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1Clarenburg Research Laboratory, Departments of Kinesiology, Anatomy and Physiology, Kansas State University, Manhattan, Kansas 66506-5802; and 2Department of Medicine, University of California-San Diego, La Jolla, California 92093-0623
Submitted 25 March 2003 ; accepted in final form 6 May 2003
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ABSTRACT |
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 TOP ABSTRACT METHODSRESULTSDISCUSSIONDISCLOSURESACKNOWLEDGMENTSREFERENCES |
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red blood cell velocity; red blood cell flux; capillary hematocrit; muscle oxygen diffusing capacity; oxygen delivery
O2) at rest and during
exercise (12,
19,
24,
34,
43,
46,
50). Systemic vasoconstriction
is elevated in CHF via elevated sympathetic nervous efferent activity
(48), impaired nitric oxide
(NO)-mediated vasodilation
(28), impaired NO-mediated
attenuation of sympathetic vasoconstriction
(45), and increased levels of
both endothelin (30) and
angiotensin (49). These
considerations imply that, in CHF, skeletal muscle blood flow during exercise
is reduced due to peripheral alterations that are superimposed on the
presiding cardiac insufficiency. This notion is supported by the reduced
capacity of arterioles to dilate in response to increased O2 demand
(10). Furthermore, a recent
investigation (39) reported
that the muscle contraction-induced reduction of venous pressure that augments
blood flow (i.e., muscle pump) concomitant with the onset of contractions in
healthy muscle (38) is
impaired in CHF. Thus, not only reduced
O2, but also slower
O2 kinetics, may be
responsible, in part, for altered muscle metabolic control
(31) and slowed oxygen uptake
(
O2) kinetics
(18,
33,
37) seen at the transition to
a given elevated metabolic demand in CHF patients. The red blood cell (RBC) surface area in contact with the myocyte is considered crucial for transcapillary O2 flux (13, 17). Thus, within the microcirculation, factors such as capillary-to-fiber ratio, the proportion of capillaries supporting RBC flow, and capillary hematocrit (Hctcap; which increases, in part, due to vasodilation; Refs. 25, 27, 36) all contribute to the capacity for O2 to move from the capillary to myocyte [i.e., muscle O2 diffusing capacity (DmO2)]. In resting CHF muscle, this capacity is severely impaired due to both capillary involution (47) and a smaller proportion of capillaries supporting RBC flow (24), although Hctcap remains unchanged due to proportional reductions in capillary RBC velocity (VRBC) and flux (FRBC) (24). However, if vasodilation is either slowed or impaired at the transition to an elevated metabolic demand, then it is possible that Hctcap might be similarly reduced, resulting in a further loss in diffusive O2 movement.
Recently, our laboratory
(11) studied microvascular
PO2 (PmO2) dynamics across the
transition from rest to contractions in muscle from control (C) rats and rats
with moderate left ventricular (LV) dysfunction (i.e., moderate CHF). In C rat
muscle, the fall in PmO2 at contraction onset was
characterized by a time delay followed by a monoexponential fall to
steady-state values, with no sign of an undershoot in
PmO2 (4,
11). Conversely, in CHF
muscle, PmO2 fell more rapidly, demonstrating a
transient undershoot below its contracting steady-state baseline
(11). As
PmO2 represents the dynamic balance between
O2 and
O2, these data were
indicative of a slowed microvascular
O2 response compared with
that for O2
(4). These findings are
consistent with slowed blood flow kinetics [and arteriolar vasodilation
(10)] and unaltered or
slightly reduced oxidative enzyme activities
(2,
8,
11), demonstrated previously
in moderate CHF. The purpose of this investigation was to study the capillary
hemodynamics at rest and in response to electrically induced contractions in
CHF rats and compare these results with data reported previously in C rats
(26). We tested the hypothesis
that capillary VRBC and FRBC kinetics would be
slowed and that the amplitude of these responses would be attenuated in CHF
compared with C muscle contractions.
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METHODS |
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Muscle preparation. The spinotrapezius was prepared in situ with minimal fascial disturbance, according to methods described previously (16, 26). The muscle was then sutured at five equidistant points to a horseshoe manifold. The manifold was attached to a swivel and a muscle-stretching apparatus that permitted precise length changes along the longitudinal axis of the muscle. In addition, this secured the muscle such that, during contractions, the scapula (origin of spinotrapezius) was drawn anteriorly, whereas the caudal region remained in place, thus allowing the capillaries to remain in focus throughout the contraction protocol. Stainless steel plate electrodes (2.5-mm radius) were placed on the dorsal spinotrapezius surface proximal to the motor point (cathode) and along the caudal periphery (anode), facilitating whole muscle, indirect muscle contractions. The rat was placed on a circulation-heated Lucite platform. The spinotrapezius muscle was superfused continuously with a Krebs-Henseleit bicarbonate-buffered solution equilibrated with 95% N2-5% CO2. All exposed surrounding tissue was protected with Saran Wrap (Dow Brands). The muscle was transilluminated, allowing for clear visualization of sarcomeres within the fibers.
Experimental design. Once the muscle was positioned on the
platform, a microvascular field containing (typically) 6-10 capillaries in the
midcaudal (dorsal surface) region of the muscle was selected, and sarcomere
length was set at 
2.8 µm, as verified via direct on-screen
measurement. Resting data were obtained after a 15-min quiescent period.
Thereafter, muscle contractions were elicited (1 Hz, 2-ms duration, 5 V)
for 3 min (model S88, Grass Instruments). Mean arterial pressure (MAP) was
monitored throughout the data-acquisition period. The experimental protocol
was no longer than 1.5-2 h in duration, during which up to 1.5 ml of sterile
isotonic saline were infused intra-arterially to compensate for
dehydration.
Intravital video microscopy. Microcirculatory images were obtained via an intravital video microscope (Nikon Eclipse E600-FN; x40 objective; 0.8 numerical aperture) equipped with a noncontact, illuminated lens and viewed on a high-resolution color monitor (Sony Trinitron PVM-1954Q, Ichinoniya, Japan) under a final magnification of x1,184. This was confirmed by initial calibration of the system by means of a stage micrometer (MA285, Meiji Techno). Images were time referenced by frame and stored on videocassettes (JVC SVHS Master XG) for subsequent off-line analysis (30 frames/s) via a videocassette recorder (JVC BR-S822U).
Off-line analysis. Initially, each microvascular field (i.e.,
capillaries and myocyte boundaries) was traced directly from the screen onto
acetate paper, and the proportion of capillaries supporting RBC flow was
assessed. For all capillaries in which hemodynamics were assessed, capillary
diameter (dc) was measured at two sites per capillary: one
before contractions (resting conditions), and the second within 5 s of the
final contraction. Both VRBC and FRBC were
measured within two 5-s periods before contraction in each intercontraction
period (i.e., relaxation) in which measurements could be made and within the
first 5 s postcontraction. Between contractions, hemodynamic assessment was
possible in 15 frames. VRBC was acquired by following
the RBC path length over several frames. FRBC was measured by
counting the number of cells passing an arbitrary point.
VRBC was measured twice over each 5-s period (pre- and
postcontraction) and once between contractions. FRBC was counted
over a 2-s period within each designated 5-s period pre- and postcontraction
and over the entire time that RBC movement could be assessed between
contractions. For each capillary in which hemodynamic data were gathered,
Hctcap was calculated as
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Statistical analysis. All data are presented as means ± SE. Data distribution was assessed via the Kilmogorov-Smirnov test for normality. Differences between C and CHF groups were tested with Student's t-test. Resting and postcontraction data between groups were tested via a one-way repeated-measures ANOVA. When the F value was significant, the Student-Newman-Keuls post hoc test was utilized for pairwise comparisons. Statistical significance was accepted at the P < 0.05 level.
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RESULTS |
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TOPABSTRACTMETHODSRESULTSDISCUSSIONDISCLOSURESACKNOWLEDGMENTSREFERENCES |
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After completion of the exteriorization procedure, MAP remained constant throughout the experimental protocol (i.e., rest to muscle contractions) for both the C and CHF group of rats (95 ± 6 mmHg). Arterial PO2 was well maintained (arterial PO2 = 98 ± 10 Torr), and systemic hematocrit measured at the end of muscle contractions averaged 47 ± 2% with all rats falling within the typical normal range for these variables.
Muscle fiber and capillary structure. Sarcomere length in CHF and C muscles was set at similar values (P > 0.05) before contractions (C, 2.8 ± 0.1; CHF, 2.8 ± 0.1 µm) and remained unchanged (P > 0.05) after the contraction bout (C, 2.9 ± 0.1; CHF, 2.8 ± 0.1 µm). Muscle fiber width was significantly less (P < 0.05) in CHF (47.2 ± 2.4 µm) compared with C muscle (56.6 ± 4.9 µm). The total number of capillaries (both RBC perfused and impeded) per unit fiber width (i.e., lineal density) was unchanged (P > 0.05) between C and CHF groups (C, 33.3 ± 2.7 vs. CHF, 35.0 ± 2.1 capillaries/mm). The dc was not different (P > 0.05) between C and CHF groups (C, 6.2 ± 0.1; CHF, 6.0 ± 0.1 µm) and was not altered (P > 0.05) by the muscle contractions in either group (C, 6.1 ± 0.1; CHF, 6.0 ± 0.1 µm).
Capillary hemodynamics. 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, which resulted in a significant reduction (P < 0.05) in the lineal density of continuously RBC-perfused vessels. Furthermore, contractions failed to induce significant (P > 0.05) recruitment of previously intermittently RBC-perfused or impeded capillaries in either group of rats, as the proportion of capillaries supporting continuous RBC flow in C and CHF contracting muscle (C, 0.89 ± 0.01; CHF, 0.63 ± 0.03) was similar to that measured at rest. At rest, VRBC (C, 270 ± 62; CHF, 179 ± 14 µm/s) and FRBC (C, 22.4 ± 5.5 vs. CHF, 15.2 ± 1.2 RBCs/s) were reduced (both P < 0.05) in the capillaries supporting continuous RBC flow in CHF compared with C muscle (Figs. 1 and 2). Contractions significantly elevated (both P < 0.05) VRBC (C, 428 ± 47 vs. CHF, 222 ± 15 µm/s) and FRBC (C, 44.3 ± 5.5 vs. CHF, 24 ± 1.2 RBCs/s) in both C and CHF muscle; however, both hemodynamic variables remained significantly (P < 0.05) less in the CHF compared with C group (Figs. 1 and 2). The speed of the VRBC and FRBC increase at contraction onset was slowed in CHF compared with C muscle. Specifically, time to 50% of the increase from baseline to end contractions (amplitude) for both VRBC (C, 8 ± 4; CHF, 56 ± 11 s; Fig. 3) and FRBC (C, 11 ± 3; CHF, 65 ± 11 s; Fig. 4) was significantly longer (P < 0.05) in CHF vs. C. Contractions elicited a significant rise (both P < 0.05) in Hctcap in C and CHF muscle (Fig. 5). Hctcap values were not different (P > 0.05) between the two groups, either at rest (C, 0.16 ± 0.01; CHF, 0.18 ± 0.01) or immediately after the contraction protocol (C, 0.21 ± 0.01; CHF, 0.23 ± 0.01) (Fig. 5). In addition, the speed of the increase in Hctcap from rest in response to muscle contractions was unchanged in CHF compared with C muscle (Fig. 6).
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DISCUSSION |
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TOPABSTRACTMETHODSRESULTSDISCUSSIONDISCLOSURESACKNOWLEDGMENTSREFERENCES |
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O2 on-kinetics in CHF
patients. Consequently, these findings provide a mechanistic explanation for
the PmO2 profiles observed across the
rest-to-contraction transition in muscle from CHF individuals
(11). Experimental model. Based on the elevated LV end-diastolic pressures and unchanged markers of lung congestion, the CHF rats in this investigation were likely in a state of moderate CHF. Thus, as reported previously in our laboratory, it would be expected that these rats would exhibit fiber atrophy (47), capillary involution (47), reduced vascular transport capacity (32), and reduced blood flow at rest (24, 34) and during submaximal exercise (34). Data presented herein confirm each of the above, thereby substantiating the level of CHF severity (i.e., moderate CHF) in the experimental rats. In addition, our laboratory has utilized both sham rats (i.e., same surgical procedures as the CHF rats minus the left main coronary artery suture ligation) and C rats (i.e., similar to those used in this investigation) in previous investigations and have shown that neither resting capillary hemodynamics nor the skeletal muscle blood flow response to exercise is significantly altered by the sham procedure (24, 26, 44). Thus only data from C rats were reported in this investigation.
CHF in rats vs. humans. Technological and ethical limitations
preclude determination of muscle microcirculatory hemodynamics at the onset of
contractions in humans. The rat model of CHF is well accepted and possesses
several significant advantages over other models. 1) The level of
physical activity is unaltered between C and CHF rats
(42). 2) The elapsed
duration post-MI is known and can be controlled. 3) Corollary
diseases that potentially confound experimental results and their
interpretation, such as hypertension, Type 2 diabetes, and emphysema, which
pervade the human CHF population, are not manifested. 4) Unlike
humans, the post-MI rat is not subjected obligatorily to a barrage of
pharmacological interventions that includes angiotensin-converting enzyme
inhibitors, 
-blockers, anti-arrhythmics, diuretics, and vasodilators.
Thus it may be argued that the rat model of CHF as utilized herein facilitates
investigation of the uncontrolled manifestations of the disease.
Acknowledgment must be made, however, that, in humans, the muscle
microcirculatory and functional deficits may be ameliorated by the longevity
of the condition (humans may remain in stable CHF for many years) and
therapeutic and lifestyle interventions. The present investigation presents a
foundation from which to investigate the specific mechanisms for CHF-induced
dysfunction and evaluate the microcirculatory consequences and efficacy of
therapeutic interventions.
Capillary hemodynamics at the rest-to-contraction transition. A large body of literature exists that demonstrates that CHF reduces skeletal muscle blood flow at rest and during steady-state exercise in most (12, 19, 24, 34, 43, 46, 50), but not all (41), instances. Neural, humoral, and mechanical mechanisms that may explain these decrements have been studied extensively, and the reader is referred to the original papers (e.g., Refs. 28, 30, 39, 45, 48, 49).
Bulk blood flow to skeletal muscle increases in an immediate and biphasic
manner at exercise onset. The first phase is thought to arise primarily as a
result of the muscle pump
(38), in contrast to the
second phase, usually initiated 15-20 s after exercise onset, which is thought
to be dependent on vasodilatory mechanisms and metabolic feedback control
(7,
40). Whereas the elevation of
bulk muscle blood flow and
O2 in response to an
elevated metabolic rate is important, determination of the temporal and
spatial distribution of RBCs within the capillary network is key to
understanding blood-myocyte O2 exchange. The data presented herein
demonstrate, for the first time, that the capillary hemodynamic responses in
skeletal muscle of CHF rats are slowed considerably (compared with C) at the
transition from rest to electrically induced rhythmic contractions.
Specifically, whereas VRBC is elevated within 2 s in C
muscle, no increase was evident for 30 s in the CHF muscle
(Fig. 3). As
VRBC increased in such a short time frame in C muscle, it
seems likely that the initial increase was due, primarily, to the muscle pump.
However, the muscle pump effect was either mitigated or nonexistent in CHF
muscle (Figs. 3 and
4). These findings support
those of Shiotani et al. (39),
where the muscle pump contribution to femoral artery blood flow was reduced
significantly in CHF patients compared with matched control subjects. The
underlying factors responsible for this are likely to include venous
congestion and constriction
(49), reduced venous vascular
capacity (32), or reductions
in muscle mass, as demonstrated in previous studies from our laboratory
(8,
47) and corroborated in the
present investigation (i.e., fiber width was reduced 17% in the CHF rats
compared with C). A biphasic capillary FRBC response is clearly
evident in the C muscle (Fig.
4), which fits well with that reported for bulk blood flow
(40). A phase I or immediate
response for FRBC appears nonexistent in the CHF muscle at
contraction onset, further supporting the lack of a muscle pump effect. In
addition, the time course for the increase in the FRBC is
significantly slowed in CHF compared with C muscles, suggesting that
arteriolar vasodilation, while present, occurs more gradually.
The present investigation suggests that the onset, speed, and magnitude of vasodilation are impaired at exercise onset in CHF. To date, the relative importance of neural (48), NO-related (28, 45), and humoral (30, 49) factors contributing to this response in CHF remains to be determined. However, previous investigations have provided evidence that the sympathetic nervous system is significantly activated (48), resulting in elevated levels of plasma norepinephrine in CHF rats, both at rest and during exercise (35). Considering that skeletal muscle arterioles are extremely sensitive to vasoconstrictive hormones that are commonly elevated in the CHF condition (i.e., angiotensin II, arginine vasopressin, and endothelin) (9), the possibility exists that a high level of vasoconstrictor tone exists in the CHF rat that contributes to the very slow hyperemic response found in the present investigation. In addition to possible increases in vasoconstrictor tone, there is substantial evidence that the relative contribution of endothelial-mediated vasodilators is reduced in the skeletal muscle of rats with CHF. In this regard, our laboratory has shown that the relative contribution of NO to the skeletal muscle blood flow response to exercise is attenuated in CHF rats (19). Moreover, Didion and Mayhan (10) have shown that skeletal muscle arteriolar reactivity to acetylcholine and calcitonin gene-related peptide is impaired in CHF rats, whereas the arteriolar reactivity to sodium nitroprusside is not. These results suggest that endothelial-mediated vasodilation is diminished in CHF rats, whereas vascular smooth muscle reactivity remains intact. Finally, McAllister and colleagues (32) have shown that postcapillary resistance is elevated significantly in skeletal muscle of rats with CHF, which is associated with a reduction in the vascular flow capacity. These findings are consistent with the hypothesis that sodium and fluid retention, along with peripheral tissue edema formation, may be contributing to the attenuated vasodilator capacity of the skeletal muscle (i.e., increased "vascular stiffness" induced by sodium and fluid retention in the vascular smooth muscle) (51). In addition, the increases in skeletal muscle postcapillary resistance, along with the significant increases in central venous pressure found in CHF, may be mechanistically linked to the reduction and/or elimination of the muscle pump effect in contracting muscle of CHF rats. In conclusion, the factors that are contributing to the very slow capillary hemodynamic response found in the CHF rat appear to be multifactorial, and elucidation of their relative importance will contribute substantially to our mechanistic understanding of the vascular dysfunction prevalent in CHF.
Implications for blood-myocyte O2 flux
during exercise. Honig and colleagues
(20) reported that there was a
substantial recruitment of previously non-RBC-perfused capillaries in response
to muscle contractions. This large increase was not corroborated in subsequent
investigations (e.g., Refs. 6,
21). As the majority of
capillaries support continuous RBC perfusion at rest under control conditions
(5,
25,
26), one would not consider
capillary recruitment a viable method for augmenting the size of the capillary
RBC-to-myocyte interface thought crucial for achieving a given O2
flux (13,
17). However, as a significant
proportion of capillaries do not support continuous RBC flow in CHF
(24), recruitment of these
vessels might represent one feasible mechanism for increasing
DmO2 and thus blood-myocyte O2 flux during
contractions. However, under neither C nor CHF conditions was there a
significant "capillary recruitment" with muscle contractions. A
secondary mechanism by which DmO2 could be increased is
via augmented Hctcap. Indeed, muscle contractions did induce a
significant increase in Hctcap in both groups
(Fig. 5) and across the
rest-to-contraction transition the kinetic profiles for Hctcap were
not different between groups (Figs.
5 and
6). As a whole, both diffusive
[lineal density of RBC-perfused capillaries (decreased) x
Hctcap (unchanged)] and conductive (FRBC x lineal
of density of RBC-perfused capillaries)
O2 are severely limited
in CHF compared with C muscle.
Inferences for slowed
O2
on-kinetics in CHF. The unequivocal identification of a single,
rate-limiting step for O2
kinetics at the transition to an elevated metabolic demand has remained
elusive. Whereas Hughson and colleagues
(22,
23) have demonstrated that
reducing O2 may slow
O2 kinetics, it has been
difficult to demonstrate a speeding of the response with increased
O2, particularly at
moderate-intensity exercise
(14,
29). Moreover, in healthy
humans, Grassi et al. (15) and
Bangsbo et al. (3) have shown
that bulk muscle O2 is in
apparent excess (or, at least, adequate) at the immediate transition to
moderate- and severe-intensity exercise. Thus a muscle
O2 limitation does not
appear to constrain O2
kinetics in healthy individuals. It has long been recognized that, at the
onset of a given absolute exercise workload, CHF patients demonstrate slowed
O2 kinetics compared with
healthy control subjects (18,
33,
37). The present results and
those of Diederich et al. (11)
suggest that the kinetics of
O2 at exercise onset in
CHF muscle are so slow that the site of
O2 kinetics limitation in
CHF muscle shifts from the oxidative machinery to
O2 (see Ref.
4 for a detailed discussion on
this issue). Moreover, data presented herein suggest that both significant
spatial and temporal impairments in O2 availability exist within
contracting skeletal muscle in CHF, and this further supports the notion that
a O2 limitation may be
responsible, in part, for slowed
O2 on-kinetics seen in
CHF patients.
Conclusions. In the present investigation, intravital microscopy
techniques were employed to study capillary hemodynamics at rest and during
contractions in C and CHF rat spinotrapezius muscle. Conductive
(FRBC) and diffusive (proportion of RBC-perfused capillaries)
O2 were reduced, both at
rest and during contractions, in the CHF compared with C muscle. Furthermore,
the speed of the rise in VRBC and FRBC at
contraction onset was slowed in the CHF condition, probably indicative of
impaired muscle pump function and a slowed vasodilatory response. These data
provide an underlying mechanism that explains the altered muscle metabolism
(i.e., increased phosphocreatine breakdown) and slowed
O2 on-kinetics manifested
at the onset of a given bout of exercise in individuals with CHF.
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DISCLOSURES |
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ACKNOWLEDGMENTS |
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TOPABSTRACTMETHODSRESULTSDISCUSSIONDISCLOSURESACKNOWLEDGMENTSREFERENCES |
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FOOTNOTES |
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The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.
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REFERENCES |
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TOPABSTRACTMETHODSRESULTSDISCUSSIONDISCLOSURESACKNOWLEDGMENTSREFERENCES |
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O2 on blood flow dynamics
at onset of forearm exercise. J Appl Physiol
81: 1619-1626,
1996.O2 kinetics in heavy
submaximal exercise by hyperoxia and prior high-intensity exercise.
J Appl Physiol 83:
1318-1325, 1997.This article has been cited by other articles:
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,
n = 20 capillaries from 4 muscles, Ref.
,
n = 20 capillaries from 4 muscles) rats from rest (time = 0) over a
3-min contraction bout. B: proportional changes as a result of muscle
contractions normalized to resting values. Time to 50% of the peak amplitude
was significantly faster (P < 0.05) in the C compared with CHF
muscle.
