Significance Airborne transmission of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) or other pathogens is probably increased during indoor exercise, but data on the emission of aerosol particles by an exercising individual are lacking. Here, we report that aerosol particle emission increases on average 132-fold from 580 ± 489 particles/min at rest to 76,200 ± 48,000 particles/min during maximal exercise. Aerosol particle emission increases moderately up to an exercise intensity of ≈2 W/kg and exponentially at higher exercise intensities. These data not only explain SARS-CoV-2 transmissions during indoor group exercise but also can be used to design better targeted mitigation measures for physical activity indoors such as physical education in school, dance events during weddings, or high-intensity gym classes such as spinning.

Pathogens such as severe acute respiratory syndrome coronavirus type 2 (SARS-CoV-2), influenza, and rhinoviruses are transmitted by airborne aerosol respiratory particles that are exhaled by infectious subjects. We have previously reported that the emission of aerosol particles increases on average 132-fold from rest to maximal endurance exercise. The aims of this study are to first measure aerosol particle emission during an isokinetic resistance exercise at 80% of the maximal voluntary contraction until exhaustion, second to compare aerosol particle emission during a typical spinning class session versus a three-set resistance training session. Finally, we then used this data to calculate the risk of infection during endurance and resistance exercise sessions with different mitigation strategies. During a set of isokinetic resistance exercise, aerosol particle emission increased 10-fold from 5,400 ± 1,200 particles/min at rest to 59,000 ± 69,900 particles/min during a set of resistance exercise. We found that aerosol particle emission per minute is on average 4.9-times lower during a resistance training session than during a spinning class. Using this data, we determined that the simulated infection risk increase during an endurance exercise session was sixfold higher than during a resistance exercise session when assuming one infected participant in the class. Collectively, this data helps to select mitigation measures for indoor resistance and endurance exercise classes at times where the risk of aerosol-transmitted infectious disease with severe outcomes is high.

Objective: Proliferating cancer cells shift their metabolism to anaerobic glycolysis even in the presence of oxygen to generate glycolytic intermediates as substrates for anabolic reactions. We hypothesise that a similar metabolic remodelling also occurs during physiological skeletal muscle hypertrophy. Methods: We used mass spectrometry in hypertrophying muscles both in C2C12 muscle cells in vitro and plantaris mice muscle in vivo and assessed metabolomic changes and the incorporation of stable isotope [U-13C6] glucose tracer compared with non-treated controls. We also performed enzyme inhibition for further mechanistic analysis and a systematic review to align any changes in metabolomics during muscle growth with previous findings. Results: Both our metabolomics analysis and the systematic review reveal altered metabolite concentrations in anabolic pathways such as in the pentose phosphate and serine synthesis pathway to build up biomass, as well as in the hexosamine biosynthetic pathway that serves as a basis for the post-translational so-called O-linked glycosylation modification. We further demonstrated that labelled carbon from [U-13C6]glucose is increasingly incorporated into the non-essential amino acids in hypertrophying myotubes. The inhibition of the key enzyme phosphoglycerate dehydrogenase (Phgdh) supresses muscle protein synthesis by 75% highlighting the importance of the serine pathway for maintaining muscle size. Conclusion: Understanding the mechanisms that regulates skeletal muscle mass will help in developing effective treatments against muscle weakness. Our results provide evidence for metabolic rewiring of glycolytic intermediates into anabolic pathways during muscle growth, such as in the serine synthesis and hexosamine biosynthetic pathways.