title: MRS Evidence of Adequate O₂ Supply in Human Skeletal Muscle at the Onset of Exercise.
abstract: OBJECTIVE
  At exercise onset, intramuscular oxidative energy production responds relatively slowly in comparison with the change in adenosine triphosphate demand. To determine whether the slow kinetics of oxidative adenosine triphosphate production is due to inadequate O2 supply or metabolic inertia, we studied the kinetics of intramyocellular deoxygenation (deoxy-myoglobin (Mb)) and metabolism (phosphocreatine (PCr)) using proton (1H) and phosphorus (31P) magnetic resonance spectroscopy in six healthy subjects (33 ± 5 yr).
  
  
  METHODS
  Specifically, using dynamic plantarflexion exercise, rest to exercise and recovery were assessed at both 60% of maximum work rate (moderate intensity) and 80% of maximum work rate (heavy intensity).
  
  
  RESULTS
  At exercise onset, [PCr] fell without delay and with a similar time constant (τ) at both exercise intensities (approximately 33 s). In contrast, the increase in deoxy-Mb was delayed at exercise onset by 5-7 s, after which it increased with kinetics (moderate τ = 37 ± 9 s; heavy τ = 29 ± 6 s) that was not different from τPCr (P > 0.05). At cessation, deoxy-Mb recovered without time delay and more rapidly (τ = ∼20 s) than PCr (τ = ∼33 s) (P < 0.05).
  
  
  CONCLUSIONS
  Using a unique combination of in vivo magnetic resonance spectroscopy techniques with high time resolution, this study revealed a delay in intramuscular deoxygenation at the onset of exercise and rapid reoxygenation kinetics upon cessation. Together, these data imply that intramuscular substrate-enzyme interactions, and not O2 availability, determine the exercise onset kinetics of oxidative metabolism in healthy human skeletal muscles.
authors.affiliation: 1Department of Medicine, Division of Geriatrics, University of Utah, Salt Lake City, UT; 2Department of Exercise and Sport Science, University of Utah, Salt Lake City, UT; 3Geriatric Research, Education and Clinical Center, Veterans Affairs Medical Center, Salt Lake City, UT; 4Institute of Myology, Paris, FRANCE; 5CEA, I2BM, MIRcen, IdM NMR Laboratory, Paris, FRANCE; 6Faculty of Medicine, Norwegian University of Science and Technology, Trondheim, NORWAY; and 7Department of Medicine, Division of Respiratory and Critical Care Physiology and Medicine, Los Angeles Biomedical Research Institute at Harbor-UCLA Medical Center, Torrance, CA.
authors.forename: Russell S
authors.initials: RS
authors.lastname: Richardson
authors.forename: Claire
authors.initials: C
authors.lastname: Wary
authors.forename: D Walter
authors.initials: DW
authors.lastname: Wray
authors.forename: Jan
authors.initials: J
authors.lastname: Hoff
authors.forename: Harry B
authors.initials: HB
authors.lastname: Rossiter
authors.forename: Gwenael
authors.initials: G
authors.lastname: Layec
authors.forename: Pierre G
authors.initials: PG
authors.lastname: Carlier
mesh_terms: D000255:Adenosine Triphosphate / Q000378:metabolism; D000328:Adult; D003402:Creatine Kinase / Q000378:metabolism; D015444:Exercise / Q000502:physiology*; D006801:Humans; D006863:Hydrogen-Ion Concentration; D009682:Magnetic Resonance Spectroscopy; D018482:Muscle, Skeletal / Q000378:metabolism*; D009211:Myoglobin / Q000378:metabolism; D010101:Oxygen Consumption; D010725:Phosphocreatine / Q000378:metabolism; D012146:Rest
chemical_list: D009211:Myoglobin; C055547:deoxymyoglobin; D010725:Phosphocreatine; D000255:Adenosine Triphosphate; D003402:Creatine Kinase
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