No abstract

compared to non-vibration exercise for both BB (p < 0.01) and TB (p < 0.05) muscles; (3) the vibration-induced increase in antagonist coactivation was proportional to vibration f out in the range 18-42 Hz and (4) the vibrationinduced increase in TB agonist activation and antagonist coactivation occurred at all loading conditions in the range 20-80 % MSL. Conclusion The use of high vibration frequencies within the range of 18-42 Hz can maximize TB agonist activation and antagonist activation of both BB and TB muscles during upper limb vibration exercise.

This study aimed to analyze the influence of different vibration frequencies, loading conditions, and exercise types on the mechanical behavior of a novel vibratory bar (VB). Fourteen healthy men were asked to hold the VB during lying row (pulling) and bench press (pushing) static exercise as steadily as possible for 10 seconds with loads of 20, 50, and 80% of the maximum sustained load (MSL) and at preset vibration frequencies (f(in)) of 20, 35, and 50 Hz. Root mean square vibration acceleration (a(RMS)), peak-to-peak displacement (D), and frequency (f(out)) were gained from a 3-dimensional accelerometer fixed to the VB. Increasing vibration frequency (from 20 to 50 Hz) resulted in a progressive and sizeable increase in VB a(RMS) and f(out) (both p ≤ 0.001) with smaller variations of D (≤5.9%, p ≤ 0.001). Adding weight to the VB (progressive overload from 20 to 80% MSL) did not affect D and minimally altered a(RMS) (<4.2%, p = 0.014) and f(out) (<1.7%, p = 0.002). Altering the type of exercise (pulling vs. pushing) did not affect VB a(RMS), D, and f(out). In conclusion, this study establishes the validity of a novel VB and legitimates its use for effective and safe upper-body static exercise with a wide range of vibration frequencies and loading conditions in the context of physical training or rehabilitation.

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Our group identified two pathogenic variants on the PKD1 gene, c.10527_10528delGA and c.7292T&gt;A from unrelated families. They came from two small counties in Granada, with 61 and 26 ADPKD individuals affected. To determine a common ancestor, healthy and ADPKD individuals from these families were genotyped by analyzing four microsatellites located on chromosome 16. Our study identified a common haplotype in all ADPKD individuals. These findings underpin our hypothesis of the founder effect and explains why there is a high frequency of ADPKD in small regions. Determining hot spots of ADPKD will help to better plan health care in the future.