We sought to determine whether acute resistance exercise (RE)-induced gene expression is modified by RE training. We studied the expression patterns of a select group of genes following an acute bout of RE in naïve and hypertrophying muscle. Thirteen untrained subjects underwent supervised RE training for 12 wk of the nondominant arm and performed an acute bout of RE 1 wk after the last bout of the training program (training+acute). The dominant arm was either unexercised (control) or subjected to the same acute exercise bout as the trained arm (acute RE). Following training, men (14.8 ± 2.8%; P < 0.05) and women (12.6 ± 2.4%; P < 0.05) underwent muscle hypertrophy with increases in dynamic strength in the trained arm (48.2 ± 5.4% and 72.1 ± 9.1%, respectively; P < 0.01). RE training resulted in attenuated anabolic signaling as reflected by a reduction in rpS6 phosphorylation following acute RE. Changes in mRNA levels of genes involved in hypertrophic growth, protein degradation, angiogenesis, and metabolism commonly expressed in both men and women was determined 4 h following acute RE. We show that RE training can modify acute RE-induced gene expression in a divergent and gene-specific manner even in genes belonging to the same ontology. Changes in gene expression following acute RE are multidimensional, and may not necessarily reflect the actual adaptive response taking place during the training process. Thus RE training can selectively modify the acute response to RE, thereby challenging the use of gene expression as a marker of exercise-induced adaptations.

Effects of neonatal nicotine exposure on the development of nicotinic acetyicholine receptor (nAChR) a2, a3, cr4, cs7, and /32 subunit mRNAs and the number of nAChR isoforms in rat brain were studied. The mRNA levels for nAChR subunits were measured by ribonuclease protection assay, and the number of nAChR isoforms was measured with (-)-[ 3H]nicotine, [3H]epibatidine, and ct-[3H}bungarotoxin ([3H]a-Bgt). Pups were divided into two groups: One group received (-)nicotine treatment (0.1 mg/kg s.c. free base twice per day) during postnatal day (P)1 to P21 and the other during P8 to P16. The period from P8 to P16 was chosen due to persistent changes that occur in brain nAChRs and in the behavior of adult mice that received (-)-nicotine treatment during PlO to P16. (-)-Nicotine exposure from P1 to P21 significantly up-regulated the number of [3H]epibatidine and high-affinity (-) -[3H]nicotine binding sites in most of the brain regions studied but did not influence the number of [3H}a-Bgtbinding sites. This effect was a transient one: The up-regulated binding sites returned to control level 1 week after withdrawal from nicotine. (-) -Nicotine exposure during P8 to P16 resulted in a significant and long-lasting increase in the number of nAChR isoforms labeled by (-)-[3H]nicotine, but not by [3H]epibatidine, in the cortex, hippocampus, and striatum of adult rat. This treatment converted the low-affinity binding sites of (-)-nicotine into a high-affinity state revealed by the competition studies of (-)-[3H]nicotine/ (-)-nicotine. No changes in the mRNA levels of the subunits studied were observed following nicotine treatment during these two periods. These results suggest that the second postnatal week is a critical period during which nicotine treatment can induce permanent effects on the nAChRs in rat brain. The underlying mechanisms involved in the up-regulation of the number of nAChRs observed in this study are posttranscriptional. Key Words: Nicotinic acetylcholine receptor-Subunit mRNA-Receptor binding sites-Development-Nicotine treatment.