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Vol. 83, Issue 6, 2019-2028, December 1997
1 Applied Exercise Science
Laboratory, ABSTRACT Crouse, Stephen F., Barbara C. O'Brien, Peter W. Grandjean,
Robert C. Lowe, J. James Rohack, and John S. Green. Effects of
training and a single session of exercise on lipids and apolipoproteins in hypercholesterolemic men. J. Appl.
Physiol. 83(6): 2019-2028, 1997.
lipoproteins; high-density-lipoprotein cholesterol; low-density-lipoprotein cholesterol; triglyceride
INTRODUCTION ENDURANCE EXERCISE is widely recommended in the
treatment paradigm of various hyperlipoproteinemias for its putative
antiatherogenic action on circulating lipids and apolipoproteins and to
improve cardiorespiratory fitness, which may lower atherosclerotic risk independent of lipids and other risk factors (12, 25). Support for this
practice, however, is largely based on research in normocholesterolemic subjects. Training studies in hypercholesterolemic subjects are rare,
and lipid results are inconclusive (19, 28, 29). Indeed, the generally
held notion that exercise training by previously sedentary,
normocholesterolemic individuals invariably results in beneficial
changes in blood lipids is not beyond dispute. Although training of
sufficient volume and duration may promote modest increases in blood
concentrations of high-density-lipoprotein (HDL) cholesterol (HDL-C),
HDL2-C,
HDL3-C, and apolipoprotein (apo)
A-I, as well as decreases in triglycerides (TG) (7, 10, 32, 38),
negligible changes in these blood constituents after training have been
reported with a considerable degree of regularity (7, 10). Explanations
advanced for these discordant findings include interstudy differences
in subject pretraining lipid concentrations, diet, weight loss, body
composition, and training volume and intensity (7, 10, 34). In addition
to these explanations, the timing of blood collection after the most
recent training session could influence study outcomes. It is apparent
that the energy demands of a single session of endurance exercise can
transiently alter lipid metabolism, causing measurable changes in
circulating lipid and apolipoprotein concentrations, as well as changes
in the distribution of lipids among lipoproteins, which persist for
hours or days after exercise. Lower blood total cholesterol (TC), TG,
and low-density-lipoprotein (LDL) cholesterol (LDL-C) concentrations,
along with higher HDL-C and
HDL2-C, all changes often
attributed to training, have been measured in trained individuals
immediately and up to 72 h after completion of exhaustive physical
exercise (9, 10, 22, 31). Because the time of blood sampling was either
not controlled or occurred Whether the transient lipid response itself is altered by training is
another dimension of this problem. Qualitatively different transient
changes in lipids and apolipoproteins have been shown to occur after a
single session of exercise in trained compared with untrained normo-
and hypercholesterolemic individuals (4, 22, 26). This naturally leads
to the conjecture that training influences lipid metabolism and that
the effect is manifested, at least in part, as an altered transient
response. This hypothesis has not been tested in a longitudinal
training study. Thus the primary objective of our study was twofold:
1) to differentiate between
transient (acute) and training (chronic) effects of exercise on blood
lipid and apolipoprotein concentrations in hypercholesterolemic men and
2) to determine the extent to which
the transient response is altered by training.
We recently reported that intensity of exercise did not influence the
transient changes in lipid and apolipoprotein concentrations that
occurred up to 48 h after exercise in untrained, hypercholesterolemic men (4). This does not, however, rule out the possibility that after
training the transient response is modified by the intensity at which
exercise is performed. Support for this notion is provided by the
findings that larger postexercise increases in HDL-C concentrations may
occur in trained runners after high- compared with low-intensity exercise (15, 17). Thus a secondary purpose of our study was to test
the hypothesis that, after training, relatively greater postexercise
changes in lipids and apolipoproteins, particularly a greater rise in
HDL-C, would occur after a single session of high- compared with
moderate-intensity exercise.
MATERIALS AND METHODS Subjects
Procedures
ABSTRACT
INTRODUCTION
MATERIALS AND METHODS
RESULTS
DISCUSSION
ACKNOWLEDGEMENTS
FOOTNOTES
REFERENCES
To differentiate
between transient (acute) and training (chronic) effects of exercise at
two different intensities on blood lipids and apolipoproteins (apo), 26 hypercholesterolemic men (cholesterol = 258 mg/dl, age = 47 yr, weight = 81.9 kg) trained three times per week for 24 wk, 350 kcal/session at
high (80% maximal O2 uptake,
n = 12) or moderate (50% maximal
O2 uptake, n = 14) intensity. Serum lipid and
apolipoprotein (apo) concentrations (plasma volume adjusted) were
measured before and immediately, 24, and 48 h after exercise on four
different occasions corresponding to 0, 8, 16, and 24 wk of training.
Data were analyzed using three-way repeated-measures multivariate
analysis of variance followed by analysis of variance and Duncan's
procedures (
= 0.05). A transient 6% rise in
low-density-lipoprotein cholesterol measured before training at the
24-h time point was no longer evident after training. Triglycerides
fell and total cholesterol, high-density-lipoprotein cholesterol
(HDL-C), HDL3-C, apo A-I, and apo
B rose 24-48 h after exercise regardless of training or intensity.
Total cholesterol, HDL3-C, apo
A-I, and apo B were lower and
HDL2-C was higher after training
than before training. Thus exercise training and a single session of
exercise exert distinct and interactive effects on lipids and
apolipoproteins. These results support the practice of training at
least every other day to obtain optimal exercise benefits.
48 h after the last training session in
the majority of published training-lipid studies, findings attributed
to training may have been confounded by transient changes in blood
lipid concentrations induced by recent exercise. On the basis of these
findings, it can be logically proposed that the lipid benefit of
exercise arises, at least in part, from a transient lipid response to
the most recent episode(s) of exercise. This proposition has been
advanced by Holloszy et al. (18) and later by Haskell (16), but we are
aware of no published training studies in which it has been tested,
even though it has important relevance for exercise recommendations to
improve public health.
90% of all supervised training sessions; only data from these 26 subjects are included in the analyses. Eighteen of the 26 men could be
classified as having high blood cholesterol (>240 mg/dl) and 8 as
having borderline-high blood cholesterol (200-239 mg/dl) on the
basis of the pretraining assessment of lipids (24). The molecular basis
for cholesterol elevation was not determined for any of the subjects.
However, the suggestion of a heritable trait for hypercholesterolemia
was evident for 2 of the 26 subjects, who self-reported blood relatives
with known high blood cholesterol on the medical history screening
instrument used in the study. Of the 11 subjects who were lost to
follow-up, 3 men relocated, 6 gave time conflicts as reason for
dropping out, and 2 developed physical problems that prohibited cycle
ergometer exercise. Lipid and physiological characteristics of the 11 dropouts were not different before training from the 26 men who
completed the study (t-test,
P > 0.05).
O2 max)] or high (80%
O2 max)-exercise-intensity
group, and completed the pretraining experimental exercise protocol.
The men began their individualized training program within 1 wk of
completing the experimental exercise protocol. All testing procedures
were repeated after 8, 16, and 24 wk of training. In general,
pretraining and posttraining blood sampling procedures were matched for
time of day (±1 h). Exercise was withheld for 60-72 h before
the preexercise blood sample was drawn at the beginning of each
experimental exercise protocol (Fig. 1).
Fig. 1.
Schematic of general study protocol. Pre ex, preexercise; IPE,
immediately postexercise; +24 h, 24 h after exercise; +48 h, 48 h after
exercise; O2 max, maximal
O2 uptake.
[View Larger Version of this Image (24K GIF file)]
O2 max was defined as
the highest observed O2 uptake
(ml/min). At least two of the following criteria were required for the
exercise test to be considered valid:
1) achievement of maximum heart rate within 10 beats/min of the age-predicted maximum,
2) rating of perceived exertion
>18, 3) respiratory exchange ratio
>1.1 at maximal exertion, or 4)
O2 uptake plateau, despite further
increases in workload.
Experimental exercise protocol.
Subjects reported to the laboratory in the morning after a 12-h fast
(water allowed ad libitum), and preexercise blood samples were drawn
after 5 min of seated rest (blood collection procedures described
below). Within 10 min of collection of the preexercise blood sample,
subjects began exercise on a stationary cycle ergometer. The exercise
protocol consisted of three successive 1-min rides at 15, 30, and 60 W
for warm-up followed by exercise at their assigned intensity (moderate
or high) for a duration required to expend 350 kcal of energy. Duration
(min) was determined by dividing 350 kcal by the rate of energy
expenditure (kcal/min) at the required exercise intensity. The rate of
energy expenditure was calculated from the
energy-O2 equivalent (23) at the
respiratory exchange ratio corresponding to 50 and 80%
O2 max. Respiratory gas exchange, exchange ratio, heart rate, and blood pressure were measured at 10-min intervals throughout the exercise session, and the
workload was adjusted as necessary to maintain the prescribed intensity. Blood samples were obtained immediately postexercise (IPE,
i.e., 5 min postexercise), then again 24 (+24 h) and 48 h (+48 h) later
(time of day controlled ±1 h). All exercise was discontinued for 48 h after the completion of the experimental exercise session until all
postexercise blood sampling procedures were completed.
Blood sampling and biochemical analysis.
After 5 min of seated rest, blood was drawn without stasis from an
antecubital vein into 15-ml Vacutainer tubes containing a separation
gel with a clot activator (no. 6432, Becton Dickinson). Hematocrit and
hemoglobin concentrations were determined in duplicate in fresh whole
blood and were used to estimate changes in plasma volume after the
experimental exercise session (8). Serum was isolated within 3 h of
collection at 4°C by centrifugation (1,500 g for 30 min). HDL and
HDL3 were separated from aliquots
of serum by precipitation (14, 35). Serum and the HDL and
HDL3 fractions were frozen at
60°C.
Aliquots of frozen serum samples collected during the
experimental exercise protocol (4 samples/subject) were thawed
within 2 wk of the completion of each training period (pretraining and 8, 16, and 24 wk) and analyzed for concentrations of TC, TG,
HDL-C, and HDL3-C (1, 3).
Serum HDL2-C concentration was
calculated as the difference between HDL-C and
HDL3-C; LDL-C was estimated (13).
All samples for apo A-I and apo B testing were thawed and analyzed
after completion of the study (27). Samples from each subject were
analyzed in the same analytic run, and assays were performed in
duplicate, then averaged for statistical analysis. Internal quality
control was maintained during each analytic run using serum of known
lipid and apolipoprotein content. No differences in the average lipid
values of the control serum among the four study training periods
(pretraining and 8, 16, and 24 wk) were significant [analysis of
variance (ANOVA), P > 0.05],
indicating that laboratory drift over the 24-wk study was negligible.
Interassay coefficients of variation were 6% for HDL-C and
HDL3-C, 4.8% for TC, 7.9% for
TG, 3.2% for apo A-I, and 3.6% for apo B.
Exercise training.
Exercise training consisted of riding a cycle ergometer at 50%
O2 max for the
moderate-intensity group or 80%
O2 max for the
high-intensity group 3 days/wk for 24 wk (72 supervised training sessions). The rate of energy expenditure, workload, and duration of
the exercise sessions were calculated from
energy-O2 equivalents as described
for the experimental exercise protocol. An individualized, progressive
training protocol was utilized so that each subject could meet the
caloric requirement of each exercise session without rest intervals.
The energy expenditure for both intensity groups was increased 50 kcal
every 2 wk from 200 kcal initially to a peak of 350 kcal by the 7th wk
of training. Each individual's exercise prescription was adjusted for
increases in O2 max
measured at weeks 8 and
16 to ensure that the prescribed
exercise intensity and caloric consumption were maintained throughout
the study.
Statistical analysis.
The independent factors were exercise intensity (moderate- and
high-intensity groups), training period (pretraining and 8, 16, and 24 wk), and time of blood sampling after a single session of exercise
(preexercise, IPE, +24 h, and +48 h). The dependent variables of
interest were TC, TG, LDL-C, HDL-C,
HDL2-C,
HDL3-C, apo A-I, and apo B
concentrations. Statistical analysis was completed using
log10-transformed TC data, since
the TC data measured before training were not normally distributed.
Data in Tables 1 and 2 are presented in original units (mg/dl).
An intensity-by-training period-by-time multivariate ANOVA (MANOVA)
with repeated measures on the second and third factors was employed for
the global analysis, since the lipid and lipoprotein variables were
interrelated. Follow-up procedures for significant MANOVA effects
included repeated-measures intensity-by-training period-by-time ANOVA
procedures; Duncan's new multiple range test was employed for post hoc
analysis where appropriate. The physiological and diet data were
analyzed using 2 (intensity)-by-4 (period) ANOVA with repeated measures
on the second factor (Table 1); Duncan's new multiple range test was employed for post hoc analyses. Correlational analyses were used to
explore relationships between 24-wk changes (calculated as the
difference between pretraining and 24-wk preexercise values) in
O2 max, weight, waist
girth, waist-to-hip ratios, and all lipids and apolipoproteins. Because
of the exploratory nature of the study, the comparisonwise level
was set at 0.05 for all statistical tests of significance. Thus the
experimentwise level may exceed 0.05 in some instances. All lipid
concentrations measured after the experimental exercise sessions (IPE,
+24 h, and +48 h) were adjusted for changes in plasma volume.
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RESULTS
Physical Characteristics and Diet
The average values for each physiological and dietary variable of interest were collapsed across intensity groups for analysis. As shown in Table 1, the endurance training program effectively raisedO2 max (~36%) and
resulted in a small but significant reduction in total body weight
(1.4 kg) and waist girth (3.2 cm). Neither estimated
total caloric intake nor diet composition changed significantly over
the 24-wk study.
Lipids and Apolipoproteins
The average values for plasma volume-adjusted lipids and apolipoproteins at each time point within each group and period are presented in Table 2. Significant factors by MANOVA included 1) training period-by-time interaction, 2) intensity-by-time interaction, 3) main effect for time, and 4) main effect for training period. Univariate ANOVA follow-up procedures revealed a significant training period-by-time interaction only for LDL-C, which supports the conclusion that the transient change in LDL-C after a single session of exercise was altered after training (Fig. 2). Furthermore, the intensity-by-time interaction was significant for LDL-C and HDL2-C, suggesting that the transient response for these two lipoprotein lipids depended on the intensity at which the exercise was performed (Fig. 3). Transient changes in plasma volume-adjusted TC, TG, HDL-C, HDL3-C, apo A-I, and apo B concentrations were significant at IPE to +48 h (main effect for time was significant for these variables), demonstrating that changes in these lipids and apolipoproteins occurred in response to a single session of exercise regardless of exercise intensity or training status (Fig. 4). Finally, in these hypercholesterolemic subjects, training was accompanied by a significant change in TC, HDL2-C, HDL3-C, apo A-I, and apo B concentrations (Fig. 5). No correlations between 24-wk changes in any lipid or apolipoprotein variable and the physiological variables oxygen uptake, body weight, waist girth, and waist-to-hip ratio approached significance.
DISCUSSION
To our knowledge, we are the first to show that the profile characteristics of the transient LDL-C response after a single session of exercise depend on the training status of hypercholesterolemic men. Before training, LDL-C concentration was elevated over preexercise values at +24 and +48 h, but after training this rise was not evident and, in fact, LDL-C fell slightly (4%) by +24 h (Fig. 2). When pretraining values were compared with those measured at corresponding time points after training, LDL-C was 6% (11 mg/dl) lower at +48 h after 8 wk of training and 9% (17 mg/dl) lower at +24 h after 24 wk of training. Exercise intensity had no detectable influence on this training response. Thus training may suppress the LDL-C rise noted in hypercholesterolemic men after a single session of exercise. Despite this effect on the transient LDL-C response, the average LDL-C concentration (mean LDL-C value collapsed across the intensity and time factors) did not change with training (main effect for training period was not significant for LDL-C), a finding consistent with most published training studies in normocholesterolemic subjects (7, 10). These results taken together suggest that the primary effect of training on LDL-C is to alter the transient, postexercise metabolism of this circulating lipoprotein, rather than to cause a long-term change in blood LDL-C concentration.
We are aware of no comparable longitudinal studies that have been published. In a cross-sectional investigation, Kantor and associates (22) reported that plasma volume-adjusted LDL-C concentrations were significantly lower than preexercise values in trained and untrained men 10 min after cycle ergometer exercise; LDL-C concentration subsequently returned to baseline (preexercise) within 24 h and remained stable over the next 2 days. Similarly, in our study the nadir of the transient LDL-C response was IPE regardless of training status, but this was followed by a 4-12% rise above preexercise and IPE values 24-48 h later, at least through 16 wk of training. As pointed out above, this postexercise rise was attenuated after 24 wk of training. This delayed rise contrasts with results of other studies in normocholesterolemic men in which LDL-C concentrations were unchanged from preexercise values 24 and 48 h after exercise (5, 15, 21, 22). We can only speculate as to why our findings differ from those of others. Our subjects were older and carried a greater proportion of body weight as fat than subjects in related studies, both factors that could conceivably influence postexercise lipid metabolism and alter the LDL-C response. It is also reasonable to propose that the abnormal resting lipid metabolism known to accompany some types of hypercholesterolemia (20, 30) may contribute to the unique response to exercise noted in our subjects. Whatever the cause, our data suggest that en- durance training for 6 mo normalizes the transient postexercise LDL-C response in hypercholesterolemic men.
In addition to this apparent training effect on the transient LDL-C response, postexercise LDL-C changes, as well as those for HDL2-C, varied with intensity (significant intensity-by-time interaction; Fig. 3). At 24 and 48 h after moderate-intensity exercise, LDL-C rose significantly, but HDL2-C concentration remained unchanged. In contrast, immediately after high-intensity exercise, LDL-C concentration was significantly reduced from preexercise values but subsequently returned to baseline by 24 h; HDL2-C concentration concurrently fell slightly, then rose significantly 16% by 48 h. This HDL2-C rise led to a significant difference between intensity groups (43% higher in the high-intensity exercise group) by 48 h. At no time point were group differences in LDL-C significant. These changes produced by high-intensity exercise would generally be interpreted as favorable with respect to atherosclerotic risk. Few comparative data have been published, and results are inconsistent. Others have shown in related studies in normocholesterolemic men that transient postexercise changes in LDL-C and HDL2-C concentrations were not influenced by exercise intensity (6, 15). Furthermore, in contrast to our null findings for other lipid and apolipoprotein variables, intensity has been shown to be an important mediator of a postexercise rise in TC, HDL-C, and apo A-I concentrations in normocholesterolemic, trained men (15, 17). We are unable to explain these divergent findings.
A unique aspect of our study was the fact that we could separate the
effects of exercise training from the transient (acute) effects of
exercise. This is especially relevant in light of the fact that blood
for lipid analysis was collected within 48 h of the most recent
training session and without regard for potential shifts in plasma
volume in a majority of published studies in which a beneficial
influence of training on lipids was reported (10, 32, 38). We measured
lipids in blood collected 60 h after the last training
session and failed to show significant training changes in the
established lipid risk markers TG and HDL-C, despite substantial
improvements in cardiorespiratory fitness. It could be argued that our
inability to detect significant changes in lipids after training in
contrast to the findings of others was due to a lack of statistical
power stemming from our relatively small sample size. However, the
modest changes in TG (2 mg/dl) and HDL-C (1 mg/dl) we
measured from pretraining to 24 wk would be of doubtful physiological
consequence even if found to be statistically significant. Previous
research suggests that beneficial lipid changes with training may not
be independent of weight loss. Because weight loss was modest in our
study (1.4 kg), one-third to one-fifth the magnitude reported in
other lipid studies designed to examine the effects of exercise and
weight loss (7, 36, 38), we cannot rule out the fact that a more
substantial decrease in body mass or in waist girth (as a measure of
abdominal fat stores) with training may have led to favorable TG and
HDL-C changes in our hypercholesterolemic subjects. To explore this
notion further in our data set, we correlated 24-wk changes in body
weight and waist girth, which ranged from 5.8 to +1.6 kg and
from 13.9 to +1.5 cm, respectively, with changes in lipids and
apolipoproteins. No significant correlations were found to support the
weight loss-lipid change hypothesis. Although weight loss may be an
important determinant of the magnitude of lipid changes, it has been
shown that exercise training without weight loss can produce favorable
alterations in lipid metabolism, at least in overweight,
normocholesterolemic men (33). It is conceivable that the effectiveness
of exercise training and weight loss to promote favorable changes in
these lipid risk markers is blunted with hypercholesterolemia.
In contrast to the lack of a training effect, transient and generally favorable changes in the plasma volume-adjusted concentrations of these two lipid risk markers were produced by a single session of exercise (Fig. 4). It is noteworthy that had our study been a simple training study in which a single blood sample for lipid analysis was collected within 48 h after exercise, increased HDL-C and reduced TG concentrations may have been falsely attributed to training. These results demonstrate the importance of controlling the time of blood sampling after an exercise training session when attempting to measure lipid training benefits and suggest that failure to do so may to lead to confusion with regard to the transient vs. chronic effects of exercise. Furthermore, on the basis of our findings, we propose that at least a portion of the lipid benefit of exercise with respect to these traditional lipid risk markers is realized within 48 h of completion of a single training session, a hypothesis previously advanced by Holloszy et al. (18) and Haskell (16).
In addition to these transient changes in TG and HDL-C, a rise in plasma volume-adjusted TC, HDL3-C, apo B, and apo A concentrations occurred 24-48 h after a single session of exercise (Fig. 4), effects that were not influenced by training status or exercise intensity. We are aware of no similarly designed longitudinal studies with which to compare our results. The magnitude and timing of the transient response reported in existing cross-sectional literature vary widely. In the majority of studies in normocholesterolemic men, plasma volume-adjusted TC, TG, apo A-I, and apo B concentrations were not significantly altered (5, 6, 15, 17, 21, 22), whereas HDL-C, HDL2-C, and HDL3-C were elevated (15, 17, 21, 22) up to 72 h after exercise. Thus the transient rise in TC, apo A-I, and apo B coincident with the fall in TG concentrations noted in our present study may be characteristic of men with elevated cholesterol, and, unlike the LDL-C response, these particular transient changes are not modified by exercise training.
Training was not without some effect, however. Average TC, HDL2-C, HDL3-C, apo A-I, and apo B concentrations were significantly different from pretraining values in our hypercholesterolemic subjects after 8-16 wk of training (Fig. 5), effects that likely reflect more long-lasting (as opposed to transient) metabolic adaptations to exercise and occur regardless of intensity and time of measurement after exercise. Caloric intake and the nutrient composition of the subject's diets remained stable by our assessment throughout the 24-wk training period. Thus it is unlikely that the lipid and apolipoprotein responses were confounded by diet. These apparent training results should be interpreted with caution, however, since a nonexercising control group was not included in our study design, and therefore we cannot rule out the influence of seasonal variation on our data. Few comparative training studies in hypercholesterolemic men have been published, although reductions in TC and TG along with increases in HDL-C after training have been variously reported (19, 28, 29). The rise in HDL2-C concentration coincident with a fall in HDL3-C in our study is indicative of subtle changes in HDL metabolism after training that would not be apparent if only HDL-C concentrations had been measured and may reflect enhanced reverse cholesterol transport in these individuals. Increased HDL2-C concentrations have been measured after training in normocholesterolemic men, especially after exercise-induced weight loss (38, 39). An increase in synthesis and a decrease in catabolism are thought to be responsible for the rise in apo A-I with training in normocholesterolemic subjects (32, 36, 37). Without kinetic data, we can only speculate that an opposite effect occurred after training in our hypercholesterolemic subjects, i.e., catabolism was enhanced or synthesis decreased (perhaps a combination of both), to cause the measured fall in apo A-I concentration. Others have shown that apo A-I synthetic rates are lower in hypertriglyceridemic than in normal subjects (11), suggesting a link between apo A-I synthesis and lipid status. Whether apo A-I metabolism is similarly affected by hypercholesterolemia remains to be determined, but a decrease in synthesis would be consistent with our data.
Although apo B has seldom been measured in exercise studies, present evidence in normocholesterolemic subjects suggests that weight loss in addition to exercise is required to induce a decrease in this putative atherogenic apolipoprotein (37, 39). Our results do not support the need for substantial weight loss, since significant reductions in apo B occurred in our hypercholesterolemic subjects with minimal changes in body weight. Furthermore, in our data, 24-wk changes in body weight and waist girth did not correlate with changes in apo B concentrations.
In conclusion, we have shown that a single session of exercise produces
transient changes in lipid and apolipoprotein concentrations in
hypercholesterolemic men that are uniquely different from those produced by exercise training. Of immediate therapeutic importance in
exercise prescription to lower heart disease risk in this population, favorable changes in the traditional lipid risk markers HDL-C and TG
may represent a transient response to the most recent episode of
exercise as opposed to an adaptive response to chronic exercise training. Furthermore, these transient changes are produced by moderate- or high-intensity caloric-equivalent exercise. Chronic exercise training appears to produce different effects. A transient rise in LDL-C concentration produced by a single session of exercise was no longer evident after training, suggesting that some aspects of
postexercise lipid metabolism are altered by training. Modest reductions in TC, HDL3-C, and apo
A-I and B concentrations, along with a rise in
HDL2-C, also accompany training by
hypercholesterolemic men, and these changes are not affected by
training intensity. Although TG and HDL-C were not responsive to
training in our study, we cannot rule out the fact that a strategy of
exercise training combined with substantial weight loss and a low-fat,
low-cholesterol diet may have produced more favorable changes in these
lipids, as has been demonstrated by others in normocholesterolemic
subjects. Because our data show that changes in lipids and
apolipoproteins are prolonged for up to 48 h after a single session of
exercise, we recommend that exercise be performed at least every other
day by hypercholesterolemic men to maintain the transient lipid benefit and carried out repeatedly over the course of several months to produce
long-term metabolic and cardiovascular adaptations conducive to good
health. Furthermore, in future studies designed to test the effect of
training on lipids, exercise should be discontinued 60 h before blood
sampling to control for the transient effects of the last episode of
exercise.
ACKNOWLEDGEMENTS
We are grateful to Jana Crouse and Susan Lee for assistance in the preparation of the manuscript and to Drs. Nicolaas Pronk and Dennis Jacobsen for technical assistance in data collection.
FOOTNOTES
Address for reprint requests: S. F. Crouse, Applied Exercise Science Laboratory, Dept. of Health and Kinesiology, Texas A & M University, College Station, TX 77843.
Received 21 January 1997; accepted in final form 22 July 1997.
REFERENCES
| 1. | Allain, C. C., L. S. Poon, C. S. G. Chan, W. Richmond, and P. C. Fu. Enzymatic determination of total cholesterol. Clin. Chem. 20: 470-474, 1974[Abstract]. |
| 2. | Brozek, J., F. Grande, T. Anderson, and A. Keys. Densitometric analysis of body composition: revision of some quantitative assumptions. Ann. NY Acad. Sci. 110: 113-140, 1963. |
| 3. | Bucolo, G., and H. David. Quantitative determination of serum triglycerides by the use of enzymes. Clin. Chem. 19: 476-482, 1973[Abstract]. |
| 4. |
Crouse, S. F.,
B. C. O'Brien,
J. J. Rohack,
R. C. Lowe,
J. S. Green,
H. Tolson,
and
J. L. Reed.
Changes in serum lipids and apolipoproteins after exercise in men with high cholesterol: influence of intensity.
J. Appl. Physiol.
79:
279-286,
1995 |
| 5. | Cullinane, E., S. Siconolfi, A. Saritelli, and P. D. Thompson. Acute decrease in serum triglycerides with exercise: is there a threshold for an exercise effect? Metabolism 31: 844-847, 1982[Medline]. |
| 6. |
Davis, P. G.,
W. P. Bartoli,
and
J. L. Durstine.
Effects of acute exercise intensity on plasma lipids and apolipoproteins in trained runners.
J. Appl. Physiol.
72:
914-919,
1992 |
| 7. | Despres, J. P., and B. Lamarche. Low-intensity endurance exercise training, plasma lipoproteins and the risk of coronary heart disease. J. Intern. Med. 236: 7-22, 1994[Medline]. |
| 8. |
Dill, D. B.,
and
D. L. Costill.
Calculation of percentage changes in volumes of blood, plasma, and red cells in dehydration.
J. Appl. Physiol.
37:
247-248,
1974 |
| 9. | Dufaux, B., U. Order, R. Muller, and W. Hollmann. Delayed effects of prolonged exercise on serum lipoproteins. Metabolism 35: 105-109, 1986[Medline]. |
| 10. | Durstine, J. L., and W. L. Haskell. Effects of exercise training on plasma lipids and lipoproteins. In: Exercise and Sport Sciences Reviews, edited by J. O. Holloszy. Baltimore, MD: Williams & Wilkins, 1994, p. 477-521. |
| 11. | Eisenberg, S. High density lipoprotein metabolism. J. Lipid Res. 25: 1017-1058, 1984[Medline]. |
| 12. |
Fletcher, G.,
S. Blair,
J. Blumenthal,
C. Caspersen,
S. Epstein,
H. Falls,
E. Froelicher,
V. Froelicher,
and
I. Pina.
Benefits and recommendations for physical activity programs for all Americans. A statement for health professionals by the Committee on Exercise and Cardiac Rehabilitation of the Council on Clinical Cardiology, American Heart Association.
Circulation
86:
340-344,
1992 |
| 13. | Friedwald, W. T., R. E. Levy, and D. S. Fredrickson. Estimation of the concentration of low-density lipoprotein cholesterol in plasma without use of preparative ultracentrifuge. Clin. Chem. 18: 499-502, 1972[Abstract]. |
| 14. | Gidez, L. I., G. J. Miller, M. Burstein, M. S. Sagle, and H. A. Eder. Separation and quantitation of subclasses of human plasma high density lipoproteins by a simple precipitation procedure. J. Lipid Res. 23: 1206-1223, 1982[Abstract]. |
| 15. | Gordon, P. M., F. L. Goss, P. S. Visich, V. Warty, B. J. Denys, K. F. Metz, and R. J. Robertson. The acute effects of exercise intensity on HDL-C metabolism. Med. Sci. Sports Exerc. 26: 671-677, 1994[Medline]. |
| 16. | Haskell, W. L. Health consequences of physical activity: understanding and challenges regarding dose-response. Med. Sci. Sports Exerc. 26: 649-660, 1994[Medline]. |
| 17. |
Hicks, A. L.,
J. D. MacDougall,
and
T. J. Muckle.
Acute changes in high-density lipoprotein cholesterol with exercise of different intensities.
J. Appl. Physiol.
63:
1956-1960,
1987 |
| 18. | Holloszy, J. O., J. S. Skinner, G. Toro, and T. K. Cureton. Effects of a six month program of endurance exercise on the serum lipids of middle-aged men. Am. J. Cardiol. 14: 753-759, 1964[Medline]. |
| 19. |
Huttunen, J. K.,
E. Lansimies,
E. Voutilainen,
C. Ehnholm,
E. Hietanen,
I. Penttila,
O. Siitonien,
and
R. Rauramaa.
Effect of moderate physical exercise on serum lipoproteins: a controlled clinical trial with special reference to serum high-density lipoproteins.
Circulation
60:
1220-1229,
1979 |
| 20. | Inazu, A., J. Koizumi, H. Mabuchi, K. Kajinami, and R. Takeda. Enhanced cholesteryl ester transfer protein activities and abnormalities of high density lipoproteins in familial hypercholesterolemia. Horm. Metab. Res. 24: 284-288, 1992[Medline]. |
| 21. | Kantor, M. A., E. M. Cullinane, P. N. Herbert, and P. D. Thompson. Acute increase in lipoprotein lipase following prolonged exercise. Metabolism 33: 454-457, 1984[Medline]. |
| 22. | Kantor, M. A., E. M. Cullinane, S. P. Sady, P. N. Herbert, and P. D. Thompson. Exercise acutely increases high density lipoprotein-cholesterol and lipoprotein lipase activity in trained and untrained men. Metabolism 36: 188-192, 1987[Medline]. |
| 23. | McArdle, W. D., F. I. Katch, and V. L. Katch. Exercise Physiology. Philadelphia, PA: Lea & Febiger, 1991. |
| 24. | National Cholesterol Education Program. Second Report of the Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults. Washington, DC: National Institutes of Health, 1993. (Publ. 93-3095: p. 0-1-R-32.) |
| 25. | Pate, R. R., M. Pratt, S. N. Blair, W. L. Haskell, C. A. Macera, C. Bouchard, D. Buchner, W. Ettinger, G. W. Heath, A. C. King, A. Kriska, A. S. Leon, B. H. Marcus, J. Morris, R. S. Paffenbarger, K. Patrick, M. L. Pollock, J. M. Rippe, J. Sallis, and J. H. Wilmore. Physical activity and public health: a recommendation from the Centers for Disease Control and Prevention and the American College of Sports Medicine. JAMA 273: 402-407, 1995[Abstract]. |
| 26. | Pay, H. E., A. E. Hardman, G. J. W. Jones, and A. Hudson. The acute effects of low-intensity exercise on plasma lipids in endurance-trained and untrained young adults. Eur. J. Appl. Physiol. 64: 182-186, 1992. |
| 27. |
Rifai, N.,
and
M. E. King.
Immunoturbidimetric assays of apolipoproteins A, A-I, A-II, and B in serum.
Clin. Chem.
32:
957-961,
1986 |
| 28. | Superko, H. R., and W. H. Haskell. The role of exercise training in the therapy of hyperlipoproteinemia. Cardiol. Clin. 5: 285-310, 1987[Medline]. |
| 29. | Sutherland, W. H. F., E. R. Nye, and S. P. Woodhouse. Red blood cell cholesterol levels, plasma cholesterol esterification rate and serum lipids and lipoproteins in men with hypercholesterolaemia and normal men during 16 weeks physical training. Atherosclerosis 47: 145-157, 1983[Medline]. |
| 30. | Tall, A., E. Granot, R. Brocia, I. Tabas, C. Hesier, K. Williams, and M. Denke. Accelerated transfer of cholesteryl esters in dyslipidemic plasma: role of cholesteryl ester transfer protein. J. Clin. Invest. 79: 1217-1225, 1987. |
| 31. | Thompson, P. D., E. Cullinane, L. O. Henderson, and P. N. Herbert. Acute effects of prolonged exercise on serum lipids. Metabolism 29: 662-665, 1980[Medline]. |
| 32. |
Thompson, P. D.,
E. M. Cullinane,
S. P. Sady,
M. M. Flynn,
D. N. Bernier,
M. A. Kantor,
A. L. Saritelli,
and
P. N. Herbert.
Modest changes in high-density lipoprotein concentration and metabolism with prolonged exercise training.
Circulation
78:
25-34,
1988 |
| 33. | Thompson, P. D., S. M. Yurgalevitch, M. M. Flynn, J. M. Zmuda, D. Spannaus-Martin, A. Saritelli, L. Bausserman, and P. N. Herbert. Effect of prolonged exercise training without weight loss on high-density lipoprotein metabolism in overweight men. Metabolism 46: 217-223, 1997[Medline]. |
| 34. | Tran, Z. V., and A. Weltman. Differential effects of exercise on serum lipid and lipoprotein levels seen with changes in body weight. JAMA 254: 919-924, 1985[Abstract]. |
| 35. | Warnick, G. R., and J. J. Albers. A comprehensive evaluation of the heparin-manganese precipitation procedure for estimating high density lipoprotein cholesterol. J. Lipid Res. 19: 65-76, 1978[Abstract]. |
| 36. | Williams, P. T., R. M. Krauss, K. M. Vranizan, J. J. Albers, and P. D. S. Wood. Effects of weight-loss by exercise and by diet on apolipoproteins A-I and A-II and the particle-size distribution of high-density lipoproteins in men. Metabolism 41: 441-449, 1992[Medline]. |
| 37. | Wood, P. D., W. L. Haskell, S. N. Blair, P. T. Williams, R. M. Krauss, F. T. Lindgren, J. J. Albers, P. H. Ho, and J. W. Farquhar. Increased exercise level and plasma lipoprotein concentration: a one-year, randomized, controlled study in sedentary, middle-aged men. Metabolism 32: 31-39, 1983[Medline]. |
| 38. | Wood, P. D., M. L. Stefanick, D. M. Dreon, B. Frey-Hewitt, S. C. Garay, P. T. Williams, H. R. Superko, S. P. Fortmann, J. J. Albers, K. M. Vranizan, N. M. Ellsworth, R. B. Terry, and W. L. Haskell. Changes in plasma lipids and lipoproteins in overweight men during weight loss through dieting as compared with exercise. N. Engl. J. Med. 319: 1173-1179, 1988[Abstract]. |
| 39. | Wood, P. D., M. L. Stefanick, P. T. Williams, and W. L. Haskell. The effects on plasma lipoproteins of a prudent weight-reducing diet, with or without exercise, in overweight men and women. N. Engl. J. Med. 325: 461-466, 1991[Abstract]. |
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