The influence of loading intensity on muscle–tendon unit behavior during maximal knee extensor stretch shortening cycle exercise

Tendon stiffness increases as the magnitude and rate of loading increases, according to its viscoelastic properties. Thus, under some loading conditions tendons should become exceptionally stiff and act almost as rigid force transducers. Nonetheless, observations of tendon behavior during multi-joint sprinting and jumping tasks have shown that tendon strain increases whilst muscle strain decreases as the loading intensity increases. The purpose of the current study was to examine the influence of external loading intensity on muscle–tendon unit (MTU) behavior during a high-speed single-joint, stretch-shortening cycle (SSC) knee extension task. Eighteen men (n = 9) and women (n = 9) performed single-leg, maximum intensity SSC knee extensions at loads of 20, 60 and 90?% of their one repetition maximum. Vastus lateralis fascicle length (L _f) and velocity (v _f) as well as MTU (L _MTU) and tendinous tissue (L _t) length were measured using high-speed ultrasonography (96 Hz). Patellar tendon force (F _t) and rate of force development (RFD_t) were estimated using inverse dynamics. Results showed that as loading intensity increased, concentric joint velocity and shortening v _f decreased whilst F _t and RFD_t increased, but no significant differences were observed in eccentric joint velocity or peak L _MTU or L _f. In addition, the tendon lengthened significantly less at the end of the eccentric phase at heavier loads. This is the first observation that tendon strain decreases significantly during a SSC movement as loading intensity increases in vivo, resulting in a shift in the tendon acting as a power amplifier at light loads to a more rigid force transducer at heavy loads.     

Force–velocity and unloaded shortening velocity during graded potassium contractures in frog skeletal muscle fibres

Steady-state conditions of contraction, at maximal and submaximal forces, were produced in intact single muscle fibres, from Rana esculenta, using full tetani and graded K⁺-contractures. The uniformity in radial direction, of spreading of activation produced in K⁺-contractures, was checked in relation to the fibre diameters. The absolute isometric force was similar in tetani and maximal contractures, for fibres with diameters between 40 and 60 m, but not for fibres with diameters greater than about 70 m in which contracture force never reached tetanic force. The force–[K⁺]_o relation was similar for fibres with diameters between 40 and 60 m, but it was right shifted and it had a minor slope for fibres with diameters greater than 65–70 m. This suggests that only in the small diameter fibres (40–60 m) the activation does not fail to penetrate uniformly from the surface towards the fibre core. For fibres selected in the diameter range between 40 and 60 m, force–velocity relations and unloaded shortening velocities were determined in tetani and maximal and submaximal contractures. Data were obtained across a force range of 0.3 to 1 P ₀ (tetanic plateau force). Controlled velocity method was used to obtain force–velocity relations, and slack test to determine the unloaded shortening velocity (V _U). The values of the parameters characterising the force–velocity relation (V ₀ and a/P ₀) and V _U as determined by the slack test did not differ significantly in tetani and contractures, independent of the activation level or absolute force developed by the fibre. These results show that, at least within the range of forces tested, crossbridge kinetics is independent of the number of cycling crossbridges, in agreement with the prediction of the recruitment model of myofilament activation.     

Acute and delayed neuromuscular adjustments of the triceps surae muscle group to exhaustive stretch–shortening cycle fatigue

Stretch–shortening cycle (SSC)-type fatigue is associated with acute and delayed functional defects, and appears to be a useful model to reveal the flexibility of both central and reflex adjustments to the contractile failure. SSC fatigue was induced in an experimental (EXP) group (n=6) on a sledge ergometer with an exhaustive rebound exercise with submaximal effort. The acute (POST) and 2-day delayed (2D) neuromuscular changes with fatigue were examined in a short submaximal rebound task (REBOUND) and in a maximal isometric plantarflexion test (ISOM). The EXP group results were compared to those of a control group (n=6) who did not perform the exhaustive SSC exercise and did not present any change in the tests. In the EXP group, the ISOM test revealed mostly a large decrease in maximal plantarflexion force at 2D that was correlated with the reduced mean soleus muscle (SOL) activation. Indicating task-dependent fatigue effects on the neural changes, the REBOUND test revealed both acute and delayed increases in SOL activation. Supporting central neural changes, SOL preactivation increased in POST and 2D. The neural flexibility along time and across muscles was demonstrated by the shifted increase in SOL activation from the braking phase in POST to the push-off phase in 2D, and associated increased gastrocnemius medialis preactivation in 2D. In contrast, activation during the stretch–reflex period was constant in POST, and decreased in 2D. These results would support the influence of musculotendinous afferents on the flexible neural adjustments to the SSC-induced contractile failure.     

The decrease in electrically evoked force production is delayed by a previous bout of stretch–shortening cycle exercise

Aim: Unaccustomed physical exercise with a large eccentric component is accompanied by muscle damage and impaired contractile function, especially at low stimulation frequencies. A repeated bout of eccentric exercise results in less damage and improved recovery of contractile function. Here we test the hypotheses that (1) a prior stretch–shortening cycle (SSC) exercise protects against impaired muscle function during a subsequent bout of SSC exercise and (2) the protection during exercise is transient and becomes less effective as the exercise progresses. Methods: Healthy untrained men (n = 7) performed SSC exercise consisting of 100 maximal drop jumps at 30 s intervals. The same exercise was repeated 4 weeks later. Peak quadriceps muscle force evoked by electrical stimulation at 15 (P15) and 50 (P50) Hz was measured before exercise, after 10, 25, 50 and 100 jumps as well as 1 and 24 h after exercise. Results: P15 and P50 were higher during the initial phase of the repeated bout compared with the first exercise bout, but there was no difference between the bouts at the end of the exercise periods. P15 and P50 were again larger 24 h after the repeated bout. The P15/P50 ratio during exercise was not different between the two bouts, but it was higher after the repeated bout. Conclusion: A prior bout of SSC exercise temporarily protects against impaired contractile function during a repeated exercise bout. The protection can again be seen after exercise, but the underlying mechanism then seems to be different.     

Activation of the skeletal α-actin promoter during muscle regeneration

Little is known conerning promoter regulation of genes in regenerating skeletal muscles. In young rats, recovery of muscle mass and protein content is complete within 21 days. During the initial 5–10 days of regeneration, mRNA abundance for IGF-I, myogenin and MyoD have been shown to be dramatically increased. The skeletal -actin promoter contains E box and serum response element (SRE) regulatory regions which are directly or indirectly activated by myogenin (or MyoD) and IGF-I proteins, respectively. We hypothesized that the skeletal -actin promoter activity would increase during muscle regeneration, and that this induction would occur before muscle protein content returned to normal. Total protein content and the percentage content of skeletal -actin protein was diminished at 4 and 8 days and re-accumulation had largely occurred by 16 days post-bupivacaine injection. Skeletal - actin mRNA per whole muscle was decreased at day 8, and thereafter returned to control values. During regeneration at day 8, luciferase activity (a reporter of promoter activity) directed by –424 skeletal -actin and –99 skeletal -actin promoter constructs was increased by 700% and 250% respectively; however, at day 16, skeletal -actin promoter activities were similar to control values. Thus, initial activation of the skeletal - actin promoter is associated with regeneration of skeletal muscle, despite not being sustained during the later stages of regrowth. The proximal SRE of the skeletal -actin promoter was not sufficient to confer a regeneration-induced promoter activation, despite increased serum response factor protein binding to this regulatory element in electrophoretic mobility shift assays. Skeletal -actin promoter induction during regeneration is due to a combination of regulatory elements, at least including the SRE and E box. © Kluwer Academic Publishers.     

Excitability of the soleus reflex arc during intensive stretch–shortening cycle exercise in two power-trained athlete groups

In several explosive types of sport events the leg extensor muscles are subjected to very high impact loads. Thus, extreme requirements exist for the neuromuscular system to develop sufficient muscle stiffness in the lower extremities in order to tolerate these high impact loads. Therefore, it would be challenging to measure reflex modulation during high impact activities, and with different athlete populations. In the present experiment, H-reflex and short latency reflex (M1) sensitivity was measured during drop jump exercises among high jumpers and sprinters. The changes in both reflex peak-to-peak amplitudes showed a significant (P < 0.05) reduction towards the end of the exercise for the sprinters. In addition, the same subject group showed a remarkable increase in serum creatine kinase (CK) activity 2 h after the jumps. Similar changes could not be observed for the high jumpers. These results clearly indicate different neural adaptation strategies for the two athlete groups. Reduction in H-reflex sensitivity and an increase in CK-activity in sprinters were taken as evidence for presynaptic inhibition, probably induced by substances related to muscle damage. Since high jump training includes more high impact loading, it was assumed that it could lead to some structural adaptation and, thus, prevents exercise induced reflex modification to a certain extent.     

Modeling of skeletal muscle: the influence of tendon and aponeuroses compliance on the force–length relationship

The aim of this study was to investigate the influence of changing elastic properties of tendon and aponeuroses on force production and muscle geometry. A three-dimensional, structural, continuum mechanics model of the cat medial gastrocnemius was used for this purpose. Increasing compliance in tendon and aponeuroses caused a decrease in the peak isometric force and a shift of the force–length relationship to the right of the length axis (i.e. toward greater muscle lengths). This result can be explained with the stability condition of the force–length relationship which produced a history dependence of force production that is conceptually in agreement with experimental observations.     

Effects of S-glutathionylation on the passive force–length relationship in skeletal muscle fibres of rats and humans

Journal of Muscle Research and Cell Motility - This study investigated the effect of S-glutathionylation on passive force in skeletal muscle fibres, to determine whether activity-related redox...     

Do cross-bridges contribute to the tension during stretch of passive muscle?

The tension rise during stretch of passive skeletal muscle is biphasic, with an initial steep rise, followed by a subsequent more gradual change. The initial rise has been interpreted as being due to the presence of numbers of long-term, stable cross-bridges in resting muscle fibres. A point of weakness with the cross-bridge interpretation is that the initial stiffness reaches its peak value at muscle lengths beyond the optimum for myofilament overlap. To explain this result it has been suggested that despite the reduced overlap at longer lengths, the closer interfilament spacing and a higher sensitivity of the myofilaments to Ca²⁺ allows more stable cross-bridges to form. Recently the stretch responses of passive muscle have been re-examined and it has been suggested that it is not necessary to invoke cross-bridge mechanisms at all. Explanations based on a viscous resistance to interfilament sliding and mechanical properties of the elastic filaments, the gap filaments, were thought to adequately account for the observed tension changes. However, an important property of passive muscle, the dependence of stretch responses on the immediate history of contraction and length changes, thixotropy, cannot be explained simply in terms of viscous and viscoelastic properties. The review discusses the cross-bridge interpretation of muscle thixotropy and the relationship of passive stiffness to filament resting tension and latency relaxation. It is proposed that cross-bridges can exist in three states; one, responsible for the resting stiffness, requires resting levels of calcium. When, during activation, calcium levels rise, cross-bridges enter a low-force, high-stiffness state, signalled by latency relaxation, before they move to the third, force-generating state. It is concluded that, compared with viscoelastic models, a cross-bridge-based explanation of passive muscle properties is better able to accommodate the currently known facts although, as new information becomes available, this view may need to be revised.     

The force–velocity relationship of the human soleus muscle during submaximal voluntary lengthening actions

In experiments on isolated animal muscle, the force produced during active lengthening contractions can be up to twice the isometric force, whereas in human experiments lengthening force shows only modest, if any, increase in force. The presence of synergist and antagonist muscle activation associated with human experiments in situ may partly account for the difference between animal and human studies. Therefore, this study aimed to quantify the force–velocity relationship of the human soleus muscle and assess the likelihood that co-activation of antagonist muscles was responsible for the inhibition of torque during submaximal voluntary plantar flexor efforts. Seven subjects performed submaximal voluntary lengthening, shortening(at angular, velocities of +5, –5, +15, –15 and +30, and –30° s^–1) and isometric plantar flexor efforts against an ankle torque motor. Angle-specific (90°) measures of plantar flexor torque plus surface and intramuscular electromyography from soleus, medial gastrocnemius and tibialis anterior were made. The level of activation (30% of maximal voluntary isometric effort) was maintained by providing direct visual feedback of the soleus electromyogram to the subject. In an attempt to isolate the contribution of soleus to the resultant plantar flexion torque, activation of the synergist and antagonist muscles were minimised by: (1) flexing the knee of the test limb, thereby minimising the activation of gastrocnemius, and (2) applying an anaesthetic block to the common peroneal nerve to eliminate activation of the primary antagonist muscle, tibialis anterior and the synergist muscles, peroneus longus and peroneus brevis. Plantar flexion torque decreased significantly (P<0.05) after blocking the common peroneal nerve which was likely due to abolishing activation of the peroneal muscles which are synergists for plantar flexion. When normalised to the corresponding isometric value, the force–velocity relationship between pre- and post-block conditions was not different. In both conditions, plantar flexion torques during shortening actions were significantly less than the isometric torque and decreased at faster velocities. During lengthening actions, however, plantar flexion torques were not significantly different from isometric regardless of angular velocity. It was concluded that the apparent inhibition of lengthening torques during voluntary activation is not due to co-activation of antagonist muscles. Results are presented as mean (SEM).     

The expression of α-dystrobrevin and dystrophin during skeletal muscle regeneration

The expression of α-dystrobrevin and dystrophin in rat tibialis anterior muscles was chronologically evaluated during a cycle of regeneration after myonecrosis induced by the injection of cardiotoxin. In immunohistochemical studies, α-dystrobrevin and dystrophin were first stained weakly at the sarcolemma of some regenerating muscle fibers on day 5. On day 7, α-dystrobrevin was still stained weakly, whereas dystrophin was stained conspicuously. After day 10, α-dystrobrevin and dystrophin were both stained conspicuously on almost all regenerating muscle fibers. In the Western blot analysis, α-dystrobrevin and dystrophin were first detected as visible bands on days 5 and 7, respectively. The bands of α-dystrobrevin and dystrophin both darkened sequentially up to day 10. The protein levels based on the densitometrical analysis of the bands on each day were converted to the percentage of the protein level on day 28, which was taken as 100%. The sequential line based on these data showed that α-dystrobrevin and dystrophin reached 50% of the protein level on day 28 by 6.6 and 5.3 days, respectively. These data provide evidence that α-dystrobrevin regenerates more slowly than dystrophin in skeletal muscle. This revised version was published online in July 2006 with corrections to the Cover Date.     

Na+–K+ pump location and translocation during muscle contraction in rat skeletal muscle

Muscle contraction may up-regulate the number of Na(+)-K(+) pumps in the plasma membrane by translocation of subunits. Since there is still controversy about where this translocation takes place from and if it takes place at all, the present study used different techniques to characterize the translocation. Electrical stimulation and biotin labeling of rat muscle revealed a 40% and 18% increase in the amounts of the Na(+)-K(+) pump alpha(2) subunit and caveolin-3 (Cav-3), respectively, in the sarcolemma. Exercise induced a 36% and 19% increase in the relative amounts of the alpha(2) subunit and Cav-3, respectively, in an outer-membrane-enriched fraction and a 41% and 17% increase, respectively, in sarcolemma giant vesicles. The Na(+)-K(+) pump activity measured with the 3-O-MFPase assay was increased by 37% in giant vesicles from exercised rats. Immunoprecipitation with Cav-3 antibody showed that 17%, 11% and 14% of the alpha(1) subunits were associated with Cav-3 in soleus, extensor digitorum longus, and mixed muscles, respectively. For the alpha(2), the corresponding values were 17%, 5% and 16%. In conclusion; muscle contraction induces translocation of the alpha subunits, which is suggested to be caused partly by structural changes in caveolae and partly by translocation from an intracellular pool.     

The expression of dystrophin and α1-syntrophin during skeletal muscle regeneration

The expression of dystrophin and 1-syntrophin in rat tibialis anterior muscles were evaluated during a cycle of regeneration after myonecrosis induced by the injection of cardiotoxin. Immunohistochemical studies were performed in cryosections of muscles on days 1, 3, 5, 7, 10, 14, 21 and 28 after injection of cardiotoxin. Western blot analysis was also examined in muscle on days 1, 3, 5, 7, 10, 14, 21 and 28. In immunohistochemical studies, dystrophin was stained weakly at the sarcolemma of some regenerating muscle fibers on day 3, and by day 10 it was stained strongly on almost all regenerating muscle fibers. 1-syntrophin was stained weakly at the sarcolemma of some regenerating fibers on day 5, and by day 14 it was detected on all regenerating muscle fibers. In Western blot analysis, dystrophin (DYS1) and 1-syntrophin (1S) were completely absent on day 1. Re-expression of DYS1 and 1S was visible by day 5 and accelerated thereafter. The Western blots of DYS1 and 1S were densitometrically analyzed on each day. The protein levels on each day were converted to the percentage of the protein level on day 28, which was taken as 100%. From the sequential line based on these data, the following results were obtained on the chronological course of DYS1 and 1S. DYS1: 25% of the protein level on day 28 was reached by 3.5 days, 50% was reached by 5.3 days, and 90% was reached by 6.9 days. 1S: 25% of the protein level on day 28 was reached by 4.6 days, 50% was reached by 6.0 days, and 90% was reached by 12.5 days. In this study, DYS1 regenerated earlier than 1S at the sarcolemma of regenerating muscle fibers.     

Do cross-bridges contribute to the tension during stretch of passive muscle? a response

Journal of Muscle Research and Cell Motility -     

Concentrically trained cyclists are not more susceptible to eccentric exercise-induced muscle damage than are stretch–shortening exercise-trained runners

Here, we test the hypothesis that continuous concentric exercise training renders skeletal muscles more susceptible to damage in response to eccentric exercise. Elite road cyclists (CYC; n = 10, training experience 8.1 ± 2.0 years, age 22.9 ± 3.7 years), long-distance runners (LDR; n = 10, 9.9 ± 2.3 years, 24.4 ± 2.5 years), and healthy untrained (UT) men (n = 10; 22.4 ± 1.7 years) performed 100 submaximal eccentric contractions at constant angular velocity of 60° s^?1. Concentric isokinetic peak torque, isometric maximal voluntary contraction (MVC), and electrically induced knee extension torque were measured at baseline and immediately and 48 h after an eccentric exercise bout. Muscle soreness was assessed and plasma creatine kinase (CK) activity was measured at baseline and 48 h after exercise. Voluntary and electrically stimulated knee extension torque reduction were significantly greater (p < 0.05) in UT than in LDR and CYC. Immediately and 48 h after exercise, MVC decreased by 32 % and 20 % in UT, 20 % and 5 % in LDR, and 25 % and 6 % in CYC. Electrically induced 20 Hz torque decreased at the same times by 61 and 29 % in UT, 40 and 17 % in LDR, and 26 and 14 % in CYC. Muscle soreness and plasma CK activity 48 h after exercise did not differ significantly between athletes and UT subjects. In conclusion, even though elite endurance athletes are more resistant to eccentric exercise-induced muscle damage than are UT people, stretch–shortening exercise-trained LDR have no advantage over concentrically trained CYC.     

β‐Adrenergic modulation of skeletal muscle contraction: key role of excitation–contraction coupling

Our aim is to describe the acute effects of catecholamines/β‐adrenergic agonists on contraction of non‐fatigued skeletal muscle in animals and humans, and explain the mechanisms involved. Adrenaline/β‐agonists (0.1–30 μm) generally augment peak force across animal species (positive inotropic effect) and abbreviate relaxation of slow‐twitch muscles (positive lusitropic effect). A peak force reduction also occurs in slow‐twitch muscles in some conditions. β₂‐Adrenoceptor stimulation activates distinct cyclic AMP‐dependent protein kinases to phosphorylate multiple target proteins. β‐Agonists modulate sarcolemmal processes (increased resting membrane potential and action potential amplitude) via enhanced Na⁺–K⁺ pump and Na⁺–K⁺–2Cl⁻ cotransporter function, but this does not increase force. Myofibrillar Ca²⁺ sensitivity and maximum Ca²⁺‐activated force are unchanged. All force potentiation involves amplified myoplasmic Ca²⁺ transients consequent to increased Ca²⁺ release from sarcoplasmic reticulum (SR). This unequivocally requires phosphorylation of SR Ca²⁺ release channels/ryanodine receptors (RyR1) which sensitize the Ca²⁺‐induced Ca²⁺ release mechanism. Enhanced trans‐sarcolemmal Ca²⁺ influx through phosphorylated voltage‐activated Ca²⁺ channels contributes to force potentiation in diaphragm and amphibian muscle, but not mammalian limb muscle. Phosphorylation of phospholamban increases SR Ca²⁺ pump activity in slow‐twitch fibres but does not augment force; this process accelerates relaxation and may depress force. Greater Ca²⁺ loading of SR may assist force potentiation in fast‐twitch muscle. Some human studies show no significant force potentiation which appears to be related to the β‐agonist concentration used. Indeed high‐dose β‐agonists (∼0.1 μm) enhance SR Ca²⁺‐release rates, maximum voluntary contraction strength and peak Wingate power in trained humans. The combined findings can explain how adrenaline/β‐agonists influence muscle performance during exercise/stress in humans. IntroductionCatecholamines such as adrenaline (epinephrine) or noradrenaline (norepinephrine), released from the adrenal medulla or sympathetic nerves, can assist exercise performance through well‐known effects such as raised heart rate and myocardial contractility, bronchodilatation, electrolyte regulation, fuel mobilization and blood flow redistribution (Bowman, 1980; Zouhal et al. 2008; Roatta & Farina, 2010; Hostrup et al. 2014 a,b). In addition catecholamines, sympathetic nerve stimulation, or β‐adrenergic agonists can enhance the contractile performance of skeletal muscles of amphibia, animals and humans (for reviews see Bowman, 1980; Williams & Barnes, 1989 a; Roatta & Farina, 2010). Such effects on contractile function include a potentiation of peak force (positive inotropic effect) (Figs 1 A and C, ​,33 B, and ​and44 C and D) and a faster relaxation of some muscles (positive lusitropic effect) (Fig. 1 A–C). However, in some situations a depression of peak force can occur (negative inotropic effect) (Fig. 1 B). The magnitude and nature of these adrenergic effects vary depending on such aspects as the fibre‐type composition of the muscle, species, concentration of agent, and the muscle condition, e.g. fatigued (Juel, 1988; Cairns & Dulhunty, 1994; Decorte et al. 2015) or K⁺ depressed (Clausen, 2003; Cairns et al. 2011). These effects all require activation of β₂‐adrenergic receptors, since they manifest with general β‐adrenergic agonists, e.g. isoprenaline (isoproterenol), or selective β₂‐adrenergic agonists such as salbutamol or terbutaline, i.e. short‐acting β₂‐agonists, and are also antagonized with general or selective β₂‐adrenoceptor blockers (Bowman, 1980). With the advent of long‐acting β₂‐agonists, e.g. clenbuterol, some caution is needed about non‐selective effects especially when high concentrations are used (Head & Ha, 2011; McCormick et al. 2010), and their chronic application promotes muscle hypertrophy (Lynch & Ryall, 2008). The focus of the present article is on acute effects of catecholamines and short‐acting β‐agonists on cellular processes and contractile function of non‐fatigued skeletal muscle.Open in a separate windowFigure 1 Representative effects of terbutaline on isometric force or power in animal and human muscles A, influence of terbutaline (10 μm for 15 min) on maximal tetanic contractions (100 Hz) in isolated rat slow‐twitch soleus fibre bundles. Supramaximal stimulation pulses delivered from parallel plate electrodes, 24°C. Reproduced from Cairns & Dulhunty, 1993 a with permission. B, influence of oral terbutaline (8 mg for 2 h+) compared with control (pre‐ingestion) on unfused tetanic contractions (10 Hz) in human soleus muscle in vivo. Stimulation of soleus muscle at body temperature (G. Crivelli, F. Borrani, R. Capt, G. Gremion & N. A. Maffiuletti, unpublished data). C, influence of inhaled terbutaline (15 mg for ∼20 min, plasma 24 ± 1 ng ml⁻¹) compared with placebo on maximal voluntary contraction for quadriceps muscles in a trained human male. D, influence of inhaled terbutaline (15 mg for ∼30 min, plasma 24 ± 1 ng ml⁻¹) compared with placebo on Wingate cycle power in a trained human male. C and D are reproduced from Hostrup et al. 2014 a with permission.Open in a separate windowFigure 3 Representative effects of 10 μm terbutaline on myoplasmic [Ca²⁺] ([Ca²⁺]_i) and tension during tetanic stimulation (100 Hz) of single, intact fast‐twitch flexor digitorum brevis fibres of the mouse in vitro [Ca²⁺]_i was measured with the fluorescent Ca²⁺ indicator Indo‐1. ‘Terbutaline’ is the maximal effect obtained after 10 min terbutaline exposure. Parallel plate stimulation electrodes, 22°C. Adapted from Cairns et al. 1993 with permission.Open in a separate windowFigure 4 Influence of 10 μm isoprenaline on sarcoplasmic reticulum [Ca²⁺] ([Ca²⁺]_SR) and cell shortening (i.e. fibre deflection) during twitch stimulation of fast‐twitch tibialis anterior fibres of the mouse in situ [Ca²⁺]_SR was measured with a cameleon Ca²⁺ sensor as the fluorescence ratio (F(535 nm)/F(450 nm)). Data are means ± SEM (25 individual twitches from 3 fibres). B and D were obtained 10 min after application of isoprenaline compared with before (control), i.e. A and C, respectively. Values are normalized to control. The positive inotropic effect is shown as the 50% increase in peak cell shortening (D). Reproduced from Rudolf et al. 2006 with permission (© 2006 Kim and Roy. Journal of Cell Biology. 173:187–193. doi:10.1083/jcb.200601160).Several reviews over the last 15 years have described β‐adrenergic effects on selected muscle processes (e.g. Catterall, 2000; Clausen, 2003; Lynch & Ryall, 2008; Capes et al. 2011) yet none have provided a wholistic appraisal of the β‐adrenergic mechanisms influencing muscle contraction since Williams & Barnes (1989 a). Moreover, a resurgence of studies on β‐adrenergic effects on human muscle (Table 2012; Roatta & Farina, 2013). Therefore, the aims of the present review are: (1) to provide a comprehensive update on the mechanisms underpinning β‐adrenergic effects on non‐fatigued skeletal muscle contraction in humans and animal models; and (2) to explain how adrenaline/β‐agonists influence muscle performance during exercise or stress in humans.

Table 1

Effects of catecholamines or β‐adrenergic agonists on skeletal muscle contraction across species

Viscoelastic creep in the human skeletal muscle–tendon unit

The purposes of the present study were to (1) characterize viscoelastic creep in vivo in the human skeletal muscle–tendon unit and (2) to examine the consistency of these responses during a single 30-s stretch. Twelve volunteers (mean ± SD = 22 ± 3 years; height = 169 ± 11 cm; mass = 70 ± 17 kg) participated in two separate experimental trials. Each trial consisted of a 30-s constant-torque stretch of the plantar flexor muscles. Position (°) values were quantified at every 5-s period (0, 5, 10, 15, 20, 25, and 30 s) and the percent change in position was quantified for each 5-s epoch (0–5, 5–10, 10–15, 15–20, 20–25, and 25–30 s) relative to the total increase in the range of motion. In addition, the intraclass correlation coefficient (ICC) and standard errors of the measurement (SEM) were calculated for test–retest reliability. These results indicated that position increased over the entire 30-s stretch (P < 0.05), while the majority of the increases in position (73–85%) occurred during the first 15–20 s. ICC values were >0.994 and SEM values (expressed as percentage of the mean) were <1.54%. In conclusion, these results demonstrate viscoelastic creep in vivo in the human skeletal muscle–tendon unit and suggest that these responses may be reliable for future studies.