consequences of leftventricular dysfunction (LVD) after myocardial infarction is adecrement in exercise capacity. Several factors have been hypothesizedto account for this decrement, including alterations in skeletal musclemetabolism and aerobic capacity. The purpose of this study was todetermine whether LVD-induced alterations in skeletal muscle enzymeactivities, fiber composition, and fiber size are1) generalized in muscles orspecific to muscles composed primarily of a given fiber type and2) related to the severity of theLVD. Female Wistar rats were divided into three groups: sham-operatedcontrols (n = 13) and rats withmoderate (n = 10) and severe(n = 7) LVD. LVD was surgicallyinduced by ligating the left main coronary artery and resulted inelevations (P < 0.05) in leftventricular end-diastolic pressure (sham, 5 ± 1 mmHg; moderate LVD,11 ± 1 mmHg; severe LVD, 25 ± 1 mmHg). Moderate LVDdecreased the activities of phosphofructokinase (PFK) and citratesynthase in one muscle composed of type IIB fibers but did not modifyfiber composition or size of any muscle studied. However, severe LVDdiminished the activity of enzymes involved in terminal and-oxidation in muscles composed primarily of type I fibers, type IIAfibers, and type IIB fibers. In addition, severe LVD induced areduction in the activity of PFK in type IIB muscle, a 10% reductionin the percentage of type IID/X fibers, and a corresponding increase inthe portion of type IIB fibers. Atrophy of type I fibers, type IIAfibers, and/or type IIB fibers occurred in soleus and plantarismuscles of rats with severe LVD. These data indicate that rats withsevere LVD after myocardial infarction exhibit1) decrements in mitochondrialenzyme activities independent of muscle fiber composition,2) a reduction in PFK activity in type IIB muscle, 3) transformationof type IID/X to type IIB fibers, and4) atrophy of type I, IIA, and IIBfibers.

     

Effect of intermittent weight bearing on soleus fiber force-velocity-power and force-pCa relationships

Bangart, J. J., J. J. Widrick, and R. H. Fitts. Effectof intermittent weight bearing on soleus fiber force-velocity-power andforce-pCa relationships. J. Appl.Physiol. 82(6): 1905-1910, 1997.Ratpermeabilized type I soleus fibers displayed a 33% reduction in peakpower output and a 36% increase in the freeCa²⁺ concentration required forone-half maximal activation after 14 days of hindlimb non-weightbearing (NWB). We examined the effectiveness of intermittent weightbearing (IWB; consisting of four 10-min periods of weight bearing/day)as a countermeasure to these functional changes. At peak power output,type I fibers from NWB animals produced 54% less force and shortenedat a 56% greater velocity than did type I fibers from controlweight-bearing animals while type I fibers from the IWB rats produced26% more absolute force than did fibers from the NWB group andshortened at a velocity that was only 80% of the NWB group mean. As aresult, no difference was observed in the average peak power of fibers from the IWB and NWB animals. Hill plot analysis of force-pCa relationships indicated that fibers from the IWB group required similarlevels of free Ca²⁺ to reachhalf-maximal activation in comparison to fibers from the weight-bearinggroup. However, at forces <50% of peak force, the force-pCa curvefor fibers from the IWB animals clearly fell between the relationshipsobserved for the other two groups. In summary, IWB treatments1) attenuated the NWB-inducedreduction in fiber Ca²⁺sensitivity but 2) failed to preventthe decline in peak power that occurs during NWB because of opposingeffects on fiber force (an increase vs. NWB) and shortening velocity (adecrease vs. NWB).

     

Contractile function of single muscle fibers after hindlimb unweighting in aged rats

Thompson, L. V., and J. A. Shoeman. Contractilefunction of single muscle fibers after hindlimb unweighting in aged rats. J. Appl. Physiol. 84(1):229-235, 1998.This investigation determined how muscle atrophyproduced by hindlimb unweighting (HU) alters the contractile functionof single muscle fibers from older animals (30 mo). After 1 wk of HU,small bundles of fibers were isolated from the soleus muscles and thedeep region of the lateral head of the gastrocnemius muscles. Singleglycerinated fibers were suspended between a motor lever and forcetransducer, functional properties were studied, and the myosin heavychain (MHC) composition was determined electrophoretically. After HU, the diameter of type I MHC fibers of the soleus declined (88 ± 2 vs. 80 ± 4 µm) and reductions were observed in peak active force (47 ± 3 vs. 28 ± 3 mg) and peak specific tension(P_o; 80 ± 5 vs. 56 ± 5 kN/m²). The maximal unloadedshortening velocity increased. The type I MHC fibers from thegastrocnemius showed reductions in diameter (14%), peak active force(41%), and P_o (24%), whereas thetype IIa MHC fibers showed reductions in peak active force andP_o. Thus 1 wk ofinactivity has a significant effect on the force-generating capacity ofsingle skeletal muscle fibers from older animals in a fibertype-specific manner (type I MHC > type IIa MHC > type I-IIa MHC).The decline in the functional properties of single skeletal musclefibers in the older animals appears to be more pronounced than what hasbeen reported in younger animal populations.

     

From single muscle fiber to whole muscle mechanics: a finite element model of a muscle bundle with fast and slow fibers

Muscles exhibit highly complex, multi-scale architecture with thousands of muscle fibers, each with different properties, interacting with each other and surrounding connective structures. Consequently, the results of single-fiber experiments are scarcely linked to the macroscopic or whole muscle behavior. This is especially true for human muscles where it would be important to understand of how skeletal muscles disorders affect patients’ life. In this work, we developed a mathematical model to study how fast and slow muscle fibers, well characterized in single-fiber experiments, work and generate together force and displacement in muscle bundles. We characterized the parameters of a Hill-type model, using experimental data on fast and slow single human muscle fibers, and comparing experimental data with numerical simulations obtained from finite element (FE) models of single fibers. Then, we developed a FE model of a bundle of 19 fibers, based on an immunohistochemically stained cross section of human diaphragm and including the corresponding properties of each slow or fast fiber. Simulations of isotonic contractions of the bundle model allowed the generation of its apparent force–velocity relationship. Although close to the average of the force–velocity curves of fast and slow fibers, the bundle curve deviates substantially toward the fast fibers at low loads. We believe that the present model and the characterization of the force–velocity curve of a fiber bundle represents the starting point to link the single-fiber properties to those of whole muscle with FE application in phenomenological models of human muscles.     

Decreased insulin action on muscle glucose transport after eccentric contractions in rats

Asp, Sven, and Erik A. Richter. Decreased insulinaction on muscle glucose transport after eccentric contractions in rats. J. Appl. Physiol. 81(5):1924-1928, 1996.We have recently shown that eccentriccontractions (Ecc) of rat calf muscles cause muscle damage anddecreased glycogen and glucose transporter GLUT-4 protein content inthe white (WG) and red gastrocnemius (RG) but not in the soleus (S) (S. Asp, S. Kristiansen, and E. A. Richter. J. Appl.Physiol. 79: 1338-1345, 1995). To study whetherthese changes affect insulin action, hindlimbs were perfused at three different insulin concentrations (0, 200, and 20,000 µU/ml) 2 daysafter one-legged eccentric contractions of the calf muscles. Comparedwith control, basal glucose transport was slightly higher (P < 0.05) in Ecc-WG and -RG,whereas it was lower (P < 0.05) atboth submaximal and maximal insulin concentrations in the Ecc-WG and atmaximal concentrations in the Ecc-RG. In the Ecc-S, the glucosetransport was unchanged in hindquarters perfused in the absence orpresence of a submaximal stimulating concentration of insulin, whereasit was slightly (P < 0.05) higherduring maximal insulin stimulation compared with control S. At the endof perfusion the glycogen concentrations were lower in bothEcc-gastrocnemius muscles compared with control muscles at all insulinconcentrations. Fractional velocity of glycogen synthase increasedsimilarly with increasing insulin concentrations in Ecc- and control WGand RG. We conclude that insulin action on glucose transport but notglycogen synthase activity is impaired in perfused muscle exposed toprior eccentric contractions.

     

Decreased contraction economy in mouse EDL muscle injured by eccentric contractions

Warren III, Gordon L., Jay H. Williams, Christopher W. Ward,Hideki Matoba, Christopher P. Ingalls, Karl M. Hermann, and R. B. Armstrong. Decreased contraction economy in mouse EDL muscleinjured by eccentric contractions. J. Appl.Physiol. 81(6): 2555-2564, 1996.The objective ofthis study was to find out whether basal and/or active energymetabolism are altered in isolated mouse extensor digitorum longusmuscle injured by eccentric (Ecc) contractions. Measurements of basalO₂ consumption and isometric tetanus O₂ recovery cost were madeat 25°C on muscles that had done either 10 Ecc, 10 isometric (Iso),or no contractions (No). In parallel experiments, rates of lactate andpyruvate production were measured to estimate the anaerobiccontribution. Basal O₂ consumptionwas unaffected by the type of protocol performed(P = 0.07). However, the tetanusO₂ cost per force-time integral was elevated by 30-36% for the Ecc protocol muscles over that forthe Iso and No protocol muscles. When including the increased lactateproduction by the Ecc protocol muscles, the total energetic cost perforce-time integral was 53% higher than that for the Iso protocolmuscles [2.35 ± 0.17 vs. 1.54 ± 0.18 µmolO₂/(N ^· m ^· s)].The decreased economy was attributed to two factors. First, in skinnedfibers isolated from the injured muscles, the ratio of maximalactomyosin adenosinetriphosphatase activity to force production was upby 37.5%, suggesting uncoupling of ATP hydrolysis from forceproduction. Second, increased reliance on anaerobic metabolism alongwith the fluorescent microscopic study of mitochondrial membranepotential and histochemical study of ATP synthase suggested anuncoupling of oxidative phosphorylation in the injured muscles.

     

Determination of fascicle length and pennation in a contracting human muscle in vivo

Fukunaga, Tetsuo, Yoshiho Ichinose, Masamitsu Ito, YasuoKawakami, and Senshi Fukashiro. Determination of fascicle lengthand pennation in a contracting human muscle in vivo.J. Appl. Physiol. 82(1): 354-358, 1997.We have developed a technique to determine fascicle length inhuman vastus lateralis muscle in vivo by using ultrasonography. Whenthe subjects had the knee fully extended passively from a position of110° flexion (relaxed condition), the fascicle length decreasedfrom 133 to 97 mm on average. During static contractions at 10% ofmaximal voluntary contraction strength (tensed condition), fascicleshortening was more pronounced (from 126 to 67 mm), especially when theknee was closer to full extension. Similarly, as the knee was extended, the angle of pennation (fascicle angle, defined as the angle between fascicles and aponeurosis) increased (relaxed, from 14 to 18°; tensed, from 14 to 21°), and a greater increase in the pennation angle was observed in the tensed than in the relaxed condition when theknee was close to extension (<40°). We conclude that there aredifferences in fascicle lengths and pennation angles when the muscle isin a relaxed and isometrically tensed conditions and that thedifferences are affected by joint angles, at least at thesubmaximal contraction level.

     

Effects of intracellular acidification and varied temperature on force, stiffness, and speed of shortening in frog muscle fibers

This study aimed to establish whether the temperature-dependent effect of acidification on maximum force observed in mammalian muscles also applies to frog muscle. Measurements of force, stiffness, and unloaded velocity of shortening in intact single muscle fibers from the anterior tibialis muscle of Rana temporaria were performed between 0 and 22°C during fused tetani in H₂CO₃-CO₂-buffered Ringer solution with pH adjusted to 7.0 and 6.3, respectively. The force-to-stiffness ratio increased as a rectilinear function of temperature between 0 and 20°C at pH 7.0. Lowering the pH to 6.3 reduced the tetanic force by 13.5 ± 1.2 and 11.5 ± 1.4% at 2.8 and 20.5°C, respectively, with only a minor reduction in fiber stiffness. The maximum speed of shortening was decreased by lowered pH by 12.9 ± 1.5 and 7.8 ± 1.1% at low and high temperature, respectively. Acidification increased the time to reach 70% of maximum force by 18.0% at 2°C; the same pH change performed at 20°C in the same fibers reduced the rise time by 24.1%. The same increase in the rate of rise of force at high temperature was also found at normal pH after the fibers were fatigued by frequent stimulation. It is concluded that, in frog muscle, the force-depressant effect of acidification does not vary significantly with temperature. By contrast, acidification affects the onset of activation in a manner that is critically dependent on temperature. muscle contraction; pH     

Sarcomere lesion damage occurs mainly in slow fibers of reloaded rat adductor longus muscles

Sarcomerelesions were previously observed with reloading of rat adductor longusmuscles after spaceflight and hindlimb unloading (HU).Spaceflown rats displayed more lesioned fibers in the"slow-fiber" region, suggesting a damage-susceptible fiber type.Unloading induces fast myosin expression in some slow fibers,generating hybrid fibers. We examined whether lesion damage differedamong slow-, hybrid-, and fast-fiber types in HU-reloaded adductorlongus muscles. Temporal HU for 5, 8, 11, 14, and 17 days revealed that hybrid fiber percent, detected by antimyosin immunostaining, peaked at29 ± 12% by 14 days. A 14-day HU followed by 12-14 h ofvoluntary reloading was performed to induce lesions.² analysis showed that slowfibers were preferentially damaged, accounting for 92 ± 5% oflesioned fibers; hybrid and fast fibers accounted for 7 ± 4 and<0.5%, respectively. Atrophy did not explain differential lesiondamage across fiber types, as slow and hybrid fibers atrophied to asimilar extent. Because active myofiber contractions are requisite forlesion formation, selective recruitment of slow fibers most likelyexplains their damage susceptibility.

     

Muscle fiber architecture of the dog diaphragm

Boriek, Aladin M., Charles C. Miller III, and Joseph R. Rodarte. Muscle fiber architecture of the dog diaphragm.J. Appl. Physiol. 84(1): 318-326, 1998.Previous measurements of muscle thickness and length ratio ofcostal diaphragm insertions in the dog (A. M. Boriek and J. R. Rodarte.J. Appl. Physiol. 77: 2065-2070,1994) suggested, but did not prove, discontinuous muscle fiberarchitecture. We examined diaphragmatic muscle fiber architecture usingmorphological and histochemical methods. In 15 mongrel dogs, transversesections along the length of the muscle fibers were analyzedmorphometrically at ×20, by using the BioQuant System IVsoftware. We measured fiber diameters, cross-sectional fiber shapes,and cross-sectional area distributions of fibers. We also determinednumbers of muscle fibers per cross-sectional area and ratio ofconnective tissue to muscle fibers along a course of the muscle fromnear the chest wall (CW) to near the central tendon (CT) for midcostalleft and right hemidiaphragms, as well as ventral, middle, and dorsalregions of the left costal hemidiaphragm. In six other mongrel dogs,the macroscopic distribution of neuromuscular junctions (NMJ) onthoracic and abdominal diaphragm surfaces was determined by stainingthe intact diaphragmatic muscle for acetylcholinesterase activity. Theaverage major diameter of muscle fibers was significantly smaller, andthe number of fibers was significantly larger midspan between CT and CWthan near the insertions. The ratio of connective tissues to musclefibers was largest at CW compared with other regions along the lengthof the muscle. The diaphragm is transversely crossed by multiplescattered NMJ bands with fairly regular intervals offset in adjacentstrips. Muscle fascicles traverse two to five NMJ, consistent withfibers that do not span the entire fascicle from CT to CW. Theseresults suggest that the diaphragm has a discontinuous fiberarchitecture in which contractile forces may be transmitted among themuscle fibers through the connective tissue adjacent to the fibers.

     

Evidence of residual force enhancement for multi-joint leg extension

Force enhancement is a well accepted property of skeletal muscle and has been observed at all structural levels ranging from single myofibrils to voluntarily activated m. quadriceps femoris in vivo. However, force enhancement has not been studied for multi-joint movements like human leg extension; therefore knowledge about its relevance in daily living remains limited. The purpose of this study was to determine whether there is force enhancement during maximal voluntary multi-joint leg extension. Human leg extension was studied (n=22) on a motor driven leg press dynamometer where external reaction forces under the feet as well as activity of 8 lower extremity muscles were measured. In addition, torque in the ankle and knee joints was calculated using inverse dynamics. The steady-state isometric force, joint torques, and muscle activation after active stretch (20° stretch amplitude at 60°/s) were compared with the corresponding values obtained during isometric reference contractions. There was consistent force enhancement during and following stretch for both forces and joint torques. Potentiation during stretch reached values between 26% and 30%, while a significant force enhancement of 10.5–12.3% and 4.3–7.4% remained 0.5–1 and 2.5–3 s after stretch, respectively. During stretch, EMG signals of m. gastrocnemius medialis and lateralis were significantly increased, while following stretch all analyzed muscles showed the same activity as during the reference contractions. We conclude from these results that force enhancement exists in everyday movements and should be accounted for when analyzing or modelling human movement.     

In vivo moment generation and architecture of the human plantar flexors after different shortening–stretch cycles velocities

The purpose of this study was to examine the moment generation of the human plantar flexors and the architecture of the gastrocnemius medialis muscle during and after shortening–stretch cycles in vivo. Fourteen male subjects (30 ± 7 years, 177 ± 7 cm, 80 ± 9 kg) performed a series of electro-stimulated shortening–stretch plantar flexion contractions. The shortening–stretch cycles were performed at three constant angular velocities (25°/s, 50°/s, 100°/s), two amplitudes (15° and 25° ankle angle changes) and at two different stimulation frequencies (30 Hz and 85 Hz). The resultant ankle joint moments were calculated through inverse dynamics. Pennation angle and fascicle length of the m. gastrocnemius medialis at rest and during contractions were measured using ultrasonography. The corresponding ankle moments, kinematics and changes in muscle architecture were analysed at seven time intervals. A three-way analysis of variance (amplitude × velocity × stimulation frequency) and post-hoc test with Bonferroni correction were used to check the amplitude, velocity and stimulation level related effects on moment enhancement (α = 0.05). The results show an ankle joint moment enhancement after shortening–stretch cycles influenced by muscle architectural changes. We found 2–3% isometric ankle joint moment enhancement at steady state, 1.5–2.0 s after the shortening–stretch cycle. However, the observed alteration in muscle architecture after the imposed perturbation, could lead to an underestimation (1–3%) of joint moment enhancement due to the force–length relationship of the triceps surae. Furthermore, the enhancement observed was independent of the shortening–stretch amplitude, velocity and stimulation frequency.