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 thatQ O 2 and fractional O 2 extraction increase as linear and hyperbolic functions, respectively, ofV 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 measureQ 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 lowerV O 2 andQ O 2 in MG and WG under each set of conditions. These data suggest that during submaximal metabolic rates, the relationship betweenQ 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. The relationship between blood flow (Q) and metabolic rate (V O 2 ) is strong and has been well characterized for both the whole body and the exercising limbs. In the exercising human, legQ andV O 2 are linearly related by the equationQ = S ×V O 2 + I, where S represents the slope (5.3) and I the intercept (2.8 l min −1 ; data from Knight et al. 1992

Other than during sleep and contrived laboratory testing protocols, humans rarely exist in prolonged metabolic steady states; rather, they transition among different metabolic rates (V O2). The dynamic transition of V O2 (V O2 kinetics), initiated, for example, at exercise onset, provides a unique window into understanding metabolic control. This brief review presents the state-of-the art regarding control of V O2 kinetics within the context of a simple model that helps explain the work rate dependence of V O2 kinetics as well as the effects of environmental perturbations and disease. Insights emerging from application of novel approaches and technologies are integrated into established concepts to assess in what circumstances O2 supply might exert a commanding role over V O2 kinetics, and where it probably does not. The common presumption that capillary blood flow dynamics can be extrapolated accurately from upstream arterial measurements is challenged. From this challenge, new complexities emerge with respect to the relationships between O2 supply and flux across the capillary-myocyte interface and the marked dependence of these processes on muscle fiber type. Indeed, because of interfiber type differences in O2 supply relative to V O2, the presence of much lower O2 levels in the microcirculation supplying fast-twitch muscle fibers, and the demonstrated metabolic sensitivity of muscle to O2, it is possible that fiber type recruitment profiles (and changes thereof) might help explain the slowing of V O2 kinetics at higher work rates and in chronic diseases such as heart failure and diabetes.

To determine whether fibre type affects the O2 exchange characteristics of skeletal muscle at the microcirculatory level we tested the hypothesis that, following the onset of contractions, muscle comprising predominately type I fibres (soleus, Sol, 86 % type I) would, based on demonstrated blood flow responses, exhibit a blunted microvascular PO2 (PO2,m, which is determined by the O2 delivery (Q̇O2) to O2 uptake (V̇O2) ratio) profile (assessed via phosphorescence quenching) compared to muscle of primarily type II fibres (peroneal, Per, 84 % type II). PO2,m was measured at rest, and following the rest‐contractions (twitch, 1 Hz, 2–4 V for 120 s) transition in Sol (n= 6) and Per (n= 6) muscles of Sprague‐Dawley rats. Both muscles exhibited a delay followed by a mono‐exponential decrease in PO2,m to the steady state. However, compared with Sol, Per demonstrated (1) a larger change in baseline minus steady state contracting PO2,m (ΔPO2,m) (Per, 13.4 ± 1.7 mmHg; Sol, 8.6 ± 0.9 mmHg, P < 0.05); (2) a faster mean response time (i.e. time delay (TD) plus time constant (τ); Per, 23.8 ± 1.5 s; Sol, 39.6 ± 4.3 s, P < 0.05); and therefore (3) a greater rate of PO2,m decline (ΔPO2,m/τ; Per, 0.92 ± 0.08 mmHg s−1; Sol, 0.42 ± 0.05 mmHg s−1, P < 0.05). These data demonstrate an increased microvascular pressure head of O2 at any given point after the initial time delay for Sol versus Per following the onset of contractions that is probably due to faster Q̇O2 dynamics relative to those of V̇O2.

No abstract

Objective: This investigation tested the hypothesis that the dynamics of muscle microvascular O pressure (PO m, which from rest to contractions and that the nature of that perturbation is dependent upon the severity of cardiac dysfunction. 

Microcirculatory red blood cell (RBC) hemodynamics are impaired within skeletal muscle of Type I diabetic rats (Kindig CA, Sexton WL, Fedde MR, and Poole DC. Respir Physiol 111: 163-175, 1998). Whether muscle microcirculatory dysfunction occurs in Type II diabetes, the more prevalent form of the disease, is unknown. We hypothesized that Type II diabetes would reduce the proportion of capillaries supporting continuous RBC flow and RBC hemodynamics within the spinotrapezius muscle of the Goto-Kakizaki Type II diabetic rat (GK). With the use of intravital microscopy, muscle capillary diameter (d(c)), capillary lineal density, capillary tube hematocrit (Hct(cap)), RBC flux (F(RBC)), and velocity (V(RBC)) were measured in healthy male Wistar (control: n = 5, blood glucose, 105 +/- 5 mg/dl) and male GK (n = 7, blood glucose, 263 +/- 34 mg/dl) rats under resting conditions. Mean arterial pressure did not differ between groups (P > 0.05). Sarcomere length was set to a physiological length ( approximately 2.7 mum) to ensure that muscle stretching did not alter capillary hemodynamics; d(c) was not different between control and GK rats (P > 0.05), but the percentage of RBC-perfused capillaries (control: 93 +/- 3; GK: 66 +/- 5 %), Hct(cap), V(RBC), F(RBC), and O(2) delivery per unit of muscle were all decreased in GK rats (P < 0.05). This study indicates that Type II diabetes reduces both convective O(2) delivery and diffusive O(2) transport properties within muscle microcirculation. If these microcirculatory deficits are present during exercise, it may provide a basis for the reduced O(2) exchange characteristic of Type II diabetic patients.

No abstract

No abstract