Immediate effect of neuromuscular electrical stimulation on the abductor hallucis muscle: A randomized controlled trial.

Hallux valgus (HV) is a foot deformity with deviation of the greater toe and the first metatarsal. There is little evidence on training the abductor hallucis muscle (AbdH) to treat HV because of the difficulty in implementing the necessary interventions. Although neuromuscular electrical stimulation (NMES) has been used to induce voluntary exercise, there is currently no study on NMES for AbdH. We aimed to verify the immediate effect of NMES on the AbdH muscle function. For the NMES group (n = 15), electrical stimulation was applied for 20 min. In the sham group (n = 15), the stimulating device was set but not turned on. Electromyogram, HV angle (HVA) at rest and during abduction of the big toe, and strength of the AbdH were evaluated. Analysis of covariance was used to investigate differences within groups using the baseline as the covariate. NMES significantly improved the maximal voluntary isometric contractions (%MVIC), HVA at exercise, and muscle strength (%MVIC: p = .00, HVA exercise: p = .00, AbdH strength: p = .00). HVA at rest showed no change (p = .12). Application of NMES on the AbdH muscle immediately improved its activity output, muscle strength, and HVA during exercise.

Comparison of sarcomere alterations after muscle contraction and tension loading in the rat soleus muscle.

Muscle contraction induced by 30 min of continuous nerve stimulation at 50 Hz resulted in sarcomere changes of the soleus muscle in the rat in our previous study. To further investigate the cause of sarcomere alterations, the sciatic nerve was electrically stimulated intermittently for 30 min. Nerve stimulation was also conducted after cutting the tendons of the soleus, gastrocnemius and plantaris muscles in order to prevent imposing tension on these muscles as a result to their own contractions. In addition, the muscles were pulled by weights via their tendons to load high tension for 30 min without nerve stimulation. Sarcomere alterations immediately after treatments were quantified by electron microscopy. The percentages of aberrant sarcomere areas of the soleus muscle were 25.7 +/- 16.4% (mean +/- SD) in the group of intermittent nerve stimulation with intact tendons and 21.1 +/- 35.4% in the group of tenotomy and continuous nerve stimulation, which were roughly equal to or more severe than the group of continuous nerve stimulation with intact tendons (18.8 +/- 15.8%) in our previous study. Sarcomere alterations consisted mainly of hypercontraction in these groups. Almost all sarcomere changes in the tension-loaded (pulled) soleus muscles were scarce myofilaments (1.7 +/- 1.0% by 600 g; 4.5 +/- 2.9% by 1200 g), and hypercontraction was not observed. These findings indicate that neither high tension nor a decrease of muscle blood flow during continuous contraction seems to be the primary cause of sarcomere alterations in the present study. There are probably other causes that produce aberrant sarcomeres.

Ischemic injury and repair process after transection in hypothyroid rat muscles.

Hindlimb ischemia for 4 h, followed by reperfusion, resulted in necrosis of most soleus muscle in euthyroid rats, whereas only slight damage occurred in hypothyroid rats. Muscle repair after transection of the tibialis anterior muscle of hypothyroid rats showed delayed debris removal, initial retardation of myotube formation, and a higher incidence of aberrant sarcomeres in newly formed muscle fibers by electron microscopy. The protective mechanism against ischemia in hypothyroid muscles can probably be attributed to decreased degradation of high-energy phosphates, reduced formation of substrates for xanthine oxidase during ischemia, and attenuated generation of harmful oxygen free radicals during reperfusion. Initial delay of myotube formation seems to reflect retarded proliferation of muscle precursor cells. Prolonged occurrence of aberrant sarcomeres in hypothyroidism is perhaps due to a delay or imbalance in the synthesis of proteins that assemble sarcomeres. These findings demonstrate the significant roles of thyroid hormones in ischemic injury and muscle repair.