Nuclear calcium release by InsP3-receptor channels plays a role in meiosis reinitiation in the mouse oocyte

Cerebral palsy (CP) is classified as a static encephalopathy. CP is a nonprogressive disorder affecting posture and movement and is commonly associated with a spectrum of developmental disabilities. Serial testing of physiological function can provide a quantitative assessment of improvement or decline in the condition of the patient. Furthermore, there are increasing numbers of children with disability who are involved in athletic activity, and the need for physiological feedback to the disabled athlete and coach is the same as for able-bodied individuals. It is acknowledged that children and adolescents with CP have a lower maximal oxygen consumption (VO2max) compared with their able-bodied peers. Children with CP also have distinctly subnormal values for peak anaerobic power and muscular endurance of the upper and lower limbs. Irrespective of the scaling method used (absolute or relative), when compared with normal data from healthy controls, children with CP scored between 2 and 4 standard deviations below the expected mean value for power. Gait abnormalities in children with CP have been shown to increase submaximal walking energy expenditure almost 3-fold compared with healthy children. Assessment of the metabolic cost alone is important but does not provide any information on the mechanisms giving rise to the high energy cost of locomotion in children with CP. Hence, a multidisciplinary (kinetic, kinematic and electromyographic) approach is an important noninvasive tool for studying some of the underlying mechanisms responsible for abnormal gait and elevated energy costs. A certain level of muscle co-contraction is necessary for achieving joint stability during locomotion, particularly at the ankle and knee. There appears, however, to be a co-contraction threshold beyond which there are associated elevated metabolic costs during locomotion in children with CP.