Bakkman 2007 ActaPhysiol: Difference between revisions
(Created page with "{{Publication |title=Bakkman L, Sahlin K, Holmberg HC, Tonkonogi M (2007) Quantitative and qualitative adaptation of human skeletal muscle mitochondria to hypoxic compared with n...") |
No edit summary |
||
Line 1: | Line 1: | ||
{{Publication | {{Publication | ||
|title=Bakkman L, Sahlin K, Holmberg HC, Tonkonogi M (2007) Quantitative and qualitative adaptation of human skeletal muscle mitochondria to hypoxic compared with normoxic training at the same relative work rate. Acta Physiol (Oxford) 190: 243–251. | |title=Bakkman L, Sahlin K, Holmberg HC, Tonkonogi M (2007) Quantitative and qualitative adaptation of human skeletal muscle mitochondria to hypoxic compared with normoxic training at the same relative work rate. Acta Physiol (Oxford) 190: 243–251. | ||
|authors=Bakkman L, Sahlin K, Holmberg HC, Tonkonogi M | |authors=Bakkman L, Sahlin K, Holmberg HC, Tonkonogi M | ||
|year=2007 | |year=2007 | ||
Line 16: | Line 16: | ||
|injuries=RONS; Oxidative Stress | |injuries=RONS; Oxidative Stress | ||
|organism=Human | |organism=Human | ||
|tissues=Skeletal | |tissues=Skeletal muscle | ||
|kinetics=Oxygen | |kinetics=Oxygen | ||
|topics=Respiration; OXPHOS; ETS Capacity | |topics=Respiration; OXPHOS; ETS Capacity | ||
|additional=latent mitochondrial dysfunction | |additional=latent mitochondrial dysfunction | ||
}} | }} |
Revision as of 03:15, 5 April 2012
Bakkman L, Sahlin K, Holmberg HC, Tonkonogi M (2007) Quantitative and qualitative adaptation of human skeletal muscle mitochondria to hypoxic compared with normoxic training at the same relative work rate. Acta Physiol (Oxford) 190: 243–251. |
Bakkman L, Sahlin K, Holmberg HC, Tonkonogi M (2007) Acta Physiol (Oxford)
Abstract: Aim: To investigate if training during hypoxia (H) improves the adaptation of muscle oxidative function compared with normoxic (N) training performed at the same relative intensity.
Method: Eight untrained volunteers performed one-legged cycle training during 4 weeks in a low-pressure chamber. One leg was trained under N conditions and the other leg under hypobaric hypoxia (526 mmHg) at the same relative intensity as during N (65% of maximal power output, Wmax). Muscle biopsies were taken from vastus lateralis before and after the training period. Muscle samples were analysed for the activities of oxidative enzymes [citrate synthase (CS) and cytochrome c oxidase (COX)] and mitochondrial respiratory function.
Results: Wmax increased with more than 30% over the training period during both N and H. CS activity increased significantly after training during N conditions (+20.8%, P < 0.05) but remained unchanged after H training (+4.5%, ns) with a significant difference between conditions (P < 0.05 H vs. N). COX activity was not significantly changed by training and was not different between exercise conditions [+14.6 (N) vs. -2.3% (H), ns]. Maximal ADP stimulated respiration (state 3) expressed per weight of muscle tended to increase after N (+31.2%, P < 0.08) but not after H training (+3.2%, ns). No changes were found in state four respiration, respiratory control index, P/O ratio, mitochondrial Ca2+ resistance and apparent Km for oxygen.
Conclusion: The training-induced increase in muscle oxidative function observed during N was abolished during H. Altitude training may thus be disadvantageous for adaptation of muscle oxidative function. • Keywords: altitude, apparent Km for oxygen, citrate synthase, cytochrome c oxidase, hypoxic exercise, mitochondrial function, oxidative capacity, respiration, latent mitochondrial dysfunction
Labels:
Stress:RONS; Oxidative Stress"RONS; Oxidative Stress" is not in the list (Cell death, Cryopreservation, Ischemia-reperfusion, Permeability transition, Oxidative stress;RONS, Temperature, Hypoxia, Mitochondrial disease) of allowed values for the "Stress" property. Organism: Human Tissue;cell: Skeletal muscle
Regulation: Respiration; OXPHOS; ETS Capacity"Respiration; OXPHOS; ETS Capacity" is not in the list (Aerobic glycolysis, ADP, ATP, ATP production, AMP, Calcium, Coupling efficiency;uncoupling, Cyt c, Flux control, Inhibitor, ...) of allowed values for the "Respiration and regulation" property.
latent mitochondrial dysfunction