Activation-induced force enhancement in human adductor pollicis

It has been known for a long time that the steady-state isometric force after muscle stretch is bigger than the corresponding force obtained in a purely isometric contraction for electrically stimulated and maximal voluntary contractions (MVC). Recent studies using sub-maximal voluntary contractions showed that force enhancement only occurred in a sub-group of subjects suggesting that force enhancement for sub-maximal voluntary contractions has properties different from those of electrically-induced and maximal voluntary contractions. Specifically, force enhancement for sub-maximal voluntary contractions may contain an activation-dependent component that is independent of muscle stretching. To address this hypothesis, we tested for force enhancement using (i) sub-maximal electrically-induced contractions and stretch and (ii) using various activation levels preceding an isometric reference contraction at 30% of MVC (no stretch). All tests were performed on human adductor pollicis muscles. Force enhancement following stretching was found for all subjects (n = 10) and all activation levels (10%, 30%, and 60% of MVC) for electrically-induced contractions. In contrast, force enhancement at 30% of MVC, preceded by 6 s of 10%, 60%, and 100% of MVC was only found in a sub-set of the subjects and only for the 60% and 100% conditions. This result suggests that there is an activation-dependent force enhancement for some subjects for sub-maximal voluntary contractions. This activation-dependent force enhancement was always smaller than the stretch-induced force enhancement obtained at the corresponding activation levels. Active muscle stretching increased the force enhancement in all subjects, independent whether they showed activation dependence or not. It appears that post-activation potentiation, and the associated phosphorylation of the myosin light chains, might account for the stretch-independent force enhancement observed here.     

Myoelectric manifestations of fatigue in vastus lateralis,medialis obliquus and medialis longus muscles

The purpose of this study was to determine whether surface electromyography (EMG) assessment of myoelectric manifestations of muscle fatigue is capable of detecting differences between the vastus lateralis and medialis muscles which are consistent with the results of previous biopsy studies. Surface EMG signals were recorded from the vastus medialis longus (VML), vastus medialis obliquus (VMO) and vastus lateralis (VL) muscles during isometric knee extension contractions at 60% and 80% of the maximum voluntary contraction (MVC) for 10 s and 60 s, respectively. Initial values and rate of change of mean frequency (MNF), average rectified value (ARV) and conduction velocity (CV) of the EMG signal were calculated. Comparisons between the two force levels revealed that the initial values of MNF for the VL muscle were greater at 80% MVC compared to 60% MVC (P < 0.01). Comparisons between the vasti muscles demonstrated lower initial values of CV for VMO compared to VL at 60% MVC (P < 0.01) and lower than VML and VL at 80% MVC (P < 0.01). In addition, initial values of MNF were higher for VL with respect to both VML and VMO at 80% MVC (P < 0.01) and initial estimates of ARV were higher for VMO compared to VML at both force levels (P < 0.01 at 60% MVC and P < 0.05 at 80% MVC). For the sustained contraction at 80% MVC, VL demonstrated a greater decrease in CV over time compared to VMO (P < 0.05).These findings suggest that surface EMG signals and their time course during sustained isometric contractions may be useful to non-invasively describe functional differences between the vasti muscles.     

Muscle activity and time to task failure differ with load compliance and target force for elbow flexor muscles

The primary purpose of this study was to determine the influence of load compliance on time to failure during sustained isometric contractions performed with the elbow flexor muscles at four submaximal target forces. Subjects pulled against a rigid restraint during the force task and maintained a constant elbow angle, while supporting an equivalent inertial load during the position task. Each task was sustained for as long as possible. Twenty-one healthy adults (23 ± 6 yr; 11 men) participated in the study. The maximal voluntary contraction (MVC) force was similar (P = 0.95) before the subjects performed the force and position tasks at each of the four target forces: 20, 30, 45, and 60% of MVC force. The time to task failure was longer for the force tasks (576 ± 80 and 325 ± 70 s) than for the position tasks (299 ± 77 and 168 ± 35 s) at target forces of 20 and 30% (P < 0.001), but was similar for the force tasks (178 ± 35 and 86 ± 14 s) and the position tasks (132 ± 29 and 87 ± 14 s) at target forces of 45 and 60% (P > 0.19). The briefer times to failure for the position task at the lower forces were accompanied by greater rates of increase in elbow flexor muscle activity, mean arterial pressure, heart rate, and rating of perceived exertion. There was no difference in the estimates of external mechanical work at any target force. The dominant mechanisms limiting time to failure of sustained isometric contractions with the elbow flexor muscles appear to change at target forces between 30 and 45% MVC, with load compliance being a significant factor at lower forces only.     

A moderate glycemic meal before endurance exercise can enhance performance

Kirwan, John P., Donal O'Gorman, and William J. Evans.A moderate glycemic meal before endurance exercise can enhance performance. J. Appl. Physiol. 84(1):53-59, 1998.The purpose of this study was to determine whetherpresweetened breakfast cereals with various fiber contents and amoderate glycemic index optimize glucose availability and improveendurance exercise performance. Six recreationally active women ate 75 g of available carbohydrate in the form of breakfast cereals: sweetenedwhole-grain rolled oats (SRO, 7 g of dietary fiber) or sweetenedwhole-oat flour (SOF, 3 g of dietary fiber) and 300 ml of water orwater alone (Con). The meals were provided 45 min before semirecumbentcycle ergometer exercise to exhaustion at 60% of peakO₂ consumption (O_{2 peak}). Diet andphysical activity were controlled by having the subjects reside in theGeneral Clinical Research Center for 2 days before each trial. Bloodsamples were drawn from an antecubital vein for glucose, free fattyacid (FFA), glycerol, insulin, epinephrine, and norepinephrinedetermination. Breath samples were obtained at 15-min intervals aftermeal ingestion and at 30-min intervals during exercise. Muscle glycogenconcentration was determined from biopsies taken from the vastuslateralis muscle before the meal and immediately after exercise. PlasmaFFA concentrations were lower (P < 0.05) during the SRO and SOF trials for the first 60 and 90 min ofexercise, respectively, than during the Con trial. Respiratory exchangeratios were higher (P < 0.05) at 90 and 120 min of exercise for the SRO and SOF trials, respectively, than for the Con trial. At exhaustion, glucose, insulin, FFA, glycerol, epinephrine, and norepinephrine concentrations, respiratory exchange ratio, and muscle glycogen use in the vastus lateralis muscle weresimilar for all trials. Exercise time to exhaustion was 16% longer(P < 0.05) during the SRO thanduring the Con trial: 266.5 ± 13 and 225.1 ± 8 min,respectively. There was no difference in exercise time for the SOF(250.8 ± 12) and Con trials. We conclude that eating ameal with a high dietary fiber content and moderate glycemic index 45 min before prolonged moderately intense exercise significantly enhancesexercise capacity.

     

Muscle inactivation: assessment of interpolated twitch technique

Behm, D. G., D. M. M. St-Pierre, and D. Perez. Muscleinactivation: assessment of interpolated twitch technique.J. Appl. Physiol. 81(5):2267-2273, 1996.The validity, reliability, and protocol for theinterpolated twitch technique (ITT) were investigated with isometricplantar flexor and leg extension contractions. Estimates of muscleinactivation were attempted by comparing a variety of superimposed withpotentiated evoked torques with submaximal and maximal voluntarycontraction (MVC) torques or forces. The use of nerve and surfacestimulation to elicit ITT was reliable, except for problems inmaintaining maximal stimulation with nerve stimulation at 20°plantar flexion and during leg extension. The interpolated twitchratio-force relationship was best described by a shallow hyperboliccurve resulting in insignificant MVC prediction errors withsecond-order polynomials (1.1-6.9%). The prediction error under40% MVC was approximately double that over 60% MVC, contributing topoor estimations of MVC in non-weight-bearing postimmobilized anklefracture patients. There was no significant difference in the ITTsensitivity when twitches, doublets, or quintuplets were used.The ITT was valid and reliable when high-intensity contractions wereanalyzed with a second-order polynomial.

     

The isometric force that induces maximal surface muscle deoxygenation

To determine the external force that induces maximal deoxygenation of brachioradialis muscle 32 trained male subjects maintained isometric contractions using the elbow flexor muscles up to the limit time (isotonic part of the isometric contraction, IIC) and beyond that time for 120 s (anisotonic part of the isometric contraction). During IIC each subject maintained relative forces of either 25% and 70% maximal voluntary contraction (MVC), 50% and 100% MVC, or 40% and 60% MVC. Muscle oxygenation was assessed using a near infrared spectroscope, and expressed as a percentage of the reference value (ΔO_2rest) which was the difference between the minimal oxygenation obtained after 6 min of ischaemia at rest and the maximal reoxygenation following the release of the tourniquet. During IIC at 25% MVC, muscle oxygenation decreased to 17 (SEM 3)% ΔO_2rest, then it levelled off [25 (SEM 1)% ΔO_2rest]. After the point at which target force could not be maintained, reoxygenation was very weak. During IIC at 40%, 50%, 60%, and 70% MVC, the lowest muscle oxygenation values were obtained after 15–20 s of contraction and corresponded to −18 (SEM 6), −59 (SEM 12) −31 (SEM 6), and −29 (SEM 6)% ΔO_2rest, respectively. For the contraction at 100% MVC, the lowest oxygenation [−19 (SEM 9)% ΔO_2rest] was obtained while force was decreasing (69% MVC). During the anisotonic part of the isometric contractions, the greatest reoxygenation rate was obtained after 50% MVC IIC (P < 0.001). Our results showed that during isometric elbow flexions between 25% and 100% MVC, there was no linear relationship between external force and muscle oxygenation, and that the maximal deoxygenation of the brachioradialis muscle was obtained at 50% MVC. Accepted: 16 February 1998     

Effects of N2O narcosis on breathing and effort sensations during exercise and inspiratory resistive loading

Fothergill, D. M., and N. A. Carlson. Effects ofN₂O narcosis on breathing andeffort sensations during exercise and inspiratory resistive loading.J. Appl. Physiol. 81(4):1562-1571, 1996.The influence of nitrous oxide(N₂O) narcosis on the responses toexercise and inspiratory resistive loading was studied in thirteen maleUS Navy divers. Each diver performed an incremental bicycle exercisetest at 1 ATA to volitional exhaustion while breathing a 23%N₂O gas mixture and a nonnarcoticgas of the same PO₂, density, andviscosity. The same gas mixtures were used during four subsequent30-min steady-state submaximal exercise trials in which the subjectsbreathed the mixtures both with and without an inspiratory resistance(5.5 vs. 1.1 cmH₂O ^· s ^· l¹at 1 l/s). Throughout each test, subjective ratings of respiratory effort (RE), leg exertion, and narcosis were obtained with acategory-ratio scale. The level of narcosis was rated between slightand moderate for the N₂O mixturebut showed great individual variation. Perceived leg exertion and thetime to exhaustion were not significantly different with the twobreathing mixtures. Heart rate was unaffected by the gas mixture andinspiratory resistance at rest and during steady-state exercise but wassignificantly lower with the N₂O mixture during incremental exercise (P < 0.05). Despite significant increases in inspiratory occlusionpressure (13%; P < 0.05),esophageal pressure (12%; P < 0.001), expired minute ventilation (4%;P < 0.01), and the work rate ofbreathing (15%; P < 0.001) when the subjects breathed the N₂O mixture,RE during both steady-state and incremental exercise was 25% lowerwith the narcotic gas than with the nonnarcotic mixture(P < 0.05). We conclude that the narcotic-mediated changes in ventilation, heart rate, and RE induced by23% N₂O are not of sufficientmagnitude to influence exercise tolerance at surface pressure.Furthermore, the load-compensating respiratory reflexes responsible formaintaining ventilation during resistive breathing are not depressed byN₂O narcosis.

     

Muscle fatigue and exhaustion during dynamic leg exercise in normoxia and hypobaric hypoxia

Fulco, Charles S., Steven F. Lewis, Peter N. Frykman, RobertBoushel, Sinclair Smith, Everett A. Harman, Allen Cymerman, and Kent B. Pandolf. Muscle fatigue and exhaustion during dynamic leg exercisein normoxia and hypobaric hypoxia. J. Appl. Physiol. 81(5): 1891-1900, 1996.Using anexercise device that integrates maximal voluntary static contraction(MVC) of knee extensor muscles with dynamic knee extension, we comparedprogressive muscle fatigue, i.e., rate of decline in force-generatingcapacity, in normoxia (758 Torr) and hypobaric hypoxia (464 Torr).Eight healthy men performed exhaustive constant work rate kneeextension (21 ± 3 W, 79 ± 2 and 87 ± 2% of 1-leg kneeextension O₂ peak uptake fornormoxia and hypobaria, respectively) from knee angles of90-150° at a rate of 1 Hz. MVC (90° knee angle) wasperformed before dynamic exercise and during 5-s pauses every 2 minof dynamic exercise. MVC force was 578 ± 29 N in normoxia and 569 ± 29 N in hypobaria before exercise and fell, at exhaustion, to similar levels (265 ± 10 and 284 ± 20 N for normoxia andhypobaria, respectively; P > 0.05)that were higher (P < 0.01) thanpeak force of constant work rate knee extension (98 ± 10 N, 18 ± 3% of MVC). Time to exhaustion was 56% shorter for hypobariathan for normoxia (19 ± 5 vs. 43 ± 7 min, respectively;P < 0.01), and rate of right leg MVC fall wasnearly twofold greater for hypobaria than for normoxia (mean slope = 22.3 vs. 11.9 N/min, respectively;P < 0.05). With increasing durationof dynamic exercise for normoxia and hypobaria, integratedelectromyographic activity during MVC fell progressively with MVCforce, implying attenuated maximal muscle excitation. Exhaustion, perse, was postulated to relate more closely to impaired shorteningvelocity than to failure of force-generating capacity.

     

Effects of fatigue duration and muscle type on voluntary and evoked contractile properties

Behm, D. G., and D. M. M. St-Pierre. Effects of fatigueduration and muscle type on voluntary and evoked contractile properties. J. Appl. Physiol. 82(5):1654-1661, 1997.The effects of fatigue duration and muscle typeon voluntary and evoked contractile properties were investigated withan isometric, intermittent, submaximal fatigue protocol. Four groupsperformed contractions of the plantar flexors and quadriceps at variousintensities to produce long (LDF; 19 min 30 s)- and short-durationfatigue (SDF; 4 min 17 s). The LDF group had a significantly greaterdecrease in muscle activation than did the SDF group (12 vs. 5.8%)during recovery, although there was no difference in the impairment of maximum voluntary contraction force beyond 30 s of recovery. The significant decrease in the compound muscle action potential of the LDFgroup (M-wave amplitude; 14.7%) contrasted with the M-wave potentiation of the SDF group (15.7%), suggesting changes in membrane excitation may affect LDF. The quadriceps group performing contractions at 50% MVC experienced a smaller decrease in agonist electromyograph activity than did other groups, indicating both muscle and fatigue duration specificity. Impairments in excitation-contraction coupling were indicated by changes in quadriceps peak twitch and time to peaktwitch while decreases in PF M-wave amplitudes suggested a disruptionof membrane potentials. Results suggest that fatigue mechanisms may beduration (activation, half relaxation time) or muscle specific(electromyograph, twitch torque) or a combination of both (M wave, timeto peak twitch torque).

     

Motor drive and metabolic responses during repeated submaximal contractions in humans

Contractile failure during various types of exercise has been attributed to intramuscular metabolic changes. We examined the temporal changes in force-generating capacity and metabolic state during intermittent isometric contractions in humans. One-legged quadriceps contractions at 30% maximum voluntary contraction (MVC) were executed for 6 s, with 4 s of rest between. The decrease in force-generating capacity was tested from brief MVC's and short bursts of 50-Hz stimulation applied at 5-min intervals. After 1 min of exercise, the MVC force declined linearly and in parallel to the 50-Hz stimulation force, indicating that the contractile failure was due to intramuscular processes. After 30 min of exercise the MVC force had declined by approximately 40% compared with the value obtained after 1 min. In separate experiments the same contraction protocol was followed, but two-legged contractions were used. Muscle biopsies taken after 5, 15, and 30 min of exercise showed only minor changes in the concentrations of glycogen, lactate, creatine phosphate (CrP), and ATP. However, at exhaustion, defined as loss of ability to sustain the target force, the concentrations of CrP and glycogen were reduced by 73 and 32%, and muscle lactate concentration had increased to 4.8 mmol/kg wet wt. Thus the gradual decline in force-generating capacity was not due to lactacidosis or lack of substrates for ATP resynthesis and must have resulted from excitation/contraction coupling failure, whereas exhaustion was closely related to phosphagen depletion, without significant lactacidosis.     

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.

     

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.

     

Evidence of long term muscle fatigue following prolonged intermittent contractions based on mechano- and electromyograms.

The focus of the present study is the long term element of muscle fatigue provoked by prolonged intermittent contractions at submaximal force levels and analysed by force, surface electromyography (EMG) and mechanomyogram (MMG). It was hypothesized that fatigue related changes in mechanical performance of the biceps muscle are more strongly reflected in low than in high force test contractions, more prominent in the MMG than in the EMG signal and less pronounced following contractions controlled by visual compared to proprioceptive feedback. Further, it was investigated if fatigue induced by 30 min intermittent contractions at 30% as well as 10% of maximal voluntary contraction (MVC) lasted more than 30 min recovery. In six male subjects the EMG and MMG were recorded from the biceps brachii muscle during three sessions with fatiguing exercise at 10% with visual feedback and at 30% MVC with visual and proprioceptive feedback. EMG, MMG, and force were evaluated during isometric test contractions at 5% and 80% MVC before prolonged contraction and after 10 and 30 min of recovery. MVC decreased significantly after the fatiguing exercise in all three sessions and was still decreased even after 30 min of recovery. In the time domain significant increases after the fatiguing exercise were found only in the 5% MVC tests and most pronounced for the MMG. No consistent changes were found for neither EMG nor MMG in the frequency domain and feedback mode did not modify the results. It is concluded that long term fatigue after intermittent contractions at low force levels can be detected even after 30 min of recovery in a low force test contraction. Since the response was most pronounced in the MMG this may be a valuable variable for detection of impairments in the excitation-contraction coupling.     

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.

     

Muscle weakness following sustained and rhythmic isometric contractions in man

The effects of sustained and rhythmically performed isometric contractions on electrically evoked twitch and tetanic force generation of the triceps surae have been investigated in 4 healthy male subjects. The isometric contractions were performed separately and on different occasions at 30%, 60% and 100% of the force of maximal voluntary contraction (MVC). The area under the maximal voluntary contraction (MVC) force/time curve during the rhythmic and sustained contractions was the same for each experiment. The results showed that following rhythmic isometric exercise there was a small decrease in low (10 and 20 Hz) and high (40 Hz) frequency tetanic tension which was associated with % MVC. However, there was no change in the 20/40 ratio of tetanic forces, MVC or the contraction times and force of the maximal twitch. In contrast, following sustained isometric exercise tetanic forces were markedly reduced, particularly at low frequencies of stimulation. The 20/40 ratio decreased and the induced muscle weakness was greater at 30% than 60% or 100% MVC. The performance of sustained isometric contractions also effected a decrease in contraction time of the twitch and MVC. The results are in accord with previous findings for dynamic work (Davies and White 1982), and show that if isometric exercise is performed rhythmically the effect on tetanic tensions is small and there is no evidence of a preferential loss of electrically evoked force at either high or low frequencies of stimulation following the contractions. For sustained contractions, however, the opposite is true, the ratio of 20/40 Hz forces is markedly reduced and following 30% sustained MVC there is a significant (p less than 0.05) change in the time to peak tension (TPT) of the maximal twitch.     

Skeletal muscle chemoreflex and pHi in exercise ventilatory control

Oelberg, David A., Allison B. Evans, Mirko I. Hrovat, PaulP. Pappagianopoulos, Samuel Patz, and David M. Systrom. Skeletal muscle chemoreflex and pH_i inexercise ventilatory control. J. Appl.Physiol. 84(2): 676-682, 1998.To determinewhether skeletal muscle hydrogen ion mediates ventilatory drive inhumans during exercise, 12 healthy subjects performed three bouts ofisotonic submaximal quadriceps exercise on each of 2 days in a 1.5-Tmagnet for ³¹P-magnetic resonancespectroscopy(³¹P-MRS). Bilaterallower extremity positive pressure cuffs were inflated to 45 Torr duringexercise (BLPP_ex) or recovery(BLPP_rec) in a randomized orderto accentuate a muscle chemoreflex. Simultaneous measurements were madeof breath-by-breath expired gases and minute ventilation, arterializedvenous blood, and by ³¹P-MRS ofthe vastus medialis, acquired from the average of 12 radio-frequencypulses at a repetition time of 2.5 s. WithBLPP_ex, end-exercise minuteventilation was higher (53.3 ± 3.8 vs. 37.3 ± 2.2 l/min;P < 0.0001), arterializedPCO₂ lower (33 ± 1 vs. 36 ± 1 Torr; P = 0.0009), and quadricepsintracellular pH (pH_i) more acid (6.44 ± 0.07 vs. 6.62 ± 0.07; P = 0.004), compared withBLPP_rec. Bloodlactate was modestly increased withBLPP_ex but without a change inarterialized pH. For each subject, pH_i was linearly relatedto minute ventilation during exercise but not to arterialized pH. Thesedata suggest that skeletal muscle hydrogen ion contributes to theexercise ventilatory response.

     

Exercise-induced changes in circulating growth factors with cyclic variation in plasma estradiol in women

Hornum, Mette, Dan M. Cooper, Jo Anne Brasel, Alina Bueno,and Kathy E. Sietsema. Exercise-induced changes in circulating growth factors and cyclic variation in plasma estradiol in women. J. Appl. Physiol. 82(6):1946-1951, 1997.The effect of 10 min of high-intensity cyclingexercise on circulating growth hormone (GH), insulin-like growthfactors I and II (IGF-I and -II), and insulin-like growth factorbinding protein 3 (IGF BP-3) was studied in nine eumenorrheic women(age 19-48 yr) at two different phases of the menstrual cycle.Tests were performed on separate mornings corresponding to thefollicular phase and to the periovulatory phase of the menstrual cycle,during which plasma levels of endogenous estradiol(E₂) were relatively low (272 ± 59 pmol/l) and high (1,112 ± 407 pmol/l), respectively. GHincreased significantly in response to exercise under bothE₂ conditions. Plasma GH before exercise (2.73 ± 2.48 vs. 1.71 ± 2.09 µg/l) and total GH over 10 min of exercise and 1-h recovery (324 ± 199 vs. 197 ± 163 ng) were both significantly greater for periovulatory phase than for follicular phase studies. IGF-I, but not IGF-II, increased acutely after exercise. IGF BP-3, assayed by radioimmunoassay, was not significantly different at preexercise, end exercise, or at 30-min recovery time points and was not different between the two study days.When assayed by Western blot, however, there was a significant increasein IGF BP-3 30 min after exercise for the periovulatory study. Thesefindings indicate that the modulation of GH secretion associated withmenstrual cycle variations in circulatingE₂ affects GH measured afterexercise, at least in part, by an increase in baseline levels. Theacute increase in IGF-I induced by exercise appears to be independentof the GH response and is not affected by menstrual cycle timing.

     

Effects of the ovarian cycle on sympathetic neural outflow during static exercise

We comparedreflex responses to static handgrip at 30% maximal voluntarycontraction (MVC) in 10 women (mean age 24.1 ± 1.7 yr) during twophases of their ovarian cycle: the menstrual phase (days 1-4) and the follicularphase (days10-12). Changes in muscle sympathetic nerve activity (MSNA; microneurography) in response tostatic exercise were greater during the menstrual compared withfollicular phase (phase effect P = 0.01). Levels of estrogen were less during the menstrual phase(75 ± 5.5 vs. 116 ± 9.6 pg/ml, days 1-4 vs.days 10-12;P = 0.002). Generated tension did not explain differences in MSNA responses (MVC: 29.3 ± 1.3 vs. 28.2 ± 1.5 kg, days 1-4 vs.days 10-12;P = 0.13). In a group of experiments with the use of ³¹P-NMRspectroscopy, no phase effect was observed forH⁺ andH₂PO₄ concentrations(n = 5). During an ischemicrhythmic handgrip paradigm (20% MVC), a phase effect was notobserved for MSNA or H⁺ orH₂PO₄ concentrations,suggesting that blood flow was necessary for the expression of thecycle-related effect. The present studies suggest that, during statichandgrip exercise, MSNA is increased during the menstrual compared withthe follicular phase of the ovarian cycle.

     

Residual force enhancement following eccentric induced muscle damage

During lengthening of an activated skeletal muscle, the force maintained following the stretch is greater than the isometric force at the same muscle length. This is termed residual force enhancement (RFE), but it is unknown how muscle damage following repeated eccentric contractions affects RFE. Using the dorsiflexors, we hypothesised muscle damage will impair the force generating sarcomeric structures leading to a reduction in RFE. Following reference maximal voluntary isometric contractions (MVC) in 8 young men (26.5±2.8y) a stretch was performed at 30°/s over a 30° ankle excursion ending at the same muscle length as the reference MVCs (30° plantar flexion). Surface electromyography (EMG) of the tibialis anterior and soleus muscles was recorded during all tasks. The damage protocol involved 4 sets of 25 isokinetic (30°/s) lengthening contractions. The same measures were collected at baseline and immediately post lengthening contractions, and for up to 10min recovery. Following the lengthening contraction task, there was a 30.3±6.4% decrease in eccentric torque (P<0.05) and 36.2±9.7% decrease in MVC (P<0.05) compared to baseline. Voluntary activation using twitch interpolation and RMS EMG amplitude of the tibialis anterior remained near maximal without increased coactivation for MVC. Contrary to our hypothesis, RFE increased (～100-250%) following muscle damage (P<0.05). It appears stretch provided a mechanical strategy for enhanced muscle function compared to isometric actions succeeding damage. Thus, active force of cross-bridges is decreased because of impaired excitation-contraction coupling but force generated during stretch remains intact because force contribution from stretched sarcomeric structures is less impaired.     

cGMP-independent mechanism of airway smooth muscle relaxation induced by S-nitrosoglutathione

This study tested the hypothesis that the NO donorS-nitrosoglutathione (GSNO) relaxescanine tracheal smooth muscle (CTSM) in part by a cGMP-independentprocess that involves reversible oxidation of intracellular thiols.GSNO caused a concentration-dependent relaxation in ACh-contractedstrips (EC₅₀ ~1.2 µM)accompanied by a concentration-dependent increase in cytosolic cGMPconcentration ([cGMP]_i). Thesoluble guanylate cyclase inhibitor methylene blue prevented theincrease in [cGMP]_iinduced by 1 and 10 µM GSNO, but isometric force decreased by 10 ± 4 and 55 ± 3%, respectively. After recovery of[cGMP]_i to baseline,GSNO-induced relaxation persisted during continuous ACh stimulation.Dithiothreitol caused a rapid recovery of isometric force to valuessimilar to those obtained with ACh alone in these strips. We concludethat GSNO relaxes CTSM contracted by ACh in part by oxidation ofintracellular protein thiols.