Prior eccentric contractions impair maximal insulin action on muscle glucose uptake in the conscious rat

Asp, Sven, Allan Watkinson, Nicholas D. Oakes, and Edward W. Kraegen. Prior eccentric contractions impair maximal insulin action on muscle glucose uptake in the conscious rat.J. Appl. Physiol. 82(4):1327-1332, 1997.Our aim was to examine the effect of prioreccentric contractions on insulin action locally in muscle in theintact conscious rat. Anesthetized rats performed one-leg eccentriccontractions through the use of calf muscle electrical stimulationfollowed by stretch of the active muscles. Two days later, basal andeuglycemic clamp studies were conducted with the rats in the awakefasted state. Muscle glucose metabolism was estimated from2-[¹⁴C(U)]deoxy-D-glucoseandD-[3-³H]glucose administration, and comparisons were made between the eccentrically stimulated and nonstimulated (control) calfmuscles. At midphysiological insulin levels, effects ofprior eccentric exercise on muscle glucose uptake were notstatistically significant. Maximal insulin stimulation revealed reducedincremental glucose uptake above basal(P < 0.05 in the red gastrocnemius;P < 0.1 in the white gastrocnemiusand soleus) and impaired net glycogen synthesis in all eccentricallystimulated muscles (P < 0.05). Weconclude that prior eccentric contractions impair maximal insulin action (responsiveness) on local muscle glucose uptake and glycogen synthesis in the conscious rat.

     

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.

     

Normal forces and myofibrillar disruption after repeated eccentric exercise

Hortobágyi, Tibor, Joseph Houmard, David Fraser,Ronald Dudek, Jean Lambert, and James Tracy. Normalforces and myofibrillar disruption after repeated eccentric exercise.J. Appl. Physiol. 84(2): 492-498, 1998.To investigate the "rapid-adaptation" phenomenon, weexamined force, neural, and morphological adaptations in 12 subjectswho performed 100 eccentric contractions with the quadriceps muscle(bout 1) and repeated the sameexercise after a 2-wk hiatus (bout2). Two days after bout1, quadriceps muscle strength and surfaceelectromyographic (EMG) activity declined ~37 and 28%, respectively,in the control group (n = 6). Atday 2 after bout 1, significant increases occurred in patellar tendonreflex amplitude (~25%), muscle soreness (fivefold), and serumcreatine kinase (220%), and 65 ± 12% of the total number of pixelsin the EMG indicated myofibrillar disruption. At day7 after bout 1, all variables returned to normal. At day 2 after bout 2, no significant changesoccurred in force, EMG, creatine kinase, or soreness, but reflexamplitude increased, and 23 ± 4% of the total number of pixels inthe EMG still indicated myofibrillar disruption. The results suggestthat the rapid force recovery following eccentric exercise is mediatedat least in part by neural factors and that this recovery may occurindependently of cell disruption.

     

Neuromuscular factors contributing to in vivo eccentric moment generation

Webber, Sandra, and Dean Kriellaars. Neuromuscularfactors contributing to in vivo eccentric moment generation.J. Appl. Physiol. 83(1): 40-45, 1997.Muscle series elasticity and its contribution to eccentricmoment generation was examined in humans. While subjects [male,n = 30; age 26.3 ± 4.8 (SD) yr; body mass 78.8 ± 13.1 kg] performed an isometric contractionof the knee extensors at 60° of knee flexion, a quick stretch was imposed with a 12°-step displacement at 100°/s. The test wasperformed at 10 isometric activation levels ranging from 1.7 to 95.2%of maximal voluntary contraction (MVC). A strong linear relationship was observed between the peak imposed eccentric moment derived fromquick stretch and the isometric activation level(y = 1.44x + 7.08; r = 0.99). This increase in theeccentric moment is consistent with an actomyosin-dependent elasticitylocated in series with the contractile element of muscle. Byextrapolating the linear relationship to 100% MVC, the predictedmaximum eccentric moment was found to be 151% MVC, consistent with invitro data. A maximal voluntary, knee extensor strength test was alsoperformed (5-95°, 3 repetitions, ±50, 100, 150, 200, and250°/s). The predicted maximum eccentric moment was 206% of theangle- and velocity-matched, maximal voluntary eccentric moments. Thiswas attributed to a potent neural regulatory mechanism that limits therecruitment and/or discharge of motor units during maximalvoluntary eccentric contractions.

     

More tetanic contractions are required for activating glucose transport maximally in trained muscle

Kawanaka, Kentaro, Izumi Tabata, and MitsuruHiguchi. More tetanic contractions are requiredfor activating glucose transport maximally in trained muscle.J. Appl. Physiol. 83(2): 429-433, 1997.Exercise training increases contraction-stimulated maximalglucose transport and muscle glycogen level in skeletal muscle.However, there is a possibility that more muscle contractions arerequired to maximally activate glucose transport in trained than inuntrained muscle, because increased glycogen level after training mayinhibit glucose transport. Therefore, the purpose of this study was toinvestigate the relationship between the increase in glucose transportand the number of tetanic contractions in trained and untrained muscle.Male rats swam 2 h/day for 15 days. In untrained epitrochlearis muscle,resting glycogen was 26.6 µmol glucose/g muscle. Ten, 10-s-longtetani at a rate of 1 contraction/min decreased glycogen level to 15.4 µmol glucose/g muscle and maximally increased2-deoxy-D-glucose(2-DG) transport. Training increasedcontraction-stimulated maximal 2-DG transport (+71%;P < 0.01), GLUT-4 protein content(+78%; P < 0.01), and restingglycogen level (to 39.3 µmol glucose/g muscle;P < 0.01) on the next day after thetraining ended, although this training effect might be due, at least inpart, to last bout of exercise. In trained muscle, 20 tetani werenecessary to maximally activate glucose transport. Twenty tetanidecreased muscle glycogen to a lower level than 10 tetani (18.9 vs.24.0 µmol glucose/g muscle; P < 0.01). Contraction-stimulated 2-DG transport was negatively correlatedwith postcontraction muscle glycogen level in trained (r = 0.60;P < 0.01) and untrained muscle(r = 0.57;P < 0.01).

     

Greater initial adaptations to submaximal muscle lengthening than maximal shortening

Hortobágyi, Tibor, Jason Barrier, David Beard, JohnBraspennincx, Peter Koens, Paul Devita, Line Dempsey, and Jean Lambert. Greater initial adaptations to submaximal muscle lengthening thanmaximal shortening. J. Appl. Physiol.81(4): 1677-1682, 1996.The purpose of this study was tocompare the short-term strength and neural adaptations to eccentric andconcentric training at equal force levels. Forty-two sedentary women(age = 21.5 yr) were ranked based on the initial quadriceps strengthscore, and trios of subjects were randomly assigned to either aneccentric (n = 14), a concentric (n = 14), or a nonexercising controlgroup (n = 14). Training involved atotal of 824 eccentric or concentric quadriceps actions at 1.05 rad ^· s¹administered in four sets of 6-10 repetitions, four times per weekfor 6 wk. Before and after training, all subjects were tested forunilateral maximal isometric and eccentric and concentric actions at1.05 rad ^· s¹and for a 40-repetition eccentric and concentric fatigue series of theleft and right quadriceps. Surface electromyographic activity of thevastus lateralis and medialis was monitored during testing. Concentrictraining increased concentric (36%, P < 0.05), isometric (18%, P < 0.05), and eccentric strength (13%), and eccentric training increasedeccentric (42%, P < 0.05),isometric (30%, P < 0.05), andconcentric (13%) strength. Eccentric training improved eccentric andisometric strength more (P < 0.05)than did concentric training. The electromyographic adaptations weregreater with eccentric training. Cross-education was 6%, and neithertraining mode modified fatigability. The data suggest that training ofthe quadriceps muscle with submaximal eccentric actions brings aboutgreater strength adaptations faster than does training withmaximal-level concentric actions in women. This greater adaptation islikely to be mediated by both mechanical and neural factors.

     

Modulation of myosin isoform expression by mechanical loading: role of stimulation frequency

Caiozzo, Vincent J., Michael J. Baker, and Kenneth M. Baldwin. Modulation of myosin isoform expression by mechanical loading: role of stimulation frequency. J. Appl.Physiol. 82(1): 211-218, 1997.This study testedthe hypothesis that mechanical loading, not stimulation frequency perse, plays a key role in determining the plasticity of myosin heavychain (MHC) protein isoform expression in muscle undergoing resistancetraining. Female Sprague-Dawley rats were randomly assigned toresistance-training programs that employed active1) shortening(n = 7) or2) lengthening contractions(n = 8). The medial gastrocnemius (MG)muscles in each group trained under loading conditions thatapproximated 90-95% of maximum isometric tetanictension but were stimulated at frequencies of 100 and~25 Hz, respectively. Lengthening and shortening contractions wereproduced by using a Cambridge ergometer system. The MG muscles trainedevery other day, performing a total of 16 training sessions. Bothtraining programs produced significant (P < 0.01) and similar reductions inthe fast type IIB MHC protein isoform in the white MG muscle, reducingits relative content to ~50% of the total MHC protein isoform pool.These changes were accompanied by increases in the relative content ofthe fast type IIX MHC protein isoform that were of similar magnitudefor both groups. The results of this study clearly demonstrate thatstimulation frequency does not play a key role in modulating MHCisoform alterations that result from high-resistance training.

     

Impact of sarcoglycan complex on mechanical signal transduction in murine skeletal muscle

Loss of the dystrophin glycoprotein complex (DGC) or a subset of its components can lead to muscular dystrophy. However, the patterns of symptoms differ depending on which proteins are affected. Absence of dystrophin leads to loss of the entire DGC and is associated with susceptibility to contractile injury. In contrast, muscles lacking -sarcoglycan (-SG) display little mechanical fragility and still develop severe pathology. Animals lacking dystrophin or -SG were used to identify DGC components critical for sensing dynamic mechanical load. Extensor digitorum longus muscles from 7-wk-old normal (C57), dystrophin- null (mdx), and -SG-null (gsg^–/–) mice were subjected to a series of eccentric contractions, after which ERK1/2 phosphorylation levels were determined. At rest, both dystrophic strains had significantly higher ERK1 phosphorylation, and gsg^–/– muscle also had heightened ERK2 phosphorylation compared with wild-type controls. Eccentric contractions produced a significant and transient increase in ERK1/2 phosphorylation in normal muscle, whereas the mdx strain displayed no significant proportional change of ERK1/2 phosphorylation after eccentric contraction. Muscles from gsg^–/– mice had no significant increase in ERK1 phosphorylation; however, ERK2 phosphorylation was more robust than in C57 controls. The reduction in mechanically induced ERK1 phosphorylation in gsg^–/– muscle was not dependent on age or severity of phenotype, because muscle from both young and old (age 20 wk) animals exhibited a reduced response. Immunoprecipitation experiments revealed that -SG was phosphorylated in normal muscle after eccentric contractions, indicating that members of the DGC are modified in response to mechanical perturbation. This study provides evidence that the SGs are involved in the transduction of mechanical information in skeletal muscle, potentially unique from the entire DGC. muscular dystrophy; eccentric contractions; extracellular signal-regulated kinase 1/2     

Doublet potentiation during eccentric and concentric contractions of cat soleus muscle

Sandercock, Thomas G., and C. J. Heckman. Doubletpotentiation during eccentric and concentric contractions of cat soleusmuscle. J. Appl. Physiol. 82(4):1219-1228, 1997.The addition of an extra stimulus pulse, ordoublet, at the beginning of a low-frequency train has been shown tosubstantially increase isometric force. This study examined the effectsof muscle movement on this doublet potentiation. The soleus muscles ofanesthetized cats were stimulated at 10 Hz for 1 s, with and without anadded doublet (0.01-s interval). Isovelocity releases reduced but didnot eliminate peak and early doublet potentiation (average 0.0-0.5s after the doublet). Large releases, >0.4 s after the doublet,completely abolished sustained doublet potentiation (average0.5-1.0 s after the doublet). In contrast, early isovelocitystretches boosted peak doublet potentiation. Yet, large stretches laterin the stimulus almost completely eliminated sustained doubletpotentiation. This suggests that a different mechanism is responsiblefor early and sustained doublet potentiations. Because peak and averageinitial doublet potentiation were not strongly affected by movement,doublets still offer a viable control strategy to increase force during movement while minimizing the number of stimulus pulses.

     

Effects of muscle kinematics on surface EMG amplitude and frequency during fatiguing dynamic contractions

Potvin, J. R. Effects of muscle kinematics on surfaceEMG amplitude and frequency during fatiguing dynamic contractions. J. Appl. Physiol. 82(1): 144-151, 1997.Fifteen male subjects performed a repetitive elbowflexion/extension task with a 7-kg mass until exhaustion. Average jointangle, angular velocity, and biceps brachii surface electromyographic(EMG) amplitude (aEMG) and mean powerfrequency (MPF) were calculated with each consecutive 250-ms segment ofdata during the entire trial. Data were separated into concentric oreccentric phases and into seven 20°-ranges from 0 to 140° ofelbow flexion. A regression analysis was used to estimate the restedand fatigued aEMG and MPF values. aEMG values were expressed as apercentage of amplitudes from maximum voluntary contractions (MVC).Under rested dynamic conditions, the average concentric aEMG amplitudewas 10% MVC higher than average eccentric values. Rested MPF valueswere similar for concentric and eccentric phases, although valuesincreased ~20 Hz from the most extended to flexed joint angles.Fatigue resulted in an average increase in concentric and eccentricaEMG of 35 and 10% MVC, respectively. The largest concentric aEMGincreases (up to 58% MVC) were observed at higher joint velocities,whereas eccentric increases appeared to be related to decreases invelocity. Fatigue had a similar effect on MPF during both concentricand eccentric phases. Larger MPF decreases were observed at shortermuscle lengths such that values within each angle range were verysimilar by the end of the trial. It was hypothesized that this findingmay reflect a biological minimum in conduction velocity beforepropagation failure occurs.

     

Stretch-induced enhancement of mechanical power output in human multijoint exercise with countermovement

Takarada, Yudai, Yuichi Hirano, Yusuke Ishige, and NaokataIshii. Stretch-induced enhancement of mechanical power output inhuman multijoint exercise with countermovement. J. Appl. Physiol. 83(5): 1749-1755, 1997.Therelation between the eccentric force developed during a countermovementand the mechanical power output was studied in squatting exercisesunder nominally isotonic load (50% of 1-repetition maximum). Thesubjects (n = 5) performed squattingexercises with a countermovement at varied deceleration rates beforelifting the load. The ground reaction force and video images wererecorded to obtain the power output of the body. Net muscle momentsacting at hip, knee, and ankle joints were calculated from videorecordings by using inverse dynamics. When an intense deceleration wastaken at the end of downward movement, large eccentric force wasdeveloped, and the mechanical power subsequently produced during thelifting movement was consistently larger than that produced without thecountermovement. Both maximal and mean power outputs during concentricactions increased initially with the eccentric force, whereas theybegan to decline when the eccentric force exceeded ~1.4 times the sumof load and body weight. Video-image analysis showed that thischaracteristic relation was predominantly determined by the torquearound the knee joint. Electromyographic analyses showed no consistentincrease in time-averaged integrated electromyograph from vastuslateralis with the power output, suggesting that the enhancement ofpower output is primarily caused by the prestretch-induced improvementof an intrinsic force-generating capability of the agonist muscle.

     

Efficiency of human skeletal muscle in vivo: comparison of isometric, concentric, and eccentric muscle action

Ryschon, T. W., Fowler, R. E. Wysong, A.-R. Anthony, and R. S. Balaban. Efficiency of human skeletal muscle in vivo: comparison of isometric, concentric, and eccentric muscle action. J. Appl. Physiol. 83(3): 867-874, 1997.The purpose of this study was to estimate the efficiency of ATPutilization for concentric, eccentric, and isometric muscle action inthe human tibialis anterior and extensor digitorum longus in vivo. Adynamometer was used to quantitate muscle work, or tension, whilesimultaneous ³¹P-nuclear magneticresonance data were collected to monitor ATP, phosphocreatine,inorganic phosphate, and pH. The relative efficiency of the actions wasestimated in two ways: steady-state effects on high-energyphosphates and a direct comparison of ATP synthesis rates with work. Inthe steady state, the cytosolic free energy dropped to the lowest valuewith concentric activity, followed by eccentric and isometric actionfor comparative muscle tensions. Estimates of ATP synthesis ratesrevealed a mechanochemical efficiency [i.e., ATP productionrate/work (both in J/s)] of 15.0 ± 1.3% in concentric and34.7 ± 6.1% in eccentric activity. The estimated maximum ATPproduction rate was highest in concentric action, suggesting anactivation of energy metabolism under these conditions. By using directmeasures of metabolic strain and ATP turnover, these data demonstrate adecreasing metabolic efficiency in human muscle action from isometric,to eccentric, to concentric action.

     

Neuromuscular drive and force production are not altered during bilateral contractions

Jakobi, J. M., and E. Cafarelli. Neuromuscular driveand force production are not altered during bilateral contractions. J. Appl. Physiol. 84(1): 200-206, 1998.Several investigators have studied the deficit in maximalvoluntary force that is said to occur when bilateral muscle groupscontract simultaneously. A true bilateral deficit (BLD) would suggest asignificant limitation of neuromuscular control; however, some of thedata from studies in the literature are equivocal. Our purpose was todetermine whether there is a BLD in the knee extensors of untrainedyoung male subjects during isometric contractions and whether thisdeficit is associated with a decreased activation of the quadriceps,increased activation of the antagonist muscle, or an alteration inmotor unit firing rates. Twenty subjects performed unilateral (UL) and bilateral (BL) isometric knee extensions at 25, 50, 75, and 100% maximal voluntary contraction. Total UL and BL force (3%) and maximal rate of force generation (2.5%) were not significantly different. Total UL and BL maximal vastus lateralis electromyographic activity (EMG; 2.7 ± 0.28 vs. 2.6 ± 0.24 mV) andcoactivation (0.17 ± 0.02 vs. 0.20 ± 0.02 mV) were also notdifferent. Similarly, the ratio of force to EMG during submaximal ULand BL contractions was not different. Analysis of force production byeach leg in UL and BL conditions showed no differences in force, rateof force generation, EMG, motor unit firing rates, and coactivation.Finally, assessment of quadriceps activity with the twitchinterpolation technique indicated no differences in the degree ofvoluntary muscle activation (UL: 93.6 ± 2.51 Hz, BL: 90.1 ± 2.43 Hz). These results provide no evidence of a significant limitationin neuromuscular control between BL and UL isometric contractions ofthe knee extensor muscles in young male subjects.

     

Contraction-induced injury to the extensor digitorum longus muscles of rats: the role of vitamin E

Van der Meulen, Jack H., Anne McArdle, Malcolm J. Jackson,and John A. Faulkner. Contraction-induced injury to the extensordigitorum longus muscles of rats: the role of vitamin E. J. Appl. Physiol. 83(3): 817-823, 1997.Three days after a protocol of 225 pliometric (lengthening)contractions was administered to in situ extensor digitorum longusmuscles of rats, the force deficit was 64 ± 7% and the percentageof damaged muscle fibers was 38 ± 5% of the control values. Wethen tested the hypothesis that at 3 h and 3 days after the protocol anelevation in the muscle vitamin E content would decrease the forcedeficit, the percentage of damaged muscle fibers, and the serumactivities of creatine kinase and pyruvate kinase. The 5-8 days ofintravenous injections of -tocopherol increased muscle vitamin Econtent threefold compared with vehicle (ethanol)-treated rats. Despite the difference in vitamin E content, the force deficit and number ofdamaged fibers were not different. After the contractionprotocol, the serum creatine kinase and pyruvate kinase activities ofthe vehicle-treated rats increased fourfold at 3 h and twofold at 3 days, whereas the vitamin E-treated rats showed no change. We concludethat vitamin E treatment did not ameliorate either the induction of theinjury or the more severe secondary injury at 3 days.Despite the absence of evidence for an antioxidant function, the lackof any increase in serum enzyme activities for vitamin E-treated ratsat 3 h and 3 days supported a role for vitamin E in the prevention ofenzyme loss after muscle damage.

     

Effects of concentric and eccentric training on muscle strength, cross-sectional area, and neural activation

Higbie, Elizabeth J., Kirk J. Cureton, Gordon L. Warren III,and Barry M. Prior. Effects of concentric and eccentric trainingon muscle strength, cross-sectional area, and neural activation.J. Appl. Physiol. 81(5):2173-2181, 1996.We compared the effects of concentric (Con) andeccentric (Ecc) isokinetic training on quadriceps muscle strength,cross-sectional area, and neural activation. Women (age 20.0 ± 0.5 yr) randomly assigned to Con training (CTG;n = 16), Ecc training (ETG;n = 19), and control (CG;n = 19) groups were tested before andafter 10 wk of unilateral Con or Ecc knee-extension training. Averagetorque measured during Con and Ecc maximal voluntary knee extensions increased 18.4 and 12.8% for CTG, 6.8 and 36.2% for ETG, and 4.7 and1.7% for CG, respectively. Increases by CTG and ETG were greater than for CG (P < 0.05). ForCTG, the increase was greater when measured with Con than with Ecctesting. For ETG, the increase was greater when measured with Ecc thanwith Con testing. The increase by ETG with Ecc testing was greater thanthe increase by CTG with Con testing. Corresponding changes in theintegrated voltage from an electromyogram measured during strengthtesting were 21.7 and 20.0% for CTG, 7.1 and 16.7% for ETG, and8.0 and 9.1% for CG. Quadriceps cross-sectional areameasured by magnetic resonance imaging (sum of 7 slices) increased morein ETG (6.6%) than in CTG (5.0%) (P < 0.05). We conclude that Ecc is more effective than Con isokinetictraining for developing strength in Ecc isokinetic muscle actions andthat Con is more effective than Ecc isokinetic training for developingstrength in Con isokinetic muscle actions. Gains in strength consequentto Con and Ecc training are highly dependent on the muscle action usedfor training and testing. Muscle hypertrophy and neural adaptationscontribute to strength increases consequent to both Con and Ecctraining.

     

Regional intramuscular pressure development and fatigue in the canine gastrocnemius muscle in situ

Ameredes, Bill T., and Mark A. Provenzano. Regionalintramuscular pressure development and fatigue in the caninegastrocnemius muscle in situ. J. Appl.Physiol. 83(6): 1867-1876, 1997.Intramuscular pressure (P_IM) was measuredsimultaneously in zones of the medial head of thegastrocnemius-plantaris muscle group (zone I, popliteal origin; zoneII, central; zone III, near calcaneus tendon) to determine regionalmuscle mechanics during isometric tetanic contractions. PeakP_IM averages were 586, 1,676, and993 mmHg deep in zones I, II, and III and 170, 371, and 351 mmHgsuperficially in zones I, II, and III, respectively. During fatigue,loss of P_IM across zones wasgreatest in zone III (81%) and least in zone I (60%) when whole muscle tension loss was 49%. Recovery ofP_IM was greatest in zone III andleast in zone II, achieving 86% and 67% of initial P_IM, respectively, when tensionrecovered to 89%. These data demonstrate that1) regional mechanical performancecan be measured as P_IM within awhole muscle, 2)P_IM is nonuniform within thecanine gastrocnemius-plantaris muscle, being greatest in the deepcentral zone, and 3) fatigue andrecovery of P_IM are dissimilaracross regions. These differences suggest distinct local effects that integrate to determine whole muscle mechanical capacity during andafter intense exercise.

     

Instantaneous force-velocity-length relationship in diaphragmatic sarcomere

Coirault, Catherine, Denis Chemla, Jean-Claude Pourny,Francine Lambert, and Yves Lecarpentier. Instantaneousforce-velocity-length relationship in diaphragmatic sarcomere.J. Appl. Physiol. 82(2): 404-412, 1997.The simultaneous analysis of muscle force, length, velocity, andtime has been shown to precisely characterize the mechanicalperformance of isolated striated muscle. We tested the hypothesis thatthe three-dimensional force-velocity-length relationship reflectsmechanical properties of sarcomeres. In hamster diaphragm strips,instantaneous sarcomere length (SL) and muscle length were simultaneously measured during afterloaded twitches. SL was measured by means of laser diffraction. Wealso studied the influence of initialSL, abrupt changes in total load, and2 × 10⁷ M dantrolene.Baseline resting SL at the apex of thelength-active tension curve was 2.2 ± 0.1 µm, whereasSL at peak shortening was 1.6 ± 0.1 µm in the preloaded twitch and 2.1 ± 0.1 µm in the "isometric" twitch. Over the whole load continuum and at anygiven level of isotonic load, there was a unique relationship between instantaneous sarcomere velocity and instantaneousSL. Part of this relationship was timeindependent and initial SL independent and was markedly downshifted after dantrolene. When five different muscle regions were considered, there were no significant variations ofSL and sarcomere kinetics along themuscle. These results indicate that the time- and initiallength-independent part of the instantaneous force-velocity-lengthrelationship previously described in muscle strips reflects intrinsicsarcomere mechanical properties.

     

Forearm training attenuates sympathetic responses to prolonged rhythmic forearm exercise

Sinoway, Lawrence, Jeffrey Shenberger, Gretchen Leaman,Robert Zelis, Kristen Gray, Robert Baily, and Urs Leuenberger. Forearm training attenuates sympathetic responses to prolonged rhythmic forearm exercise. J. Appl.Physiol. 81(4): 1778-1784, 1996.We previouslydemonstrated that nonfatiguing rhythmic forearm exercise at 25%maximal voluntary contraction (12 2-s contractions/min) evokessympathoexcitation without significant engagement ofmetabolite-sensitive muscle afferents (B. A. Batman, J. C. Hardy, U. A. Leuenberger, M. B. Smith, Q. X. Yang, and L. I. Sinoway.J. Appl. Physiol. 76: 1077-1081,1994). This is in contrast to the sympathetic nervous system responsesobserved during fatiguing static forearm exercise wheremetabolite-sensitive afferents are the key determinants of sympatheticactivation. In this report we examined whether forearm exercisetraining would attenuate sympathetic nervous system responses torhythmic forearm exercise. We measured heart rate, mean arterial bloodpressure (MAP), muscle sympathetic nerve activity (microneurography),plasma norepinephrine (NE), and NE spillover and clearance (tritiatedNE kinetics) during nonfatiguing rhythmic forearm exercise before andafter a 4-wk unilateral forearm training paradigm. Training had noeffect on forearm mass, maximal voluntary contraction, or heart ratebut did attenuate the increase in MAP (increase in MAP: from 15.2 ± 1.8 before training to 11.4 ± 1.4 mmHg after training;P < 0.017), muscle sympathetic nerve activity (increase in bursts: from 10.8 ± 1.4 before training to6.2 ± 1.1 bursts/min after training;P < 0.030), and the NE spillover(increase in arterial spillover: from 1.3 ± 0.2 before training to0.6 ± 0.2 nmol ^· min^{1 ·} m²after training, P < 0.014; increasein venous spillover: from 2.0 ± 0.6 beforetraining to 1.0 ± 0.5 nmol ^· min^{1 ·} m²after training, P < 0.037) seen inresponse to exercise performed by the trained forearm. Thus forearmtraining reduces sympathetic responses during a nonfatiguing rhythmichandgrip paradigm that does not engage muscle metaboreceptors. Wespeculate that this effect is due to a conditioning-inducedreduction in mechanically sensitive muscle afferentdischarge.

     

Augmented sympathetic tone alters muscle metabolism with exercise: lack of evidence for functional sympatholysis

Shoemaker, J. Kevin, Prasant Pandey, Michael D. Herr, DavidH. Silber, Qing X. Yang, Michael B. Smith, Kristen Gray, and LawrenceI. Sinoway. Augmented sympathetic tone alters muscle metabolismwith exercise: lack of evidence for functional sympatholysis. J. Appl. Physiol. 82(6):1932-1938, 1997.It is unclear whether sympathetic tone opposesdilator influences in exercising skeletal muscle. We examined highlevels of sympathetic tone, evoked by lower body negative pressure(LBNP, 60 mmHg) on intramuscular pH and phosphocreatine (PCr)levels (³¹P-nuclear magnetic resonance spectroscopy) duringgraded rhythmic handgrip (30 contractions/min; ~17, 34, 52 and 69%maximal voluntary contraction). Exercise was performedwith LBNP and without LBNP (Control). At the end of exercise, LBNPcaused lower levels of muscle pH (6.59 ± 0.09) comparedwith Control (6.78 ± 0.05; P < 0.05). PCr recovery, an index of mitochondrial respiration, was lessduring the recovery phase of the LBNP trial. Exercise mean arterialpressure was not altered by LBNP. The protocols were repeated withmeasurements of forearm blood flow velocity and deep venous samples(active forearm) of hemoglobin (Hb) saturation, pH, and lactate. WithLBNP, mean blood velocity was reduced at rest, during exercise, andduring recovery compared with Control (P < 0.05). Also, venous Hbsaturation and pH levels during exercise and recovery were lower withLBNP and lactate was higher compared with Control(P < 0.05). We concludethat LBNP enhanced sympathetic tone and reduced oxygen transport. Athigh workloads, there was a greater reliance on nonoxidativemetabolism. In other words, sympatholysis did not occur.

     

Impaired calcium pump function does not slow relaxation in human skeletal muscle after prolonged exercise

Booth, John, Michael J. McKenna, Patricia A. Ruell, Tom H. Gwinn, Glen M. Davis, Martin W. Thompson, Alison R. Harmer, Sandra K. Hunter, and John R. Sutton. Impaired calcium pump function doesnot slow relaxation in human skeletal muscle after prolonged exercise.J. Appl. Physiol. 83(2): 511-521, 1997.This study examined the effects of prolonged exercise on humanquadriceps muscle contractile function and homogenate sarcoplasmicreticulum Ca²⁺ uptake andCa²⁺-adenosinetriphosphataseactivity. Ten untrained men cycled at 75 ± 2% (SE) peak oxygenconsumption until exhaustion. Biopsies were taken from theright vastus lateralis muscle at rest, exhaustion, and 20 and 60 minpostexercise. Peak tension and half relaxation time of the leftquadriceps muscle were measured during electrically evoked twitch andtetanic contractions and a maximal voluntary isometric contraction atrest, exhaustion, and 10, 20, and 60 min postexercise. At exhaustion,homogenate Ca²⁺ uptake andCa²⁺ adenosinetriphosphataseactivity were reduced by 17 ± 4 and 21 ± 5%, respectively, andremained depressed after 60 min recovery (P  0.01). Muscle ATP, creatinephosphate, and glycogen were all depressed at exhaustion(P  0.01). Peak tension during a maximal voluntary contraction, a twitch, and a 10-Hz stimulation werereduced after exercise by 28 ± 3, 45 ± 6, 65 ± 5%,respectively (P  0.01), but noslowing of half relaxation times were found. Thus fatigue induced byprolonged exercise reduced muscleCa²⁺ uptake, but this did notcause a slower relaxation of evoked contractions.