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David C Poole

Publications and source records attributed to David C Poole.

At least 37 records · Page 2Linked to original sources
PubMed2004

Effects of chronic heart failure in rats on the recovery of microvascular PO2 after contractions in muscles of opposing fibre type.

Chronic heart failure (CHF) impairs muscle O2 delivery (QO2) and, at a given O2 uptake (VO2), lowers microvascular O2 pressures (PmvO2: determined by the QO2-to-VO2 ratio), which may impair recovery of high-energy phosphates following exercise. Because CHF preferentially decreases QO2 to slow-twitch muscles, we hypothesized that recovery PmvO2 kinetics would be slowed to a greater extent in soleus (SOL: approximately 84% type I fibres) than in peroneal (PER: approximately 14% type I) muscles of CHF rats. PmvO2 dynamics were determined in SOL and PER muscles of control (CON: n= 6; left ventricular end-diastolic pressure, LVEDP: approximately 3 mmHg), moderate CHF (MOD: n= 7; LVEDP: approximately 11 mmHg) and severe CHF (SEV: n= 4; LVEDP: approximately 25 mmHg) following cessation of electrical stimulation (180 s; 1 Hz). In PER, neither the recovery PmvO2 values nor the mean response time (MRT; a weighted average of the time to 63% of the overall response) were altered by CHF (CON: 66.8 +/- 8.0, MOD: 72.4 +/- 11.8, SEV: 69.1 +/- 9.5 s). In marked contrast, SOL PmvO2, at recovery onset, was reduced significantly in the SEV group ( approximately 6 Torr) and PmvO2 MRT was slowed with increased severity of CHF (CON: 45.1 +/- 5.3, MOD: 63.2 +/- 9.4, SEV: 82.6 +/- 12.3 s; P < 0.05 CON vs. MOD and SEV). These data indicate that CHF slows PmvO2 recovery following contractions and lowers capillary O2 driving pressure in slow-twitch SOL, but not in fast-twitch PER muscle. These results may explain, in part, the slowed recovery kinetics (phosphocreatine and VO2) and pronounced fatigue following muscular work in CHF patients.

Animals↗
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↗
PubMed2004

Measurement of muscle microvascular oxygen pressures: compartmentalization of phosphorescent probe.

OBJECTIVE: To determine whether the phosphorescent probe Oxyphor R2 (a palladium porphyrin dendrimer) becomes extravasated within normotensive skeletal muscle, R2 perfusion and washout studies were performed using a perfused rat hindlimb preparation. METHODS: Phosphorescence signals were monitored in tibialis anterior muscles after 35 min of R2 blood perfusion and across a subsequent washout period that included vasodilation (sodium nitroprusside, SNP, approximately 3 x 10(-2) M). RESULTS: Two responses were evident: Group 1 (n = 4)--Inflowing blood pressure and vascular conductance remained stable close to initial values and subsequently a marked vasodilation was evident with SNP (vascular conductance; R2 blood perfusion, 0.096 +/- 0.005; washout, pre-SNP, 0.085 +/- 0.005, post-SNP, 0.110 +/- 0.005 mL/min/mmHg, p <.05, for pre- vs. post-SNP). Baseline phosphorescence signals could be monitored up to 99 +/- 36 s post-SNP when the phosphorescence signal disappeared. For these muscles, palladium content was undetectable. Group 2 (n = 3)--Inflowing blood pressure increased 112% and vascular conductance fell approximately 50%. These hindlimbs were unresponsive to SNP, phosphorescence signal was undiminished by washout and SNP, and muscles became edematous. CONCLUSIONS: These results suggest that in normotensive muscle (i.e., Group 1 above), extravasation of phosphorescent probe R2 over 35 min of perfusion is insufficient to yield a detectable phosphorescence signal in skeletal muscle.

Animals↗
PubMed2003

Recovery of microvascular PO2 during the exercise off-transient in muscles of different fiber type.

The speed with which muscle energetic status recovers after exercise is dependent on oxidative capacity and vascular O(2) pressures. Because vascular control differs between muscles composed of fast- vs. slow-twitch fibers, we explored the possibility that microvascular O(2) pressure (Pmv(O(2)); proportional to the O(2) delivery-to-O(2) uptake ratio) would differ during recovery in fast-twitch peroneal (Per: 86% type II) compared with slow-twitch soleus (Sol: 84% type I). Specifically, we hypothesized that, in Per, Pmv(O(2)) would be reduced immediately after contractions and would recover more slowly during the off-transient from contractions compared with Sol. The Per and Sol muscles of six female Sprague-Dawley rats (weight = approximately 220 g) were studied after the cessation of electrical stimulation (120 s; 1 Hz) to compare the recovery profiles of Pmv(O(2)). As hypothesized, Pmv(O(2)) was lower throughout recovery in Per compared with Sol (end contraction: 13.4 +/- 2.2 vs. 20.2 +/- 0.9 Torr; end recovery: 24.0 +/- 2.4 vs. 27.4 +/- 1.2 Torr, Per vs. Sol; P <or= 0.05). In addition, the mean response time for recovery was significantly faster for Sol compared with Per (45.1 +/- 5.3 vs. 66.3 +/- 8.1 s, Sol vs. Per; P < 0.05). Despite these findings, Pmv(O(2)) rose progressively in both muscles and at no time fell below end-exercise values. These data indicate that, during the recovery from contractions (which is prolonged in Per), capillary O(2) driving pressure (i.e., Pmv(O(2))) is reduced in fast-compared with slow-twitch muscle. In conclusion, the results of the present investigation may partially explain the slowed recovery kinetics (phosphocreatine and O(2) uptake) found previously in 1) fast- vs. slow-twitch muscle and 2) various patient populations, such as those with congestive heart failure and diabetes mellitus.

Animals↗
PubMed2003

Altered regional blood flow responses to submaximal exercise in older rats.

Maximal aerobic capacity and the ability to sustain submaximal exercise (Ex) declines with advancing age. Whether altered muscle blood flow (BF) plays a mechanistic role in these effects remains to be resolved. The present investigation determined the effects of aging on the hemodynamic and regional BF response to submaximal Ex in rats. Heart rate (HR), mean arterial pressure (MAP), and BF to different organs (kidneys, splanchnic organs, and 28 hindlimb muscles) were determined at rest and during submaximal treadmill Ex (20 m/min, 5% grade) with radiolabeled microspheres in young (Y; 6-8 mo old, 339 +/- 8 g, n = 9) and old (O; 27-29 mo old, 504 +/- 18 g, n = 7) Fischer 344 x Brown Norway rats. Results demonstrated that HR, MAP, and BF to the pancreas, small and large intestine, and total hindlimb musculature were similar between Y and O rats at rest. BF to the kidneys, spleen, and stomach were 33, 60, and 43% lower, respectively, in O compared with Y rats. BF to the total hindlimb musculature increased (P < 0.05) during Ex and was similar for both Y and O rats (Y: 16 +/- 3 to 124 +/- 7 vs. O: 20 +/- 3 to 137 +/- 12 ml.min-1.100 g-1). However, in O vs. Y rats, BF was reduced in 6 (highly oxidative) and elevated in 8 (highly glycolytic) of the 28 individual hindquarter muscles or muscle parts examined (P < 0.05). During Ex, BF to the spleen and stomach decreased (P < 0.05) from rest in Y rats, whereas BF decreased in the kidneys, pancreas, spleen, stomach, as well as the small and large intestines of O rats. In conclusion, these data demonstrate that, despite similar increases in total hindlimb BF in Y and O rats during submaximal Ex, there is a profound BF redistribution from highly oxidative to highly glycolytic muscles.

Aging↗
PubMed2003

Effect of sampling strategy on measures of VO2peak obtained using commercial breath-by-breath systems.

The purpose of this study was to determine the effect of sampling strategy (i.e., number of breaths) on measured peak rate of oxygen uptake ( VO(2peak)) elicited by a range of severe intensity exercise bouts. The hypothesis was that a smaller sample (i.e., fewer breaths) would produce a higher measure of VO(2peak) and that this effect would be greater in shorter tests than in longer tests. Thirty-three university students performed constant-power cycle ergometer tests at intensities selected to elicit fatigue in ~3.0 min (short duration), approximately 5.5 min (medium duration), and approximately 8.0 min (long duration). Values for VO(2peak) were the highest rates of oxygen uptake obtained using the following sampling methods: single breath, and 3-, 5-, 15- and 30-breath rolling averages. As hypothesized, measures of VO(2peak) increased systematically with decreasing sample size. Contrary to the hypothesis, the effect of sample size was greater in medium duration and long duration tests than in the short duration tests. The interaction between test duration and sample size on measures of VO(2peak) highlights the importance of standardizing the analysis protocol for exercise in the severe domain. If such standardization is not feasible, it should be recognized that specific analysis protocols may exert a substantial effect upon the reported VO(2peak).

Adult↗
PubMed2003

Effects of chronic heart failure on skeletal muscle capillary hemodynamics at rest and during contractions.

Chronic heart failure (CHF) reduces muscle blood flow at rest and during exercise and impairs muscle function. Using intravital microscopy techniques, we tested the hypothesis that the speed and amplitude of the capillary red blood cell (RBC) velocity (VRBC) and flux (FRBC) response to contractions would be reduced in CHF compared with control (C) spinotrapezius muscle. The proportion of capillaries supporting continuous RBC flow was less (P < 0.05) in CHF (0.66 +/- 0.04) compared with C (0.84 +/- 0.01) muscle at rest and was not significantly altered with contractions. At rest, VRBC (C, 270 +/- 62; CHF, 179 +/- 14 microm/s) and FRBC (C, 22.4 +/- 5.5 vs. CHF, 15.2 +/- 1.2 RBCs/s) were reduced (both P < 0.05) in CHF vs. C muscle. Contractions significantly (both P < 0.05) elevated VRBC (C, 428 +/- 47 vs. CHF, 222 +/- 15 microm/s) and FRBC (C, 44.3 +/- 5.5 vs. CHF, 24.0 +/- 1.2 RBCs/s) in C and CHF muscle; however, both remained significantly lower in CHF than C. The time to 50% of the final response was slowed (both P < 0.05) in CHF compared with C for both VRBC (C, 8 +/- 4; CHF, 56 +/- 11 s) and FRBC (C, 11 +/- 3; CHF, 65 +/- 11 s). Capillary hematocrit increased with contractions in C and CHF muscle but was not different (P > 0.05) between CHF and C. Thus CHF impairs diffusive and conductive O2 delivery across the rest-to-contractions transition in rat skeletal muscle, which may help explain the slowed O2 uptake on-kinetics manifested in CHF patients at exercise onset.

Algorithms↗
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↗
PubMed2003

Effects of aging on capillary geometry and hemodynamics in rat spinotrapezius muscle.

The effects of aging on muscle microvascular structure and function may play a key role in performance deficits and impairment of O2 exchange within skeletal muscle of senescent individuals. To determine the effects of aging on capillary geometry, red blood cell (RBC) hemodynamics, and hematocrit in a muscle of mixed fiber type, spinotrapezius muscles from Fischer 344 x Brown Norway hybrid rats aged 6-8 mo [young (Y); body mass 421 +/- 10 g, n = 6] and 26-28 mo [old (O); 561 +/- 12 g, n = 6] were observed by high-resolution transmission light microscopy under resting conditions. The percentage of RBC-perfused capillaries (Y: 78 +/- 3%; O: 75 +/- 2%) and degree of tortuosity and branching (Y: 13 +/- 2%; O: 13 +/- 2%, additional capillary length) were not different in O vs. Y muscles. Lineal density of RBC-perfused capillaries in O was significantly reduced (Y: 30.7 +/- 1.8, O: 22.8 +/- 3.1 capillaries/mm; P < 0.05). However, RBC-perfused capillaries from O rats (n = 78) exhibited increased RBC velocity (VRBC) (Y: 219 +/- 12, O: 310 +/- 14 microm/s; P < 0.05) and RBC flux (FRBC) (Y: 27 +/- 2, O: 41 +/- 2 RBC/s; P < 0.05) vs. Y rats (n = 66). Thus O2 delivery per unit of muscle was not different between groups (Y: 894 +/- 111, O: 887 +/- 118 RBC. s-1. mm muscle-1). Capillary hematocrit was not different in Y vs. O rats (Y: 26 +/- 1%, O: 28 +/- 1%: P > 0.05). These data indicate that in resting spinotrapezius muscle, aging decreases the lineal density of RBC-perfused capillaries while increasing mean VRBC and FRBC within those capillaries. Whereas muscle conductive O2 delivery and capillary hematocrit were unchanged, elevated VRBC reduces capillary RBC transit time and may impair the diffusive transport of O2 from blood to myocyte particularly under exercise conditions.

Aging↗
PubMed2003

Arterial blood gas control in the upright versus recumbent Asian elephant.

In the elephant, there is concern that lateral recumbency (LR) impairs respiratory muscle and lung function resulting in clinically significant arterial hypoxemia. Using healthy adult female Asian elephants (Elephas maximus, n=6), the hypothesis was tested that, given the O(2) binding characteristics of elephant blood, substantial reductions in arterial O(2) pressure (Pa(O(2))) in LR could be tolerated without lowering arterial O(2) content appreciably. Fifteen minutes of LR decreased Pa(O(2)) from 103+/-2 (upright, U) to 77+/-4 mmHg (P<0.05) and hemoglobin O(2) saturation (U, 97.8+/-0.1, LR, 95.3+/-0.5%, P<0.05). However, due to a recumbency-induced hemoconcentration, arterial O(2) content was unchanged (U, 18.2+/-2.4, LR, 18.3+/-2.1 ml O(2) per 100 ml). In addition, there was a mild hyperventilation in LR that reduced arterial CO(2) pressure (P(CO(2))) from 39.4+/-0.3 to 37.1+/-1.0 mmHg (P<0.05). These data indicate that the Asian elephant can endure at least short periods of LR without lowering arterial O(2) content.

Acid-Base Equilibrium↗
PubMed2003

Cortical bone dynamics, strength, and densitometry after induction of emphysema in hamsters.

Recent evidence suggests that patients suffering from chronic obstructive pulmonary disease are also at an increased risk of developing osteoporosis. The pathophysiological mechanism(s) linking these progressive diseases is unknown. The goal of this investigation was to determine whether there were alterations in bone mineral density and content, cortical bone structure and strength, and indexes of bone formation and resorption in the elastase-induced emphysematous hamster. At 3 wk after induction of emphysema, the femoral bone mineral content was 8% less (P = 0.026) and the femoral fracture strength was 6% less (P = 0.032) in the emphysematous hamster than in controls. The cortical area was 8.4% less (P = 0.013) and the periosteal mineral appositional rate was 27% less (P = 0.05) than in controls. Additionally, the endocortical eroded surface in the emphysematous group was about twice that in the control group (P = 0.003). Differences in some indexes of bone formation and resorption, paralleled by differences in bone structure and strength, were observed 3 wk after induction of emphysema. These differences in skeletal metabolism and strength may help explain some of the skeletal changes associated with chronic obstructive pulmonary disease in humans.

Animals↗
PubMed2002

Dynamics of oxygen uptake following exercise onset in rat skeletal muscle.

Technical limitations have precluded measurement of the V(O(2)) profile within contracting muscle (mV(O(2))) and hence it is not known to what extent V(O(2)) dynamics measured across limbs in humans or muscles in the dog are influenced by transit delays between the muscle microvasculature and venous effluent. Measurements of capillary red blood cell flux and microvascular P(O(2)) (P(O(2)m)) were combined to resolve the time course of mV(O(2)) across the rest-stimulation transient (1 Hz, twitch contractions). mV(O(2)) began to rise at the onset of contractions in a close to monoexponential fashion (time constant, J = 23.2 +/- 1.0 sec) and reached it's steady-state value at 4.5-fold above baseline. Using computer simulation in healthy and disease conditions (diabetes and chronic heart failure), our findings suggest that: (1) mV(O(2)) increases essentially immediately (< 2 sec) following exercise onset; (2) within healthy muscle the J blood flow (thus O(2) delivery, J Q(O(2)m)) is faster than JmV(O(2)) such that oxygen delivery is not limiting, and 3) a faster P(O(2)m) fall to a P(O(2)m) value below steady-state values within muscle from diseased animals is consistent with a relatively sluggish Q(O(2)m) response compared to that of mV(O(2)).

Animals↗
PubMed2002

Nitric oxide synthase inhibition speeds oxygen uptake kinetics in horses during moderate domain running.

Within the moderate exercise intensity domain, the speed of oxygen uptake (V(O(2))) kinetics at the transition to a higher metabolic rate is thought to be limited by an inertia of the oxidative machinery. Nitric oxide (NO)-induced inhibition of O(2) consumption within the electron transport chain may contribute to this inertia. This investigation tested the hypothesis that a reduction or removal of any such NO effect via infusion of N(omega)-nitro-L-arginine methyl ester (L-NAME; a NOS inhibitor) would speed V(O(2)) kinetics at the onset of moderate exercise. Five Thoroughbred geldings underwent four transitions to running speeds of 7 m sec(-1) (two control, C, 2 L-NAME [20 mg kg(-1)]) on an equine treadmill during which pulmonary gas exchange was determined using a bias flow system. Consistent with exercise in the moderate intensity domain, in none of the transitions was a V(O(2)) slow component elicited. The L-NAME treatment significantly accelerated V(O(2)) kinetics via a reduction of the primary amplitude time constant (C, 17.3 +/- 1.7; L-NAME, 11.8 +/- 1.5 sec, P < 0.05) concomitant with faster overall dynamics (i.e. T(50) and T(75) both P < 0.05) and a trend toward a decreased O(2) deficit (C, 6.4 +/- 0.7; L-NAME, 4.7 +/- 1.2 L; P = 0.06). These data support the notion that NO contributes prominently to the oxidative enzyme inertia and thus the speed of V(O(2)) kinetics at the onset of moderate intensity exercise in the horse.

Analysis of Variance↗
PubMed2002

Effects of prior contractions on muscle microvascular oxygen pressure at onset of subsequent contractions.

In humans, pulmonary oxygen uptake (.V(O2)) kinetics may be speeded by prior exercise in the heavy domain. This "speeding" arises potentially as the result of an increased muscle O(2) delivery (.Q(O2)) and/or a more rapid elevation of oxidative phosphorylation. We adapted phosphorescence quenching techniques to determine the.Q(O2)-to-O(2) utilization (.Q(O2)/.V(O2)) characteristics via microvascular O(2) pressure (P(O2,m)) measurements across sequential bouts of contractions in rat spinotrapezius muscle. Spinotrapezius muscles from female Sprague-Dawley rats (n = 6) were electrically stimulated (1 Hz twitch, 3-5 V) for two 3 min bouts (ST(1) and ST(2)) separated by 10 min rest. P(O2,m) responses were analysed using an exponential + time delay (TD) model. There was no significant difference in baseline and DeltaP(O2,m) between ST(1) and ST(2) (28.5 +/- 2.6 vs. 27.9 +/- 2.4 mmHg, and 13.9 +/- 1.8 vs. 14.1 +/- 1.3 mmHg, respectively). The TD was reduced significantly in the second contraction bout (ST(1), 12.2 +/- 1.9; ST(2), 5.7 +/- 2.2 s, P < 0.05), whereas the time constant of the exponential P(O2,m) decrease was unchanged (ST(1), 16.3 +/- 2.6; ST(2), 17.6 +/- 2.7 s, P > 0.1). The shortened TD found in ST(2) led to a reduced time to reach 63 % of the final response of ST(2) compared to ST(1) (ST(1), 28.3 +/- 3.0; ST(2), 20.2 +/- 1.8 s, P < 0.05). The speeding of the overall response in the absence of an elevated P(O2,m) baseline (which had it occurred would indicate an elevated.Q(O2)/.V(O2) or muscle blood flow suggests that some intracellular process(es) (e.g. more rapid increase in oxidative phosphorylation) may be responsible for the increased speed of P(O2,m) kinetics after prior contractions under these conditions.

Animals↗
PubMed2002

The relationship between power and the time to achieve .VO(2max).

PURPOSE: The severe exercise intensity domain may be defined as that range of work rates over which .VO(2max) can be elicited during constant-load exercise. The purpose of this study was to help characterize the .VO(2) response within this domain. METHODS: Eleven participants performed cycle ergometer exercise tests to fatigue at several discrete work rates between 95% and 135% of the maximum power (P(max)) achieved during an incremental exercise test. RESULTS: As previously demonstrated, the relationship between power and time to fatigue was hyperbolic. The asymptote of power (critical power, P(critical)) was 198 +/- 44 W. The rapidity of the .VO(2) response increased systematically at higher work rates such that the relationship between power and time to .VO(2max) was also well fit by a hyperbola. The power asymptote of this relationship (196 +/- 42 W) was not different from P(critical)(P > 0.05). The two hyperbolic relationships converged at 342 +/- 70 W (136% P(max)). CONCLUSION: These data suggest that, for this population of male and female university students, the upper boundary of the severe exercise intensity domain is approximately 136% P(max). This upper boundary is the highest work rate for which exercise duration is prolonged sufficiently (in this study, 136 +/- 17 s) to allow .VO(2) to rise to its maximal value. The lower boundary for severe exercise is just above P(critical), which is the highest work rate that is sustainable for a prolonged duration and that will not elicit .VO(2max).

Adult↗
PubMed2002

The effect of treadmill incline on maximal oxygen uptake, gas exchange and the metabolic response to exercise in the horse.

In healthy man, conditions that change muscle O2 delivery affect the achievable maximum rate of O2 uptake as well as the metabolic (e.g. lactate threshold, LT) and gas exchange (e.g. gas exchange threshold, Tge) responses to incremental exercise. Inclined (I) compared to level (L) running increases locomotory muscle EMG at a given speed in the horse, indicative of elevated metabolic demand. To our knowledge, the effect of treadmill incline on VO2,max, LT and Tge has not been addressed in the exercising quadruped. We used blood sampling and breath-by-breath expired gas analysis to test the hypothesis that I (10% gradient) would increase VO2,max and the rate of O2 uptake (VO2) at LT and Tge in six Thoroughbred horses during incremental running to volitional fatigue. VO2,max was significantly higher for I (I, 77.8 +/- 4.1; L, 65.5 +/- 5.3 1 min(-1); P < 0.05), but peak plasma lactate concentration was not (I, 28.0 +/- 3.7; L, 25.9 +/- 3.0 mM). Arterial Pco2 increased to 62.1 +/- 3.3 and 57.9 +/- 2.7 Torr (I vs. L; P < 0.05), yet despite this relative hypoventilation, a distinct Tge was present. This Tge occurred at a significantly different absolute (I, 49.6 +/- 3.2; L, 42.4 +/- 3.21 min(-1); P < 0.05), but nearly identical relative VO2 (I, 63.6 +/- 1.2; L, 63.9 +/- 1.6% VO2max) in I and L. Similarly, LT occurred at a significantly greater absolute VO2 (I, 37.3 +/- 2.8; L, 26.9 +/- 2.1 1 min(-1)), but a relative VO2 that was not different (I, 47.9 +/- 2.1; L, 43.9 +/- 4.5% VO2,max). In addition, Tge occurred at a significantly higher (P < or = 0.05) absolute and relative VO2 than LT for both I and L tests. In conclusion, VO2,max is higher during inclined than level running and both LT and Tge in the horse occur at a similar percentage of VO2,max irrespective of the absolute level of VO2,max. In contrast to humans, LT is a poor analogue of Tge in the horse.

Animals↗
PubMed2002

Dynamics of microvascular oxygen pressure during rest-contraction transition in skeletal muscle of diabetic rats.

Type I diabetes reduces dramatically the capacity of skeletal muscle to receive oxygen (QO(2)). In control (C; n = 6) and streptozotocin-induced diabetic (D: n = 6, plasma glucose = 25.3 +/- 3.9 mmol/l and C: 8.3 +/- 0.5 mmol/l) rats, phosphorescence quenching was used to test the hypothesis that, in D rats, the decline in microvascular PO(2) [Pm(O(2)), which reflects the dynamic balance between O(2) utilization (VO(2)) and QO(2)] of the spinotrapezius muscle after the onset of electrical stimulation (1 Hz) would be faster compared with that of C rats. Pm(O(2)) data were fit with a one or two exponential process (contingent on the presence of an undershoot) with independent time delays using least-squares regression analysis. In D rats, Pm(O(2)) at rest was lower (C: 31.2 +/- 3.2 mmHg; D: 24.3 +/- 1.3 mmHg, P < 0.05) and at the onset of contractions decreased after a shorter delay (C: 13.5 +/- 1.8 s; D: 7.6 +/- 2.1 s, P < 0.05) and with a reduced mean response time (C: 31.4 +/- 3.3 s; D: 23.9 +/- 3.1 s, P < 0.05). Pm(O(2)) exhibited a marked undershoot of the end-stimulation response in D muscles (D: 3.3 +/- 1.1 mmHg, P < 0.05), which was absent in C muscles. These results indicate an altered VO(2)-to-QO(2) matching across the rest-exercise transition in muscles of D rats.

Animals↗