Genetics and voice production in childhood and adolescence - a review.

Adolescence is a challenging time of change in voicing, normally and in pathology. An increased focus on voice production in relation to genetics can expand our knowledge of the onset of puberty and voice change. Our aim with this review was to connect research of genetics to voice production in adolescence. We need further understanding of the developmental background of voice in childhood and adolescence, because many genetic multi handicaps include voice production. Genetic development related to voice production was the focus in a search made by the Royal English Society of Medicine, with only a few results. We supplemented with references to genetic studies of adults and animals as well as adjacent areas of voice production. The genetic development of voice production is steered from the hypothalamus probably related to growth hormone. The genetic voice production in adults form the basis for understanding development. Some research results were found related to the pubertal steps. The findings are important in the future, using advanced voice analysis and artificial intelligence methods in patients with Multi handicaps.

Losartan has no additive effect on the response to heavy-resistance exercise in human elderly skeletal muscle.

Our purpose here was to investigate the potential of blocking the angiotensin II type I receptor (AT1R) on the hypertrophy response of elderly human skeletal muscle to 4 mo of heavy-resistance exercise training. Fifty-eight healthy elderly men (+65 yr) were randomized into three groups, consuming either AT1R blocker (losartan, 100 mg/day) or placebo for 4 mo. Two groups performed resistance training (RT) and were treated with either losartan or placebo, and one group did not train but was treated with losartan. Quadriceps muscle biopsies, MR scans, and strength tests were performed at baseline and after 8 and 16 wk. Biopsies were sectioned for immunohistochemistry to determine the number of satellite cells, capillaries, fiber type distribution, and fiber area. Gene expression levels of myostatin, connective tissue, and myogenic signaling pathways were determined by real-time RT-PCR. Four months of heavy-resistance training led in both training groups to expected improvements in quadriceps (∼3-4%) and vastus lateralis (∼5-6%), cross-sectional area, and type II fiber area (∼10-18%), as well as dynamic (∼13%) and isometric (∼19%) quadriceps peak force, but with absolutely no effect of losartan on these outcomes. Furthermore, no changes were seen in satellite cell number with training, and most gene targets failed to show any changes induced by training or losartan treatment. We conclude that there does not appear to be any effect of AT1R blocking in elderly men during 4 mo of resistance training. Therefore, we do not find any support for using AT1R blockers for promoting muscle adaptation to training in humans. NEW & NOTEWORTHY Animal studies have suggested that blocking angiotensin II type I receptor (AT1R) enhances muscle regeneration and prevents disuse atrophy, but studies in humans are limited. Focusing on hypertrophy, satellite cells, and gene expression, we found that AT1R blocking did not result in any greater responses with 4 mo of resistance training. These results do not support previous findings and question the value of blocking AT1R in the context of preserving aging human muscle.