Adaptations of lumbar biomechanics after four weeks of running training with minimalist footwear and technique guidance: Implications for running-related lower back pain.

OBJECTIVES: To investigate the changes in lumbar kinematic and paraspinal muscle activation before, during, and after a 4-week minimalist running training. DESIGN: Prospective cohort study. SETTING: University research laboratory. PARTICIPANTS: Seventeen habitually shod recreational runners who run 10-50 km per week. MAIN OUTCOME MEASURES: During stance phases of running, sagittal lumbar kinematics was recorded using an electrogoniometer, and activities of the lumbar paraspinal muscles were assessed by electromyography. Runners were asked to run at a prescribed speed (3.1 m/s) and a self-selected speed. RESULTS: For the 3.1 m/s running speed, significant differences were found in the calculated mean lumbar posture (p = 0.001) during the stance phase, including a more extended lumbar posture after minimalist running training. A significant reduction in the contralateral lumbar paraspinal muscle activation was also observed (p = 0.039). For the preferred running speed, similar findings of a more extended lumbar posture (p = 0.002) and a reduction in contralateral lumbar paraspinal muscle activation (p = 0.047) were observed. CONCLUSION: A 4-week minimalist running training program produced significant changes in lumbar biomechanics during running. Specifically, runners adopted a more extended lumbar posture and reduced lumbar paraspinal muscle activation. These findings may have clinical implications for treating individuals with running-related lower back pain.

Increased TMEM16A-encoded calcium-activated chloride channel activity is associated with pulmonary hypertension.

Pulmonary artery smooth muscle cells (PASMCs) are more depolarized and display higher Ca(2+) levels in pulmonary hypertension (PH). Whether the functional properties and expression of Ca(2+)-activated Cl- channels (Cl(Ca)), an important excitatory mechanism in PASMCs, are altered in PH is unknown. The potential role of Cl(Ca) channels in PH was investigated using the monocrotaline (MCT)-induced PH model in the rat. Three weeks postinjection with a single dose of MCT (50 mg/kg ip), the animals developed right ventricular hypertrophy (heart weight measurements) and changes in pulmonary arterial flow (pulse-waved Doppler imaging) that were consistent with increased pulmonary arterial pressure and PH. Whole cell patch experiments revealed an increase in niflumic acid (NFA)-sensitive Ca(2+)-activated Cl(-) current [I(Cl(Ca))] density in PASMCs from large conduit and small intralobar pulmonary arteries of MCT-treated rats vs. aged-matched saline-injected controls. Quantitative RT-PCR and Western blot analysis revealed that the alterations in I(Cl(Ca)) were accompanied by parallel changes in the expression of TMEM16A, a gene recently shown to encode for Cl(Ca) channels. The contraction to serotonin of conduit and intralobar pulmonary arteries from MCT-treated rats exhibited greater sensitivity to nifedipine (1 µM), an l-type Ca(2+) channel blocker, and NFA (30 or 100 µM, with or without 10 µM indomethacin to inhibit cyclooxygenases) or T16A(Inh)-A01 (10 µM), TMEM16A/Cl(Ca) channel inhibitors, than that of control animals. In conclusion, augmented Cl(Ca)/TMEM16A channel activity is a major contributor to the changes in electromechanical coupling of PA in this model of PH. TMEM16A-encoded channels may therefore represent a novel therapeutic target in this disease.