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Problem Statement: Both the aerobic and the anaerobic metabolic systems contribute to the majority of competitive swimming events with a significant energy supply coming from glycolysis, which can lead to blood lactate accumulation. Importantly, stroke technique is a significant determinant of the energy cost of swimming. Head turning for inhalation can potentially affect hydrodynamic resistance, in turn influencing performance, while breathing restriction may contribute to fatigue. Purpose: Sufficient breathing is more important in longer distances with greater aerobic demand, thus, it is expected that restricting oxygen delivery would alter the metabolic contribution of these durations. Therefore, the aim of this investigation was to compare metabolic responses to an incremental swim test with different breathing patterns in young competitive swimmers in the 200-m front crawl. Approach: Competitive male youth swimmers were recruited (n=8, Age=15-2, Height=177.5-9.6, Body weight=65.3-11.8) from a local swim club. A 7 x 200m incremental swim test was conducted with two different breathing rates: 1, breathing every three strokes (BR3) 2, breathing every five strokes (BR5) in a counterbalanced fashion and blood lactate and heart rate (HR) responses were recorded. Data were compared using a 2-way Analysis of Variance (ANOVA) with repeated measures. Results: Although there was a main effect for time (p=0.000), lactate and HR responses did not show significant condition by time interaction for the BR3 and BR5 breathing conditions (p=0.098 and p=0.262, respectively). Rating of perceived exertion (RPE) scores were almost identical on the 10-point Borg-scale between the two conditions at the completion of the swim test without any statistically significant difference (p=0.402). Conclusions: Experienced swimmers may attempt to control their breathing in order to increase swimming velocity by reducing drag without compromising performance due to lactate accumulation and fatigue. The current findings demonstrate that restricted breathing is feasible for longer (e.g. 200m) swimming distances. [ABSTRACT FROM AUTHOR]

A controlled laboratory experiment was used to assess the efficacy of the cognitive processes that underlie risk taking decision making in young and elderly people. Thirty-six participants took part in the study: half the subjects were elderly (mean age of 74) and the other half were young adults (mean age of 19). The elderly participants made equivalent decisions to those of the control young adults. Both age-groups of participants systematically and comparably changed their behavior as a function of risk levels. Furthermore, the elderly participants, relative to young adults, did not exhibit any slowing down in the speed of processing the information involved in making risk taking decisions, reflecting that healthy elderly people are cognitively apt to making risk taking decisions. Both age-groups took comparably less time on the easy trials (trials with either low or high levels of risk) and comparably more time on the difficult trials (trials with medium levels of risk). [ABSTRACT FROM AUTHOR]

The mitochondrial calcium uniporter channel (MCUC) mediates mitochondrial calcium entry, regulating energy metabolism and cell death. Although several MCUC components have been identified, the molecular basis of mitochondrial calcium signaling networks and their remodeling upon changes in uniporter activity have not been assessed. Here, we map the MCUC interactome under resting conditions and upon chronic loss or gain of mitochondrial calcium uptake. We identify 89 high-confidence interactors that link MCUC to several mitochondrial complexes and pathways, half of which are associated with human disease. As a proof-of-concept, we validate the mitochondrial intermembrane space protein EFHD1 as a binding partner of the MCUC subunits MCU, EMRE, and MCUB. We further show a MICU1-dependent inhibitory effect of EFHD1 on calcium uptake. Next, we systematically survey compensatory mechanisms and functional consequences of mitochondrial calcium dyshomeostasis by analyzing the MCU interactome upon EMRE, MCUB, MICU1, or MICU2 knockdown. While silencing EMRE reduces MCU interconnectivity, MCUB loss-of-function leads to a wider interaction network. Our study provides a comprehensive and high-confidence resource to gain insights into players and mechanisms regulating mitochondrial calcium signaling and their relevance in human diseases., (© 2024. The Author(s).)