Acute Effects of Static and Proprioceptive Neuromuscular Facilitation Stretching of the Plantar Flexors on Ankle Range of Motion and Muscle-Tendon Behavior in Children with Spastic Cerebral Palsy-A Randomized Clinical Trial.

Stretching is considered a clinically effective way to prevent muscle contracture development in children with spastic cerebral palsy (CP). Therefore, in this study, we assessed the effects of a single session of proprioceptive neuromuscular facilitation (PNF) or static stretching (SS) on ankle joint range of motion (RoM) and gastrocnemius muscle-tendon behavior in children with CP. During the SS (n = 8), the ankle joint was held in maximum dorsiflexion (30 s). During the PNF stretching (n = 10), an isometric contraction (3-5 s) was performed, followed by stretching (~25 s). Ten stretches were applied in total. We collected data via dynamometry, 3D motion capture, 2D ultrasound, and electromyography, before and after the stretching sessions. A mixed ANOVA was used for the statistical analysis. Both ankle RoM and maximum dorsiflexion increased over time (F(1,16) = 7.261, p < 0.05, η² = 0.312; and F(1,16) = 4.900, p < 0.05, η² = 0.234, respectively), without any difference between groups. An interaction effect (F(1,12) = 4.768, p = 0.05, η² = 0.284) was observed for muscle-tendon unit elongation (PNF: -8.8%; SS: +14.6%). These findings suggest a positive acute effect of stretching on ankle function. However, SS acutely increased muscle-tendon unit elongation, while this decreased after PNF stretching, indicating different effects on the spastic muscles. Whether PNF stretching has the potential to cause positive alterations in individuals with CP should be elucidated in future studies.

Notoginsenoside R1 attenuates oxidative stress-induced osteoblast dysfunction through JNK signalling pathway.

Oxidative stress (OS)-induced mitochondrial damage and the subsequent osteoblast dysfunction contributes to the initiation and progression of osteoporosis. Notoginsenoside R1 (NGR1), isolated from Panax notoginseng, has potent antioxidant effects and has been widely used in traditional Chinese medicine. This study aimed to investigate the protective property and mechanism of NGR1 on oxidative-damaged osteoblast. Osteoblastic MC3T3-E1 cells were pretreated with NGR1 24 h before hydrogen peroxide administration simulating OS attack. Cell viability, apoptosis rate, osteogenic activity and markers of mitochondrial function were examined. The role of C-Jun N-terminal kinase (JNK) signalling pathway on oxidative injured osteoblast and mitochondrial function was also detected. Our data indicate that NGR1 (25 µM) could reduce apoptosis as well as restore osteoblast viability and osteogenic differentiation. NGR1 also reduced OS-induced mitochondrial ROS and restored mitochondrial membrane potential, adenosine triphosphate production and mitochondrial DNA copy number. NGR1 could block JNK pathway and antagonize the destructive effects of OS. JNK inhibitor (SP600125) mimicked the protective effects of NGR1while JNK agonist (Anisomycin) abolished it. These data indicated that NGR1 could significantly attenuate OS-induced mitochondrial damage and restore osteogenic differentiation of osteoblast via suppressing JNK signalling pathway activation, thus becoming a promising agent in treating osteoporosis.

Effects of alfacalcidol on circulating cytokines and growth factors in rat skeletal muscle.

Supra-physiological levels of vitamin D induce skeletal muscle atrophy, which may be particularly detrimental in already sarcopaenic elderly. Neither the cause nor whether the atrophy is fibre type specific are known. To obtain supraphysiological levels of circulating vitamin D (1,25(OH)(2)D(3)) 27.5-month-old female Fischer(344) × Brown Norway F1 rats were orally treated for 6 weeks with vehicle or the vitamin D analogue alfacalcidol. Alfacalcidol treatment induced a 22% decrease in body mass and 17% muscle atrophy. Fibre atrophy was restricted to type IIb fibres in the low-oxidative part of the gastrocnemius medialis only (-22%; P < 0.05). There was a concomitant 1.6-fold increase in mRNA expression of the ubiquitin ligase MuRF-1 (P < 0.001), whereas those of insulin-like growth factor 1 and myostatin were not affected. Circulating IL-6 was unaltered, but leptin and adiponectin were decreased (-39%) and increased (64%), respectively. The treated rats also exhibited a reduced food intake. In conclusion, supraphysiological levels of circulating 1,25(OH)(2)D(3) cause preferential atrophy of type IIb fibres, which is associated with an increased expression of MuRF-1 without evidence of systemic inflammation. The atrophy and loss of body mass in the presence of supra-physiological levels of vitamin D are primarily due to a reduced food intake.