EFFECT OF LOWER LIMB PROXIMAL TO DISTAL MUSCLE IMBALANCE CORRECTION ON FUNCTIONAL PES PLANUS DEFORMITY IN YOUNG ADULTS

The pes planus deformity is seen more in adults. Pes planus or low foot medial longitudinal arch, contributes to lower extremity injury due to the muscular imbalance. This deformity causes proximal to distal muscle imbalance in lower limb. Effective correction of muscle imbalance is prime important in correction of pes planus. The purpose of the study was to find the effect of exercise in pes planus to correct the imbalance, improve the condition & prevent the injuries along with the long-term effect of the pes planus deformity. To study and find the effect of lower limb proximal to distal muscle imbalance correction in pes planus deformity in young adults. 40 people with functional pes planus deformity were randomly assigned to a group that received the baseline treatment for the muscle imbalance along with the intrinsic muscle strengthening exercises (experimental group) or a group that received only intrinsic muscle strengthening exercises (control group). Each group received 6 weeks treatment. Statistical analysis were performed using paired t test and unpaired t test. In pre-intervention, there was no statistically significant difference seen with p values for the navicular drop test for the right leg and left leg 0.1127, 0.1504 respectively. Ink test p values for the right leg, left leg 0.4184, 0.8719 respectively. While on comparing the post-interventional values using the unpaired t test, revealed that there was extremely significant difference seen with p value for both legs the navicular drop test was 0.0001 and for the ink test (right leg=0.0008, left leg=0.0318). Our study reported that muscular imbalance corrective exercises along with the intrinsic muscle strengthening was more effective in improving the condition and muscle imbalance caused by the pes planus. So, muscular imbalance corrective exercises and intrinsic muscle strengthening exercises should be recommended to correct the deformity or prevent the abnormalities in people with functional pes planus.

Molecular Mechanisms of Muscle Tone Impairment under Conditions of Real and Simulated Space Flight

Kozlovskaya et al. [1] and Grigoriev et al. [2] showed that enormous loss of muscle stiffness (atonia) develops in humans under true (space flight) and simulated microgravity conditions as early as after the first days of exposure. This phenomenon is attributed to the inactivation of slow motor units and called reflectory atonia. However, a lot of evidence indicating that even isolated muscle or a single fiber possesses substantial stiffness was published at the end of the 20th century. This intrinsic stiffness is determined by the active component, i.e. the ability to form actin-myosin cross-bridges during muscle stretch and contraction, as well as by cytoskeletal and extracellular matrix proteins, capable of resisting muscle stretch. The main facts on intrinsic muscle stiffness under conditions of gravitational unloading are considered in this review. The data obtained in studies of humans under dry immersion and rodent hindlimb suspension is analyzed. The results and hypotheses regarding reduced probability of cross-bridge formation in an atrophying muscle due to increased interfilament spacing are described. The evidence of cytoskeletal protein (titin, nebulin, etc.) degradation during gravitational unloading is also discussed. The possible mechanisms underlying structural changes in skeletal muscle collagen and its role in reducing intrinsic muscle stiffness are presented. The molecular mechanisms of changes in intrinsic stiffness during space flight and simulated microgravity are reviewed.

Impaired Limb Functional Outcome of Peripheral Nerve Regeneration Is Marked by Incomplete Recovery of Paw Muscle Atrophy and Brain Functional Connectivity in a Rat Forearm Nerve Repair Model

Skilled sensorimotor deficit is an unsolved problem of peripheral nerve injury (PNI) led by limb trauma or malignancies, despite the improvements in surgical techniques of peripheral nerve anastomosis. It is now accepted that successful functional recovery of PNI relies tremendously on the multilevel neural plasticity from the muscle to the brain. However, animal models that recapitulate these processes are still lacking. In this report, we developed a rat model of PNI to longitudinally assess peripheral muscle reinnervation and brain functional reorganization using noninvasive imaging technology. Based on such model, we compared the longitudinal changes of the rat forepaw intrinsic muscle volume and the seed-based functional connectivity of the sensorimotor cortex after nerve repair. We found that the improvement of skilled limb function and the recovery of paw intrinsic muscle following nerve regeneration are incomplete, which correlated with the functional connectivity between the primary motor cortex and dorsal striatum. Our results were highly relevant to the clinical observations and provided a framework for future investigations that aim to study the peripheral central sensorimotor circuitry underlying skilled limb function recovery after PNI.