The effects of training in hyperoxia vs. normoxia on skeletal muscle enzyme activities and exercise performance.
Inspiring a hyperoxic (H) gas permits subjects to exercise at higher power outputs while training, but there is controversy as to whether this improves skeletal muscle oxidative capacity, maximal O(2) consumption (Vo(2 max)), and endurance performance to a greater extent than training in normoxia (N). To determine whether the higher power output during H training leads to a greater increase in these parameters, nine recreationally active subjects were randomly assigned in a single-blind fashion to train in H (60% O(2)) or N for 6 wk (3 sessions/wk of 10 x 4 min at 90% Vo(2 max)). Training heart rate (HR) was maintained during the study by increasing power output. After at least 6 wk of detraining, a second 6-wk training protocol was completed with the other breathing condition. Vo(2 max) and cycle time to exhaustion at 90% of pretraining Vo(2 max) were tested in room air pre- and posttraining. Muscle biopsies were sampled pre- and posttraining for citrate synthase (CS), beta-hydroxyacyl-coenzyme A dehydrogenase (beta-HAD), and mitochondrial aspartate aminotransferase (m-AsAT) activity measurements. Training power outputs were 8% higher (17 W) in H vs. N. However, both conditions produced similar improvements in Vo(2 max) (11-12%); time to exhaustion (approximately 100%); and CS (H, 30%; N, 32%), beta-HAD (H, 23%; N, 21%), and m-AsAT (H, 21%; N, 26%) activities. We conclude that the additional training stimulus provided by training in H was not sufficient to produce greater increases in the aerobic capacity of skeletal muscle and whole body Vo(2 max) and exercise performance compared with training in N.
Perry
Christopher G R
CG
Dept. of Human Health and Nutritional Sciences, University of Guelph, Guelph, Ontario, Canada N1G 2W1. perryc@uoguelph.ca
Talanian
Jason L
JL
Heigenhauser
George J F
GJ
Spriet
Lawrence L
LL
D015094:3-Hydroxyacyl CoA Dehydrogenases / Q000378:metabolism; D000328:Adult; D024442:Aspartate Aminotransferase, Mitochondrial / Q000378:metabolism; D001786:Blood Glucose; D002950:Citrate (si)-Synthase / Q000378:metabolism; D018592:Cross-Over Studies; D015444:Exercise / Q000502:physiology*; D005080:Exercise Test; D005230:Fatty Acids, Nonesterified / Q000097:blood; D005260:Female; D005990:Glycerol / Q000097:blood; D006801:Humans; D018496:Hyperoxia / Q000503:physiopathology*; D019344:Lactic Acid / Q000097:blood; D008297:Male; D008931:Mitochondria, Muscle / Q000201:enzymology*; D018482:Muscle, Skeletal / Q000201:enzymology*; D010101:Oxygen Consumption / Q000502:physiology*
D001786:Blood Glucose; D005230:Fatty Acids, Nonesterified; D019344:Lactic Acid; D015094:3-Hydroxyacyl CoA Dehydrogenases; D002950:Citrate (si)-Synthase; D024442:Aspartate Aminotransferase, Mitochondrial; D005990:Glycerol