title: Control of microvascular oxygen pressures in rat muscles comprised of different fibre types.
abstract: In response to an elevated metabolic rate ((.-)V(O(2)), increased microvascular blood-muscle O(2) flux is the product of both augmented O(2) delivery ((.-)Q(O(2)), and fractional O(2) extraction. Whole body and exercising limb measurements demonstrate that (.-)Q(O(2) and fractional O(2) extraction increase as linear and hyperbolic functions, respectively, of (.-)V(O(2). Given the presence of disparate vascular control mechanisms among different muscle fibre types, we tested the hypothesis that, in response to muscle contractions, (.-)Q(O(2) would be lower and fractional O(2) extraction (as assessed via microvascular O(2) pressure, P(mvO(2))) higher in fast- versus slow-twitch muscles. Radiolabelled microsphere and phosphorescence quenching techniques were used to measure (.-)Q(O(2) and P(mvO(2)), respectively at rest and across the transition to 1 Hz twitch contractions at low (Lo, 2.5 V) and high intensities (Hi, 4.5 V) in rat (n = 20) soleus (Sol, slow-twitch, type I), mixed gastrocnemius (MG, fast-twitch, type IIa) and white gastrocnemius (WG, fast-twitch, type IIb) muscle. At rest and for Lo and Hi (steady-state values) transitions, P(mvO(2)) was lower (all P < 0.05) in MG (mmHg: rest, 22.5 +/- 1.0; Lo, 15.3 +/- 1.3; Hi, 10.2 +/- 1.6) and WG (mmHg: rest, 19.0 +/- 1.3; Lo, 12.2 +/- 1.1; Hi, 9.9 +/- 1.1) than in Sol (rest, 33.1 +/- 3.2 mmHg; Lo, 19.0 +/- 2.3 mmHg; Hi, 18.7 +/- 1.8 mmHg), despite lower (.-)V(O(2) and (.-)Q(O(2) in MG and WG under each set of conditions. These data suggest that during submaximal metabolic rates, the relationship between (.-)Q(O(2) and O(2) extraction is dependent on fibre type (at least in the muscles studied herein), such that muscles comprised of fast-twitch fibres display a greater fractional O(2) extraction (i.e. lower P(mvO(2))) than their slow-twitch counterparts. These results also indicate that the greater sustained P(mvO(2)) in Sol may be important for ensuring high blood-myocyte O(2) flux and therefore a greater oxidative contribution to energetic requirements.
authors.affiliation: Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, TX 75309-9034, USA.
authors.forename: Paul
authors.initials: P
authors.lastname: McDonough
authors.forename: Brad J
authors.initials: BJ
authors.lastname: Behnke
authors.forename: Danielle J
authors.initials: DJ
authors.lastname: Padilla
authors.forename: Timothy I
authors.initials: TI
authors.lastname: Musch
authors.forename: David C
authors.initials: DC
authors.lastname: Poole
mesh_terms: D000818:Animals; D001783:Blood Flow Velocity / Q000502:physiology; D005260:Female; D008833:Microcirculation / Q000502:physiology*; D009119:Muscle Contraction / Q000502:physiology*; D018485:Muscle Fibers, Skeletal / Q000502:physiology*; D018482:Muscle, Skeletal / Q000098:blood supply* / Q000502:physiology*; D010100:Oxygen / Q000097:blood*; D010101:Oxygen Consumption / Q000502:physiology*; D005082:Physical Exertion / Q000502:physiology*; D051381:Rats; D017207:Rats, Sprague-Dawley
chemical_list: D010100:Oxygen