(Hypertension. 2000;35:919.)
© 2000 American Heart Association, Inc.
Scientific Contributions |
Physical Exercise, Aortic Blood Pressure, and Aortic Wall Elasticity and Composition in Rats
From the Laboratoire de Pharmacologie Cardio-vasculaire (N.N., P.K., I.L.-I., J.A.), Faculté de Pharmacie de l’Université Henri Poincaré, Nancy I, France; and Center National de la Recherche Scientifique UMR 5578 (D.D., M.-H.S.), Université Claude Bernard, Lyon, France.
Correspondence to Dr Jeffrey Atkinson, Laboratoire de Pharmacologie Cardio-vasculaire, Faculté de Pharmacie de l’Université Henri Poincaré, Nancy I, 5 rue Albert Lebrun, 54000 Nancy, France. E-mail atkinson{at}pharma.u-nancy.fr
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Abstract |
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Abstract—With a training schedule (8 weeks’ treadmill running at 30 m/min up a 10% incline 5 d/wk for 90 min/day), we investigated whether exercise modifies aortic wall dimensions, composition (calcium and elastin content), or stiffness in normotensive 6-month-old male Wistar WAG/Rij rats. Maximal oxygen uptake was measured in half of the rats (n=10 per group). Wall stiffness was evaluated in the other half (9 trained and 10 untrained) on the basis of changes in thoracoabdominal pressure pulse wave velocity and differences in amplitude between the peripheral and central aortic pressure signals. Experiments were performed in nonanesthetized, unrestrained rats and then after pithing. The impact of exercise on the oxidative capacity of the plantaris muscles was evaluated with the measurement of citrate synthase activity. Training increased maximal oxygen uptake by 34% and citrate synthase activity by 40%. Mean peripheral aortic pressure increased by 6% and 19% in trained rats, under awake and pithed conditions, whereas mean central aortic pressure increased by 16%, after pithing only. All indexes of aortic stiffness were similar in trained and control rats, as were aortic wall dimensions, composition, cardiac mass, and heart rate. In conclusion, physical exercise in young rats appears to have no effect on aortic stiffness.
Key Words: exercise • aorta • elasticity • calcium • rats
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Introduction |
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Medial calcification of the aortic wall leads to the destruction of elastic fibers and an increase in stiffness.1 2 This process can be reversed with pharmacological (chronic treatment with an angiotensin I–converting enzyme inhibitor)2 and with nonpharmacological (exercise3 ) interventions. Matsuda et al3 showed that forced swimming in rats decreased the calcium content of elastin, increased the elastin content of the aortic wall, and improved the aortic wall elastic properties. Exercise training may not be the only element involved. Forced swimming was used, and other components, such as excitement, prolonged submergence (and hence stimulation of the diving reflex), and the maintenance of temperature homeostasis, may have been involved in the cardiovascular changes that were observed. Treadmill running may be a more suitable model that overcomes these difficulties.4
The objective of this study was therefore to measure aortic wall
elasticity and composition in nonanesthetized, freely moving
rats after an 8-week period of treadmill running. Maximal
O2 uptake (
O2
max) was measured in the first experiment, and aortic wall
stiffness was measured in the second.
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Methods |
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Animals and Training
Six-month-old normotensive male Wistar rats (WAG/Rij; Center d’Etudes Atomiques de Saclay) were divided into 2 groups: 21 untrained rats (mean weight 309±10 g) and 20 trained rats (mean weight 316±11 g). Exercise training consisted of running on a motor-driven treadmill (Gymrol SA) at 30 m/min up a 10% incline for 5 days a week. During the first 4 weeks, the duration of exercise was gradually increased from 10 to 90 min/day and then maintained at this level for an additional 4 weeks. At the end of the training period, 10 rats from each group were used for
O2 max measurement.
The remainder were transferred to the facility in Nancy, where
aortic wall mechanics and composition were evaluated. Experiments were
performed in accordance with the guidelines of the European Union and
the French Ministry of Agriculture.
Maximal Oxygen Uptake
The treadmill used for the measurement of maximal oxygen uptake
(O2 max) was placed in an
airtight Plexiglas chamber. Air was drawn through the system with a
vacuum pump; flow rate, which was maintained at 4 L/min, was controlled
daily with a gas meter. A smaller pump delivered airflow to an
O2 analyzer (model OA 137; Servomex) and
a CO2 analyzer (UNOR S.2; Schlumberger)
through a flowmeter (200 mL/min). The treadmill exercise protocol
consisted of a 3-minute warm-up at 10 m/min on a 0% gradient followed
by increases in treadmill speed, gradient, or both every 3 min.
O2 max was defined as the
point at which O2 uptake did not increase with
increasing workload or when the rat stopped running.
Aortic Blood Pressure, Pulse Wave Velocity, Pulse Amplification,
and Wave Reflections in Nonanesthetized, Unrestrained
Rats
Experiments were performed from the third to the fifth day after
the end of the training period. Experiments in untrained rats were
performed 1 week later.
Polyethylene cannulas (0.96/0.58 mm OD/ID) were implanted under 2% halothane/O2 anesthesia, into the descending thoracic aorta, abdominal aorta, and abdominal vena cava.1 5 During the 24-hour recovery period, rats lost 4±1% of their body weight. There were 2 deaths after surgery (1 per group).
At 24 hours after catheterization, the aortic cannulas of nonanesthetized, unrestrained rats were filled with heparinized (5 IU/ml), gas-free 0.15 mol/L NaCl and connected to low-volume pressure transducers (Baxter; Bentley Laboratories Europe) via 15 cm of polyethylene cannula. The frequency response of the whole recording systems (3 cannulas, previously implanted for 24 hours in vivo in a rat aorta, filled with gas-free saline solution plus transducer and amplifier) was evaluated up to 30 Hz with a sinusoidal wave generator6 and compared with that of a Millar Mikro-Tip pressure transducer (0.67 mm, SPR 407; Millar Instruments). The frequency response of the cannula system was flat up to 25 Hz and then slightly underdamped from 25 to 30 Hz (maximal value +7.2±1.2% at 30 Hz, Figure 1, top). Phase lag was slightly but significantly different from 0 (Figure 1, bottom).
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) and polyethylene cannula (
) pressure
recording systems (cannulas were previously implanted for 24
hours in a rat aorta), expressed as variations in amplitude (top: A,
%) and phase lag (bottom: 
, °). *P<0.05 vs
A=100% or The pressure signals were converted into digital form and recorded online at a sampling rate of 256 Hz. After a 30-minute habituation period, baseline parameters were determined on a beat-to-beat basis and averaged over periods of 4 s/min for 1 hour. An algorithm was used to detect the maximal and minimal values of each pressure signal and to calculate the mean aortic blood pressure (mm Hg) on the basis of the waveform area, pulse pressure as the diastolic-systolic difference, and heart rate (bpm) on the basis of a count of the entire number of cycles during the 4-second period.
Pulse wave velocity (cm/s) was calculated as the distance between the 2 cannula tips, measured in situ after postmortem fixation by sticking a damp cotton thread onto the aorta (7.6±0.2 cm [24±1 cm/kg] in untrained rats, 7.5±0.2 cm [24±1 cm/kg] in trained rats, P>0.05), divided by transit time. Transit times (ms) were measured online for each 4-second period (1024 sampling points, 25 heartbeats) with an algorithm that systematically shifted in time the peripheral pressure waveform with respect to the central pressure waveform and determined the value of the time shift that provided the highest correlation.1 5 This is based on least-squares analysis of the differences in the amplitudes of the central and peripheral pressure signals at a given point in time; the analysis was repeated following increments of the peripheral sampling points and the creation of intermediate points with linear interpolation. Because the sampling rate was 1/3.9 ms and 10 intermediate points were created, the theoretical resolution of the calculated transit time was ±0.39 ms (ie, ±2.5% error for a wave traveling at 455 cm/s). In a separate experiment performed on 3 anesthetized adult male Wistar rats, transit times were determined with the same method after the chronic implantation of polyethylene cannulas, which were then replaced with 2 Millar Mikro-Tip pressure transducers (SPR 407). Pulse wave velocity was similar in both cases (polyethylene 598±99 cm/s, Millar 573±53 cm/s, P>0.05, n=60 observations). Pulse wave velocity was used for the calculation of 2 indexes of wall stiffness: elastic modulus and isobaric elasticity (see later).
A third index of wall stiffness, aortic pressure wave amplification, was calculated as the ratio of peripheral aortic pulse pressure to central aortic pulse pressure. This reflects the progressive increase in aortic pulse pressure from central to distal sites, with the abdominal aorta being stiffer than the thoracic aorta. Aortic pressure wave amplification decreases with central aortic stiffening.7 Pulse amplification may also be modified simply because of alterations in peripheral wave reflection, independent of changes in stiffness of the central aorta. To distinguish between the 2 mechanisms, we studied pressure transfer function and wave reflection analysis.
A fourth index of wall stiffness was the pressure transfer function. Fourier analysis was performed on the central and peripheral pressure waveforms recorded during a 4-second period at a mean arterial blood pressure of 100 mm Hg. An arbitrary level of 100 mm Hg, which is lower than the mean of the groups, was chosen so that all animals would be included in the analysis. Power spectra were calculated over the first 5 harmonics. Frequency-dependent amplification was determined by dividing the amplitude of the peripheral pressure signal by the amplitude of the corresponding harmonic of the central pressure signal and plotted versus the harmonic. This relationship is shifted upward and to higher frequency values with central aortic stiffening.7
The possible impact of wall stiffness on end-systolic pressure
was evaluated by measuring wave reflections on the central pressure
signal. Ninety-five percent of the pressure waveforms were of the type
A as defined by Murgo et al,8 and the following
parameters were calculated on type A waveforms during a
1-second period (
6 heartbeats) and averaged: (1) the height from the
shoulder of the reflected wave to the systolic peak (
P,
mm Hg), (2) the augmentation index (the ratio of P to pulse
pressure, %), (3) the travel time of the reflected wave (time from the
foot of the pressure wave to the shoulder [t], ms), and (4) the
left ventricular ejection time (time from the foot of the
pressure wave to the diastolic incisura [LVET], ms). In a
separate experiment (see earlier), the timings of arterial
wave reflections were similar whether they were measured with
polyethylene cannulas or Millar Mikro-Tip pressure transducers (t
30±2 and 35±2 ms, respectively). P was lower when measured with
Millar Mikro-Tip pressure transducers (2±0.3 mm Hg;
P<0.05 versus 6±1 mm Hg when measured with cannula),
but augmentation index was not significantly different, because there
was a simultaneous decrease in central aortic pulse
pressure (Millar, 13±4 and 22±2 mm Hg, P>0.05
versus cannula, 21±4 and 27±2 mm Hg, for augmentation index and
central aortic pulse pressure, respectively).
Aortic Blood Pressure, Pulse Wave Velocity, and Pulse Amplification
in Pithed Rats
Animals were anesthetized with 2%
halothane/O2. A femoral venous cannula was
implanted for the continuous infusion of the
1-adrenoceptor agonist
phenylephrine.9 10 Animals were pithed and
immediately ventilated with a rodent respirator (1.2 mL/100 g, 50
strokes/min; rodent respirator 601; Harvard Apparatus).
Arterial cannulas were connected to the recording system, and baseline aortic blood pressures and pulse wave velocity were measured. Phenylephrine was infused (400 to 800 nmol/kg) so as to raise central aortic mean blood pressure from baseline to the level measured in the nonanesthetized, unrestrained state. Arterial blood pressure and transit time were recorded every 30 seconds for 30 minutes. Values for aortic pulse wave velocity (dependent variable) were expressed as a function of central aortic mean blood pressure (independent variable) according to a linear model; we previously showed that the linear model gives similar results to an exponential model over a range of pressure of 40 to 120 mm Hg (results not shown). "Isobaric elasticity" is defined as the slope relating pulse wave velocity to central aortic mean blood pressure.1 5 9 10
Aortic Wall Composition and Structure, Wall Stress, Elastic
Modulus, and Cardiac Mass
Rats were perfused for 30 minutes at their normotensive central
aortic mean blood pressure levels (measured before pithing) with 10%
formol containing PBS. A 1-cm sample of the thoracic descending aorta
(just below the aortic arch) was excised, immersed in 10% formol,
dehydrated in graded ethanol solutions, and embedded in paraffin.
Sixteen sections (thickness 20 µm) were stained with
hematoxylin-eosin for the determination of aortic internal diameter and
medial thickness (Saisam algorithm; Microvision Instruments).
Elastic modulus and wall stress (106
dyne/cm2) were calculated as
(PWV2 · Di ·
)/h and (CMABP · Di)/2h, from
the Moens-Korteweg and Lamé equations, respectively, where PWV is
baseline pulse wave velocity in awake rats (cm/s),
Di is internal diameter (cm), h is medial
thickness (cm), is blood density (1.05
g/cm3), and CMABP is central mean aortic blood
pressure measured in awake rats (dyne/cm2).
A 0.1-cm sample of the abdominal aorta was removed, and the aortic wall content of the elastin-specific cross-linking amino acids desmosine and isodesmosine (µg/g aortic wet wt) was determined with capillary zone electrophoresis and UV detection after acid hydrolysis.11 Tissue calcium content (µmol/g aortic dry wt) was determined on a 0.5-cm sample of the thoracic descending aorta with atomic absorption spectrophotometry (AA10; Varian Ltd) after mineralization and acid digestion of the tissue.12 The heart was removed, and the left ventricle was dissected free and weighed.
Muscle Enzyme Analysis
The plantaris muscles from both legs were removed from all rats
of both series and processed for citrate synthase (EC 4.1.3.7)
activity. This enzyme is responsive to endurance exercise and was
selected as a marker of the oxidative capacity of the muscle. Tissue
samples (10 mg) were homogenized at 4°C in 0.3 mol/L
phosphate buffer containing 0.05% bovine serum albumin (pH
7.7) with a glass Potter-Elvehjem homogenizer. The
samples were frozen at -80°C and thawed 3 times to disrupt the
mitochondrial membrane. Citrate synthase activity (µmol
substrate · min-1 ·
g-1) was measured spectrophotometrically at
30°C according to Srere.13
Statistics
Values are given as mean±SEM. Linear regression ANOVA was
performed with standard parametric techniques, and results are
expressed as slopes and intercepts. For any given
parameter, missing values per group were 
2. Differences
between groups were evaluated with ANOVA plus the Bonferroni test. A
value of P<0.05 was chosen to indicate statistical
significance.
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Results |
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O2 max and Muscle Citrate
Synthase ActivityO2 max increased by 34%,
from 83±3 mL O2 ·
kg-1 · min-1 in
control rats to 111±3 mL O2 ·
kg-1 · min-1 in
trained rats (P<0.05). Citrate synthase activity of
plantaris muscles in trained rats from the
O2 max series of
experiments was increased by 44% (25±2 versus 17±1 µmol
· min-1 · g-1 in
untrained rats, P<0.05). A similar increase was observed in
the series in which aortic mechanics was measured (+39%, from
19±1 µmol · min-1 ·
g-1 in untrained rats to 26±2 µmol
· min-1 · g-1 in
trained rats, P<0.05).
Aortic Blood Pressures, Indexes of Aortic Wall Stiffness, Wave
Reflection, and Heart Rate in Nonanesthetized,
Unrestrained Rats
During the recording period, rats were calm, and the
values for aortic blood pressure were stable (intraobserver and
interobserver coefficients of variability were <4%). Central aortic
blood pressure values were similar in both groups (Table 1). Peripheral aortic
mean, systolic, and diastolic blood pressures were
significantly increased in trained rats (+6%, +5%, and +7%,
respectively); central and peripheral pulse pressures were
not modified.
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Pulse wave velocity was unchanged after training. Pulse pressure increased by 30% to 35% between central and peripheral aortic recording sites in both groups; pulse amplification values were similar in trained and untrained rats. Frequency-dependent amplification increased up to a maximum at the second harmonic and then decreased at higher harmonics (Figure 2). There were no differences between the 2 groups, and there were no significant differences in intensity or timing of arterial wave reflection (Table 1). The heart rate was unchanged after training.
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) rats.
Aortic Blood Pressures and Isobaric Elasticity in
Phenylephrine-Infused Pithed Rats
Baseline postpithing values for aortic blood pressures, pulse
amplification, heart rate, and pulse wave velocity were significantly
lower than those measured before pithing in all rats (Table 2). Central and peripheral
aortic mean and diastolic blood pressures were greater in
trained than in untrained rats. Heart rate was similar in both groups.
There were no differences in pulse wave velocity, in central and
peripheral pulse pressures, or in pulse amplification
between the 2 groups.
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The continuous infusion of phenylephrine produced a gradual increase in aortic pulse wave velocity and arterial blood pressure. Over the arterial pressure range studied (40– 50 to 110–120 mm Hg), there was a significant linear relationship between the aortic pulse wave velocity (dependent variable) and central aortic mean blood pressure (independent variable). Slopes (3.1±0.4 and 2.8±0.4 cm · s-1 · mm Hg-1) and intercepts (132±22 and 173±27 cm/s) were similar in trained and untrained rats, respectively.
Aortic Wall Composition and Structure, Wall Stress, Elastic
Modulus, and Cardiac Mass
Thoracic aortic geometry (internal diameter, wall thickness, and
wall thickness/internal diameter ratio) was similar in the 2 groups
(Table 3), as were wall stress and
elastic modulus. There was a significant linear relationship between
elastic modulus (dependent variable) and wall stress (independent
variable) that was similar in both groups (slopes 2.7±0.8 and
2.0±0.7, intercepts 0.22±0.96x106 and
0.98±0.79x106 dyne/cm2 in
trained and untrained rats, respectively). Physical training had no
effect on aortic calcium or desmosine-plus-isodesmosine content.
Neither cardiac nor left ventricular mass was significantly
modified with physical training.
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Aortic Wall Structure and Elasticity
Training had no effect on aortic dimensions (length, internal diameter, or wall thickness) or on wall elastin content (as judged from the lack of change in the content of desmosines) or calcium content. The 4 indicators of aortic elasticity (elastic modulus, pulse wave amplification, pressure transfer function, and isobaric elasticity) were similar in trained and untrained rats. The relationship between elastic modulus and wall stress was unchanged.
These results do not confirm the hypothesis of Matsuda et
al3 (see the introduction). The length of the training
period in their experiments (16 weeks) was longer than that of the
present study (8 weeks). In the present study, an 8-week period
of treadmill running was used because such a forced running program is
used to induce modifications of the skeletal muscle function and
aerobic capacity in our laboratory.14 15 Albeit, changes
in the structure and mechanical properties of central arteries can
occur relatively rapidly and over a time span similar to that of the
present study. Structural and functional arterial
alterations can develop in 2 months after the induction of
hypertension16 or elastocalcinosis,1 2 and
these alterations can be reversed equally rapidly.2 16
Furthermore, our training program produced marked increases in
O2 max (+34%) and skeletal
muscle citrate synthase activity. These increases are similar to those
obtained in previous studies, showing that aerobic capacity of the
skeletal muscle is increased after the same training
program14 and that such a program is able to modify the
mRNA expression of uncoupled proteins related to energy dissipation in
skeletal and heart muscles.15
A more plausible explanation for the difference between our results and those of Matsuda et al3 resides in their use of forced swimming as exercise training. As stated in the introduction, such a program has elements other than physical training that may induce cardiovascular changes. Moreover, Matsuda et al3 also reported results obtained after 16 weeks of forced running (at 30 m/min, 60 min/day, 6 d/wk), and in this case, as in the present study, the calcium content of elastin, the elastin content, and the elastic properties of the aortic wall were unaltered.3 All of these observations lead to the conclusion that a forced running program, as currently used to evaluate skeletal muscle conditioning and adaptation of aerobic capacity, does not modify aortic function and mechanics, at least not in young animals.
The lack of an effect of physical training on elasticity and the structure of large elastic arteries agrees with some reports in young or adult humans17 18 but not all.19 20 In the latter reports, however, because athletes were compared with untrained subjects, subjects with certain genetically determined vascular features may be selected out of the general population. Thus, a greater aortic elasticity may be causal rather than an adaptive response to physical exercise.
Cardiovascular Fitness
In the present study, physical exercise did not improve
cardiovascular fitness; heart rate and central aortic
blood pressures were not changed in trained awake rats. In the pithed
preparation, both central and peripheral aortic mean blood
pressures increased after physical training. This suggests that
physical training produced an increase in peripheral
resistance, because perfusion pressure at maximal dilation (which is
the case in the pithed rat) is directly related to the wall-to-lumen
ratio of resistance vessels.21 This merits further
investigation because although some reports suggest that physical
training produces a decrease in vascular resistance,22
other reports do not.23 In the unanesthetized
baseline condition, peripheral aortic mean and
diastolic pressures were also greater in trained rats.
Because aortic dimensions were unaltered, the drop in mean pressure
along the aorta was therefore smaller in trained rats. This may
indicate a smaller cardiac output in trained rats. In the light of this
observation, the lack of resting bradycardia after exercise may
represent an adaptation to maintain stroke volume. Gleeson et
al24 used a program that increases
O2 max by 16% and citrate
synthase activity by 38% and found no resting bradycardia in young
rats. In older animals (18-month-old normotensive WAG/Rij rats), we
observed that 6 weeks’ treadmill running induced resting bradycardia
(377±30 bpm in awake trained rats [n=4], P<0.05 versus
442±3 bpm in control rats [n=6]) and lowered central aortic pulse
pressure (36±4 mm Hg in trained rats, P<0.05 versus
48±3 mm Hg in control rats) with no change in the elastic
properties of the aortic wall (elastic modulus 8.6±4.7
106 dyne/cm2 in trained
rats, P>0.05 versus 3.4±0.5 106
dyne/cm2 in control rats). This pattern of
reduced heart rate and pulse pressure with no change in elasticity
suggests a fall in stroke volume.
Finally, our physical training did not induce cardiac hypertrophy. Some authors have reported an increase in cardiac or left ventricular mass, or both, relative to body weight after physical training.25 26 This has not been confirmed by others.24 It has been suggested that this may be due to a substantial decrease in body weight with relatively little change in cardiac mass.4 27
Wave reflections were similar in trained and untrained rats. It should
be noted, however, that in 95% of waveforms of the central aortic
pulse pressure contour in the untrained rat are characterized by rapid
wave reflection and a large augmentation index such that the wave is of
type A as defined by Murgo et al.8 Therefore, modification
of the reflected wave may be difficult to obtain in rats. One also
cannot exclude the possibility that the pressure recording
system that was used does not allow accurate detection of the
inflection point, which requires the presence of at least the seventh
or eighth harmonic (ie, a frequency component of 50 Hz). If a
second-order underdamped response of the pressure recording
system is assumed (as predicted by the frequency response measured up
to 30 Hz), the components at 50 Hz may well be attenuated, and this may
preclude accurate detection of the inflection point, and explain (not
statistically significant) differences in augmentation index values
obtained with the polyethylene cannula or Mikro-Tip transducer. All of
these arguments may temper our comments regarding wave reflection on
the basis of the augmentation index calculation.
In conclusion, a forced running program that conditions skeletal muscle and increases aerobic capacity does not modify aortic mechanics or improve cardiovascular fitness in young rats.
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Acknowledgments |
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This work was supported by grants from the Foundation "CNP Sport et Santé" (CNP, Paris, France), LIPHA Pharmaceutical Company (Lyon, France), the French Education and Research Ministry (Paris, France), the Regional Development Committee (Metz, France), and the Greater Nancy Urban Council (Nancy, France). Drs Desplanches and Sornay thank Dr Bruno Corman (Center d’Etudes Atomiques de Saclay, Gif sur Yvette, France) for the generous gift of the WAG/Rij rats and Dr Roland Favier (Center National de la Recherche Scientifique UMR 5578, Lyon, France) for his advice and assistance with the maximal oxygen uptake study. Drs Niederhoffer, Kieffer, Lartaud-Idjouadiene, and Atkinson thank Drs René Peslin, Claude Duvivier, and Philippe Giummelly (Institut National de la Santé et de la Recherche Médicale U14 and Laboratoire de Pharmacologie Cardiovasculaire, Faculté de Pharmacie, Nancy, France) for their help with the analysis of the hemodynamic signals. Drs Niederhoffer, Kieffer, Lartaud-Idjouadiene, and Atkinson were part of the EU Biomed network "EureCa."
Received September 21, 1999; first decision October 12, 1999; accepted December 1, 1999.
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