Changes in the Second Ventilatory Threshold Following Individualised versus Standardised Exercise Prescription among Physically Inactive Adults: A Randomised Trial

The second ventilatory threshold (VT2) is established as an important indicator of exercise intensity tolerance. A higher VT2 allows for greater duration of higher intensity exercise participation and subsequently greater reductions in cardiovascular disease (CVD) risk. This study aimed to compare the efficacy of standardised and individualised exercise prescription on VT2 among physically inactive adults. Forty-nine physically inactive male and female participants (48.6 ± 11.5 years) were recruited and randomised into a 12-week standardised (n = 25) or individualised (n = 24) exercise prescription intervention. The exercise intensity for the standardised and individualised groups was prescribed as a percentage of heart rate reserve (HRR) or relative to the first ventilatory threshold (VT1) and VT2, respectively. Participants were required to complete a maximal graded exercise test at pre-and post-intervention to determine VT1 and VT2. Participants were categorised as responders to the intervention if an absolute VT2 change of at least 1.9% was attained. Thirty-eight participants were included in the analysis. A significant difference in VT2 change was found between individualised (pre vs. post: 70.6% vs. 78.7% maximum oxygen uptake (VO2max)) and standardised (pre vs. post: 72.5% vs. 72.3% VO2max) exercise groups. Individualised exercise prescription was significantly more efficacious (p = 0.04) in eliciting a positive response in VT2 (15/19, 79%) when compared to the standardised exercise group (9/19, 47%). Individualised exercise prescription appears to be more efficacious than standardised exercise prescription in eliciting a positive VT2 change among physically inactive adults. Increasing VT2 allows for greater tolerance to higher exercise intensities and therefore greater cardiovascular health outcomes

Treino de força muscular de membros superiores orientado à tarefa na distrofia miotônica do tipo 1: estudo de caso

O objetivo do presente estudo foi verificar os efeitos do treino de força muscular dos membros superiores a partir da abordagem orientada à tarefa, com relação à força muscular, à funcionalidade e à qualidade de vida de um indivíduo adulto com distrofia miotônica do tipo1. Foi realizado um treino de força muscular submáximo (60% da resistência máxima), na freqüência de três terapias semanais, num período de 16 semanas, constituído de três avaliações, a inicial, a final e a de seguimento de um mês do término do protocolo, com base na Medical Research Council scale (MRC), no Total Muscle Score (TMS), na Medida de Função Motora (MFM) e na versão brasileira do questionário de qualidade de vida SF-36. Com relação à força muscular, houve um incremento de 5% no TMS. Na funcionalidade, a MFM apresentou um acréscimo de 1,04% na avaliação final, o qual se perdurou na avaliação de seguimento. Na SF-36, o participante apresentou um acréscimo de 2,12% na segunda avaliação, retornando à pontuação inicial após um mês do protocolo; porém no domínio de capacidade funcional manteve-se o aumento de 20%. O treino de força muscular submáximo orientado à tarefa mostrou-se benéfico com base na força muscular e no domínio de capacidade funcional do questionário de qualidade de vida; porém denotou restrita variação quantitativa no âmbito da funcionalidade.This study aimed to assess the effects of upper limb strength training using a task-oriented approach with respect to muscle strength, func-tionality and quality of life in an adult with myotonic dystrophy type1. Submaximal muscular strength training (60% maximum resistance) was performed three times a week for a period of 16 weeks, consisting of three evaluations, an initial, a final, and then a follow-up one month after protocol completion based on the Medical Research Council scale (MRC), Total Muscle Score (TMS), Motor Function Measure (MFM), and the Brazilian version of the quality of life questionnaire SF-36. Regard-ing muscle strength, there was an increase of 5% in the TMS. In terms of functionality, the MFM showed an increase of 1.04% in the final evalua-tion and remained the same in the follow-up evaluation. In the SF-36, the participant had an increase of 2.12% in the second evaluation, returning to the initial score one month after protocol. However, concerning func-tional capacity the same 20% increase was observed. The task-oriented submaximal muscle strength training proved to be beneficial based on the information reported about muscle strength and functional capacity in the quality of life questionnaire; nonetheless, a small quantitative vari-ation regarding functionality was seen

ProtoDESI: First On-Sky Technology Demonstration for the Dark Energy Spectroscopic Instrument

The Dark Energy Spectroscopic Instrument (DESI) is under construction to measure the expansion history of the universe using the baryon acoustic oscillations technique. The spectra of 35 million galaxies and quasars over 14,000 square degrees will be measured during a 5-year survey. A new prime focus corrector for the Mayall telescope at Kitt Peak National Observatory will deliver light to 5,000 individually targeted fiber-fed robotic positioners. The fibers in turn feed ten broadband multi-object spectrographs. We describe the ProtoDESI experiment, that was installed and commissioned on the 4-m Mayall telescope from August 14 to September 30, 2016. ProtoDESI was an on-sky technology demonstration with the goal to reduce technical risks associated with aligning optical fibers with targets using robotic fiber positioners and maintaining the stability required to operate DESI. The ProtoDESI prime focus instrument, consisting of three fiber positioners, illuminated fiducials, and a guide camera, was installed behind the existing Mosaic corrector on the Mayall telescope. A Fiber View Camera was mounted in the Cassegrain cage of the telescope and provided feedback metrology for positioning the fibers. ProtoDESI also provided a platform for early integration of hardware with the DESI Instrument Control System that controls the subsystems, provides communication with the Telescope Control System, and collects instrument telemetry data. Lacking a spectrograph, ProtoDESI monitored the output of the fibers using a Fiber Photometry Camera mounted on the prime focus instrument. ProtoDESI was successful in acquiring targets with the robotically positioned fibers and demonstrated that the DESI guiding requirements can be met.Comment: Accepted versio

Direct and indirect control of the initiation of meiotic recombination by DNA damage checkpoint mechanisms in budding yeast

Meiotic recombination plays an essential role in the proper segregation of chromosomes at meiosis I in many sexually reproducing organisms. Meiotic recombination is initiated by the scheduled formation of genome-wide DNA double-strand breaks (DSBs). The timing of DSB formation is strictly controlled because unscheduled DSB formation is detrimental to genome integrity. Here, we investigated the role of DNA damage checkpoint mechanisms in the control of meiotic DSB formation using budding yeast. By using recombination defective mutants in which meiotic DSBs are not repaired, the effect of DNA damage checkpoint mutations on DSB formation was evaluated. The Tel1 (ATM) pathway mainly responds to unresected DSB ends, thus the sae2 mutant background in which DSB ends remain intact was employed. On the other hand, the Mec1 (ATR) pathway is primarily used when DSB ends are resected, thus the rad51 dmc1 double mutant background was employed in which highly resected DSBs accumulate. In order to separate the effect caused by unscheduled cell cycle progression, which is often associated with DNA damage checkpoint defects, we also employed the ndt80 mutation which permanently arrests the meiotic cell cycle at prophase I. In the absence of Tel1, DSB formation was reduced in larger chromosomes (IV, VII, II and XI) whereas no significant reduction was found in smaller chromosomes (III and VI). On the other hand, the absence of Rad17 (a critical component of the ATR pathway) lead to an increase in DSB formation (chromosomes VII and II were tested). We propose that, within prophase I, the Tel1 pathway facilitates DSB formation, especially in bigger chromosomes, while the Mec1 pathway negatively regulates DSB formation. We also identified prophase I exit, which is under the control of the DNA damage checkpoint machinery, to be a critical event associated with down-regulating meiotic DSB formation

Budding yeast ATM/ATR control meiotic double-strand break (DSB) levels by down-regulating Rec114, an essential component of the DSB-machinery

An essential feature of meiosis is Spo11 catalysis of programmed DNA double strand breaks (DSBs). Evidence suggests that the number of DSBs generated per meiosis is genetically determined and that this ability to maintain a pre-determined DSB level, or "DSB homeostasis", might be a property of the meiotic program. Here, we present direct evidence that Rec114, an evolutionarily conserved essential component of the meiotic DSB-machinery, interacts with DSB hotspot DNA, and that Tel1 and Mec1, the budding yeast ATM and ATR, respectively, down-regulate Rec114 upon meiotic DSB formation through phosphorylation. Mimicking constitutive phosphorylation reduces the interaction between Rec114 and DSB hotspot DNA, resulting in a reduction and/or delay in DSB formation. Conversely, a non-phosphorylatable rec114 allele confers a genome-wide increase in both DSB levels and in the interaction between Rec114 and the DSB hotspot DNA. These observations strongly suggest that Tel1 and/or Mec1 phosphorylation of Rec114 following Spo11 catalysis down-regulates DSB formation by limiting the interaction between Rec114 and DSB hotspots. We also present evidence that Ndt80, a meiosis specific transcription factor, contributes to Rec114 degradation, consistent with its requirement for complete cessation of DSB formation. Loss of Rec114 foci from chromatin is associated with homolog synapsis but independent of Ndt80 or Tel1/Mec1 phosphorylation. Taken together, we present evidence for three independent ways of regulating Rec114 activity, which likely contribute to meiotic DSBs-homeostasis in maintaining genetically determined levels of breaks

Overview of the Dark Energy Spectroscopic Instrument

The Dark Energy Spectroscopic Instrument (DESI) is under construction to measure the expansion history of the Universe using the Baryon Acoustic Oscillation technique. The spectra of 35 million galaxies and quasars over 14000 square degrees will be measured during the life of the experiment. A new prime focus corrector for the KPNO Mayall telescope will deliver light to 5000 fiber optic positioners. The fibers in turn feed ten broad-band spectrographs. We present an overview of the instrumentation, the main technical requirements and challenges, and the current status of the project.Comment: 11 pages, 4 figure

Budding Yeast Pch2, a Widely Conserved Meiotic Protein, Is Involved in the Initiation of Meiotic Recombination

Budding yeast Pch2 protein is a widely conserved meiosis-specific protein whose role is implicated in the control of formation and displacement of meiotic crossover events. In contrast to previous studies where the function of Pch2 was implicated in the steps after meiotic double-strand breaks (DSBs) are formed, we present evidence that Pch2 is involved in meiotic DSB formation, the initiation step of meiotic recombination. The reduction of DSB formation caused by the pch2 mutation is most prominent in the sae2 mutant background, whereas the impact remains mild in the rad51 dmc1 double mutant background. The DSB reduction is further pronounced when pch2 is combined with a hypomorphic allele of SPO11. Interestingly, the level of DSB reduction is highly variable between chromosomes, with minimal impact on small chromosomes VI and III. We propose a model in which Pch2 ensures efficient formation of meiotic DSBs which is necessary for igniting the subsequent meiotic checkpoint responses that lead to proper differentiation of meiotic recombinants