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Danielle J Padilla

Publications and source records attributed to Danielle J Padilla.

10 recordsLinked to original sources
PubMed2006

Effects of Type II diabetes on muscle microvascular oxygen pressures.

We tested the hypothesis that muscle microvascular O2 pressure (PmvO2; reflecting the O2 delivery (QO2) to O2 uptake (VO2) ratio) would be lowered in the spinotrapezius muscle of Goto-Kakizaki (GK) Type II diabetic rats (n=7) at rest and during twitch contractions when compared to control (CON; n=5) rats. At rest, PmvO2 was lower in GK versus CON rats (CON: 29+/-2; GK: 18+/-2Torr; P<0.05). At the onset of contractions, GK rats evidenced a faster change in PmvO2 than CON (i.e., time constant (tau); CON: 16+/-4; GK: 6+/-2s; P<0.05). In contrast to the monoexponential fall in PmvO2 to the steady-state level seen in CON, GK rats exhibited a biphasic PmvO2 response that included a blunted (or non-existent) PmvO2 decrease followed by recovery to a steady-state PmvO2 that was at, or slightly above, resting values. Compared with CON, this decreased PmvO2 across the transition to a higher metabolic rate in Type II diabetes would be expected to impair blood-muscle O2 exchange and contractile function.

Analysis of Variance↗
PubMed2006

Effects of Type II diabetes on capillary hemodynamics in skeletal muscle.

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.

Animals↗
PubMed2006

Temporal profile of rat skeletal muscle capillary haemodynamics during recovery from contractions.

In skeletal muscle capillaries, red blood cell (RBC) flux (F(RBC)), velocity (V(RBC)) and haematocrit (Hct(CAP)) are key determinants of microvascular O2 exchange. However, the mechanisms leading to the changes in F(RBC), V(RBC) and Hct(CAP) during muscle contractions and recovery thereafter are not fully understood. To address this issue we used intravital microscopy to investigate the temporal profile of the rat spinotrapezius muscle (n = 5) capillary haemodynamics during recovery from 3 min of twitch muscle contractions (1 Hz, 4-6 V). Specifically, we hypothesized that (1) during early recovery F(RBC) and V(RBC) would decrease rapidly and F(RBC) would display a biphasic response (consistent with a muscle pump effect on capillary haemodynamics), and (2) there would be a dynamic relationship between changes (Delta) in V(RBC) and Hct(CAP). The values at rest (R) and end-recovery (ER) were significantly lower (P < 0.05) than at end-contraction (EC) for F(RBC) (in cells s(-1), R = 30.1 +/- 7.8, EC = 46.2 +/- 7.3 and ER = 26.0 +/- 6.1), V(RBC) (in microm s(-1), R = 368 +/- 83, EC = 497 +/- 62 and ER = 334 +/- 59) and Hct(CAP) (R = 0.193 +/- 0.016, EC = 0.214 +/- 0.023 and ER = 0.185 +/- 0.019). The first data point where a significant decrease in F(RBC), Hct(CAP) and V(RBC) occurred was at 5, 5 and 20 s post-contraction, respectively. The decrease in F(RBC) approximated a monoexponential response (half-time of approximately 26 s). The relationship between DeltaV(RBC) and DeltaHct(CAP) was not significant (P > 0.05). Based on the early decrease in F(RBC) (within 5 s), overall dynamic profile of F(RBC) and the approximately 20 s 'delay' to the decrease in V(RBC) we conclude that the muscle pump does not appear to contribute substantially to the steady-state capillary haemodynamics in the contracting rat spinotrapezius muscle. Moreover, our findings suggest that alterations in V(RBC) do not obligate proportional changes in Hct(CAP) within individual capillaries following muscle contractions.

Animals↗
PubMed2005

Effects of arterial hypotension on microvascular oxygen exchange in contracting skeletal muscle.

In healthy animals under normotensive conditions (N), contracting skeletal muscle perfusion is regulated to maintain microvascular O2 pressures (PmvO2) at levels commensurate with O2 demands. Hypovolemic hypotension (H) impairs muscle contractile function; we tested whether this condition would alter the matching of O2 delivery (Qo2) to O2 utilization (Vo2), as determined by PmvO2 at the onset of muscle contractions. PmvO2 in the spinotrapezius muscles of seven female Sprague-Dawley rats (280+/-6 g) was measured every 2 s across the transition from rest to 1-Hz twitch contractions. Measurements were made under N (mean arterial pressure, 97+/-4 mmHg) and H (induced by arterial section; mean arterial pressure, 58+/-3 mmHg, P<0.05) conditions; PmvO2 profiles were modeled using a multicomponent exponential fitted with independent time delays. Hypotension reduced muscle blood flow at rest (24+/-8 vs. 6+/-1 ml-1.min-1.100 g-1 for N and H, respectively; P<0.05) and during contractions (74+/-20 vs. 22+/-4 ml-1.min-1.100 g-1 for N and H, respectively; P<0.05). H significantly decreased resting PmvO2 and steady-state contracting PmvO2(19.4+/-2.4 vs. 8.7+/-1.6 Torr for N and H, respectively, P<0.05). At the onset of contractions, H reduced the time delay (11.8+/-1.7 vs. 5.9+/-0.9 s for N and H, respectively, P<0.05) before the fall in PmvO2 and accelerated the rate of PmvO2 decrease (time constant, 12.6+/-1.4 vs. 7.3+/-0.9 s for N and H, respectively, P<0.05). Muscle Vo2 was reduced by 71% at rest and 64% with contractions in H vs. N, and O2 extraction during H averaged 78% at rest and 94% during contractions vs. 51 and 78% in N. These results demonstrate that H constrains the increase of skeletal muscle Qo2 relative to that of Vo2 at the onset of contractions, leading to a decreased PmvO2. According to Fick's law, this scenario will decrease blood-myocyte O2 flux, thereby slowing Vo2 kinetics and exacerbating the O2 deficit generated at exercise onset.

Animals↗
PubMed2005

Effects of eccentric exercise on microcirculation and microvascular oxygen pressures in rat spinotrapezius muscle.

A single bout of eccentric exercise results in muscle damage, but it is not known whether this is correlated with microcirculatory dysfunction. We tested the following hypotheses in the spinotrapezius muscle of rats either 1 (DH-1; n = 6) or 3 (DH-3; n = 6) days after a downhill run to exhaustion (90-120 min; -14 degrees grade): 1) in resting muscle, capillary hemodynamics would be impaired, and 2) at the onset of subsequent acute concentric contractions, the decrease of microvascular O(2) pressure (Pmv(o(2))), which reflects the dynamic balance between O(2) delivery and O(2) utilization, would be accelerated compared with control (Con, n = 6) rats. In contrast to Con muscles, intravital microscopy observations revealed the presence of sarcomere disruptions in DH-1 and DH-3 and increased capillary diameter in DH-3 (Con: 5.2 +/- 0.1; DH-1: 5.1 +/- 0.1; DH-3: 5.6 +/- 0.1 mum; both P < 0.05 vs. DH-3). At rest, there was a significant reduction in the percentage of capillaries that sustained continuous red blood cell (RBC) flux in both DH running groups (Con: 90.0 +/- 2.1; DH-1: 66.4 +/- 5.2; DH-3: 72.9 +/- 4.1%, both P < 0.05 vs. Con). Capillary tube hematocrit was elevated in DH-1 but reduced in DH-3 (Con: 22 +/- 2; DH-1: 28 +/- 1; DH-3: 16 +/- 1%; all P < 0.05). Although capillary RBC flux did not differ between groups (P > 0.05), RBC velocity was lower in DH-1 compared with Con (Con: 324 +/- 43; DH-1: 212 +/- 30; DH-3: 266 +/- 45 mum/s; P < 0.05 DH-1 vs. Con). Baseline Pmv(O(2)) before contractions was not different between groups (P > 0.05), but the time constant of the exponential fall to contracting Pmv(O(2)) values was accelerated in the DH running groups (Con: 14.7 +/- 1.4; DH-1: 8.9 +/- 1.4; DH-3: 8.7 +/- 1.4 s, both P < 0.05 vs. Con). These findings are consistent with the presence of substantial microvascular dysfunction after downhill eccentric running, which slows the exercise hyperemic response at the onset of contractions and reduces the Pmv(O(2)) available to drive blood-muscle O(2) delivery.

Animals↗
PubMed2005

Control of microvascular oxygen pressures in rat muscles comprised of different fibre types.

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.

Animals↗
PubMed2005

Dynamics of muscle microcirculatory oxygen exchange.

PURPOSE: Beyond the initial cardiodynamic "Phase I," pulmonary oxygen uptake (VO(2)) kinetics are dictated largely by, and resemble closely, the VO(2) of the exercising muscles (VO(2)m). Within those muscles, the microcirculation is responsible for affecting almost all blood-myocyte O(2) transfer, and thus, observations at this site may provide key insights into muscle oxidative function in health and dysfunction in disease. METHODS: Recently, a novel combination of microscopy and phosphorescence quenching techniques has been utilized to understand the dynamics of microvascular O(2) delivery (VO(2)m) and muscle O(2) utilization (VO(2)m) at the onset of muscle contractions. RESULTS: These experiments have addressed longstanding questions regarding the site of control of VO(2)m kinetics and provide a first look at capillary hemodynamics at exercise onset in healthy muscle and their derangements resulting from chronic diseases such as heart failure and diabetes. CONCLUSION: This paper will review these novel findings within our current understanding of microcirculatory control and blood-myocyte O(2) transfer.

Cardiovascular Diseases↗
PubMed2004

Ventilatory dynamics and control of blood gases after maximal exercise in the Thoroughbred horse.

Despite enormous rates of minute ventilation (Ve) in the galloping Thoroughbred (TB) horse, the energetic demands of exercise conspire to raise arterial Pco(2) (i.e., induce hypercapnia). If locomotory-respiratory coupling (LRC) is an obligatory facilitator of high Ve in the horse such as those found during galloping (Bramble and Carrier. Science 219: 251-256, 1983), Ve should drop precipitously when LRC ceases at the galloptrot transition, thus exacerbating the hypercapnia. TB horses (n = 5) were run to volitional fatigue on a motor-driven treadmill (1 m/s increments; 14-15 m/s) to study the dynamic control of breath-by-breath Ve, O(2) uptake, and CO(2) output at the transition from maximal exercise to active recovery (i.e., trotting at 3 m/s for 800 m). At the transition from the gallop to the trot, Ve did not drop instantaneously. Rather, Ve remained at the peak exercising levels (1,391 +/- 88 l/min) for approximately 13 s via the combination of an increased tidal volume (12.6 +/- 1.2 liters at gallop; 13.9 +/- 1.6 liters over 13 s of trotting recovery; P < 0.05) and a reduced breathing frequency [113.8 +/- 5.2 breaths/min (at gallop); 97.7 +/- 5.9 breaths/min over 13 s of trotting recovery (P < 0.05)]. Subsequently, Ve declined in a biphasic fashion with a slower mean response time (85.4 +/- 9.0 s) than that of the monoexponential decline of CO(2) output (39.9 +/- 4.7 s; P < 0.05), which rapidly reversed the postexercise arterial hypercapnia (arterial Pco(2) at gallop: 52.8 +/- 3.2 Torr; at 2 min of recovery: 25.0 +/- 1.4 Torr; P < 0.05). We conclude that LRC is not a prerequisite for achievement of Ve commensurate with maximal exercise or the pronounced hyperventilation during recovery.

Animals↗
PubMed2003

Oxygen exchange profile in rat muscles of contrasting fibre types.

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 (QO2) to O2 uptake (VO2) 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 (DeltaPO2,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 (tau); 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 (DeltaPO2,m/tau; 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 QO2 dynamics relative to those of VO2.

Animals↗