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Before answering this question, we highlight a key difference in terms of anabolism between proliferating cells and hype...
11/01/2023

Before answering this question, we highlight a key difference in terms of anabolism between proliferating cells and hypertrophying muscle fibres. Proliferating cells need to replicate their entire genome during each cell cycle. This means that each proliferating human cell will synthesise 6.4 billion nucleotides plus nucleotides for mRNA and ribosomal biogenesis before dividing into two daughter cells. In contrast, a hypertrophying muscle fibre “only” synthesises nucleotides for mRNA and ribosome biogenesis [16] as it has “outsourced” replication and the generation of new myonuclei to proliferating satellite cells. The fact that ribose, the pentose sugar in RNA, and deoxyribose, the pentose sugar in DNA, are primarily synthesised from glucose [17] is one reason for why proliferating cells take up more glucose. However, the ribosome biogenesis of hypertrophying muscle fibres [16] will also require glucose to synthesise the nucleotides and rRNA from which ribosomes are made. Hosios et al. have directly compared the contribution of radioactive or stable isotope tracers such as 14C/13C-glucose or 14C/13C-glutamine to the cell mass of proliferating C2C12 myoblasts and differentiated C2C12 myotubes [10]. They found that glucose and glutamine contributed 15% and 8% to cell mass in proliferating C2C12 myoblasts in a steady state and 6% and 3% to cell mass in differentiated but not hypertrophy-stimulated C2C12 myotubes after 6 days of incubation, respectively [10]. In summary, proliferating and hypertrophying cells both generate biomass via anabolic reactions but only proliferating cells synthesise DNA for replication.

Some general guidelines for physical activity during lockdown have been suggested, although these indirectly touched upo...
09/01/2023

Some general guidelines for physical activity during lockdown have been suggested, although these indirectly touched upon exercise without empirical data on athletes’ training practices. Other recommendations were largely generic and likely insufficient for different levels of athletes, such as state and world-class levels. During early phases of the pandemic, “return to sport” considerations were focused on higher-level athletes. These studies provided useful insights related to the safety of training and competition during the pandemic but fell short of evidence-based guidelines for athletes across all competitive levels.

The coronavirus disease 2019 (COVID-19) pandemic caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) ...
09/01/2023

The coronavirus disease 2019 (COVID-19) pandemic caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) compromised the ability of many populations to engage in physical activity and benefit from sport participation. Both recreational and elite competition schedules were decimated by postponements and cancellations, including the 2020 Tokyo Olympic Games. Athlete training was compromised for numerous reasons, most crucially the periods of recurring local/national lockdowns (including movement restrictions, social distancing, and facility closures). Closures of specialist athlete training facilities were widespread, hindering athlete access to these and their multidisciplinary teams (e.g., coaches, sports science, medical and allied health professionals). Team or contact sports have been particularly challenged because social distancing prevents physical interaction and much team-based technical and tactical training. In combination, these challenges have compromised the ability of high-performance athletes to conduct their physical, technical, or tactical training.

A larger than normal decline in pulmonary function (i.e., FEV1) in otherwise healthy aging individuals may limit VO2max....
07/01/2023

A larger than normal decline in pulmonary function (i.e., FEV1) in otherwise healthy aging individuals may limit VO2max. In very fit people, this effect may become apparent relatively early due to their greater ventilatory requirements. It is well established that even FEV1 threshold values above the lower limits of normal pulmonary function modulate individual VO2max levels, and thus also morbidity and mortality from various diseases. Importantly, recent research provides growing evidence for the beneficial effects of regular PA on factors related to pulmonary function and consequently on VO2max and associated health benefits. Although well-designed studies are required to confirm this preliminary evidence, the current knowledge indicates that PA might slow down the age-related deterioration of pulmonary function and thus provides a further powerful argument to start and/or maintain regular PA.

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