The optimal complex training rest interval for athletes from anaerobic sports

Complex training research has indicated that 3-4 minutes may be an optimum intracomplex rest interval. The purpose of this study was to determine if a heavy resistive exercise causes performance enhancement of a slow stretch-shortening cycle exercise and if there is an optimal rest interval. Eighteen subjects performed countermovement jumps (CMJs) before and after a 5 repetition maximum back squat lifting protocol. This procedure was repeated 4 times over 2 days using rest intervals of 30 seconds and 2, 4, and 6 minutes. Flight time and peak ground reaction force (GRF) were the dependent variables. All jumps were performed on a specially constructed sledge and force platform apparatus. Repeated measures analysis of variance found a significant reduction in flight time at the 30-second and 6-minute interval (p < 0.05). No significant difference was found between men and women. Only the men showed an enhancement in jump performance after the 4-minute interval. The improvement window was different for each subject, and an analysis of the greatest increase and decrease in flight time and peak GRF was conducted, showing a significant decrease for men and women and a significant increase in flight time for men and peak ground reaction force for women. The results suggest that complex training can benefit or inhibit CMJ performance depending on the rest interval. The individual determination of the intracomplex rest interval may be necessary in the practical setting.     

Cyanobacterial soil crusts and woody shrub canopies in Kalahari rangelands

Intensive grazing of Kalahari rangelands has led to woody plant encroachment, notably of Acacia mellifera and Grewia flava. The mechanisms causing this process, and the ecological stability of woody plant encroached ecosystems, remain uncertain. Past studies suggest that canopy–soil relations may enhance woody plant competitive dominance. This study aims to investigate one element of this ecological change by examining the spatial distribution of cyanobacterial soil crusts in two vegetation sub‐habitats at sites of different disturbance. Crust burial by litter was also assessed to analyse the dynamics of canopy–crust relations. Our results show there is enhanced cyanobacterial crust cover under A. mellifera canopies and that unlike G. flava canopies, the crust cover remains under A. mellifera even at highly disturbed sites. This canopy–crust association suggests A. mellifera encroachment exhibits intrinsic resilience because of the crusts ability to stabilize the soil surface and increase nutrient retention. Crust burial by litter that accumulates under larger woody plants restricts crust development under canopies. Disturbance restricts crust development in plant interspaces and under G. flava. These two mechanisms combine to restrict crust development to an observed 40% threshold, with nonlinear models required to explain spatial patterns of crust dynamics.     

Resolution of large and small differences in gene expression using models for the Bayesian analysis of gene expression levels and spotted DNA microarrays

Background  

The detection of small yet statistically significant differences in gene expression in spotted DNA microarray studies is an ongoing challenge. Meeting this challenge requires careful examination of the performance of a range of statistical models, as well as empirical examination of the effect of replication on the power to resolve these differences.     

The role of muscarinic acetylcholine receptor-mediated activation of extracellular signal-regulated kinase 1/2 in pilocarpine-induced seizures

Pilocarpine-induced seizures are mediated by the M(1) subtype of muscarinic acetylcholine receptor (mAChR), but little is known about the signaling mechanisms linking the receptor to seizures. The extracellular signal-regulated kinase (ERK) signaling cascade is activated by M(1) mAChR and is elevated during status epilepticus. Yet, the role of ERK activation prior to seizure has not been evaluated. Here, we examine the role of pilocarpine-induced ERK activation in the induction of seizures in mice by pharmacological and behavioral approaches. We show that pilocarpine induces ERK activation prior to the induction of seizures by both western blot and immunocytochemistry with an antibody to phosphorylated ERK. In addition, we show that the ERK pathway inhibitor SL327 effectively blocks the pilocarpine-induced ERK activation. However, SL327 pretreatment has no effect on the initiation of seizures. In fact, animals treated with SL327 had higher seizure-related mortality than vehicle-treated animals, suggesting activated ERK may serve a protective role during seizures. In addition, ERK inhibition had no effect on the development of the long-term sequelae of status epilepticus (SE), including mossy fiber sprouting, neuronal death and spontaneous recurrent seizures.