Difference between revisions of "Larsen 2020 Acta Physiol (Oxf)"

Revision as of 20:12, 18 March 2020

Larsen FJ, Schiffer TA, Zinner C, Willis SJ, Morales-Alamo D, Calbet J5, Boushel R, Holmberg HC (2020) Mitochondrial oxygen affinity increases after sprint interval training and is related to the improvement in peak oxygen uptake. Acta Physiol (Oxf) [Epub ahead of print].

» PMID: 32144872 Open Access

Larsen FJ, Schiffer TA, Zinner C, Willis SJ, Morales-Alamo D, Calbet JA, Boushel R, Holmberg HC (2020) Acta Physiol (Oxf)

Abstract: The body responds to exercise training by profound adaptations throughout the cardiorespiratory and muscular systems, which may result in improvements in maximal oxygen consumption (VO₂peak) and mitochondrial capacity. By convenience, mitochondrial respiration is often measured at supra-physiological oxygen levels, an approach that ignores any potential regulatory role of mitochondrial affinity for oxygen (p50_mito) at physiological oxygen levels.

In this study, we examined the p50_mito of mitochondria isolated from the Vastus lateralis and Triceps brachii in 12 healthy volunteers before and after a training intervention with 7 sessions of sprint interval training using both leg cycling and arm cranking. The changes in p50_mito were compared to changes in whole-body VO2 peak.

We here show that p50_mito is similar in isolated mitochondria from the Vastus (40 ± 3.8 Pa) compared to Triceps (39 ± 3.3) but decreases (mitochondrial oxygen affinity increases) after 7 sessions of sprint interval training (to 26 ± 2.2 Pa in Vastus and 22 ± 2.7 Pa in Triceps, both p<0.01). The change in VO₂peak modeled from changes in p50_mito was correlated to actual measured changes in VO₂peak (R2 =0.41, p=0.002).

Together with mitochondrial respiratory capacity, p50_mito is a critical factor when measuring mitochondrial function, it can decrease with sprint interval training and should be considered in the integrative analysis of the oxygen cascade from lung to mitochondria.

This article is protected by copyright. All rights reserved. • Keywords: Mitochondria, Exercise, High intensity training, Maximal oxygen consumption, Oxygen affinity, Sprint training, Training • Bioblast editor: Plangger M • O2k-Network Lab: SE Stockholm Larsen FJ, SE Stockholm Weitzberg E, ES CN Las Palmas Calbet JAL, CA Vancouver Boushel RC

Labels: MiParea: Respiration

HRR: Oxygraph-2k

2020-03

@@ Line 5: / Line 5: @@
 |year=2020
 |journal=Acta Physiol (Oxf)
-|abstract=The body responds to exercise training by profound adaptations throughout the cardiorespiratory and muscular systems, which may result in improvements in maximal oxygen consumption (VO2 peak) and mitochondrial capacity. By convenience, mitochondrial respiration is often measured at supra-physiological oxygen levels, an approach that ignores any potential regulatory role of mitochondrial affinity for oxygen (p50mito ) at physiological oxygen levels.
+|abstract=The body responds to exercise training by profound adaptations throughout the cardiorespiratory and muscular systems, which may result in improvements in maximal oxygen consumption (VO<sub>2</sub>peak) and mitochondrial capacity. By convenience, mitochondrial respiration is often measured at supra-physiological oxygen levels, an approach that ignores any potential regulatory role of mitochondrial affinity for oxygen (p50<sub>mito</sub>) at physiological oxygen levels.
-In this study, we examined the p50mito of mitochondria isolated from the Vastus lateralis and Triceps brachii in 12 healthy volunteers before and after a training intervention with 7 sessions of sprint interval training using both leg cycling and arm cranking. The changes in p50mito were compared to changes in whole-body VO2 peak.
+In this study, we examined the p50<sub>mito</sub> of mitochondria isolated from the ''Vastus lateralis'' and ''Triceps brachii'' in 12 healthy volunteers before and after a training intervention with 7 sessions of sprint interval training using both leg cycling and arm cranking. The changes in p50<sub>mito</sub> were compared to changes in whole-body VO2 peak.
-We here show that p50mito is similar in isolated mitochondria from the Vastus (40 ± 3.8 Pa) compared to Triceps (39 ± 3.3) but decreases (mitochondrial oxygen affinity increases) after 7 sessions of sprint interval training (to 26 ± 2.2 Pa in Vastus and 22 ± 2.7 Pa in Triceps, both p<0.01). The change in VO2 peak modeled from changes in p50mito was correlated to actual measured changes in VO2 peak (R2 =0.41, p=0.002).
+We here show that p50<sub>mito</sub> is similar in isolated mitochondria from the Vastus (40 ± 3.8 Pa) compared to Triceps (39 ± 3.3) but decreases (mitochondrial oxygen affinity increases) after 7 sessions of sprint interval training (to 26 ± 2.2 Pa in Vastus and 22 ± 2.7 Pa in Triceps, both p<0.01). The change in VO<sub>2</sub>peak modeled from changes in p50<sub>mito</sub> was correlated to actual measured changes in VO<sub>2</sub>peak (R2 =0.41, p=0.002).
-Together with mitochondrial respiratory capacity, p50mito is a critical factor when measuring mitochondrial function, it can decrease with sprint interval training and should be considered in the integrative analysis of the oxygen cascade from lung to mitochondria.
+Together with mitochondrial respiratory capacity, p50<sub>mito</sub> is a critical factor when measuring mitochondrial function, it can decrease with sprint interval training and should be considered in the integrative analysis of the oxygen cascade from lung to mitochondria.
 <small>This article is protected by copyright. All rights reserved.</small>