Human Muscle Function Research Articles

The neuropeptide secretoneurin stimulates adhesion of human monocytes to arterial and venous endothelial cells in vitro

Monocytes appear to play a central role in inflammatory processes like atherogenesis or lung inflammation both as the progenitors of foam cells and as a potential source of factors mediating further inflammatory processes. However, signals mediating the influx of monocytes into the inflammatory focus remain partly unknown. Secretoneurin (SN) is a more recently characterised 33-amino acid neuropeptide that is co-released from afferent nerve endings together with substance P (SP) and calcitonin gene-related peptide (CGRP). Furthermore, SN has been shown to affect human fibroblast, endothelial, smooth muscle, eosinophil and monocyte functions in vitro. An activity of SN on monocyte adhesion to the vascular wall has not yet been reported. The aim of this study was to investigate whether the adhesion properties of human monocytes (U937 and Mono Mac-6) to endothelial cells could be influenced by SN. In an in vitro model of the vascular wall, incubation of arterial (rat aortic endothelial cells) and venous endothelial cells (immortalised human umbilical vein endothelial line: EA.hy 926) with SN resulted in a time- and concentration-dependent increase in monocyte adhesion with a maximal effect seen after 4–6 h at a concentration of 10 −8 M SN. Increased monocyte adhesion seems not to be tissue-specific as SN-induced adhesion was observed on both arterial and venous endothelial cells. A specific antibody preparation against SN completely abolished increased monocyte adhesion toward SN-stimulated endothelium. Since adhesion was enhanced to a similar degree and with similar time kinetics as responses evoked by interleukin-1 (IL-1, 1 ng/ml) or lipopolysaccharide (LPS, 100 ng/ml), involvement of identical adhesion molecules can be suggested. Our observations provide substantial evidence that in inflammatory processes, SN might play a role in recruitment of monocytes to inflamed tissue.

Do you really need your oblique muscles? Adaptations and exaptations.

Primitive adaptations in lateral-eyed animals have programmed the oblique muscles to counterrotate the eyes during pitch and roll. In humans, these torsional movements are rudimentary. To determine whether the human oblique muscles are vestigial. Review of primitive oblique muscle adaptations and exaptations in human binocular vision. Primitive adaptations in human oblique muscle function produce rudimentary torsional eye movements that can be measured as cycloversion and cyclovergence under experimental conditions. The human torsional regulatory system suppresses these primitive adaptations and exaptively modulates cyclovergence to facilitate stereoscopic perception in the pitch plane. It also recruits the oblique muscles to generate cycloversional saccades that preset torsional eye position immediately preceding volitional head tilt, permitting instantaneous nonstereoscopic tilt perception in the roll plane. The evolution of frontal binocular vision has exapted the human oblique muscles for stereoscopic detection of slant in the pitch plane and nonstereoscopic detection of tilt in the roll plane. These exaptations do not erase more primitive adaptations, which can resurface when congenital strabismus and neurologic disease produce evolutionary reversion from exaptation to adaptation.

Effects of fatigue and training on sarcoplasmic reticulum Ca(2+) regulation in human skeletal muscle.

Little is known about fatigue and training effects on sarcoplasmic reticulum (SR) function in human muscle, and we therefore investigated this in eight untrained controls (UT), eight endurance-trained (ET), and eight resistance-trained athletes (RT). Muscle biopsies (vastus lateralis) taken at rest and after 50 maximal quadriceps contractions (180 degrees/s, 0.5 Hz) were analyzed for fiber composition, metabolites and maximal SR Ca(2+) release, Ca(2+) uptake, and Ca(2+)-ATPase activity. Fatigue reduced (P < 0.05) Ca(2+) release (42.1 +/- 3.8%, 43.4 +/- 3.9%, 31.3 +/- 6.1%), Ca(2+) uptake (43.0 +/- 5.2%, 34.1 +/- 4.6%, 28.4 +/- 2.8%), and Ca(2+)-ATPase activity (38.6 +/- 4.2%, 48.5 +/- 5.7%, 29.6 +/- 5.0%), in UT, RT, and ET, respectively. These decreases were correlated with fatigability and with type II fiber proportion (P < 0.05). Resting SR measures were correlated with type II proportion (r > or = 0.51, P < 0.05). ET had lower resting Ca(2+) release, Ca(2+) uptake, and Ca(2+)-ATPase (P < 0.05) than UT and RT (P < 0.05), probably because of their lower type II proportion; only minor effects were found in RT. Thus SR function is markedly depressed with fatigue in controls and in athletes, is dependent on fiber type, and appears to be minimally affected by chronic training status.

Mitochondrial function and antioxidative defence in human muscle: effects of endurance training and oxidative stress.

The influence of endurance training on oxidative phosphorylation and the susceptibility of mitochondrial oxidative function to reactive oxygen species (ROS) was investigated in skeletal muscle of four men and four women. Mitochondria were isolated from muscle biopsies taken before and after 6 weeks of endurance training. Mitochondrial respiration was measured before and after exposure of mitochondria to exogenous ROS (H2O2 + FeCl2). Endurance training increased peak pulmonary O2 uptake (VO2,peak) by 24 % and maximal ADP-stimulated mitochondrial oxygen consumption (state 3) by 40% (P<0.05). Respiration in the absence of ADP (state 4), the respiratory control ratio (RCR = state 3/state 4) and the ratio between added ADP and consumed oxygen (P/O) remained unchanged by the training programme. Exposure to ROS reduced state 3 respiration but the effect was not significantly different between pre- and post-training samples. State 4 oxygen consumption increased after exposure to ROS both before (+189 %, P< 0.05) and after training (+243 %, P<0.05) and the effect was significantly higher after training (P<0.05, pre- vs. post-training). The augmented state 4 respiration could in part be attenuated by atractyloside, which indicates that ADP/ATP translocase was affected by ROS. The P/O ratio in ROS-treated mitochondria was significantly lower (P<0.05) compared to control conditions, both before (-18.6+/-2.2 %) and after training (-18.5+/-1.1%). Muscle activities of superoxide dismutase (mitochondrial and cytosolic), glutathione peroxidase and muscle glutathione status were unaffected by training. There was a positive correlation between muscle superoxide dismutase activity and age (r = 0.75; P<0.05; range of age 20-37 years), which may reflect an adaptation to increased generation of ROS in senescent muscle. The muscle glutathione pool was more reduced in subjects with high activity of glutathione peroxidase (r = 0.81; P<0.05). The influence of short-term training on mitochondrial oxygen consumption has for the first time been investigated in human skeletal muscle. The results showed that maximal mitochondrial oxidative power is increased after endurance training but that the efficiency of energy transfer (P/O ratio) remained unchanged. Antioxidative defence was unchanged after training when expressed relative to muscle weight. Although this corresponds to a reduced antioxidant protection per individual mitochondrion, the sensitivity of aerobic energy transfer to ROS was unchanged. However, the augmented ROS-induced non-coupled respiration after training indicates an increased susceptibility of mitochondrial membrane proton conductance to oxidative stress.

Delayed rectifier and Ca(2+)-dependent K(+) currents in human esophagus: roles in regulating muscle contraction.

We have examined K(+) channels and their function in human esophageal smooth muscle using perforated patch recording, RT-PCR to identify channel mRNA, and muscle contraction to study the effects of channel blockers. Depolarization revealed at least two types of currents: a 4-aminopyridine (4-AP)-sensitive transient delayed rectifier K(+) (K(V)) and a Ca(2+)-dependent K(+) (K(Ca)) current. K(Ca) current was active at positive potentials and was blocked by tetraethylammonium (TEA), iberiotoxin, and charybdotoxin but was insensitive to 4-AP. The mRNA encoding the gene products of Kv1.2 and Kv1.5 was identified in muscle and dissociated cells, consistent with these channel types contributing to K(V) current. 4-AP increased resting tension of muscle strips, suggesting a role for K(V) in setting the membrane potential. TEA, but not 4-AP, augmented the amplitude and duration of electrically evoked contraction, effects that were abolished by nifedipine. Here we provide the first description of macroscopic K(+) currents in human esophagus. K(V) channels participate in regulation of resting tension, whereas the K(Ca) channel limits depolarization and contraction during excitation.

The effects of zinc depletion on peak force and total work of knee and shoulder extensor and flexor muscles.

In this study we tested the effect of zinc (Zn) on muscle function in human. After receiving 12 mg Zn/day for 17 days, 8 male subjects received 0.3 mg Zn/day for either 33 or 41 days. Subjects were divided into two groups for repletion. Group A subjects received overnight infusions of 66 mg Zn on Days 1 and 10 and then were fed 12 mg Zn/day for another 16 days. Group B subjects were fed 12 mg Zn/day for 3 weeks. Peak force and total work capacity of the knee and shoulder extensor and flexor muscle groups were assessed using an isokinetic dynamometer at baseline, at two points during depletion, and at repletion. Plasma Zn declined significantly during depletion and remained below baseline levels after repletion. The peak force of the muscle groups tested was not affected by acute Zn depletion, however, total work capacity for the knee extensor muscles and shoulder extensor and flexor muscles declined significantly. The data suggest that acute Zn depletion alters the total work capacity of skeletal muscle.

Magnetic fields produced by single motor units in human skeletal muscles

Objective: To develop new non-invasive ways of analyzing human skeletal muscle function, biomagnetic measurement was applied to the vastus lateralis and vastus medialis of 3 healthy adult males using a 64 channel superconducting quantum interference device system.Methods: Discharges from single motor units were detected by simultaneously recorded surface electromyography. Magnetic signals were averaged 64–158 times at zero-crossing timing in the surface electromyographic signal.Results: Six motor units detected in the 3 subjects produced large magnetic fields with peak-to-peak amplitudes of 1–2 pT. Magnetomyographic isofield maps showed current sources arising from motor endplate regions and propagating in directions opposite to fiber ends. The absolute intensity of current moments in muscle fibers within motor units was estimated based on dipole fitting. The estimated moment was 23.9–114.3 nAm for repolarization dipole. Dividing these moment values by the typical dipole moment of 0.286 nAm in a single muscle fiber, the number of muscle fibers in motor unit was estimated to be 84–400.Conclusions: Magnetic recording may provide a new non-invasive way of analyzing and diagnosing human muscle function.

Biophysical interaction between phospholamban and protein phosphatase 1 regulatory subunit GM

Regulation of the sarco(endo)plasmic reticulum Ca 2+-ATPase (SERCA 2a) depends on the phosphorylation state of phospholamban (PLB). When PLB is phosphorylated, its inhibitory effect towards SERCA 2a is relieved, leading to an enhanced myocardial performance. This process is reversed by a sarcoplasmic reticulum (SR)-associated type 1 protein phosphatase (PP1) composed of a catalytic subunit PP1C and a regulatory subunit GM. Human GM and PLB have been produced in an in vitro transcription/translation system and used for co-immunoprecipitation and biosensor experiments. The detected interaction between the two partners suggests that cardiac PP1 is targeted to PLB via GM and we believe that this process occurs with the identified transmembrane domains of the two proteins. Thus, the interaction between PLB and GM may represent a specific way to modulate the SR function in human cardiac muscle.

Automated segmentation of muscle fiber images using active contour models.

The cross-sectional area of different fiber types is an important anatomic feature in studying the structure and function of healthy and diseased human skeletal muscles. However, such studies are hampered by the thousands of fibers involved when manual segmentation has to be used. We have developed a semiautomatic segmentation method that uses computational geometry and recent computer vision techniques to significantly reduce the time required to accurately segment the fibers in a sample. The segmentation is achieved by simply pointing to the approximate centroid of each fiber. The set of centroids is then used to automatically construct the Voronoi polygons, which correspond to individual fibers. Each Voronoi polygon represents the initial shape of one active contour model, called a snake. In the energy minimization process, which is executed in several stages, different external forces and problem-specific knowledge are used to guide the snakes to converge to fiber boundaries. Our results indicate that this approach for segmenting muscle fiber images is fast, accurate, and reproducible compared with manual segmentation performed by experts.

Exercise training in chronic hypoxia has no effect on ventilatory muscle function in humans

At the highest altitude, aerobic work is limited by environmental oxygen availability. We therefore reasoned that the hyperpnea associated with endurance training at altitude should provide a strong stimulus for adaptation of the ventilatory muscles. We measured peak inspiratory muscle pressure-flow characteristics (inspiring through graded resistors) and maximum sustainable ventilation capacity in ten permanent residents of La Paz, Bolivia (3600 m) prior to and immediately following 6 weeks of incremental endurance training. Additionally, eight local residents did no training and functioned as controls for the capacity test. While V O 2 max measured in hypoxia increased by 19% (Favier et al., 1995b. J. Appl Physiol. 78, 2286–2293.), none of the tested ventilatory variables showed significant changes. The values for the group mean slopes of maximum inspiratory pressure-flow pairs (−10.5 vs. −9.8 cm H 2O·sec·L −1, P=0.301; before versus after training, respectively), maximum inspiratory pressure (112.1±8.9 vs. 106.9±8.6 cmH 2O, P=0.163), peak inspiratory flow (9.8±0.41 vs. 10.2±0.55 L·sec −1, P=0.172) and the maximum volitional volume in 12 sec (43.9±2.4 vs. 45.6±2.4 L in 12 sec, P=0.133) were unchanged with exercise training. Likewise, maximal sustainable minute volume was not different between post-training and control subjects (177.4±7.9 vs. 165.4±8.4 L·min −1, P=0.141). These data support the concept that endurance training fails to elicit functional adaptations in ventilatory muscles in humans, even when exercise is done in hypoxia.

Techniques to evaluate elderly human muscle function: a physiological basis.

Elderly persons appear to exhibit muscle weakness and a slowing in their speed of muscle movement. Objective quantification of these characteristics requires reliable and practical tests to assess the muscle contractile characteristics of elderly people. This review discusses the advantages and limitations of voluntary and electrically stimulated muscle testing techniques used to assess the strength, speed, and fatigability of elderly muscle with a brief explanation of the physiological basis. This review presents the practice and theory underlying the scientific measurement of elderly human muscle function, bridging the gap between the practical issues of measurement and the physiological significance of such measurements.

A stiffness-varying model of human gait

We report on a conceptual two degrees of freedom (2 DOF) human gait model, which incorporates nonlinear joint stiffness as a stabilizing agent. Specifically, muscle spring-like property provides inherent stability during gait movement using a nonlinear angular spring and dash pot at each joint. The instability problem of the gait model in direct dynamic analysis is overcome by simulating the human co-contraction muscle function. By developing dynamic system stability requirements and hypothesizing a minimum joint stiffness criterion, we determine time-varying joint stiffness. Optimum joint stiffnesses are present for varying gait pattern, stride lengths and cadences. We conclude that nonlinear joint stiffness can be incorporated into gait models to overcome stability problems inherent in such linkage models.

Muscle architecture and function in humans

The present study focused on architectural factors which are considered to influence the linkage of muscle fiber and joint actions. By means of real-time ultrasonography we can observe clearly and noninvasively in vivo the movement of fascicle and aponeurosis in human muscle and measure directly the changes in pennation angle and length of fascicle during muscle contraction. During dorsi and plantar flexion without load the movement of tendinous tissue in human tibialis anterior muscle (TA) appeared to synchronize with the displacement of the ankle joint, indicating that the muscle-tendon complexes are stiff relative to the applied force, which is fairly small in the case of foot shaking motion. On the other hand, when the ankle joint was fixed and the TA contracted ‘statically” the ultrasonic echo from deep aponeurosis in the TA was observed to move proximally, indicating the elastic component (i.e. mainly tendinous tissue) was stretched significantly by the contraction force of muscle. In the case of the knee joint, a length of fascicle in vastus lateralis decreased by 18% with the extension of the knee passively from a 100% flexed position. When the knee extensors contracted ‘statically’ the fascicle length decreased at every joint angles and its magnitude was greater (30%) when the knee was closer to full extension than (5%) at the flexed positions. The present results clearly show that the architecture of actively contracting muscle libers differ considerably than that which occurs when movement is passively induced. The use of cadaver data in the study of architecture and modeling of muscle functions would result in inaccurate, and in some cases even erroneous results.

Contractile properties of rat, rhesus monkey, and human type I muscle fibers.

It is well known that skeletal muscle intrinsic maximal shortening velocity is inversely related to species body mass. However, there is uncertainty regarding the relationship between the contractile properties of muscle fibers obtained from commonly studied laboratory animals and those obtained from humans. In this study we determined the contractile properties of single chemically skinned fibers prepared from rat, rhesus monkey, and human soleus and gastrocnemius muscle samples under identical experimental conditions. All fibers used for analysis expressed type I myosin heavy chain as determined by sodium dodecyl sulfate-polyacrylamide gel electrophoresis. Allometric coefficients for type I fibers from each muscle indicated that there was little change in peak tension (force/fiber cross-sectional area) across species. In contrast, both soleus and gastrocnemius type I fiber maximal unloaded shortening velocity (Vo), the y-intercept of the force-velocity relationship (Vmax), peak power per unit fiber length, and peak power normalized for fiber length and cross-sectional area were all inversely related to species body mass. The present allometric coefficients for soleus fiber Vo (-0.18) and Vmax (-0.11) are in good agreement with published values for soleus fibers obtained from common laboratory and domesticated mammals. Taken together, these observations suggest that the Vo of slow fibers from quadrupeds and humans scale similarly and can be described by the same quantitative relationships. These findings have implications in the design and interpretation of experiments, especially those that use small laboratory mammals as a model of human muscle function.

Tendinous movement of a human muscle during voluntary contractions determined by real-time ultrasonography.

The degree of shortening or lengthening of muscles during joint actions has not been clarified in humans, although such information is essential in understanding human muscle functions. In this study, the tendinous movement of a muscle was determined by real-time ultrasonography during voluntary contractions. The tibialis anterior muscle (TA) was tested in five healthy men who performed dorsi- and plantar flexion movements (shortening and lengthening of TA) at two frequencies (0.1 and 1.5 Hz). The insertion point (eta) of fascicles onto the aponeurosis was clearly visualized on the ultrasonogram, and its position relative to a fixed marker moved proximally and distally according to dorsi- and plantar flexion of ankle joint. The movement of eta occurred in phase with the angular change of ankle joint, giving high correlations (r = 0.93 to 0.97) between the displacement of eta and the angle. The displacement of eta for one radian of joint angle change, 46.5 +/- 1.7 (SD) mm, was comparable to the reported moment arm of TA. The present method has many potential applications in the field of muscle physiology and biomechanics in humans.

The utility of isokinetic dynamometry in the assessment of human muscle function.

Isokinetic dynamometry has become a favoured method for the assessment of dynamic muscle function in both clinical research and sports environments. Several indices, such as peak torque, are used in the literature to characterise individual, group or larger population performance via these sophisticated data acquisition systems. Research suggests that there are several competing demands on the design of the measurement protocol which may affect the measurement of isokinetic strength and subsequent suitability of data for meaningful evaluation and interpretation. There is a need to increase measurement rigour, reliability and sensitivity to a level which is commensurate with the intended application, via more elaborate multiple-trial protocols. However, this may be confounded by logistical and financial constraints or reduced individual compliance. The net effect of the interaction of such demands may be considered to be the utility of the isokinetic dynamometry protocol. Of the factors which impinge on utility, those which relate to reliability afford the most control by the test administrator. Research data suggest that in many measurement applications, the reliability and sensitivity associated with all frequently-used indices of isokinetic leg strength which are estimated via single-trial protocols, are not sufficient to differentiate either performance change within the same individual or between individuals within a homogeneous group. While such limitation may be addressed by the use of protocols based on 3 to 4 inter-day trials for the index of peak torque, other indices which demonstrate reduced reliability, for example the composite index of the ratio of knee flexion to extension peak torque, may require many more replicates to achieve the same level of sensitivity. Here, the measurement utility of the index may not be sufficient to justify its proper deployment.

Inspiratory Muscle Training During Treatment With Corticosteroids in Humans

In a previous study performed by us, functional alterations in the inspiratory muscles were evaluated in patients receiving corticosteroids for diseases other than respiratory. We have shown that patients who received high-dose steroids for several weeks developed inspiratory muscle weakness that was reversible following withdrawal of the drug treatment. The present study was designed to evaluate the ability of specific inspiratory muscle training (SIMT) to prevent the effects of a therapeutic dosage of corticosteroids on inspiratory muscle function in patients receiving the drug for diseases other than pulmonary, with no underlying respiratory or muscular disease. Twelve patients, 5 men and 7 women, with ages ranging from 19 to 41 years, who received corticosteroids for diseases other than respiratory were recruited into two groups: 6 patients were assigned to the control group and got sham training and 6 patients received SIMT while receiving corticosteroids in a single-blind group-comparative trial. In both groups, there was no difference between the post-treatment and pretreatment values as regard to the FEV1/FVC relationship. However, in the control group but not in the training group, there was a small but significant decrease, from 99.2 +/- 3.0 to 94.3 +/- 2.8 (mean +/- SEM, p < 0.01) in FEV1 (percent of predicted normal values) and from 103.5 +/- 4.0 to 88.7 +/- 3.1 (p < 0.001) in the FVC, following treatment. All subjects had normal inspiratory muscle strength, as expressed by the maximal inspiratory mouth pressure (PImax) at residual volume, and inspiratory muscle endurance as expressed by the relationship between peak pressure and the PImax before treatment. Following administration of corticosteroids, there was a gradual decrease in both inspiratory muscle strength (from 117.5 +/- 9.4 to 80.5 +/- 3.3 cm H2O, p < 0.005) and endurance (from 82.7 +/- 2.6 to 40.2 +/- 1.7%, p < 0.001) in the control group. On the contrary, despite corticosteroid therapy, there were no significant changes in the inspiratory muscle function in the patients whose inspiratory muscles were specifically trained. We conclude that corticosteroids have a significant deteriorating effect on respiratory muscle function in humans. This weakness is preventable by using SIMT during corticosteroid treatment.

The Effect of Corticosteroids on Inspiratory Muscle Performance in Humans

Functional alterations in the inspiratory muscles were evaluated in patients receiving corticosteroids for diseases other than respiratory. Inspiratory muscle strength, as expressed by the maximal inspiratory mouth pressure (PImax), and inspiratory muscle endurance (PmPeak/PImax), using a pressure threshold breathing device, were evaluated in eight patients with normal pulmonary and inspiratory muscle functions (two patients with rapidly progressive glomerulonephritis, two with glomerulonephritis with minimal changes, two with idiopathic thrombocytopenic purpura, and two with subacute thyroiditis). There was a gradual decrease in both inspiratory muscle strength and endurance following corticosteroid administration. After 8 weeks of treatment PmPeak/PImax decreased from 84.4 +/- 2.4 to 67.9 +/- 3.1 percent (p < 0.001), while inspiratory muscle strength dropped from 126.9 +/- 9.6 to 86.5 +/- 7.4 cm H2O (p < 0.005). Gradual steroid dosage tapering resulted in marked improvement in both strength and endurance; the inspiratory muscle strength rose significantly to 112.2 +/- 8.1 cm H2O (p < 0.0005) when steroid treatment was stopped, and even more significantly 6 months later (to 123.1 +/- 8.1 cm H2O [p < 0.0001]), and the PmPeak/PImax rose to 60.6 +/- 3.4 percent (p < 0.001) and to 74.7 +/- 3.2 percent (p < 0.0001), respectively. We conclude that corticosteroids have a significant deteriorating effect on respiratory muscle function in humans. This weakness is reversible while tapering steroid dosage. Steroid therapy should be reconsidered in patients with underlying lung disease.

Experimental design of 31P MRS assessment of human forearm muscle function: Restrictions imposed by functional anatomy

The restrictions imposed by the functional anatomy of the finger flexor muscles on the experimental design of 31P MRS assessment of human forearm muscle function employing surface coil localization and voluntary exercise were investigated. It was found that 31P MRS metabolic data of finger flexor muscle should be correlated with mechanical data of combined flexion of only the ring and little fingers, rather than all four fingers as has been commonly the case in previously reported studies.

Salbutamol, a β2-adrenoceptor agonist, increases skeletal muscle strength in young men

1. beta 2-Adrenoceptor agonists have been shown to increase rapidly lean body mass and reverse muscle wasting in several animal models of human illness. However, no published information is available for humans. In the present study, we investigated the effects of a slow-release preparation of salbutamol or a placebo on skeletal muscle functional capacity in 12 healthy men. The strength of different muscle groups was measured on two occasions before and after 14 and 21 days of treatment. 2. No significant changes in muscle strength were observed with placebo during the trial. In contrast, the strength of both quadriceps muscles increased significantly (12 +/- 3%) after 14 days on salbutamol, and remained elevated at 21 days. Whereas the strength of the hamstring muscles of the dominant leg significantly increased after 21 days on salbutamol (22 +/- 6%), the strength of the non-dominant hamstring muscles returned to baseline values. 3. There was no significant change in the grip strength of either hand in these subjects during the trial. The maximal static inspiratory mouth pressure increased significantly (7 +/- 2%) after 14 days on salbutamol, and increased further after 21 days (15 +/- 4%); the expiratory mouth pressure remained constant. No significant changes in body weight, skinfold thickness, lean body mass or limb circumferences were measured in either group. 4. These data demonstrate that short-term administration of salbutamol increases voluntary muscle strength in man. However, the magnitude and duration of this effect vary between muscle groups. This study implies that the beta 2-adrenoceptor agonists may be of therapeutic potential in altering skeletal muscle function in humans.