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D C Poole

Publications and source records attributed to D C Poole.

At least 19 recordsLinked to original sources
PubMed1994

Red blood cell transit time in man: theoretical effects of capillary density.

These data indicate that through the reduction in exercise time and recruitment of trained subjects, the exercising muscle in the human dynamic knee-extension model can reach even higher work rates, VO2, and Q than previously reported (Andersen & Saltin, 1985; Andersen et al., 1985; Rowell et al., 1986). Despite these high muscle Q, the achievement of high O2 extractions is possible (Richardson et al., 1993). Previously, this was attributed almost exclusively to the elevated WRMAX, and it was therefore concluded that O2 extraction is not limited by the high Q to any greater extent than in conventional two legged cycle ergometry (Richardson et al., 1993). It is now apparent from the analysis of the data in this paper that it is possible that a difference in capillary density between the subjects in the original studies and the present research may have played a role in the increase in O2 extraction with increasing muscle Q. Although, it should be recognized that a) the capillary density necessary to reduce red cell transit time suitably to match the range of measured femoral venous hemoglobin saturation is high (Gayeski et al., 1988), however it is within the measured values for man (Brodal et al., 1977), and b) where comparable, during low WR knee-extensor exercise and whole body VO2MAX, subjects across the studies did not differ. This would be expected if capillary density differed greatly (Brodal et al., 1977). It can therefore be concluded that both the rapid protocol during knee-extensor exercise and the potential increased capillarity of the trained subjects in the present study may have combined to produce the amplified physiologic and WR responses.

Adult↗
PubMed1992

Ventilation-perfusion relationships in the lung during head-out water immersion.

Water immersion can cause airways closure during tidal breathing, and his may result in areas of low ventilation-perfusion (VA/Q) ratios (VA/Q less than or equal to 0.1) and/or shunt and, ultimately, hypoxemia. We studied this in 12 normal males: 6 young (Y; aged 20-29 yr) with closing volume (CV) less than expiratory reserve volume (ERV), and six older (O; aged 40-54 yr) with CV greater than ERV during seated head-out immersion. Arterial and expired inert gas concentrations and dye-dilution cardiac output (Q) were measured before and at 2, 5, 10, 15, and 20 min in 35 degrees C water. During immersion, Y showed increases in expired minute ventilation (VE; 8.3-10.3 l/min), Q (6.1-8.2 l/min), and arterial PO2 (PaO2; 91-98 Torr; P less than or equal to 0.05). However, O2 uptake (VO2), shunt, amount of low-VA/Q areas (% of Q), and the log standard deviation of the perfusion distribution (log SDQ) were unchanged. During immersion, O showed increases in shunt (0.6-1.8% of Q), VE (8.5-11.4 l/min), and VO2 (0.31-0.40 l/min) but showed no change in low-VA/Q areas, log SDQ, Q, or PaO2. Throughout, O showed more VA/Q inequality (greater log SDQ) than Y (O, 0.69 vs. Y, 0.47).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1992

Pulmonary and leg VO2 during submaximal exercise: implications for muscular efficiency.

Insights into muscle energetics during exercise (e.g., muscular efficiency) are often inferred from measurements of pulmonary gas exchange. This procedure presupposes that changes of pulmonary O2 (VO2) associated with increases of external work reflect accurately the increased muscle VO2. The present investigation addressed this issue directly by making simultaneous determinations of pulmonary and leg VO2 over a range of work rates calculated to elicit 20-90% of maximum VO2 on the basis of prior incremental (25 or 30 W/min) cycle ergometry. VO2 for both legs was calculated as the product of twice one-leg blood flow (constant-infusion thermodilution) and arteriovenous O2 content difference across the leg. Measurements were made 3-5 min after each work rate imposition to avoid incorporation of the VO2 slow component above the lactate threshold. For all 17 subjects, the slope of pulmonary VO2 (9.9 +/- 0.2 ml O2.W-1.min-1) was not different (P greater than 0.05) from that for leg VO2 (9.2 +/- 0.6 ml O2.W-1.min-1). Estimation of "delta" efficiency (i.e., delta work accomplished divided by delta energy expended, calculated from slope of VO2 vs. work rate and a caloric equivalent for O2 of 4.985 cal/ml) using pulmonary VO2 measurements (29.1 +/- 0.6%) was likewise not significantly different (P greater than 0.05) from that made using leg VO2 measurements (33.7 +/- 2.4%). These data suggest that the net VO2 cost of metabolic "support" processes outside the exercising legs changes little over a relatively broad range of exercise intensities. Thus, under the conditions of this investigation, changes of VO2 measured from expired gas reflected closely those occurring within the exercising legs.

Adult↗
PubMed1992

VA/Q distribution during heavy exercise and recovery in humans: implications for pulmonary edema.

Ventilation-perfusion (VA/Q) inequality has been shown to increase with exercise. Potential mechanisms for this increase include nonuniform pulmonary vasoconstriction, ventilatory time constant inequality, reduced large airway gas mixing, and development of interstitial pulmonary edema. We hypothesized that persistence of VA/Q mismatch after ventilation and cardiac output subside during recovery would be consistent with edema; however, rapid resolution would suggest mechanisms related to changes in ventilation and blood flow per se. Thirteen healthy males performed near-maximal cycle ergometry at an inspiratory PO2 of 91 Torr (because hypoxia accentuates VA/Q mismatch on exercise). Cardiorespiratory variables and inert gas elimination patterns were measured at rest, during exercise, and between 2 and 30 min of recovery. Two profiles of VA/Q distribution behavior emerged during heavy exercise: in group 1 an increase in VA/Q mismatch (log SDQ of 0.35 +/- 0.02 at rest and 0.44 +/- 0.02 at exercise; P less than 0.05, n = 7) and in group 2 no change in VA/Q mismatch (n = 6). There were no differences in anthropometric data, work rate, O2 uptake, or ventilation during heavy exercise between groups. Group 1 demonstrated significantly greater VA/Q inequality, lower vital capacity, and higher forced expiratory flow at 25-75% of forced vital capacity for the first 20 min during recovery than group 2. Cardiac index was higher in group 1 both during heavy exercise and 4 and 6 min postexercise. However, both ventilation and cardiac output returned toward baseline values more rapidly than did VA/Q relationships. Arterial pH was lower in group 1 during exercise and recovery. We conclude that greater VA/Q inequality in group 1 and its persistence during recovery are consistent with the hypothesis that edema occurs and contributes to the increase in VA/Q inequality during exercise. This is supported by observation of greater blood flows and acidosis and, presumably therefore, higher pulmonary vascular pressures in such subjects.

Acid-Base Equilibrium↗
PubMed1992

Capillary and fiber geometry in rat diaphragm perfusion fixed in situ at different sarcomere lengths.

To determine the potential range of diaphragm sarcomere lengths in situ and the effect of changes in sarcomere length on capillary and fiber geometry, rat diaphragms were perfusion fixed in situ with glutaraldehyde at different airway pressures and during electrical stimulation. The lengths of thick (1.517 +/- 0.007 microns) and thin (1.194 +/- 0.048 microns) filaments were not different from those established for rat limb muscle. Morphometric techniques were used to determine fiber cross-sectional area, sarcomere length, capillary orientation, and capillary length and surface area per fiber volume. All measurements were referenced to sarcomere length, which averaged 2.88 +/- 0.08 microns at -20 to -25 cmH2O airway pressure (residual volume) and 2.32 +/- 0.05 microns at +20 to +26 cmH2O airway pressure (total lung capacity). The contribution of capillary tortuosity and branching to total capillary length was dependent on sarcomere length and varied from 5 to 22%, consistent with that shown previously for mammalian limb muscles over this range of sarcomere lengths. Capillary length per fiber volume [Jv(c,f)] was significantly greater at residual volume (3,761 +/- 193 mm-2) than at total lung capacity (3,142 +/- 118 mm-2) and correlated with sarcomere length [l; r = 0.628, Jv(c,f) = 876l + 1,156, P less than 0.01; n = 18]. We conclude that the diaphragm is unusual in that the apparent in situ minimal sarcomere length is greater than 2.0 microns.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1992

Effects of training on muscle O2 transport at VO2max.

To quantify the relative contributions of convective and peripheral diffusive components of O2 transport to the increase in leg O2 uptake (VO2leg) at maximum O2 uptake (VO2max) after 9 wk of endurance training, 12 sedentary subjects (age 21.8 +/- 3.4 yr, VO2max 36.9 +/- 5.9 ml.min-1.kg-1) were studied. VO2max, leg blood flow (Qleg), and arterial and femoral venous PO2, and thus VO2leg, were measured while the subjects breathed room air, 15% O2, and 12% O2. The sequence of the three inspirates was balanced. After training, VO2max and VO2leg increased at each inspired O2 concentration [FIO2; mean over the 3 FIO2 values 25.2 +/- 17.8 and 36.5 +/- 33% (SD), respectively]. Before training, VO2leg and mean capillary PO2 were linearly related through the origin during hypoxia but not during room air breathing, suggesting that, at 21% O2, VO2max was not limited by O2 supply. After training, VO2leg and mean capillary PO2 at each FIO2 fell along a straight line with zero intercept, just as in athletes (Roca et al. J. Appl. Physiol. 67: 291-299, 1989). Calculated muscle O2 diffusing capacity (DO2) rose 34% while Qleg increased 19%. The relatively greater rise in DO2 increased the DO2/Qleg, which led to 9.9% greater O2 extraction. By numerical analysis, the increase in Qleg alone (constant DO2) would have raised VO2leg by 35 ml/min (mean), but that of DO2 (constant Qleg) would have increased VO2leg by 85 ml/min, more than twice as much. The sum of these individual effects (120 ml/min) was less (P = 0.013) than the observed rise of 164 ml/min (mean). This synergism (explained by the increase in DO2/Qleg) seems to be an important contribution to increases in VO2max with training.

Adaptation, Physiological↗
PubMed1992

Relationship between body and leg VO2 during maximal cycle ergometry.

It is not known whether the asymptotic behavior of whole body O2 consumption (VO2) at maximal work rates (WR) is explained by similar behavior of VO2 in the exercising legs. To resolve this question, simultaneous measurements of body and leg VO2 were made at submaximal and maximal levels of effort breathing normoxic and hypoxic gases in seven trained male cyclists (maximal VO2, 64.7 +/- 2.7 ml O2.min-1.kg-1), each of whom demonstrated a reproducible VO2-WR asymptote during fatiguing incremental cycle ergometry. Left leg blood flow was measured by constant-infusion thermodilution, and total leg VO2 was calculated as the product of twice leg flow and radial arterial-femoral venous O2 concentration difference. The VO2-WR relationships determined at submaximal WR's were extrapolated to maximal WR as a basis for assessing the body and leg VO2 responses. The differences between measured and extrapolated maximal VO2 were 235 +/- 45 (body) and 203 +/- 70 (leg) ml O2/min (not significantly different). Plateauing of leg VO2 was associated with, and explained by, plateauing of both leg blood flow and O2 extraction and hence of leg VO2. We conclude that the asymptotic behavior of whole body VO2 at maximal WRs is a direct reflection of the VO2 profile at the exercising legs.

Adult↗
PubMed1992

Capillary geometrical changes with fiber shortening in rat myocardium.

Capillary-to-fiber geometrical relations constitute an integral component of peripheral gas exchange. Determination of capillary length and surface area density necessitates quantification of capillary orientation (i.e., tortuosity and branching). In skeletal muscle, capillary tortuosity increases in a curvilinear fashion at reduced sarcomere length, and this compensates for decreased capillary density as fiber cross-sectional area increases. To investigate these relations in myocardium, rat hearts were glutaraldehyde perfusion-fixed in calcium- or barium-induced "systole" to provide varying degrees of fiber shortening. Morphometric techniques were used to analyze capillary geometry in subepicardium (EPI) and subendocardium (ENDO) using 1-micron sections cut transverse and longitudinal to the muscle fiber axis. Capillary density on transverse and longitudinal sections, capillary diameter, fiber cross-sectional area, and sarcomere length were determined in each region. Capillary surface density was computed, and values were related to sarcomere length and compared with published data for diastolic hearts. Sarcomere length in systole ranged from 2.06 +/- 0.03 to 1.35 +/- 0.02 microns (EPI) and from 1.93 +/- 0.04 to 1.44 +/- 0.04 microns (ENDO). Fiber cross-sectional area (EPI, 344 +/- 13 microns2; ENDO, 343 +/- 12 microns2) was significantly larger, and capillary density on transverse sections was significantly smaller (EPI, 4,105 +/- 318 mm-2; ENDO, 4,145 +/- 267 mm-2) than in hearts arrested in diastole. Compared with skeletal muscle, capillary tortuosity was substantially less increased by fiber shortening. Capillary tortuosity and branching did not differ between EPI and ENDO and contributed a maximum of 33% (range, 13-33%) to capillary length density and surface area at a sarcomere length of 1.45 +/- 0.04 microns. Compared with diastolic hearts, capillary length density decreased on average by 19.6% (EPI) and 17.7% (ENDO); similarly, capillary surface density decreased 19.9% (EPI) and 13.7% (ENDO). We conclude that, with fiber shortening in the heart, fiber cross-sectional area increases and capillary numerical density decreases as predicted from reduced sarcomere length. Combined with the minimal geometrical changes of the capillary bed at shorter fiber lengths, this results in a lower capillary length and surface area per fiber volume in systole. Consequently, the structural potential for O2 diffusion into myocytes is determined, in part, by fiber length.

Animals↗
PubMed1991

Contribution of exercising legs to the slow component of oxygen uptake kinetics in humans.

Rates of performing work that engender a sustained lactic acidosis evidence a slow component of pulmonary O2 uptake (VO2) kinetics. This slow component delays or obviates the attainment of a stable VO2 and elevates VO2 above that predicted from considerations of work rate. The mechanistic basis for this slow component is obscure. Competing hypotheses depend on its origin within either the exercising limbs or the rest of the body. To resolve this question, six healthy males performed light nonfatiguing [approximately 50% maximal O2 uptake (VO2max)] and severe fatiguing cycle ergometry, and simultaneous measurements were made of pulmonary VO2 and leg blood flow by thermodilution. Blood was sampled 1) from the femoral vein for O2 and CO2 pressures and O2 content, lactate, pH, epinephrine, norepinephrine, and potassium concentrations, and temperature and 2) from the radial artery for O2 and CO2 pressures, O2 content, lactate concentration, and pH. Two-leg VO2 was thus calculated as the product of 2 X blood flow and arteriovenous O2 difference. Blood pressure was measured in the radial artery and femoral vein. During light exercise, both pulmonary and leg VO2 remained stable from minute 3 to the end of exercise (26 min). In contrast, during severe exercise [295 +/- 10 (SE) W], pulmonary VO2 increased 19.8 +/- 2.4% (P less than 0.05) from minute 3 to fatigue (occurring on average at 20.8 min). Over the same period, leg VO2 increased by 24.2 +/- 5.2% (P less than 0.05). Increases of leg and pulmonary VO2 were highly correlated (r = 0.911), and augmented leg VO2 could account for 86% of the rise in pulmonary VO2.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1990

Experimental support for the theory of diffusion limitation of maximum oxygen uptake.

The four experiments summarized above demonstrate that there is a strong relationship between both measured muscle venous PO2 and calculated mean muscle capillary PO2 and VO2max. This is true for whole body or exercising muscle VO2max, and is seen both in isolated canine gastrocnemius and intact man. This behavior is exactly what would be expected if the diffusing properties for oxygen in skeletal muscle play a constraining role in setting maximum VO2. These data therefore support the hypothesis we advanced (Wagner, 1988a; Wagner, 1988b), that it is a quantitative integrative relationship between convective and diffusive phenomena that combine to set maximum VO2. A specific prediction of this integrative hypothesis (i.e., the non-uniqueness of VO2max as a function of convective oxygen delivery) was confirmed (Experiment 3). While at this point in time phenomena such as perfusion heterogeneity and muscle shunts cannot be quantitatively taken into account in such analyses, the remarkable concurrence between expectations of the hypothesis and experimental data continue to lend support to the basic idea that maximum VO2 is not limited by any single step of the oxygen transport pathway from atmosphere to mitochondria, but rather by the way in which each and every step combines with every other step to determine oxygen supply.

Animals↗
PubMed1990

The effects of training on the metabolic and respiratory profile of high-intensity cycle ergometer exercise.

The tolerable work duration (t) for high-intensity cycling is well described as a hyperbolic function of power (W): W = (W'.t-1) + Wa, where Wa is the upper limit for sustainable power (lying between maximum W and the threshold for sustained blood [lactate] increase, theta lac), and W' is a constant which defines the amount of work which can be performed greater than Wa. As training increases the tolerable duration of high-intensity cycling, we explored whether this reflected an alteration of Wa, W' or both. Before and after a 7-week regimen of intense interval cycle-training by healthy males, we estimated ( ) theta lac and determined maximum O2 uptake (mu VO2); Wa; W'; and the temporal profiles of pulmonary gas exchange, blood gas, acid-base and metabolic response to constant-load cycling at and above Wa. Although training increased theta lac (24%), mu VO2 (15%) and Wa (15%), W' was unaffected. For exercise at Wa, a steady state was attained for VO2, [lactate] and pH both pre- and post-training, despite blood [norepinephrine] and [epinephrine] ([NE], [E]) and rectal temperature continuing to rise. For exercise greater than Wa, there was a progressive increase in VO2 (resulting in mu VO2 at fatigue), [lactate], [NE], [E] and rectal temperature, and a progressive decrease for pH. We conclude that the increased endurance capacity for high-intensity exercise following training reflects an increased W asymptote of the W-t relationship with no effect on its curvature; consequently, there is no appreciable change in the amount of work which can be performed above Wa.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1990

Effects of hypoxia on capillary orientation in anterior tibialis muscle of highly active mice.

The plasticity of capillary orientation in response to combined hypoxic hypoxia and high activity levels was investigated in anterior tibialis muscle of Japanese waltzing mice (Mus wagneri rotans). Following 2 weeks of normobaric, normothermic hypoxia (PIO2 congruent to 87 Torr), muscles were perfusion-fixed in situ with glutaraldehyde and analyzed morphometrically. Muscles from hypoxic waltzers, HW, were compared with those from normoxic waltzers, NW, and normoxic control mice, N. At sarcomere lengths from 2.84 to 1.69 microns, tortuosity and branching increased capillary length 3 to 38%. When capillary orientation was related to sarcomere length, muscles from HW were not different from NW or N. At group-averaged sarcomere lengths of 2.22 microns (HW), 2.33 microns (NW) and 2.35 microns (N), tortuosity and branching contributed 16,20 and 18% respectively, to capillary length. We conclude that high activity levels under normoxic or hypoxic conditions in Japanese waltzing mice do not augment muscle capillary length by means of increased capillary tortuosity and/or branching.

Animals↗
PubMed1990

Analysis of capillary geometry in rat subepicardium and subendocardium.

The sustained high-energy turnover of cardiac muscle presents a formidable challenge to the O2 delivery systems. One major determinant of blood-tissue gas exchange potential is capillary surface area per volume of muscle fiber, Sv(c,f). Estimation of Sv(c,f) necessitates quantification of capillary orientation. Capillary geometry was analyzed systematically in subepi- (epi) and subendocardium (endo) of glutaraldehyde perfusion-fixed rat heart (n = 4). On 1-micron sections cut rigorously transverse and longitudinal to the muscle fiber axis we determined capillary number per fiber square millimeter on transverse, QA(0), and longitudinal, QA(pi/2), sections, capillary diameter, d(c), fiber cross-sectional area, a(f), and sarcomere length, l. Sv(c,f) was computed as pi.d(c).Jv(c,f), where Jv(c,f) is capillary length per fiber volume determined on the basis of a directional distribution model of capillary segments (Fisher axial). Analysis of capillary density, QA(alpha), in sections taken at angles alpha [from 0 to 90 degrees (pi/2) to fiber axis] showed that the Fisher axial distribution provides a good fit to capillary segment orientation in cardiac muscle. No systematic difference was found in fiber size (epi = 269.7 +/- 28.9, endo = 283.8 +/- 16.3 microns 2), capillary diameter (epi = 4.9 +/- 0.3; endo = 4.5 +/- 0.2 microns), Jv(c,f) (epi = 6,302 +/- 558; endo = 5,957 +/- 492 mm-2), or capillary surface per volume of muscle fiber (epi = 968.1 +/- 76.5; endo = 838.2 +/- 93.0 cm-1) between epi and endo. Contribution of capillary tortuosity and branching to Jv(c,f) ranged from 6-27% (epi) and 8-21% (endo) over the small ranges of l considered (epi = 2.09-2.23; endo = 2.04-2.17 microns).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1989

Muscle fiber size and chronic exposure to hypoxia.

Sarcomere length is practically never considered when fiber size and dependent variables are compared between muscles or experimental conditions. Because of the direct dependence of fiber cross-sectional area on muscle shortening, it is imperative to normalize measurements of fiber size, and related variables (e.g. capillary number/mm2 of fiber) to sarcomere length. We examined the relationship between fiber cross-sectional area and sarcomere length in muscles of animals chronically exposed to high altitude (deer mice, Peromyscus maniculatus, native to 3800 m, and rats, Sprague-Dawley, kept at the same altitude for 5 months) compared to sea-level controls. We found no difference in fiber cross-sectional area, normalized to sarcomere length, between high altitude and control animals in either species. It has been demonstrated that sarcomere length can vary by as much as 30-44% and 43-76% in biopsy and perfusion-fixed muscles, respectively. Therefore, identifying relatively small changes in fiber size in response to a given experimental condition in such material without normalizing for sarcomere length is difficult if not impossible. Furthermore, if the conditions of the investigation induce differences in sarcomere length between experimental and control animals, artifactual changes in fiber cross-sectional area will be produced.

Altitude↗
PubMed1989

Fitness as a determinant of oxygen uptake response to constant-load exercise.

Exercise performed above the lactate threshold (OLa) produces a slowly-developing phase of oxygen uptake (VO2) kinetics which elevates VO2 above that predicted from the sub-OLa VO2-work rate relationship. This phenomenon has only been demonstrated, to date, in subjects who were relatively homogeneous with respect to fitness. This investigation therefore examined whether this behaviour occurred at a given absolute VO2 or whether it was a characteristic of supra-OLa exercise in a group of subjects with over a threefold range of OLa (990-3000 ml O2.min-1) and peak VO2 (1600-5260 ml O2.min-1). Twelve healthy subjects performed: 1) exhausting incremental cycle ergometer exercise for estimation of OLa (OLa) and peak VO2, and 11) a series of constant-load tests above and below OLa for determination of the VO2 profile and efficiency of work. During all tests expired ventilation, VO2 and carbon dioxide production were monitored breath-by-breath. The efficiency of work determined during incremental exercise (28.1 +/- 0.7%, means +/- SE, n = 12) did not differ from that determined during sub-OLa constant-load exercise (27.4 +/- 0.5%, p greater than 0.05). For constant-load exercise, VO2 rose above that predicted, from the sub-OLa VO2-work rate relationship, for all supra-OLa work rates. This was evident above 990 ml O2.min-1 in the least fit subject but only above 3000 ml O2.min-1 in the fittest subject. As a consequence the efficiency of work was reduced from 27.4 +/- 0.5% for sub-OLa exercise to 22.6 +/- 0.4% (p less than 0.05) at the lowest supra-OLa work rate (i.e. OLa + 20 W, on average).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1989

Skeletal muscle capillary geometry: adaptation to chronic hypoxia.

The potential for gas and metabolite exchange across the capillary bed is determined largely by the capillary length and surface area available for blood-tissue transfer. It has been suggested that chronic exposure to hypoxia increases capillary tortuosity; however, the degree of orientation of capillaries in muscles of sea level animals chronically exposed to hypoxia has never been quantified rigorously. An augmented capillary tortuosity would increase capillary length per volume of muscle fiber, Jv(c,f), irrespective of whether new capillaries are formed. To resolve this issue, female rats (278 +/- 5 g) were maintained for 5 months in a temperate environment at 3800 m (PIO2 = 91 Torr). Capillary tortuosity and Jv(c,f) were estimated from transverse and longitudinal sections in perfusion-fixed M. Soleus and M. Gastrocnemius. Values were compared with weight-matched controls (274 +/- 7 g). Neither capillary density (normalized to sarcomere length 2.1 microns, hypoxic = 1292 +/- 79, control = 1282 +/- 43 mm-2) nor capillary-to-fiber ratio (hypoxic = 2.50 +/- 0.15, control = 2.57 +/- 0.05) were changed after altitude exposure. Capillary tortuosity was a function of sarcomere length in all animals and this relationship was not changed by hypoxia. Capillary length per volume of muscle fiber was unchanged (hypoxic = 1541 +/- 72, control = 1531 +/- 44 mm-2) as was mean capillary diameter. We conclude that chronic exposure to 3800 m does not change capillary tortuosity or surface area in rat M. Soleus or M. Gastrocnemius.

Adaptation, Physiological↗
PubMed1989

Capillary tortuosity in rat soleus muscle is not affected by endurance training.

The total capillary length available for blood-tissue transfer is determined by the number and orientation of the capillaries. Therefore, whether capillary tortuosity changes with exercise training has important implications for peripheral gas exchange. To determine the effects of exercise training on capillary orientation and capillary length per volume of muscle fiber [Jv(c,f)] female rats were trained by treadmill running (30 m/min, up to 60 min/day, 5 days/wk) for 4 wk. Muscles from control and trained rats were perfusion fixed at sarcomere lengths (l) ranging from 1.59 to 2.15 microns, and morphometric techniques were used to estimate capillary orientation and Jv(c,f). Training increased (P less than 0.05) musculus soleus oxidative capacity 35% [as estimated from citrate synthase activity: 24.7 +/- 1.4 to 34.7 +/- 1.0 (SE) mumol.g-1.min-1], capillary-to-fiber ratio 30% (2.17 +/- 0.06 to 2.83 +/- 0.05), and Jv(c,f) 32% (1,886 +/- 73 to 2,496 +/- 180 mm-2). Capillary tortuosity (as determined from comparisons of transverse and longitudinal sections) was a direct function of l in control and trained rats and contributed 17-73% of capillary length above that estimated from capillary counts on transverse sections. We conclude that capillary tortuosity in m. soleus is unchanged by training. Therefore, Jv(c,f) increases as a consequence of increased capillary number. M. soleus citrate synthase activity is best correlated with Jv(c,f) and not with capillary counts on transverse sections. We hypothesize that training-induced muscle changes of capillary geometry improve O2 delivery to skeletal muscle and may therefore alter the metabolic response (e.g., lactate accumulation) to exercise after training.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗