Increased fat oxidation and regulation of metabolic genes with ultraendurance exercise.
OBJECTIVE
Regular endurance exercise stimulates muscle metabolic capacity, but effects of very prolonged endurance exercise are largely unknown. This study examined muscle substrate availability and utilization during prolonged endurance exercise, and associated metabolic genes.


METHODS
Data were obtained from 11 competitors of a 4- to 5-day, almost continuous ultraendurance race (seven males, four females; age: 36 +/- 11 years; cycling Vo(2peak): males 57.4 +/- 5.9, females 48.1 +/- 4.0 mL kg(-1) min(-1)). Before and after the race muscle biopsies were obtained from vastus lateralis, respiratory gases were sampled during cycling at 25 and 50% peak aerobic power output, venous samples were obtained, and fat mass was estimated by bioimpedance under standardized conditions.


RESULTS
After the race fat mass was decreased by 1.6 +/- 0.4 kg (11%; P < 0.01). Respiratory exchange ratio at the 25 and 50% workloads decreased (P < 0.01) from 0.83 +/- 0.06 and 0.93 +/- 0.03 before, to 0.71 +/- 0.01 and 0.85 +/- 0.02, respectively, after the race. Plasma fatty acids were 3.5 times higher (from 298 +/- 74 to 1407 +/- 118 micromol L(-1); P < 0.01). Muscle glycogen content fell 50% (from 554 +/- 28 to 270 +/- 25 nmol kg(-1) d.w.; n = 7, P < 0.01), whereas the decline in muscle triacylglycerol (from 32 +/- 5 to 22 +/- 3 mmol kg(-1) d.w.; P = 0.14) was not statistically significant. After the race, muscle mRNA content of lipoprotein lipase and glycogen synthase increased (P < 0.05) 3.9- and 1.7-fold, respectively, while forkhead homolog in rhabdomyosarcoma, pyruvate dehydrogenase kinase 4 and vascular endothelial growth factor mRNA tended (P < 0.10) to be higher, whereas muscle peroxisome proliferator-activated receptor gamma co-activator-1beta mRNA tended to be lower (P = 0.06).


CONCLUSIONS
Very prolonged exercise markedly increases plasma fatty acid availability and fat utilization during exercise. Exercise-induced regulation of genes encoding proteins involved in fatty acid recruitment and oxidation may contribute to these changes.
Helge
J W
JW
Department of Biomedical Sciences, Copenhagen Muscle Research Centre, University of Copenhagen, Copenhagen, Denmark. jhelge@mfi.ku.dk
Rehrer
N J
NJ
Pilegaard
H
H
Manning
P
P
Lucas
S J E
SJ
Gerrard
D F
DF
Cotter
J D
JD
D000222:Adaptation, Physiological; D000328:Adult; D000704:Analysis of Variance; D001706:Biopsy; D001823:Body Composition; D002352:Carrier Proteins / Q000235:genetics; D017097:Electric Impedance; D005227:Fatty Acids / Q000097:blood; D005260:Female; D000071161:Forkhead Box Protein O1; D051858:Forkhead Transcription Factors / Q000235:genetics; D005786:Gene Expression Regulation; D006003:Glycogen / Q000032:analysis; D006006:Glycogen Synthase / Q000235:genetics; D006801:Humans; D050356:Lipid Metabolism; D008071:Lipoprotein Lipase / Q000235:genetics; D008297:Male; D008875:Middle Aged; D018482:Muscle, Skeletal / Q000737:chemistry / Q000378:metabolism; D010084:Oxidation-Reduction; D010807:Physical Endurance / Q000502:physiology*; D011494:Protein Kinases / Q000235:genetics; D011659:Pulmonary Gas Exchange; D012333:RNA, Messenger / Q000032:analysis; D016601:RNA-Binding Proteins; D042461:Vascular Endothelial Growth Factor A / Q000235:genetics
D002352:Carrier Proteins; C085126:FOXO1 protein, human; D005227:Fatty Acids; D000071161:Forkhead Box Protein O1; D051858:Forkhead Transcription Factors; C455622:PPARGC1B protein, human; D012333:RNA, Messenger; D016601:RNA-Binding Proteins; D042461:Vascular Endothelial Growth Factor A; D006003:Glycogen; D006006:Glycogen Synthase; D011494:Protein Kinases; C403287:pyruvate dehydrogenase kinase 4; D008071:Lipoprotein Lipase