The aim of this study was to determine the extent of ankle muscle weakness in children with cerebral palsy (CP) and to identify potential causes. Maximal voluntary contractions of plantar (PF) and dorsiflexors (DF) were determined at optimal angles in knee flexion and extension in both legs of 14 children with hemiplegia (7 males, 7 females) and 14 with diplegia (8 males, 6 females). Their results were compared to 14 age- and weight-matched control participants (5 males, 9 females). Muscle cross-sectional areas of soleus, posterior, and anterior compartment muscles were determined from MRIs in 14 children with CP (eight diplegia, six hemiplegia) and 18 control children. Specific tension (torque/unit area) of PF and DF was determined from torque and cross-sectional area results. Muscle volumes of PF and DF were also determined in both legs of five control children and five with hemiplegia. Muscle EMG was recorded from soleus, medial gastrocnemius, and tibialis anterior during each maximal voluntary contraction. Mean amplitude was significantly reduced in PF and DF in both CP groups and significantly higher levels of coactivation of antagonists were found compared to control participants. Strength of PF and DF was significantly reduced in both CP groups, but more importantly the muscles were found to be weak based on significantly reduced specific tensions. The PF were most affected, particularly in the group with hemiplegia. It is believed that an inability to maximally activate their muscles contributed to this weakness. A combination of incomplete activation and high levels of PF coactivation are thought to have contributed to DF weakness.

The purpose of this study was to investigate whether acute passive stretching (APS) reduced maximal isometric voluntary contraction (MVC) of the plantar flexors (PF) and if so, by what mechanisms. The PF in 15 female volunteers were stretched for 10 min (5 x 120 s) by a torque motor to within 2 degrees of maximum dorsiflexion (D) range of motion (ROM). MVC with twitch interpolation, maximal Hoffmann reflex (H(max)) and compound action potentials (M(max)) were recorded at 20 degrees D. Stretch reflexes (SR) were mechanically induced at 200 degrees s(-1) between 0 degrees and 10 degrees ( )D and SR torque and EMG amplitude were determined. All tests were assessed pre- (pre) and post-APS (post-test(1)). MVC, SR, and M(max) were again assessed after additional stretch was applied [mean 26 (1) degrees D; post-test(2)] to test if the optimal angle had been altered. EMG was recorded from soleus (SOL), medial gastrocnemius (MG) and tibialis anterior (TA) using bipolar surface electrodes. APS resulted in a 27% decrease in mean peak passive torque (P<0.05). MVC and SR torque were 7% (P<0.05) and 13% lower at post-test(1) (P<0.05), respectively. SR EMG amplitude of SOL and MG was reduced by 27% (P<0.05) and 22% (P<0.05), respectively. The H(max)/M(max) EMG and H(max)/M(max) torque ratios were unchanged at post-test(1). At post-test(2), MVC and SR EMG recovered to pre-APS values, while the SR and M(max) torque increased by 19% and 13%, respectively (P<0.05). The decrease in MVC during post-test(1) was attributed to changes in the mechanical properties of PF and not to reduced muscle activation.

Muscle ultrastructure of a group of subjects possessing extreme hypertrophy was compared with that of a control group which had undergone 6 months of heavy resistance training. Two needle biopsies were taken from triceps brachii of two international calibre powerlifters and five elite bodybuilders. In addition, samples were taken from five healthy volunteers before and after 6 months of training of the elbow extensors. One biopsy was prepared for electron microscopy and analyzed stereologically, and the other was stained for myosin ATPase activity and photographed under the light microscope. Despite large differences in elbow extension strength and arm girth there was no significant difference in fibre areas or percentages of fibre types between the elite group and the trained controls. This suggests that the elite group possessed a greater total number of muscle fibres than the controls did. Mitochondrial volume density of the elite group was similar to that of the control group following training but significantly less (p less than 0.05) than the pretraining control measurements. Myofibrillar volume density was significantly lower and cytoplasmic volume density significantly higher in the elite group than in the trained controls. There was a considerably higher incidence of structural abnormalities including central nuclei and atrophied fibres in the elite group than in the control group, which might possibly have been associated with the use of anabolic steroids by the elite group.

Seven healthy male subjects were studied under control conditions and following 5-6 months of heavy resistance training and 5-6 weeks of immobilization in elbow casts. Cross-sectional fibre areas and nuclei-to-fibre ratios were calculated from cryostat sections of needle biopsies taken from triceps brachii. Training resulted in a 98% increase in maximal elbow extension strength as measured by a Cybex dynamometer, while immobilization resulted in a 41% decrease in strength. Both fast twitch (FT) and slow twitch (ST) fibre areas increased significantly with training by 39% and 31%, respectively. Immobilization resulted in significant decreases in fibre area by 33% for FT and 25% for ST fibres. The observed nuclei-to-fibre ratio was 10% greater following the training programme. However, this change was non-significant. There was also a non-significant correlation between the magnitude of the changes in fibre size and the changes in maximal strength following either training or immobilization.

The aim of this study was to determine the extent of ankle muscle weakness in children with cerebral palsy (CP) and to identify potential causes. Maximal voluntary contractions of plantar (PF) and dorsiflexors (DF) were determined at optimal angles in knee flexion and extension in both legs of 14 children with hemiplegia (7 males, 7 females) and 14 with diplegia (8 males, 6 females). Their results were compared to 14 age‐ and weight‐matched control participants (5 males, 9 females). Muscle cross‐sectional areas of soleus, posterior, and anterior compartment muscles were determined from MRIs in 14 children with CP (eight diplegia, six hemiplegia) and 18 control children. Specific tension (torque/unit area) of PF and DF was determined from torque and cross‐sectional area results. Muscle volumes of PF and DF were also determined in both legs of five control children and five with hemiplegia. Muscle EMG was recorded from soleus, medial gastrocnemius, and tibialis anterior during each maximal voluntary contraction. Mean amplitude was significantly reduced in PF and DF in both CP groups and significantly higher levels of coactivation of antagonists were found compared to control participants. Strength of PF and DF was significantly reduced in both CP groups, but more importantly the muscles were found to be weak based on significantly reduced specific tensions. The PF were most affected, particularly in the group with hemiplegia. It is believed that an inability to maximally activate their muscles contributed to this weakness. A combination of incomplete activation and high levels of PF coactivation are thought to have contributed to DF weakness.