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David C Poole

Publications and source records attributed to David C Poole.

At least 19 recordsLinked to original sources
PubMed2006

Oxygen exchange in muscle of young and old rats: muscle-vascular-pulmonary coupling.

Sustained performance of muscular exercise is contingent upon increasing muscle O(2) delivery (Qo2; the product of blood flow and arterial O(2) content, i.e. Q X Cao2) and utilization (Vo2m ) rapidly at exercise onset and sustaining necessary conductive and diffusive O(2) fluxes throughout exercise. A tight co-ordination of pulmonary, cardiovascular and muscle system responses is therefore required to prevent muscle microvascular O(2) pressures (P(mvO(2))) from falling to levels that impair blood-muscle O(2) exchange and/or impact metabolic control and reduce exercise tolerance. Microvascular O(2) pressures are determined by the balance between and Qo2 and Vo2m, and emerging evidence indicates that this balance is regulated differently across muscle fibre types and also in aged muscle. Moreover, disease states such as diabetes (type I and II) and chronic heart failure (CHF) also impact P(mvO(2)). This brief review primarily examines evidence obtained in animals that ageing: (1) redistributes exercising away from highly oxidative muscles and muscle fibres; (2) alters muscle capillary haemodynamics; and (3) reduces the O(2) pressure head within the microcirculation (P(mvO(2))) that serves to facilitate blood-muscle O(2) transfer. In many respects, these alterations found in healthy ageing animals bear a striking resemblance to those present in some chronic diseases (e.g. diabetes, CHF) and may help explain the compromised exercise tolerance present in aged individuals. Putative mechanistic insights are explored within the context of current knowledge and future investigative approaches.

Aging↗
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↗
PubMed2006

Human critical power-oxygen uptake relationship at different pedalling frequencies.

Critical power (CP) is lower at faster rather than slower pedalling frequencies and traditionally reported in watts (W). Faster pedalling frequencies also engender a greater metabolic rate (VO2) at low work rates, but with progressive increases in power output, the initial difference in VO2 between fast and slower pedalling frequencies is reduced. We tested the hypothesis that CP represents a unique metabolic rate for any given individual which would be similar at different pedalling frequencies. Eleven collegiate athletes (five cross-country runners, END; six sprinters, SPR), aged 18-23 years, performed exhaustive rides at either 60 or 100 r.p.m. on separate days for the determination of the pedal rate-specific CP. The VO2 at CP (CP-VO2) was determined from an 8 min ride at the CP for each pedal frequency. The group mean CP was significantly lower at 100 r.p.m. (189 +/- 50 W) compared to 60 r.p.m. (207 +/- 53 W, P < 0.05). However, the group mean CP-VO2 values at 60 (2.53 +/- 0.60 l min(-1)) and 100 r.p.m. (2.58 +/- 0.53 l min(-1)) were not significantly different. Critical power was significantly higher in the END athletes (242 +/- 50 W at 60 r.p.m.; 221 +/- 56 W at 100 r.p.m.) compared to SPR athletes at both pedal frequencies (177 +/- 38 W at 60 r.p.m.; 162 +/- 27 W at 100 r.p.m., P < 0.05), but the CP-VO2 was not (P > 0.05). However, when the CP-VO2 was scaled to body weight, the END athletes had a significantly greater CP-VO2 (41.3 +/- 4.1 ml min(-1) kg(-1) at 60 r.p.m.; 40.8 +/- 5.5 ml min(-1) kg(-1) at 100 r.p.m.) compared to the SPR athletes at both pedal frequencies (27.7 +/- 4.6 ml min(-1) kg(-1) at 60 r.p.m.; 29.4 +/- 2.8 ml min(-1) kg(-1) at 100 r.p.m., P < 0.05). We conclude that CP represents a specific metabolic rate (VO2) which can be achieved at different combinations of power outputs and pedalling frequencies.

Adult↗
PubMed2005

Blood flow and O2 extraction as a function of O2 uptake in muscles composed of different fiber types.

We examined how the greater vasodilatory capacity of slow--(ST) versus fast-twitch (FT) muscles impacts the relationship between blood flow (Q ) and O2 uptake (VO2) and, consequently, the O2 extraction (a-vO2 diff.)-to-VO2 relationship. Q was measured with radiolabelled microspheres, while VO2 was calculated by the Fick principle using measurements of microvascular O2 pressure (phosphorescence quenching) at rest, low--(2.5 V) and high-intensity contractions (4.5 V) for soleus (Sol; ST, n=5), mixed-gastrocnemius (MG; FT, n=7) and white-gastrocnemius (WG; FT, n=7). The slope of the Q-to-VO2 relationship (delta Q/delta VO2] ) was not different among muscles (Sol = 5.5 +/- 0.2, MG = 6.0 +/- 0.11 and WG = 5.8 +/- 0.06; P > 0.05). In contrast, the intercept was greater (P < 0.05) for Sol (16.3 +/- 2.7 ml min(-1) 100 g(-1)) versus MG and WG (in ml min(-1) 100 g(-1): 1.39 +/- 0.26 and 1.45 +/- 0.23, respectively; MG and WG, P > 0.05). In addition, the a-vO2 diff.-to-VO2] relationship for Sol was shifted rightward compared to MG and WG. These data suggest that the increase in Q for a given change in VO2 is similar for slow- and fast-twitch muscles, at least for the range of metabolic rates and muscles studied herein and that a-vO2 diff. differences result from the lower resting Q in FT muscles.

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

Muscle blood flow-O2 uptake interaction and their relation to on-exercise dynamics of O2 exchange.

A computer model was developed to provide a theoretical framework for interpreting the dynamics of muscle capillary O(2) exchange in health and disease. We examined the effects of different muscle oxygen uptake (V O(2m)) and CvO(2) profiles on muscle blood flow (Q (m)) kinetics (Q (m)=V O(2m)/[CaO(2)-CvO(2)]). Further, we simulated V O(2m) and Q (m) responses to predict the CvO(2) profile and the underlying dynamics of capillary O(2) exchange (CvO(2)=CaO(2)-V O(2m)/Q (m)). Exponential equations describing V O(2m), CvO(2) and Q (m) responses in vivo were used in the simulations. The results indicated that Q (m) kinetics were relatively insensitive to CvO(2) parameters, but directly associated with V O(2m) kinetics. The biphasic Q (m) response produced a substantial fall in CvO(2) within the first 15-20s of the exercise transition (phase 1 of Q (m)). These results revealed that the main determinant of CvO(2) (or O(2) extraction) kinetics was the dynamic interaction of Q (m) and V O(2m) kinetics during phase 1 of Q (m).

Capillaries↗
PubMed2005

Effects of aging on microvascular oxygen pressures in rat skeletal muscle.

Aging alters skeletal muscle vascular geometry and control such that the dynamics of muscular blood flow (Q) and O2 delivery (Q(O2)) may be impaired across the rest-exercise transition. If, at the onset of muscle contractions, Q dynamics are slowed disproportionately to those of muscle O2 uptake (V(O2), microvascular PO2 (PO2m) would be reduced and blood-tissue O2 transfer compromised. This investigation determined the effects of aging on PO2m (a direct reflection of the Q(O2)-to-V(O2) ratio), at rest and across the rest-contractions transition in the spinotrapezius of young (approximately 6 months, n = 9) and old (>24 months, n = 10) male Fisher 344/Brown Norway hybrid rats. Phosphorescence quenching techniques were used to quantify PO2m, and test the hypothesis that, across the rest-contractions (twitch, 1 Hz; 4-6 V, 240 s) transition, aging would transiently reduce the Q(O2)-to-V(O2) ratio causing a biphasic profile in which PO2m fell below steady-state contracting values. Old rats had a lower pre-contraction baseline PO2m than young (27.1+/-1.9 versus 33.8+/-1.6 mmHg, P<0.05, respectively). In addition, in old rats PO2m demonstrated a pronounced difference between the absolute nadir and end-contracting values (2.5+/-0.9 mmHg), which was absent in young rats. In conclusion, unlike their young counterparts, old rats exhibited a transiently reduced PO2m across the rest-contractions transition that may impair blood-tissue O2 exchange and elevate the O2 deficit, thereby contributing to premature fatigue.

Age Factors↗
PubMed2005

Impact of aging on muscle blood flow in chronic heart failure.

Chronic heart failure (CHF) is manifested principally in the elderly population. Therefore, to understand the causes of exercise intolerance in CHF patients, it is imperative to resolve the effects of aging on muscle blood flow (BF) in CHF. To address this issue, we determined the muscle BF response to submaximal treadmill exercise (20 m/min, 5% grade) in young (Y(CHF): 6-8 mo, 412 +/- 11 g, n = 11) and old (O(CHF): 27-29 mo, 494 +/- 10 g, n = 8) Fischer 344 x Brown Norway rats with similar degrees of myocardial infarction-induced left ventricular (LV) dysfunction [resting LV end-diastolic pressure: Y(CHF) = 24 +/- 2, O(CHF) = 22 +/- 2 mmHg; derivative of LV pressure over time: Y(CHF) = 5,168 +/- 285; O(CHF) = 5,050 +/- 165 mmHg/s; lung weight normalized to body weight: Y(CHF) = 9.14 +/- 0.72; O(CHF) = 8.21 +/- 0.29 mg/g (all P > 0.05)]. The exercising heart rate response was blunted in O(CHF) compared with Y(CHF) rats (Y(CHF) = 454 +/- 8, O(CHF) = 395 +/- 9 beats/min; P < 0.05). BF (radiolabeled microspheres) to the total hindlimb musculature and to each of the 28 individual muscles examined was similar between Y(CHF) and O(CHF) rats under resting conditions. During exercise, BF to five of the hindlimb muscles that normally possess a majority of slow-twitch oxidative and fast-twitch oxidative glycolytic muscle fibers increased significantly less (-25 to -42%) for O(CHF) compared with Y(CHF) rats. In contrast, BF to 14 of the hindlimb muscles that normally possess a majority of fast-twitch glycolytic muscle fibers was increased (+22 to +337%) for O(CHF) vs. Y(CHF) rats, which contributed to a greater mass-specific total hindlimb BF response in O(CHF) rats (Y(CHF) = 78 +/- 5, O(CHF) = 100 +/- 11 ml.min(-1).100 g(-1); P < 0.05) and coincided with greater reductions in BF to the kidneys and splanchnic organs during exercise in O(CHF) vs. Y(CHF). In conclusion, there appears to be a profound age-related redistribution of BF from the highly oxidative to the highly glycolytic muscles of the hindlimb during exercise in O(CHF) compared with Y(CHF) rats. This phenomenon is qualitatively similar to that reported previously for healthy young and old rats.

Aging↗
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

Oxygen uptake dynamics: from muscle to mouth--an introduction to the symposium.

The purpose of this paper is to provide an introduction to the study of oxygen uptake (VO(2)) dynamics or kinetics. Following the onset of exercise, both muscle and pulmonary VO(2) rise in a near-exponential fashion towards the anticipated "steady-state" VO(2) demand. However, it can take 2-4 min, or even longer at higher work rates, before this steady state is attained. Slow VO(2) kinetics increase the so-called O(2) deficit and obligate a greater contribution from anaerobic mechanisms of ATP production (involving the breakdown of muscle high energy phosphates and lactate production from glycogen) to meet the ATP requirement of the exercise task. A primary goal in this area of research is therefore to elucidate the physiological mechanisms which control and/or limit the rate at which muscle VO(2) increases following the onset of exercise. At higher intensities of exercise, a continued increase in both muscle and pulmonary VO(2) is observed with time despite the external work rate remaining constant. This continued rise in VO(2), beyond the anticipated steady-state requirement for the work rate, has been termed the VO(2) "slow component," and establishing the mechanistic basis for this phenomenon is another important goal of research in this field. This paper provides an overview of some of the factors which might contribute to both the fundamental and slow phases of the VO(2) kinetics and, in so doing, provides general background material for the more specific papers that follow.

Exercise↗
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

Comparison of oxygen uptake kinetics during knee extension and cycle exercise.

The knee extension exercise (KE) model engenders different muscle and fiber recruitment patterns, blood flow, and energetic responses compared with conventional cycle ergometry (CE). This investigation had two aims: 1) to test the hypothesis that upright two-leg KE and CE in the same subjects would yield fundamentally different pulmonary O(2) uptake (pVo(2)) kinetics and 2) to characterize the muscle blood flow, muscle Vo(2) (mVo(2)), and pVo(2) kinetics during KE to investigate the rate-limiting factor(s) of pVo(2) on kinetics and muscle energetics and their mechanistic bases after the onset of heavy exercise. Six subjects performed KE and CE transitions from unloaded to moderate [< ventilatory threshold (VT)] and heavy (>VT) exercise. In addition to pVo(2) during CE and KE, simultaneous pulsed and echo Doppler methods, combined with blood sampling from the femoral vein, were used to quantify the precise temporal profiles of femoral artery blood flow (LBF) and mVo(2) at the onset of KE. First, the gain (amplitude/work rate) of the primary component of pVo(2) for both moderate and heavy exercise was higher during KE ( approximately 12 ml.W(-1).min(-1)) compared with CE ( approximately 10), but the time constants for the primary component did not differ. Furthermore, the mean response time (MRT) and the contribution of the slow component to the overall response for heavy KE were significantly greater than for CE. Second, the time constant for the primary component of mVo(2) during heavy KE [25.8 +/- 9.0 s (SD)] was not significantly different from that of the phase II pVo(2). Moreover, the slow component of pVo(2) evident for the heavy KE reflected the gradual increase in mVo(2). The initial LBF kinetics after onset of KE were significantly faster than the phase II pVo(2) kinetics (moderate: time constant LBF = 8.0 +/- 3.5 s, pVo(2) = 32.7 +/- 5.6 s, P < 0.05; heavy: LBF = 9.7 +/- 2.0 s, pVo(2) = 29.9 +/- 7.9 s, P < 0.05). The MRT of LBF was also significantly faster than that of pVo(2). These data demonstrate that the energetics (as gain) for KE are greater than for CE, but the kinetics of adjustment (as time constant for the primary component) are similar. Furthermore, the kinetics of muscle blood flow during KE are faster than those of pVo(2), consistent with an intramuscular limitation to Vo(2) kinetics, i.e., a microvascular O(2) delivery-to-O(2) requirement mismatch or oxidative enzyme inertia.

Adolescent↗
PubMed2004

Downhill running: a model of exercise hyperemia in the rat spinotrapezius muscle.

To utilize the rat spinotrapezius muscle as a model to investigate the microcirculatory consequences of exercise training, it is necessary to design an exercise protocol that recruits this muscle. There is evidence that the spinotrapezius is derecruited during standard treadmill exercise protocols performed on the uphill treadmill (i.e., 6 degrees incline). This investigation tested the hypothesis that downhill running would effectively recruit the spinotrapezius muscle as assessed by the presence of an exercise hyperemia response. We used radioactive 15-microm microspheres to determine blood flows in the spinotrapezius and selected hindlimb muscles of female Sprague-Dawley rats at rest and during downhill (i.e., -14 degrees incline; 331 +/- 5 g body wt, n = 7) and level (i.e., 0 degrees incline; 320 +/- 11 g body wt, n = 5) running at 30 m/min. Both level and downhill exercise increased blood flow to all hindlimb muscles (P < 0.01). However, in marked contrast to the absence of a hyperemic response to level running, blood flow to the spinotrapezius muscle increased from 26 +/- 6 ml.min(-1).100 g(-1) at rest to 69 +/- 8 ml.min(-1).100 g(-1) during downhill running (P < 0.01). These findings indicate that downhill running represents an exercise paradigm that recruits the spinotrapezius muscle and thereby constitutes a tenable physiological model for investigating the adaptations induced by exercise training (i.e., the mechanisms of altered microcirculatory control by transmission light microscopy).

Adaptation, Physiological↗