English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Zendy Plus

Presents the access of premium content as premium feature

Premium Content

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the summarisation as premium feature

Summarisation

Insights

Presents the pdf analysis as premium feature

PDF Analysis

Presents the zaia usage as premium feature

ZAIA

Zendy Tools

Zendy Open

In order to identify peripheral biomarkers of impaired oxidative metabolism during exercise following a 10‐day bed rest, 10 males performed an incremental exercise (to determine peak pulmonary V̇O 2  (V̇O 2  p )) and moderate‐intensity exercises, before (PRE) and after (POST) bed rest. Blood flow response was evaluated in the common femoral artery by Eco‐Doppler during 1 min of passive leg movements (PLM). The intramuscular matching between O 2  delivery and O 2  utilization was evaluated by near‐infrared spectroscopy (NIRS). Mitochondrial respiration was evaluated  ex vivo  by high‐resolution respirometry in isolated muscle fibres, and  in vivo  by NIRS by the evaluation of skeletal muscle V̇O 2  (V̇O 2  m ) recovery kinetics. Resting V̇O 2  m  was estimated by NIRS. Peak V̇O 2  p  was lower in POST  vs . PRE. The area under the blood flow  vs . time curve during PLM was smaller ( P  = 0.03) in POST (274 ± 233 mL)  vs . PRE (427 ± 291). An increased ( P  = 0.03) overshoot of muscle deoxygenation during a metabolic transition was identified in POST. Skeletal muscle citrate synthase activity was not different ( P  = 0.11) in POST (131 ± 16 nmol min –1  mg –1 )  vs . PRE (138 ± 19). Maximal ADP‐stimulated mitochondrial respiration (66 ± 18 pmol s –1  mg –1  (POST)  vs . 72 ± 14 (PRE),  P  = 0.41) was not affected by bed rest. Apparent  K  m  for ADP sensitivity of mitochondrial respiration was reduced in POST  vs . PRE ( P  = 0.04). The V̇O 2  m  recovery time constant was not different ( P  = 0.79) in POST (22 ± 6 s)  vs . PRE (22 ± 6). Resting V̇O 2  m  was reduced by 25% in POST  vs . PRE ( P  = 0.006). Microvascular‐endothelial function was impaired following a 10‐day bed rest, whereas mitochondrial mass and function (both  in vivo  and  ex vivo ) were unaffected or slightly enhanced.    Key points    Ten days of horizontal bed rest impaired  in vivo  oxidative function during exercise.  Microvascular impairments were identified by different methods.  Mitochondrial mass and mitochondrial function (evaluated both  in vivo  and  ex vivo ) were unchanged or even improved (i.e. enhanced mitochondrial sensitivity to submaximal [ADP]).  Resting muscle oxygen uptake was significantly lower following bed rest, suggesting that muscle catabolic processes induced by bed rest/inactivity are less energy‐consuming than anabolic ones.

Peripheral impairments of oxidative metabolism after a 10‐day bed rest are upstream of mitochondrial respiration