265
Clinical Science ( 1 989) 77,265-272
Effects of meal composition on the postprandial blood
pressure, catecholamine and insulin changes in elderly
subjects
J. F. POTTER, D. HESELTINE, G. HARTLEY*, J. MATTHEWST, I. A. MACDONALDS
AND 0. F. W. JAMES
Departments of Geriatric Medicine, *Dietetics and tMedical Statistics, University of Newcastle upon Tyne, Newcastle upon Tyne, U.K.,
and $Department of Physiology and Pharmacology, Medical School, Queen’s Medical Centre, Nottingham, U.K.
(Received 18 October 1988/6 February 1989; accepted 13 February 1989)
SUMMARY
1. The effects of four meals of similar energy, but
different nutritional, composition on postprandial blood
pressure, heart rate, autonomic function, catecholamines,
insulin and packed cell volume levels were studied in
seven fit elderly subjects.
2. The high carbohydrate and high protein meals led
to a significant overall fall in supine systolic and diastolic
blood pressure compared either with no change or a rise
after the normal (i.e. mixed) and high fat meals. Similar
between-meal differences were seen with erect diastolic
but not erect systolic blood pressure. No significant
postural blood pressure fall occurred after any of the
meals. Supine heart rate was unaffected by meal type or
by time, and although erect heart rate showed a small
increase during the study there was no between-meal
difference.
3. Parasympathetic function was unaffected by meal
type. Plasma noradrenaline rose after the high carbohydrate and mixed meals only, remaining elevated for 120
min after meal consumption. This increase was not
related to the changes in blood pressure or plasma insulin
levels.
4. Plasma insulin and glucose rose after the high
carbohydrate and mixed meals, but were unchanged after
the high protein and high fat meals. Packed cell volume
showed a small decrease towards the end of the study,
although there was no between-meal variation.
5. The differences in the cardiovascular changes after
the different meals could not be ascribed to alterations in
autonomic function, insulin release or fall in plasma
volume. We propose that the postprandial changes in
blood pressure are due to the nutrient composition of the
meal rather than the actual energy load.
Correspondence: Dr J. F. Potter, University Department of
Geriatric Medicine, Leicester General Hospital, Leicester LE5
4PW, U.K.
Key words: ageing, autonomic function, catecholamines,
insulin, postprandial blood pressure.
Abbreviations: CHO, carbohydrate; DBP, diastolic blood
pressure; NA, noradrenaline; PCV, packed cell volume;
SBP, systolic blood pressure; SED, standard error of the
difference; SNS, sympathetic nervous system.
INTRODUCTION
Ageing alters the normal homoeostatic responses to
certain cardiovascular stresses [ 1, 21. This has recently
been highlighted by reports showing that marked postprandial falls in blood pressure occur in both fit [3]and
institutionalized [4] elderly subjects, but not in young
subjects [ 5 , 61. The exact clinical effects of these blood
pressure changes in old people are, as yet, speculative, but
could be important in the pathogenesis of falls, post-meal
angina or even stroke.
Several reports have documented the fall in blood
pressure which occurs after meals without attempting to
establish the underlying mechanisms responsible [3, 61.
Plasma insulin [7, 81, glucose [9] and gut peptides [lo]
could cause a fall in blood pressure by a direct vasodilatory effect on splanchnic and skeletal muscle vessels,
and it has been proposed that insulin may also reduce
blood volume [ 111. The largest postprandial falls in blood
pressure occur in subjects with autonomic dysfunction
[ 121. Autonomic, including baroreceptor, activity is
known to become impaired with increasing age [ 131and is
further compromised by raised blood glucose levels [ 141.
Thus the postprandial cardiovascular changes may be
secondary to an alteration in autonomic control. Whatever the initial cause of the reduction in blood pressure,
the elderly appear to be unable to maintain an adequate
homoeostatic reflex response.
J. F. Potter et al.
266
From the results of previous work it is uncertain
whether the postprandial fall in blood pressure seen in the
elderly is due solely to the calorie load or is dependent
upon the nutrient and electrolyte composition or bulk of
the meal. In fact many of the studies have used nonphysiological calorie loads, i.e. pure glucose [5, 151,
fructose or xylose drinks [ 161.
This present study was undertaken both to investigate
the possible physiological mechanisms whereby postprandial hypotension occurs in the elderly and to define
the relative importance of different 'meal factors' in
producing these changes.
METHODS
Subjects
Seven fit, ambulant, community-living volunteers
[mean age 70.7 zk 1.9 (SEM) years, range 61-77 years] were
drawn from local pensioners' clubs. Subjects were
screened to exclude hypertension [systolic blood pressure
(SBP)2 160 mmHg and/or diastolic blood pressure
(DBP)2 95 mmHg ( 21.3/12.6 kPa)], ischaemic heart
disease, cerebrovascular disease, autonomic neuropathy
(by standard methods [ 17]), postural hypotension (SBP
fall > 20 mmHg (2.7 kPa)] and diabetes mellitus. None
was taking any medication at the time of the study and all
were within 10% of ideal body weight [mean 68.8 f 3.9
(SEM) kg, range 49.5-80 kg, Quetelet index 24.0 zk 1.0
(SEM) kg/m-*]. All subjects gave their informed consent
and the study was approved by the local Joint Ethical
Committee.
Protocol
Each subject was studied on four separate occasions at
least 3 days apart. On the morning of each study, subjects
were allowed a light breakfast (taken at least 5 h before
the study), having avoided caffeinated products, smoking
and alcohol for 12 h before the study. Subjects were asked
to micturate before being weighed; they then rested
supine and an intravenous cannula was inserted retrogradely into a superficial hand vein and kept patent by
flushing with heparinized saline (Hepsal CP Pharmaceuticals). The hand and forearm were placed in a electrically
heated thermostatically controlled box at 55°C to obtain
arterialized venous blood samples. Subjects rested supine
for 6 0 min before entering the study.
Blood pressure and heart rate were recorded in the
other arm using a semi-automatic recorder (Dinamap
1100; Critikon, Tampa, FL, U.S.A.), taking the mean of
three readings on each occasion. Autonomic function was
assessed by the standard methods of Ewing & Clarke [ 171.
The heart rate variation during deep breathing was
measured using a standard paper-recording electrocardiograph set at 5 cm/s with the subjects having a set
respiratory rate of 6 breaths/min. Subjects timed this
using a clock with a second hand, readings being taken on
the third of such inspiratory/expiratory cycles. The
maximum expiratory and minimum inspiratory R-R
intervals were measured using a ruler during each respiratory cycle (the expiration/inspiration ratio). The heart rate
response to standing unaided was also noted, measuring
the shortest R-R interval at around the beat 15 and the
longest R-R interval at around beat 30 (the 30:15 ratio).
Erect blood pressure was taken 2 min after standing.
All subjects were familiarized with the protocol before
any measurements were taken and they rested supine
between measurements. At 30 and 15 min before entry
into the study, haemodynamic measurements were made
and at time 0 (baseline)blood was also taken for measurement of packed cell volume (PCV), plasma osmolality,
blood glucose, plasma insulin, plasma noradrenaline (NA)
and plasma adrenaline. Subjects then received in a
double-blind, randomized cross-over fashion, one of the
four different meals. These were matched as closely as
possible: all consisted of chicken, vegetables and potatoes
(see Table 1) so that they were isocaloric (2420 kJ) with
similar sodium, potassium and calcium contents. The
electrolyte content was balanced by the use of supplements given in 100 ml of water with each of the meals.
Meals were consumed sitting over a 10-15 min period,
the time when the subjects finished being noted. They
then rested supine and the first postprandial measurements were taken 15 min after finishing the meal. Haemodynamic and autonomic function measurements were
made every 15 niin for the first 60 min then at 90 and 120
min. Blood samples were taken supine at 30, 60, 90 and
120 min. The hand was kept constantly in the heated
compartment until the end of the study.
Table 1. Energy and electrolyte content of the four test meals
Each of the four meals contained 2420 kJ. Sodium, potassium and calcium supplements were
given so that each meal contained 370 mg of sodium, 1800 mg of potassium and 460 mg of
calcium.
Meal type.. . High CHO
Carbohydrate(%oftotal energy)
Fat (% of total energy)
Protein ("/o of total energy)
Sodium (mg)
Potassium (mg)
Calcium (mg)
Fibre (g)
72
7
21
330
1841
456
11
High fat
19
66
15
243
613
89
3
High protein
Mixed
17
30
53
368
1458
325
6
49
21
24
299
1504
244
8
Postprandial blood pressure in the elderly
Assay methods
267
RESULTS
Catecholamine samples were taken into chilled
tubes containing ethyleneglycolbis(aminoethylether)tetraacetate and glutathione, spun at 4°C and then stored at
- 80°C. Duplicate samples were assayed by h.p.1.c. with
electrochemical detection, using the modified method of
Macdonald & Lake [18]. Sensitivity for NA was 0.05
nmol/l and for adrenaline 0.08 nmol/l, with an interassay
coefficient of variation of 8.4% for N A and 13.9% for
adrenaline. Plasma insulin was measured by the method
of Soeldner & Slone [ 191with an interassay coefficient of
variation of 7%. PCV was measured with a Coulter
counter and had a coefficient of variation of 1%. Blood
glucose was measured by the glucose oxidase method
(Camlab) and osmolality by depression of freezing point
using an automatic micro-osmometer (Camlab).
Statistical analysis
Results are presented as means fSEM and 95% confidence intervals are also given where indicated. The differences between the responses to the meals were
analysed in two ways. First, the profiles for each subject
within each pre-defined supine and erect time zone were
summarized by calculating the area under the curve for
each variable (by the trapezium method) divided by the
duration of the time zone. This gives an overall summary
statistic for each subject covering the whole study period
for that meal. The differences of these mean values from
baseline were compared by two-way analysis of variance.
Secondly, the maximum changes within the 120 min study
period were compared by analysis of covariance, using
the baseline value as a covariate. Where an overall difference was detected, differences between diets were
assessed by t-tests using the standard error of the difference ( SED) as calculated from the residual mean square
from the analysis of variance. Pearson correlation coefficients were also calculated.
Postprandial blood pressure and heart rate responses
All subjects consumed each of the four meals completely; none experienced any adverse side effects.
There were no significant differences between baseline
supine and erect blood pressures before the four meals,
although overall erect heart rates were higher than supine
( + 6 beats/min, 95% confidence interval + 4 to + 8
beats/min, P < 0.0 1, Table 2).
,The supine blood pressure and pulse rate changes over
the 120 min study period are shown in Fig. 1. There was a
significant between-meal effect on supine SBP ( P < 0.01).
After the high fat meal there was an overall rise in supine
SBP of + 5 mmHg (0.7 kPa) (95% confidence interval - 1
to + 1 1 mmHg) compared with a fall of - 6 mmHg (0.8
kPa) ( - 12 to 0 mmHg) with the high carbohydrate
(CHO) meal ( P < O . O l ) . The changes in supine DBP also
differed between meals (P<O.O5); after the mixed meal
there was a rise of + 2 mmHg (0.3 kPa) ( - 2 to + 6
mmHg) but a fall of - 5 mmHg (0.7 kPa) ( - 9 to - 1
mmHg) after the high CHO meal ( P < 0.05). There were
no differences between the high CHO and the high
protein meals in supine SBP or DBP. Supine heart rate
remained unchanged during the 120 min study period
with no between-meal variation.
Erect DBP (Fig. 2) showed a similar between-meal difference (P<O.Ol). The high CHO meal led to the largest
overall fall, - 8 mmHg (1.1 kPa) ( - 13 to + 3 mmHg),
smaller falls occurring after the high protein and mixed
meals, compared with a + 1 mmHg (0.1 P a ) ( - 3 to + 5
mmHg) increase with the high fat meal ( P < 0 . 0 5 ) . Postprandial erect SBP showed no statistically significant
between-meal effects, although at 60 min (the time of
maximum change) after the high CHO meal there was a
mean fall of - 14 mmHg (1.9 kPa) ( - 20 to - 8 mmHg)
compared with a rise of + 4 mmHg (0.5 kPa) ( - 4 to + 12
mmHg) with the high fat meal. Erect heart rate, although
Table 2. Baseline supine and erect blood pressures and heart rate for each of the four meals (high
CHO, high fat, high protein and mixed, i.e. normal)
Data are presented as mean f SEM ( n = 7). Ranges are given in parentheses. Baseline supine and
erect blood pressures were similar, although overall erect heart rates were greater than supine
( P < 0.01). To convert mmHg to kPa, divide by 7.5.
Meal type.. .
Supine
SBP (mmHg)
DBP (mmHg)
Heart rate (beats/min)
Erect
SBP (mmHg)
DBP (mmHg)
Heart rate (beats/min)
CHO
High fat
High protein
Mixed
123f4
(1 11- 136)
71 f 3
(60-78)
58+ I
(56-62)
122f4
(106-138)
74+3
(62-88)
57f 1
(51-62)
122f4
(109-138)
69f4
(52-84)
59f 1
(54-65)
126f4
(112-140)
69f4
(64-82)
60f2
(49-68)
121f5
124f2
(116-132)
73f4
(56-86)
65f2
(58-70)
125f2
(117-136)
77f4
(66-90)
64f2
(58-76)
122f4
(109- 134)
77f5
(60-88)
63fl
(58-67)
( 104- 138)
75f5
(61-94)
61 f 2
(57-72)
J. F. Potter et al.
1
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a
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+lo-
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n--,
+5-
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9-
-5-
.9z
5
+lor
0-
-10-15-15L
/-
-30
1
30
1
I
60
Time after meal (min)
0
90
120
Fig. 1. Changes from baseline in supine SBP, DBP and
pulse rate during the 30 min run-in period and for 120
min after the four meals (m, high CHO; 0,high fat; 0,high
protein; 0 , mixed, i.e. normal). Values are means fSEM for
seven subjects. Occasional SEM bars are omitted for
clarity. To convert mmHg to kPa, divide by 7.5.
0
io
60
I
I
90
120
.
Time after meal (min)
Fig. 2. Changes from baseline in erect SBP, DBP and
pulse rate after the four meals (m, high CHO; 0,high fat;
high protein; 0 , mixed, i.e. normal). Values are
means fSEM. Occasional SEM bars are omitted for clarity.
To convert mmHg to kPa, divide by 7.5.
0,
showing a small rise with time, did not differ between
meals.
The maximum changes in blood pressure and heart
rate seen during the study period with each of the four
meals are illustrated in Table 3. There was a significant
between-meal effect on maximum supine SBP fall
( P < 0.001), being greater after the high CHO [ - 13
mmHg ( 1.7 kPa), - 19 to - 7 mmHg] than the high fat
diet [0 mmHg, - 6 to + 6 mmHg, P<O.Ol) or mixed
meals [ - 7 mmHg (0.9 kPa), - 13 to - 1 mmHg,
P < 0.051, but not the high protein meal [ - 9 mmHg (1.2
kPa), - 15 to - 3 d g ] . There was no statistical difference in the maximum fall in DBP or the heart rate
changes between meals. The maximum drop in erect
DBP, however, did differ between meals ( P < 0.02), being
greater after the high CHO meal [ - 1 1 mmHg (1.5 kPa),
- 16 to - 6 mmHg] than either the high fat [ - 4 mmHg
(0.5 kPa), - 9 to + 1 mmHg, P<O.O5] or high protein
[ - 5 mmHg (0.7 kPa), - 10 to 0 mmHg, P<0.05]but not
the mixed [-8 mmHg (1.1 kPa), - 1 3 to - 3 mmHg]
meal. Erect SBP and heart rate did not differ between
meals and there was no difference in the maximum rises in
supine or erect blood pressure or heart rate between
meals.
No subject showed a postural SBP fall of more than 20
mmHg (2.7 kPa) after any meal. This resulted from both
erect and supine blood pressures falling to a similar extent
such that SBP and DBP were maintained on standing.
Maximum haemodynamic changes occurred within 45-60
min of finishing the meal in all cases.
Parasympatheticand sympathetic function
Parasympathetic function was assessed by two
standard methods. All subjects had baseline values within
the normal age standardized range [20], with a coefficient
of variation for baseline values for the four meals of 3.3%
for the expiration/inspiration ratio and 7.9%for the 30:15
ratio (Table 4). There was no difference between meals
over the study period for each of the two methods used.
Baseline supine plasma NA levels for all four meals were
similar (Fig. 3). However, there was a significant difference in the NA response to the four meals (P<O.Ol):
the high C H O and mixed meals resulted in similar
responses with a maximum increase of 74% and 72%,
respectively. Plasma NA levels were little changed after
the high fat or high protein meals, with a significant difference between the response to the high CHO and mixed
meals compared with the high fat or high protein meals
(P<0.05).After 120 min plasma NA levels were still
rising after the C H O meal, but reached a peak at 90 min
with the mixed meal, although NA levels were still higher
than baseline values at the end of the study (P<O.O5).
269
Postprandial blood pressure in the elderly
Table 3. Maximum changes in blood pressure and heart rate during the 120 min study period after each of the four meals
(high CHO, high fat, high protein and mixed, i.e. normal) for the seven elderly subjects
Values given are means with SED as calculated from the analysis of covariance. Where an overall difference was found,
differences between the diets were calculated using t-tests with the SED: *P<0.05, **P< 0.01. Abbreviation: NS, not
significant. To convert mmHg tokPa, divide by 7.5.
Baseline
High
CHO
meal
High
fat
meal
High
protein
meal
Mixed
meal
SED
P
114
131
63
74
57
63
116
134
67
77
57
64
2.6
3.4
2.2
3.8
1.2
2.0
< 0.00 1
117
133
4.2
3.6
NS
NS
67
77
64
77
2.2
2.4
1.2
3.2
< 0.02
*
Supine
SBP (mmHg)
123
DBP (mmHg)
71
Heart rate (beats/min)
59
Erect
SBP (mmHg)
123
DBP (mmHg)
75
Heart rate (beats/min)
65
I
Fall
Rise
Fall
Rise
Fall
Rise
321- ;
125
61
71
58
66
133
65
75
56
62
Fall
Rise
107
I24
I15
133
I15
64*
71
70
73
68
79
83
63
73
81
66
73
Fall
Rise
Fall
Rise
I34
NS
NS
NS
NS
NS
NS
NS
NS
Table 4. R-R interval changes between expiration/inspiration and for the 30: 15 ratio during the
120 min study period after the four meals (high CHO, high fat, high protein and mixed, i.e.
normal) for the seven elderly subjects
Values are means (SEM). No significant between-meal differences were seen with either test of
parasympathetic activity. All baseline values were within normal age standardized ranges [20].
Time (min)... 0
15
30
R-R ratio interval changes between expiration/inspiration
1.13
1.14
1.1 1
High CHO
(0.01)
(0.02)
(0.01)
High fat
1.18
1.13
1.12
(0.03)
(0.03)
(0.03)
High protein
1.15
1.12
1.13
(0.02)
(0.02)
(0.01)
Mixed
1.14
1.1 1
1.1 1
(0.01)
(0.01)
(0.01)
R-R ratio interval change for the 30: I5 ratio
High CHO
1.06
1.04
(0.03)
(0.02)
High fat
1.1 1
0.97
(0.04)
(0.04)
High protein
1.11
1.07
(0.03)
(0.03)
Mixed
1.08
1.01
(0.03)
(0.03)
1.01
(0.01)
1.04
(0.04)
1.09
(0.03)
1.04
(0.03)
Plasma adrenaline levels showed no change with meal
composition or time.
Changes in plasma insulin, plasma glucose and PCV
Plasma insulin changes with the four meals are shown
in Fig. 4. Baseline values were similar. although peak
levels were higher and occurred later, at 6 0 min, with the
high CHO and mixed meals than with the high protein
and fat meals. There was a significant difference in overall
insulin response between meals ( P < 0.0 1): the high CHO
45
60
90
120
1.10
(0.01)
1.09
(0.02)
1.1 1
(0.03)
1.12
(0.01)
1.13
(0.03)
1.13
(0.03)
1.13
(0.02)
1.09
(0.01)
1.12
).
(0.01
.
1.15
(0.03)
1.12
(0.03)
1.12
(0.01)
1.05
(0.02)
1.03
(0.04)
1.05
(0.02)
1.08
(0.02)
1.15
(0.01)
1.01
(0.02)
1.04
(0.03)
1.08
(0.03)
1.07
(0.02)
1.1 1
(0.01)
1.14
(0.01)
1.00
(0.03)
1.06
(0.05)
1.07
(0.02)
1.12
(0.01)
1.15
(0.01)
1.07
(0.03)
1.05
(0.04)
1.07
(0.02)
1.10
(0.03)
meal resulted in a greater increase than either the mixed
( P < 0.02), high protein or high fat ( P < 0.01) meals.
Although the patterns of the insulin and NA response
curves to each meal were similar, there was no significant
correlation between the actual levels or the changes in
insulin and NA. Baseline blood glucose levels were again
similar for all four meals and reached maximum levels at
30 min after the meal (Table 5). As expected, the high
CHO meal produced the highest blood glucose levels but
mean levels were only minimally raised after the high
protein meal; there was a significant between-meal effect
270
J. F. Potter et al.
31
O J d /
0
1
I
I
30
60
90
t
120
Time after meal (min)
Fig. 3. Changes in supine plasma NA after the four meals
(m, high CHO; 0,high fat; 0,high protein; 0 , mixed, i.e.
normal). Values are means fSEM.
50
-
40
-
30
-
20
-
10
-
T
P
,
0
/
1
0
30
I
60
I
1
90
120
Time after meal (min)
Fig. 4. Changes in insulin levels after the four meals (u,
high CHO; 0,high fat; 0, high protein; 0 , mixed, i.e.
normal). Values are means fSEM.
(P<0.05). At the end of the study blood glucose had
returned to basal levels with all except the high C H O
meal. Osmolality showed the largest rise after the high
CHO meal but there was no significant overall meal
effect. PCV showed a small fall with both the mixed and
high CHO meals; the greatest changes occurred between
90 and 120 min after the meals, but again no overall differences between meals was found.
DISCUSSION
As far as we are aware this is the first study to assess the
effects of differing meal composition on the postprandial
cardiovascular changes in old people. After the high CHO
and high protein meals there were similar reductions in
both supine and erect blood pressure, the normal (i.e.
mixed) meal led to a less pronounced fall, whereas after
the high fat meal there was either no change or a small
overall rise in blood pressure. None of the meals
appeared to impair orthostatic control of blood pressure
and no subject developed a significant postural blood
pressure drop. Despite the fall in blood pressure with the
high CHO and high protein meals, there were no changes
in supine heart rate and although erect heart rate
increased (especially after the high CHO intake) there was
no overail between-meal effect on heart rate. The postprandial fall in blood pressure appears therefore to be
dependent on the nutritional composition of meal and not
the actual calorie load.
Previous studies in the elderly have shown that blood
pressure decreases after a normal meal in both fit and
institutionalized subjects when compared with a control
period when no food is taken [3, 211; thus the changes in
blood pressure in the present study are not likely to be
due solely to repeated measurements or failure to achieve
a stable baseline blood pressure. This fall is dependent on
age, the largest changes occurring in the elderly [5,6] and
on the energy load being taken orally and not intravenously [ 151. The blood pressure fall may result from a
decrease in plasma volume or total peripheral resistance
without a full compensatory increase in cardiac output.
Gundersen & Christensen [ 1 11 suggested that insulin decreased plasma volume by causing a loss of intravascular
water and albumin, although others have failed to confirm
these findings [8]. Plasma volume changes were not
measured directly, but PCV fell rather than increased
after the high CHO, high protein and mixed meals (and
remained unchanged after the high fat meal). It is unlikely
therefore that plasma volume decreased. We did not
measure total peripheral resistance but this has been
shown to fall after meals [22, 231. Lipsitz et af. [4] also
noted that the elderlv failed to increase heart rate with a
fall in blood pressure after a meal, although this has not
been shown in all postprandial studies IS]. This lack of a
comDensatorv increase in heart rate mav result from an
age-related impairment of baroreceptor function [ 131,
which is further compromised by the elevated blood
glucose levels [14]. Ageing per se also decreases
myocardial inotropic [24] and chronotropic responses to
B-adrenergic stimulation or stress [25].
As the largest falls in postprandial blood pressure
occur in subjects with an autonomic neuropathy, and autonomic activity is known to decrease with age, it is possible
that the postprandial fall in blood pressure in this study
was due to impairment of autonomic control. We found
only small changes in cardiac parasympathetic activity
with no between-meal differences. Similarly, no differences were seen in the postural change in blood
pressure after the four meals, although this is only a crude
guide to sympathetic impairment. Plasma NA levels, a
better indicator than postural change in blood pressure of
postprandial sympathetic nervous system (SNS) activity,
were markedly increased after the high CHO and mixed
meals but little changed after the high fat and high protein
meals. This rise in plasma NA after the high CHO and
mixed meals was similar to that reported in other postprandial studies in elderly subjects. Welle et al. [26] also
Postprandial blood pressure in the elderly
noted a rise in NA after glucose but not after a high fat or
high protein intake. The increase in NA may thus be
related to changes in glucose or insulin, as NA levels were
only minimally elevated after the high protein and high fat
meals in which changes in plasma glucose and insulin
were small. It is improbable, however, that the rise in NA
is due solely to SNS stimulation resulting from the fall in
blood pressure, as NA levels were still rising at 120 min
after the high C H O meal when the blood pressure had
returned to baseline values. Furthermore, plasma NA
levels were unchanged after the high protein meal despite
a similar fall in blood pressure to that seen after the high
CHO meal.
Insulin can stimulate the SNS during euglycaemia [27],
as well as antagonizing the actions of NA [28]. Both
insulin and NA levels increased after the high C H O and
mixed meals, but there was no relationship between the
changes in the two variables. Jansen et af. [ 5 ] noted, in
elderly normotensive subjects, a fall in mean arterial
pressure after glucose, but not fructose, although both
calorie loads produced similar NA responses. They also
found a greater increase in plasma insulin after glucose
than after fructose, so it seems unlikely the rise in NA is
due primarily to an insulin-mediated stimulation of the
SNS. Finally, the elevated NA levels could be due to
diminished clearance, secondary to the elevated blood
glucose levels (insulin does not appear to alter NA
clearance rates [27]),although this has not been formally
studied and is unlikely as splanchnic blood flow will be
increased postprandially.
The variation in insulin response after the four meal
types reflects the differences in the postprandial blood
glucose levels. As the fall in blood pressure after the high
CHO and high protein meals was similar despite marked
difference in insulin levels, it seems unlikely that the postprandial changes are due directly to insulin. The findings
of Jansen & Hoefnagels [ 151support this view. They gave
271
similar energy loads (in the form of glucose) orally and
intravenously, but only after the oral load did blood pressure fall, despite similar insulin levels being produced in
both studies. We cannot exclude the role of vasoactive
gut-associated peptides, such as neurotensin, released due
to the direct effect of nutrients on the gut, as a cause for
the postprandial cardiovascular changes seen. Hoeldtke et
af [29] found that a somatostatin analogue blocked the
postprandial hypotensive effect, but were unable to
identify any gut hormone responsible. However, their
findings could be explained by a direct pressor effect of
somatostatin analogue. One possible. hypothesis for the
postprandial fall in blood pressure in the elderly is as a
result of an increase in splanchnic blood flow and a fall in
total peripheral resistance induced by certain gut peptides
or by insulin. This fall is not fully compensated for by an
increase in heart rate, perhaps due to a resetting of baroreceptor activity (either due to elevated insulin and/or
glucose levels). However, it is unlikely that there is
marked baroreceptor impairment as heart rate still
increased on standing after the meals. This failure to
increase heart rate despite the fall in blood pressure and
increase in NA levels may be compounded by an insulininduced antagonism of the action of NA, especially its
chronotropic action on the heart [30].The high C H O and
high protein meals that caused the greatest postprandial
falls in blood pressure could have different hypotensive
mechanisms, i.e. the high protein meal may lead to a more
marked increase in splanchnic blood flow [31], whereas
the high CHO meal with the subsequent greater increases
in NA, insulin and glucose levels may alter baroreceptor
activity o r lead to an insulin-mediated impairment of NAinduced vasoconstriction.
In conclusion, we have found that isocaloric high CHO
and to a lesser extent high protein or normal (mixed)
meals result in a postprandial fall in blood pressure in fit
elderly subjects, whereas a high fat meal causes no such
Table 5. PCV, osmolality and blood glucose changes during the 120 min study period after the
four test meals (high CHO, high protein, high fat and mixed, i.e. normal) in the seven elderly
subjects
Results are shown as means k SEM.
Tirne(min)...
0
30
60
90
120
0.394 f 0.0 10
0.391 fO.O1l
0.399 f 0.008
0.390 f 0.0 1 1
0.399 f 0.0 10
0.394f0.010
0.403 f 0.0 1 I
0.386 f 0.009
0.394 f 0.0 I0
0.394f0.010
0.399 f 0.009
0.383 It 0.008
0.388 f 0.0 1 1
0.390f0.01 I
0.394 f 0.009
0.377f0.011
0.382 f 0.0 11
0.391 f0.013
0.389 f 0.0 1 1
0.378 f 0.008
PCV
Mixed
High fat
High protein
High CHO
Plasma osmolality (mosmol/kg)
Mixed
293 f 3
High fat
292 f 2
High protein
295 f 3
High CHO
291 + 3
Blood glucose (mrnol/l)
Mixed
5.2 f 0.5
High fat
4.9 f 0.4
High protein
5.4 f 0.4
High CHO
5.2 f 0.3
29452
295 f 2
295 f 2
296 f 2
7.6 f 0.6
6.2 f0.4
6.3 f 0.5
8.8 f 0.5
296+3
294 f 2
297 f 2
296 f 2
7.2 f 0.8
6.2 f0.6
5.8 f 0.6
8.5f 1.1
244s
293 f 2
295 f 2
294f2
6.4 f 0.6
5.4 k 0.6
5.1 f 0 . 3
7.5 1.0
+
293 f 2
293 f 2
295 f 2
293 f 2
5.9 f 0.5
5.2 f 0.4
5.0 f 0.3
6.6 f 0.5
272
J. F. Potter et al.
decrease. The mechanisms for these changes are unclear,
but d o not appear to be due to alterations in autonomic
function, insulin release or a fall in plasma volume. In
these healthy elderly subjects postprandial orthostatic
control of blood pressure was unaffected. However, such
blood pressure changes in the 'frail' elderly and in those
with autonomic impairment may be clinically important
as a cause of dizziness, falls and post-meal angina, and
may perhaps explain some of the diurnal variation in
cerebral thrombosis [32].
ACKNOWLEDGMENTS
We thank Miss P. A. Craik for typing the manuscript, and
the dietitians at Freeman Hospital for their help in preparing the meals.
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