Difference between revisions of "Robach 2012 Br J Sports Med"

Revision as of 09:19, 20 July 2012

Robach P, Siebenmann C, Jacobs RA, Rasmussen P, Nordsborg N, Pesta D, Gnaiger E, Díaz V, Christ A, Fiedler J, Crivelli N, Secher NH, Pichon A, Maggiorini M, Lundby C (2012) The role of haemoglobin mass on VO_2max following normobaric 'live high-train low' in endurance-trained athletes. Br J Sports Med Jul 12. [Epub ahead of print].

Robach P, Siebenmann C, Jacobs RA, Rasmussen P, Nordsborg N, Pesta D, Gnaiger E, Díaz V, Christ A, Fiedler J, Crivelli N, Secher NH, Pichon A, Maggiorini M, Lundby C (2012) Br J Sports Med

Abstract: It remains unclear by which mechanism 'live high-train low' (LHTL) altitude training increases exercise performance. Haematological and skeletal muscle adaptations have both been proposed. To test the hypotheses that (i) LHTL improves maximal oxygen uptake (VO_2max ) and (ii) this improvement is related to hypoxia-induced increases in total haemoglobin mass (Hb(mass)) and not to improved maximal oxidative capacity of skeletal muscle, we determined VO_2max before LHTL and after LHTL, before and after the altitude-induced increases in Hb(mass) (measured by carbon-monoxide rebreathing) had been abolished by isovolumic haemodilution. We obtained skeletal muscle biopsies to quantify mitochondrial oxidative capacity and efficiency. Sixteen endurance-trained athletes were assigned (double-blinded, placebo controlled) to ≥16;h/day over 4;weeks to normoxia (placebo, n=6) or normobaric hypoxia equivalent to 3000;m altitude (LHTL, n=10). Four-week LHTL did not increase VO_2max , irrespective of treatment (LHTL: 1.5%; placebo: 2.0%). Hb(mass) was slightly increased (4.6%) in 5 (of 10) LHTL subjects but this was not accompanied by a concurrent increase in VO_2max . In the subjects demonstrating an increase in Hb(mass), isovolumic haemodilution elicited a 5.8% decrease in VO_2max . Cycling efficiency was altered neither with time nor by LHTL. Neither maximal capacity of oxidative phosphorylation nor mitochondrial efficiency was modified by time or LHTL. The present results suggest that LHTL has no positive effect on VO_2max in endurance-trained athletes because (i) muscle maximal oxidative capacity is not improved following LHTL and (ii) erythrocyte volume expansion after LHTL, if any, is too small to alter O₂ transport.

Labels:

Stress:Hypoxia Organism: Human Tissue;cell: Skeletal muscle Preparation: Permeabilized tissue

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.

HRR: Oxygraph-2k

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 {{Publication
-|title=Robach P, Siebenmann C, Jacobs RA, Rasmussen P, Nordsborg N, Pesta D, Gnaiger E, Díaz V, Christ A, Fiedler J, Crivelli N, Secher NH, Pichon A, Maggiorini M, Lundby C (2012) The role of haemoglobin mass on VO2max following normobaric 'live high-train low' in endurance-trained athletes. Br J Sports Med Jul 12. [Epub ahead of print].
+|title=Robach P, Siebenmann C, Jacobs RA, Rasmussen P, Nordsborg N, Pesta D, Gnaiger E, Díaz V, Christ A, Fiedler J, Crivelli N, Secher NH, Pichon A, Maggiorini M, Lundby C (2012) The role of haemoglobin mass on VO<sub>2max</sub>  following normobaric 'live high-train low' in endurance-trained athletes. Br J Sports Med Jul 12. [Epub ahead of print].
 |authors=Robach P, Siebenmann C, Jacobs RA, Rasmussen P, Nordsborg N, Pesta D, Gnaiger E, Díaz V, Christ A, Fiedler J, Crivelli N, Secher NH, Pichon A, Maggiorini M, Lundby C
 |year=2012
 |journal=Br J Sports Med
-|abstract=It remains unclear by which mechanism 'live high-train low' (LHTL) altitude training increases exercise performance. Haematological and skeletal muscle adaptations have both been proposed. To test the hypotheses that (i) LHTL improves maximal oxygen uptake (VO(2)max) and (ii) this improvement is related to hypoxia-induced increases in total haemoglobin mass (Hb(mass)) and not to improved maximal oxidative capacity of skeletal muscle, we determined VO(2)max before LHTL and after LHTL, before and after the altitude-induced increases in Hb(mass) (measured by carbon-monoxide rebreathing) had been abolished by isovolumic haemodilution. We obtained skeletal muscle biopsies to quantify mitochondrial oxidative capacity and efficiency. Sixteen endurance-trained athletes were assigned (double-blinded, placebo controlled) to ≥16&emsp14;h/day over 4&emsp14;weeks to normoxia (placebo, n=6) or normobaric hypoxia equivalent to 3000&emsp14;m altitude (LHTL, n=10). Four-week LHTL did not increase VO(2)max, irrespective of treatment (LHTL: 1.5%; placebo: 2.0%). Hb(mass) was slightly increased (4.6%) in 5 (of 10) LHTL subjects but this was not accompanied by a concurrent increase in VO(2)max. In the subjects demonstrating an increase in Hb(mass), isovolumic haemodilution elicited a 5.8% decrease in VO(2)max. Cycling efficiency was altered neither with time nor by LHTL. Neither maximal capacity of oxidative phosphorylation nor mitochondrial efficiency was modified by time or LHTL. The present results suggest that LHTL has no positive effect on VO(2)max in endurance-trained athletes because (i) muscle maximal oxidative capacity is not improved following LHTL and (ii) erythrocyte volume expansion after LHTL, if any, is too small to alter O(2) transport.
+|abstract=It remains unclear by which mechanism 'live high-train low' (LHTL) altitude training increases exercise performance. Haematological and skeletal muscle adaptations have both been proposed. To test the hypotheses that (i) LHTL improves maximal oxygen uptake (VO<sub>2max</sub> ) and (ii) this improvement is related to hypoxia-induced increases in total haemoglobin mass (Hb(mass)) and not to improved maximal oxidative capacity of skeletal muscle, we determined VO<sub>2max</sub>  before LHTL and after LHTL, before and after the altitude-induced increases in Hb(mass) (measured by carbon-monoxide rebreathing) had been abolished by isovolumic haemodilution. We obtained skeletal muscle biopsies to quantify mitochondrial oxidative capacity and efficiency. Sixteen endurance-trained athletes were assigned (double-blinded, placebo controlled) to ≥16;h/day over 4;weeks to normoxia (placebo, n=6) or normobaric hypoxia equivalent to 3000;m altitude (LHTL, n=10). Four-week LHTL did not increase VO<sub>2max</sub> , irrespective of treatment (LHTL: 1.5%; placebo: 2.0%). Hb(mass) was slightly increased (4.6%) in 5 (of 10) LHTL subjects but this was not accompanied by a concurrent increase in VO<sub>2max</sub> . In the subjects demonstrating an increase in Hb(mass), isovolumic haemodilution elicited a 5.8% decrease in VO<sub>2max</sub> . Cycling efficiency was altered neither with time nor by LHTL. Neither maximal capacity of oxidative phosphorylation nor mitochondrial efficiency was modified by time or LHTL. The present results suggest that LHTL has no positive effect on VO<sub>2max</sub>  in endurance-trained athletes because (i) muscle maximal oxidative capacity is not improved following LHTL and (ii) erythrocyte volume expansion after LHTL, if any, is too small to alter O<sub>2</sub>  transport.
 }}
 {{Labeling