Mechanomyographic and electromyographic responses during submaximal to maximal eccentric isokinetic muscle actions of the biceps brachii

The purpose of this investigation was to determine the mechanomyography (MMG) and electromyography (EMG) amplitude and mean power frequency (MPF) vs. eccentric isokinetic torque relationships for the biceps brachii muscle. Nine adults (mean +/- SD age = 23.1 +/- 2.9 years) performed submaximal to maximal eccentric isokinetic muscle actions of the dominant forearm flexors. After determination of isokinetic peak torque (PT), the subjects randomly performed submaximal step muscle actions in 10% increments from 10 to 90% PT. Polynomial regression analyses indicated that the MMG amplitude vs. eccentric isokinetic torque relationship was best fit with a quadratic model (R(2) = 0.951), where MMG amplitude increased from 10 to 60% PT and then plateaued from 60 to 100% PT. There were linear increases in MMG MPF (r(2) = 0.751) and EMG amplitude (r(2) = 0.988) with increases in eccentric isokinetic torque, but there was no significant change in EMG MPF from 10 to 100% PT. The results suggested that for the biceps brachii, eccentric isokinetic torque was increased to approximately 60% PT through concurrent modulation of the number of active motor units and their firing rates, whereas additional torque above 60% PT was produced only by increases in firing rates. These findings contribute to current knowledge of motor-control strategies during eccentric isokinetic muscle actions and could be useful in the design of training programs.     

Differences in muscle activation between submaximal and maximal 6-minute rowing tests

This study aimed to establish the differences in muscle activation between a 6-minute simulated race (all-out test) and a submaximal (blood lactate [LA] concentration 4 mmol·L(-1)) 6-minute effort (submax test) on a rowing ergometer. Eleven healthy, well-trained subjects performed the submax test followed after 1-hour rest by the all-out test. Surface electromyographic (sEMG) signal of muscles gastrocnemius medialis (GC), rectus femoris (RF), vastus lateralis (VL), biceps femoris, gluteus maximus (GM), erector spinae (ES), lower latissimus dorsi (LD_lo), upper latissimus dorsi (LD_up), brachioradialis (BR) and biceps brachii (BB), and other biomechanical, biochemical, and respiratory parameters were monitored during rowing. During the all-out test, the subjects covered a longer distance with larger average power output, higher stroke frequency, LA concentration, and oxygen consumption compared to the submax test (p < 0.05). During the submax test, the average rectified values (ARVs) of sEMG signal increased significantly only in the RF and LD_lo muscles. During the all-out test, the ARVs of the RF, VL, and GM muscles increased (p < 0.05), whereas the MDFs of the RF, ES, and LD_lo muscles decreased (p < 0.05). Compared to the submax test, the ARVs of the GC, RF, VL, LD_lo, LD_up, and BB muscles were significantly higher during the all-out test. However, only for the RF muscle, the all-out test resulted in a significantly lower MDF value compared to the submax test. The most involved muscles that would need special attention in training seem to be the leg and shoulder girdle extensors and arm flexors but not the trunk and hip extensors.     

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.

     

Differential control during maximal concentric and eccentric loading revealed by characteristics of the electromyogram

Maximal eccentric loading has been associated with higher levels of spindle afferent activity but lower levels of integrated EMG as compared to maximal concentric loading. Elbow flexor EMG was recorded from 17 subjects during concentric (CONC) and eccentric (ECC) elbow flexion at 70° s⁻¹ using a Kin-Com dynamometer. We hypothesized that peak EMG amplitude would be more sensitive to fluctuations in facilitation by the spindle primary afferents via the segmental stretch reflex pathway, and that the mean EMG would be more reflective of the ongoing level of muscle activation. A ratio of peak to mean EMG (P/M EMG ratio) was predicted to be larger during maximal eccentric loading than maximal concentric loading. The peak EMG (P<0.013) and the P/M EMG ratio (P<0.001) were significantly greater during the ECC condition than the CONC condition. In a subgroup of three subjects who underwent 3 weeks of eccentrically biased weight training, EMG, peak torque and torque variability were assessed before and after training. P/M EMG ratio decreased, while peak torque and torque variability increased following the training. Differences in the P/M EMG ratio appear to reflect differences in the way eccentric and concentric muscle actions are controlled and do not simply represent less control during the eccentric task.     

Walking kinematics and kinetics following eccentric exercise-induced muscle damage

The goal of this investigation was to investigate how walking patterns are affected following muscle-damaging exercise by quantifying both lower limb kinematics and kinetics. Fifteen young women conducted a maximal isokinetic eccentric exercise (EE) muscle damage protocol (5 × 15) of the knee extensors and flexors of both legs at 60°/s. Three-dimensional motion data and ground reaction forces (GRFs) were collected 24 h pre-EE while the participants walked at their preferred self-selected walking speed (SWS). Participants were asked to perform two gait conditions 48 h post-EE. The first condition (COND1) was to walk at their own speed and the second condition (COND2) to maintain the SWS (±5%) they had 24 h pre-EE. Walking speed during COND1 was significantly lower compared to pre-exercise values. When walking speed was controlled during COND2, significant effects of muscle damage were noticed, among other variables, for stride frequency, loading rate, lateral and vertical GRFs, as well as for specific knee kinematics and kinetics. These findings provide new insights into how walking patterns are adapted to compensate for the impaired function of the knee musculature following muscle damage. The importance to distinguish the findings caused by muscle damage from those exhibited in response to changes in stride frequency is highlighted.     

Lovastatin use and muscle damage in healthy volunteers undergoing eccentric muscle exercise.

We did a double-blind, placebo-controlled crossover study of 10 healthy young men taking no medications to determine if ingesting lovastatin is associated with more severe muscle damage after exercise. Five men in the first group took 40 mg of lovastatin daily for 30 days while those in the second group took an identical-appearing placebo. Each volunteer then walked downhill on a -14-degree incline on a treadmill at 3 km per hour for an hour. After a 2-week rest, the subjects were crossed over. Serial serum creatine kinase activity was measured immediately before and 8, 24, 48, 72, 120, and 144 hours after each treadmill session. With each subject serving as his own control, peak mean serum creatine kinase activity (/+- SEM) following treadmill after lovastatin therapy was similar to that following placebo (168.4 +/- 25.8 U per liter versus 146.7 +/- 14.7 U per liter, respectively [P = .9]). With an alpha value of .05, we had greater than a 99% chance of detecting a difference in the rise of serum creatine kinase activity of 200 U per liter between groups. Our data suggest that lovastatin is not an independent risk factor for developing exercise-induced muscle damage using this model of exercise in our study population.     

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.     

Agonist and antagonist muscle activation during maximal and submaximal isokinetic fatigue tests of the knee extensors

The purpose of this study was to examine the differences in electromyographic activity of agonist and antagonist knee musculature between a maximal and a submaximal isokinetic fatigue protocol. Fourteen healthy males (age: 24.3 ± 2.5 years) performed 25 maximal (MIFP) and 60 submaximal (SIFP) isokinetic concentric efforts of the knee extensors at 60° s⁻¹, across a 90° range of motion. The two protocols were performed a week apart. The EMG activity of vastus medialis (VM), vastus lateralis (VL) and biceps femoris (BF) were recorded using surface electrodes. The peak torque (PT) and average EMG (aEMG) were expressed as percentages of pre-fatigue maximal value. One-way analysis of variance indicated a significant (p < 0.05) decline of PT during the maximal (45.7%) and submaximal (46.8%) protocols. During the maximal test, the VM and VL aEMG initially increased and then decreased. In contrast, VM and VL aEMG continuously increased during submaximal testing (p < 0.05). The antagonist (BF) aEMG remained constant during maximal test but it increased significantly and then declined during the submaximal testing. The above results indicate that agonist and antagonist activity depends on the intensity of the selected isokinetic fatigue test.     

Indices of skeletal muscle damage and connective tissue breakdown following eccentric muscle contractions

 Indirect indices of exercise-induced human skeletal muscle damage and connective tissue breakdown were studied following a single bout of voluntary eccentric muscle contractions. Subjects (six female, two male), mean (SD) age 22 (2) years performed a bout of 50 maximum voluntary eccentric contractions of the knee extensors of a single leg. The eccentric exercise protocol induced muscle soreness (P < 0.05 Wilcoxon test), chronic force loss, and a decline in the 20:100 Hz percutaneous electrical myostimulation force ratio [P < 0.01, repeated measures analysis of variance (ANOVA)]. Serum creatine kinase (CK) and lactate dehydrogenase (LDH) activities were elevated (P < 0.01, repeated measures ANOVA) following the bout. The mean (SD) CK and LDH levels recorded 3 days post-exercise were 2815 (4144) IU · l^–1 and 375 (198) IU · l^–1, respectively. Serum alkaline phosphatase activity showed no changes throughout the study, and a non-significant increase (P = 0.058, repeated measures ANOVA) in pyridinoline was recorded following the bout. Urinary hydroxyproline (HP) and hydroxylysine (HL) excretion, expressed in terms of creatinine (Cr) concentration, increased after exercise (P < 0.05 and P < 0.01, respectively, repeated measures ANOVA). An increased HP:Cr was recorded 2 days post-exercise and HL:Cr was increased above baseline on days 2, 5, and 9 post-exercise. This indirect evidence of exercise-induced muscle damage suggests that myofibre disruption was caused by the eccentric muscle contractions. Elevated urine concentrations of indirect indices of collagen breakdown following eccentric muscle contractions suggests an increased breakdown of connective tissue, possibly due to a localised inflammatory response. Accepted: 9 October 1996     

Experimental knee pain impairs submaximal force steadiness in isometric,eccentric, and concentric muscle actions

IntroductionPopulations with knee joint damage, including arthritis, have noted impairments in the regulation of submaximal muscle force. It is difficult to determine the exact cause of such impairments given the joint pathology and associated neuromuscular adaptations. Experimental pain models that have been used to isolate the effects of pain on muscle force regulation have shown impaired force steadiness during acute pain. However, few studies have examined force regulation during dynamic contractions, and these findings have been inconsistent. The goal of the current study was to examine the effect of experimental knee joint pain on submaximal quadriceps force regulation during isometric and dynamic contractions.MethodsThe study involved fifteen healthy participants. Participants were seated in an isokinetic dynamometer. Knee extensor force matching tasks were completed in isometric, eccentric, and concentric muscle contraction conditions. The target force was set to 10 % of maximum for each contraction type. Hypertonic saline was then injected into the infrapatella fat pad to generate acute joint pain. The force matching tasks were repeated during pain and once more 5 min after pain had subsided.ResultsHypertonic saline resulted in knee pain with an average peak pain rating of 5.5 ± 2.1 (0–10 scale) that lasted for 18 ± 4 mins. Force steadiness significantly reduced during pain across all three muscle contraction conditions. There was a trend to increased force matching error during pain but this was not significant.ConclusionExperimental knee pain leads to impaired quadriceps force steadiness during isometric, eccentric, and concentric contractions, providing further evidence that joint pain directly affects motor performance. Given the established relationship between submaximal muscle force steadiness and function, such an effect may be detrimental to the performance of tasks in daily life. In order to restore motor performance in people with painful arthritic conditions of the knee, it may be important to first manage their pain more effectively.     

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.

     

MR measurements of muscle damage and adaptation after eccentric exercise.

The purposes of this study were, first, to clarify the long-term pattern of T2 relaxation times and muscle volume changes in human skeletal muscle after intense eccentric exercise and, second, to determine whether the T2 response exhibits an adaptation to repeated bouts. Six young adult men performed two bouts of eccentric biceps curls (5 sets of 10 at 110% of the 1-repetition concentric maximum) separated by 8 wk. Blood samples, soreness ratings, and T2-weighted axial fast spin-echo magnetic resonance images of the upper arm were obtained immediately before and after each bout; at 1, 2, 4, 7, 14, 21, and 56 days after bout 1; and at 2, 4, 7 and 14 days after bout 2. Resting muscle T2 [27.6 +/- 0.2 (SE) ms] increased immediately postexercise by 8 +/- 1 ms after both bouts. T2 peaked 7 days after bout 1 at 47 +/- 4 ms and remained elevated by 2.5 ms at 56 days. T2 peaked lower (37 +/- 4 ms) and earlier (2-4 days) after bout 2, suggesting an adaptation of the T2 response. Peak serum creatine kinase values, pain ratings, and flexor muscle swelling were also significantly lower after the second bout (P < 0.05). Total volume of the imaged arm region increased transiently after bout 1 but returned to preexercise values within 2 wk. The exercised flexor compartment swelled by over 40%, but after 2 wk it reverted to a volume 10% smaller than that before exercise and maintained this volume loss through 8 wk, consistent with partial or total destruction of a small subpopulation of muscle fibers.     

Cellular adaptation to repeated eccentric exercise-induced muscle damage.

Eccentrically biased exercise results in skeletal muscle damage and stimulates adaptations in muscle, whereby indexes of damage are attenuated when the exercise is repeated. We hypothesized that changes in ultrastructural damage, inflammatory cell infiltration, and markers of proteolysis in skeletal muscle would come about as a result of repeated eccentric exercise and that gender may affect this adaptive response. Untrained male (n = 8) and female (n = 8) subjects performed two bouts (bout 1 and bout 2), separated by 5.5 wk, of 36 repetitions of unilateral, eccentric leg press and 100 repetitions of unilateral, eccentric knee extension exercises (at 120% of their concentric single repetition maximum), the subjects' contralateral nonexercised leg served as a control (rest). Biopsies were taken from the vastus lateralis from each leg 24 h postexercise. After bout 2, the postexercise force deficit and the rise in serum creatine kinase (CK) activity were attenuated. Women had lower serum CK activity compared with men at all times (P < 0.05), but there were no gender differences in the relative magnitude of the force deficit. Muscle Z-disk streaming, quantified by using light microscopy, was elevated vs. rest only after bout 1 (P < 0.05), with no gender difference. Muscle neutrophil counts were significantly greater in women 24 h after bout 2 vs. rest and bout 1 (P < 0.05) but were unchanged in men. Muscle macrophages were elevated in men and women after bout 1 and bout 2 (P < 0.05). Muscle protein content of the regulatory calpain subunit remained unchanged whereas ubiquitin-conjugated protein content was increased after both bouts (P < 0.05), with a greater increase after bout 2. We conclude that adaptations to eccentric exercise are associated with attenuated serum CK activity and, potentially, an increase in the activity of the ubiquitin proteosome proteolytic pathway.     

Contrast of directional influence upon motor overflow between submaximal and maximal static exertions

This study investigated exertion-dependent motor overflow among healthy adults when they performed isometric tasks with contralateral joints in different task directions. Twenty healthy adults (10 males and 10 females, mean age = 26.2 yrs) were instructed to complete a set of isometric contractions of various force vectors with the shoulder, elbow, and wrist joints, in a total of ten motor tasks at submaximal and maximal intensities (50%, 100% maximal voluntary contractions). The electromyographical activities from eight muscles of the unexercised upper limb were recorded to characterize intensity of motor overflow during sustained isometric contraction. Both occurrence frequency and magnitude of motor overflow in terms of standardized net excitation (SNE) increased with exertion level for all joint movements (P < 0.001). Additionally, the motor overflow magnitude depended strongly on the task direction of maximal isometric contraction (P < 0.05). Motor overflow was particularly augmented by the contralateral isometric contractions where task directions were opposed to gravity. However, such a directional effect upon SNE was not evident during submaximal contraction (P > 0.05). The difference of the net excitation between maximal and submaximal contraction (DNE(100%-50%MVC) data) indicated that the pectoralis major and triceps brachii consistently exhibited a marked recruitment in reaction to change in task direction of isometric contraction. Patterned motor overflow may be physiologically relevant to topological mapping of the ipsilateral pathways and altered effectiveness of use-dependent interhemispherical connectivity. The current observations provide better insight into gain in muscle strength due to contralateral exercise.     

Energetics of kayaking at submaximal and maximal speeds

The energy cost of kayaking per unit distance (C(k), kJ x m(-1)) was assessed in eight middle- to high-class athletes (three males and five females; 45-76 kg body mass; 1.50-1.88 m height; 15-32 years of age) at submaximal and maximal speeds. At submaximal speeds, C(k) was measured by dividing the steady-state oxygen consumption (VO(2), l x s(-1)) by the speed (v, m x s(-1)), assuming an energy equivalent of 20.9 kJ x l O(-1)(2). At maximal speeds, C(k) was calculated from the ratio of the total metabolic energy expenditure (E, kJ) to the distance (d, m). E was assumed to be the sum of three terms, as originally proposed by Wilkie (1980): E = AnS + alphaVO(2max) x t-alphaVO(2max) x tau(1-e(-t x tau(-1))), were alpha is the energy equivalent of O(2) (20.9 kJ x l O(2)(-1)), tau is the time constant with which VO(2max) is attained at the onset of exercise at the muscular level, AnS is the amount of energy derived from anaerobic energy utilization, t is the performance time, and VO(2max) is the net maximal VO(2). Individual VO(2max) was obtained from the VO(2) measured during the last minute of the 1000-m or 2000-m maximal run. The average metabolic power output (E, kW) amounted to 141% and 102% of the individual maximal aerobic power (VO(2max)) from the shortest (250 m) to the longest (2000 m) distance, respectively. The average (SD) power provided by oxidative processes increased with the distance covered [from 0.64 (0.14) kW at 250 m to 1.02 (0.31) kW at 2000 m], whereas that provided by anaerobic sources showed the opposite trend. The net C(k) was a continuous power function of the speed over the entire range of velocities from 2.88 to 4.45 m x s(-1): C(k) = 0.02 x v(2.26) (r = 0.937, n = 32).     

Assessment of eccentric exercise-induced muscle damage of the elbow flexors by tensiomyography

Exercise induced muscle damage (EIMD) impairs maximal torque production which can cause a decline in athletic performance and/or mobility. EIMD is commonly assessed by using maximal voluntary contraction (MVC), creatine kinase (CK) and muscle soreness. We propose as an additional technique, tensiomyography (TMG), recently introduced to measure mechanical and muscle contractile characteristics. The purpose of this study was to determine the validity of TMG in detecting changes in maximal torque following EIMD. Nineteen participants performed eccentric elbow flexions to achieve EIMD on the non- dominant arm and used the dominant elbow flexor as a control. TMG parameters, MVC and rate of torque development (RTD) were measured prior to EIMD and repeated for another six consecutive days. Creatine kinase, muscle soreness and limb girth were also measured during this period. Twenty four hours after inducing EIMD, MVC torque, RTD and TMG maximal displacement had significantly (p<0.01) declined by 37%, 44% and 31%, respectively. By day 6 MVC, RTD and TMG recovered to 12%, 24% and 17% of respective pre-EIMD values. In conclusion, as hypothesised TMG maximal displacement significantly followed other standard EIMD responses. This could therefore be useful in detecting muscle damage from impaired muscle function and its recovery following EIMD.     

Repeated high-force eccentric exercise: effects on muscle pain and damage

Five women and three men (aged 24-43 yr) performed maximal eccentric contractions of the elbow flexors (for 20 min) on three occasions, spaced 2 wk apart. Muscle pain, strength and contractile properties, and plasma creatine kinase (CK) were studied before and after each exercise bout. Muscle tenderness was greatest after the first bout and thereafter progressively decreased. Very high plasma CK levels (1,500-11,000 IU/l) occurred after the first bout, but the second and third bouts did not significantly affect the plasma CK. After each bout the strength was reduced by approximately 50% and after 2 wk had only recovered to 80% of preexercise values. Each exercise bout produced a marked shift of the force-frequency curve to the right which took approximately 2 wk to recover. The recovery rate of both strength and force-frequency characteristics was faster after the second and third bouts. Since the adaptation occurred after the performance of maximal contractions it cannot have been a result of changes in motor unit recruitment. The observed training effect of repeated exercise was not a consequence of the muscle becoming either stronger or more resistant to fatigue.