Effects of 30 days bed rest and exercise countermeasures on <scp>PBMC</scp> bioenergetics

Buescher, F.‐M.; Schmitz, M. T.; Frett, T.; Kramme, J.; de Boni, L.; Elmenhorst, E. M.; Mulder, E.; Moestl, S.; Heusser, K.; Frings‐Meuthen, P.; Jordan, J.; Rittweger, J.; Pesta, D.

doi:10.1111/apha.14102

Cited by 1 publication

(1 citation statement)

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“…Recent advances in exercise protocols aimed specifically at astronauts targeted different muscles and monitored the divergent responses to atrophy of soleus and vastus lateralis 70 . In addition, the relationship between exercise countermeasures during bed rest and mitochondrial respiration was investigated in peripheral blood mononuclear cells 71 . This type of studies will be instrumental to advance readouts to monitor mitochondrial health and progress countermeasures during spaceflight.…”

Section: Discussionmentioning

confidence: 99%

Spaceflight on the ISS changed the skeletal muscle proteome of two astronauts

Murgia,

Rittweger,

Reggiani

et al. 2024

npj Microgravity

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Skeletal muscle undergoes atrophy and loss of force during long space missions, when astronauts are persistently exposed to altered gravity and increased ionizing radiation. We previously carried out mass spectrometry-based proteomics from skeletal muscle biopsies of two astronauts, taken before and after a mission on the International Space Station. The experiments were part of an effort to find similarities between spaceflight and bed rest, a ground-based model of unloading, focused on proteins located at the costameres. We here extend the data analysis of the astronaut dataset and show compartment-resolved changes in the mitochondrial proteome, remodeling of the extracellular matrix and of the antioxidant response. The astronauts differed in their level of onboard physical exercise, which correlated with their respective preservation of muscle mass and force at landing in previous analyses. We show that the mitochondrial proteome downregulation during spaceflight, particularly the inner membrane and matrix, was dramatic for both astronauts. The expression of autophagy regulators and reactive oxygen species scavengers, however, showed partially opposite expression trends in the two subjects, possibly correlating with their level of onboard exercise. As mitochondria are primarily affected in many different tissues during spaceflight, we hypothesize that reactive oxygen species (ROS) rather than mechanical unloading per se could be the primary cause of skeletal muscle mitochondrial damage in space. Onboard physical exercise might have a strong direct effect on the prevention of muscle atrophy through mechanotransduction and a subsidiary effect on mitochondrial quality control, possibly through upregulation of autophagy and anti-oxidant responses.

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Section: Discussionmentioning

confidence: 99%