title: Nitric oxide bioavailability modulates the dynamics of microvascular oxygen exchange during recovery from contractions.
abstract: OBJECTIVE
  lowered microvascular PO(2) (PO(2) mv) during the exercise off-transient likely impairs muscle metabolic recovery and limits the capacity to perform repetitive tasks. The current investigation explored the impact of altered nitric oxide (NO) bioavailability on PO(2) mv during recovery from contractions in healthy skeletal muscle. We hypothesized that increased NO bioavailability (sodium nitroprusside: SNP) would enhance PO(2) mv and speed its recovery kinetics while decreased NO bioavailability (l-nitro arginine methyl ester: l-NAME) would reduce PO(2) mv and slow its recovery kinetics.
  
  
  METHODS
  PO(2) mv was measured by phosphorescence quenching during transitions (rest-1 Hz twitch-contractions for 3 min-recovery) in the spinotrapezius muscle of Sprague-Dawley rats under SNP (300 microm), Krebs-Henseleit (CONTROL) and l-NAME (1.5 mm) superfusion conditions.
  
  
  RESULTS
  relative to recovery in CONTROL, SNP resulted in greater overall microvascular oxygenation as assessed by the area under the PO(2) mv curve (PO(2 AREA) ;
  
  
  METHODS
  3471 ± 292 mmHg s; SNP: 4307 ± 282 mmHg s; P < 0.05) and faster off-kinetics as evidenced by the mean response time (MRToff;
  
  
  METHODS
  60.2 ± 6.9 s; SNP: 34.8 ± 5.7 s; P < 0.05), whereas l-NAME produced lower PO(2 AREA) (2339 ± 444 mmHg s; P < 0.05) and slower MRToff (86.6 ± 14.5s; P < 0.05).
  
  
  CONCLUSIONS
  no bioavailability plays a key role in determining the matching of O(2) delivery-to-O(2) uptake and thus the upstream O(2) pressure driving capillary-myocyte O(2) flux (i.e. PO(2) mv) following cessation of contractions in healthy skeletal muscle. Additionally, these data support a mechanistic link between reduced NO bioavailability and prolonged muscle metabolic recovery commonly observed in ageing and diseased populations.
authors.affiliation: Department of Anatomy and Physiology, Kansas State University, Manhattan, KS 66506-5802, USA.
authors.forename: D M
authors.initials: DM
authors.lastname: Hirai
authors.forename: S W
authors.initials: SW
authors.lastname: Copp
authors.forename: L F
authors.initials: LF
authors.lastname: Ferreira
authors.forename: T I
authors.initials: TI
authors.lastname: Musch
authors.forename: D C
authors.initials: DC
authors.lastname: Poole
mesh_terms: D000818:Animals; D019540:Area Under Curve; D001682:Biological Availability; D005260:Female; D008163:Luminescent Measurements; D055806:Microvessels / Q000378:metabolism*; D009119:Muscle Contraction / Q000502:physiology*; D018482:Muscle, Skeletal / Q000098:blood supply / Q000502:physiology*; D009569:Nitric Oxide / Q000378:metabolism / Q000493:pharmacokinetics*; D010101:Oxygen Consumption / Q000502:physiology*; D051381:Rats; D017207:Rats, Sprague-Dawley
chemical_list: D009569:Nitric Oxide