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Cluster sets allow for velocity and power output maintenance, but the literature routinely uses highly fatiguing traditional set protocols. Although such studies have merit, others suggest fatigue should be avoided when training to improve power output, making those cluster set studies less practical. Therefore, the purpose of this study was to compare these set structures when truncating sets using a power-based threshold. Nine males (23.4 ± 0.6 yr) with various sport backgrounds performed 6 sets of back squats with individualized loads that elicited the greatest mean power (MPmax) output (112.7 ± 12.1% of body mass). Each set during the traditional set (TS) protocol included as many repetitions as possible until two consecutive repetitions dropped below 90% MPmax, which was followed by 120 s inter-set rest. The design was identical for cluster sets (CS) but with an additional 20 s intra-set rest after every 2 repetitions. The number of repetitions performed, mean velocity, and mean power output, were analyzed using 2(protocol)*6(set) repeated measures ANOVA. The number of repetitions during CS (51.8 ± 14.4) was greater than TS (31.9 ± 3.7) (p = 0.001), but the average velocity (CS = 0.711 ± 0.069, TS = 0.716 ± 0.081 m·s-1; p = 0.732) and power output (CS = 630.3 ± 59.8, TS = 636.0 ± 84.3 W; p = 0.629) of those repetitions were similar. These data indicate that CS are a viable option for increasing training volume during contemporary training where sets are ended when repetitions drop below velocity or power thresholds., Competing Interests: The authors have declared that no competing interests exist.

RNF213/Mysterin has been identified as a susceptibility gene for moyamoya disease, a cerebrovascular disease characterized by occlusive lesions in the circle of Willis. The p.R4810K (rs112735431) variant is a founder polymorphism that is strongly associated with moyamoya disease in East Asia. Many non-p.R4810K rare variants of RNF213 have been identified in white moyamoya disease patients, although the ethnic mutations have not been investigated in this population. In the present study, we screened for RNF213 variants in 19 Slovakian and Czech moyamoya disease patients. A total of 69 RNF213 coding exons were directly sequenced in 18 probands and one relative who suffered from moyamoya disease in Slovakia and the Czech Republic. We previously reported one proband harboring RNF213 p.D4013N. Results from the present study identified four rare variants other than p.D4013N (p.R4019C, p.E4042K, p.V4146A, and p.W4677L) in four of the patients. P.V4146A was determined to be a novel de novo mutation, and p.R4019C and p.E4042K were identified as double mutations inherited on the same allele. P.W4677L, found in two moyamoya disease patients and an unaffected subject in the same pedigree, was a rare single nucleotide polymorphism. Functional analysis showed that RNF213 p.D4013N, p.R4019C and p.V4146A-transfected human umbilical vein endothelial cells displayed significant lowered migration, and RNF213 p.V4146A significantly reduced tube formation, indicating that these are disease-causing mutations. Results from the present study identified RNF213 rare variants in 22.2% (4/18 probands) of Slovakian and Czech moyamoya disease patients, confirming that RNF213 may also be a major causative gene in a relative large population of white patients., Competing Interests: We have read the journal's policy and the authors of this manuscript have the following competing interest: Prof. Koizumi has a patent JP2010068737 'MOYAMOYA DISEASE-RELATED GENE AND UTILIZATION OF SAME' registered regarding with MMD. This does not alter our adherence to PLOS ONE policies on sharing data and materials. Other authors have declared that no competing interests exist.