CHD is responsible for more deaths in the United Kingdom (24), the United States (22), and globally (33) than any other single cause, and prevention and treatment of CHD remain a public health priority. The prevalence of CHD varies among nations and ethnic groups, and one group that is particularly susceptible is the South Asian group, a heterogeneous group originating from the Indian subcontinent, e.g., India, Pakistan, Bangladesh, Sri Lanka, and Nepal. Possibly the first to highlight this issue were Danaraj et al. (4) who reported a relatively high prevalence of CHD among Indian compared with Chinese people living in Singapore. More recent reports have confirmed high prevalence rates of CHD among South Asians living in the United Kingdom (30), the United States (17), and Canada (25), and estimates suggest a three- to fivefold increased risk of myocardial infarction and cardiovascular death among migrant South Asians compared with other ethnic groups (7).
A variety of interacting factors may explain the elevated risk of CHD in South Asians, and one of these is physical inactivity. In their review of physical activity levels among South Asians living in the United Kingdom, Fischbacher et al. (8) identifed 12 studies in adults and five in children, all of which reported lower levels of physical activity among UK South Asians than the general population. These findings have since been confirmed by data from a diabetes screening program in Leicester, United Kingdom (34), and by the Health Survey for England (31). Moreover, it has been estimated that physical inactivity explains >20% of the excess CHD mortality experienced by UK South Asians even after adjustment for potential confounders including socioeconomic status, smoking, diabetes, and existing cardiovascular disease (32). Outside of the United Kingdom, the INTERHEART study found that only 6.1% of South Asians reported participation in moderate- or high-intensity exercise compared with 21.6% of participants from other countries (12). In light of such findings, consensus physical activity guidelines for Asian Indians have recently been published in an attempt to promote physical activity among this group (15).
Despite the high prevalence of CHD and low levels of physical activity among South Asians, few studies have examined the effects of physical activity/exercise on CHD or on risk factors for CHD in this group, although observational evidence suggests a protective role (20). Hence, the purpose of the present study was to compare the effects of a single bout of exercise on CHD risk markers in those of South Asian (predominantly Indian) versus white European descent. The primary outcome variable in this study was postprandial triacylglycerol (TAG) concentration, an established CHD risk factor (16) that is frequently reported to be lowered by acute bouts of exercise (13). Several other disease risk markers were examined in this study, including total cholesterol, HDL cholesterol, glucose, insulin, interleukin-6 (IL-6), and soluble intercellular adhesion molecule-1 (sICAM-1).
With the approval of Loughborough University’s Ethics Advisory Committee, 10 South Asian men and 10 men of white European descent were recruited, and they gave their written informed consent to participate in this study. G Power (version 3.1.3; Franz Faul, Universitat Kiel, Kiel, Germany) was used to calculate the study sample size, and this indicated that 10 participants per group would be sufficient to detect a difference in TAG (the primary outcome variable) with a power of 0.75 and a 5% level of significance. Participants were healthy and recreationally active and ranged in age from 20 to 28 yr. Participants were nonsmokers, with no personal history of cardiovascular disease or metabolic disease, and none of them reported taking medication. Participants had a body mass index (BMI) <30 kg·m−2 and blood pressure <140/90 mm Hg. Participants were not dieting and did not have any extreme dietary habits. To verify ethnicity, each South Asian participant completed a form providing details of their place and country of birth, their mother tongue language, their religion and race, the country of their parents’ birth, and their family history of migration. This revealed that seven of the participants were Indian nationals, two were UK Indians, and one was from Pakistan. All of the European participants were white with white parents, and all were British citizens. All of the participants (South Asian and European) were students (some undergraduate, some postgraduate) studying at Loughborough University. Most of the European participants had lived in the United Kingdom for all of their lives, whereas most of the South Asian participants had been living in the United Kingdom for less than 2 yr.
Before the main trials, participants attended the laboratory for a screening and familiarization visit lasting approximately 2 h. During this visit, they completed a participant information form and questionnaires assessing health status, usual physical activity, and ethnicity (South Asians only). Subsequently, weight was measured to the nearest 0.01 kg using a digital scale (Seca Ltd, Hamburg Germany), and height was measured to the nearest 0.1 cm using a stadiometer (Avery Industrial Ltd, Leicester, UK). Skinfold thickness was measured with calipers (Harpenden, Burgess Hill, UK) on the right-hand side of the body at the biceps, triceps, subscapular, and suprailiac. The sum of these four skinfold measurements was used to determine body density (6) and body fat percentage (26). In addition, waist circumference was determined at the narrowest part of the torso above the umbilicus and below the xiphoid process using a measuring tape. Lastly, blood pressure was measured using a digital monitor (Omron M5-1; Matsusaka Co., Ltd., Matsusaka, Mie, Japan).
After familiarization with motorized treadmill running (RUNRACE; Technogym, Gambettola, Italy), participants completed two preliminary exercise tests: a submaximal, incremental treadmill running test (to determine the relation between running speed and oxygen uptake) and a maximal oxygen uptake (V˙O2max) test. The submaximal test was performed on a level treadmill and involved four 4-min stages of increasing intensity. The initial running speed was set between 6 and 9.5 km·h−1, and the speed was increased by 0.5 or 1 km·h−1 (depending on each participant’s level of fitness) at the end of each stage. After a 30-min recovery, V˙O2max was determined with the use of an incremental uphill protocol at a constant speed until participants reached volitional exhaustion (27). The initial treadmill gradient was set at 3.5% for this test, and the gradient was increased by 2.5% every 3 min. Short range telemetry (Sports tester PE3000; Polar Electro Oy, Kempele, Finland) was used to evaluate heart rate throughout both tests. RPE was assessed periodically during these tests using the Borg scale (2).
Expired air samples were collected into Douglas bags (Plysu Protection Systems, Milton Keynes, UK) during both of the preliminary exercise tests. An O2/CO2 analyzer (Servomex 1440; Crowborough, Sussex, UK) was used to measure the oxygen and carbon dioxide percentages within the expired air samples. The analyzers were calibrated using gases of known concentration before testing. A dry gas meter (Harvard Apparatus, Edenbridge, UK) was used to measure expired air volumes, which were corrected to standard temperature and pressure dry. The oxygen consumption values from the two preliminary exercise tests were used together to determine the running speed required to elicit 70% of each participant’s V˙O2max.
Participants completed two 2-day trials (exercise and control) in a random order separated by an interval of at least 1 wk. Trials were undertaken in block random order (block size of two) using software available at http://www.randomization.com/. The lead author enrolled the participants and assigned them to their trials. The lead author also supervised all of the data collection. On day 1 of the exercise trial, participants arrived at the laboratory between 8:00 and 9:00 a.m. and rested (reading, working at computer, watching television, listening to music or playing video games) throughout the day until 5:00 p.m. Participants consumed a standardized lunch at approximately 12:00 p.m. containing white bread, chocolate spread, butter, whole fat milk, chocolate muffin, apple, pear, and water. At 3:30 p.m., participants performed a 60-min run at a speed predicted to elicit 70% of their V˙O2max. One-minute samples of expired air were collected at 15-min intervals during the run to monitor the exercise intensity, i.e., minutes 14–15, 29–30, 44–45, and 59–60 during the run. If necessary, adjustments were made to the treadmill speed to ensure that participants were at the correct intensity. Heart rate and RPE were also monitored during the run. During day 1 of the control trial, procedures were exactly the same as on day 1 of the exercise trial, except that no running was performed, and four 5-min resting expired air samples were collected at the time when running was performed on day 1 of the exercise trial. Oxygen consumption and carbon dioxide production were calculated from expired air samples as described previously. Energy expenditure was estimated from oxygen consumption and carbon dioxide production values using stoichiometric equations (9).
On day 2 of the main trials, participants arrived at the laboratory between 7:45 and 8:00 a.m. having fasted overnight (no food or drink, except water) for 10 h. On arrival at the laboratory, participants sat on a bed in a semisupine position for 5 min while a cannula (BD Venflon; Becton-Dickinson, Helsingborg, Sweden) was inserted into an antecubital vein and a baseline blood sample was collected. Participants then consumed a prescribed test meal (see the succeeding part of this article) for breakfast. A clock was started the moment they commenced their meal, and this was identified as the 0 h. The trial continued on for 9 h during which a total of 14 (including the fasting sample) 9 mL of venous blood samples were collected. At 4 h, a second test meal, identical with the first, was served to participants. Participants rested throughout day 2 of both the control and exercise trials, and hence, day 2 of these trials was identical.
Control of diet and exercise
The day before each main trial and on the first day of each main trial, participants recorded their food intake using a weighed food diary. Participants replicated this food intake for the next main trial. Participants were told not to consume tea, coffee, or alcohol on the day before and during the main trials. Participants were also asked to refrain from strenuous physical activity during the day preceding the main trials and on days 1 and 2 of the main trials.
The test meals consisted of white bread, butter, cheese, mayonnaise, crisps, chocolate milk shake powder, and high-fat milk. The amount of food consumed was adjusted for each participant on the basis of their body weight and was kept constant throughout the trials. The macronutrient content of the test meal was 57% fat, 32% carbohydrate, and 11% protein, and each meal provided 60 kJ (14.3 kcal) per kilogram body mass for a 70-kg participant. Participants consumed each meal within 15 min, and water was available ad libitum.
Venous blood samples were collected for the measurement of total cholesterol, HDL cholesterol, TAG, glucose, insulin, IL-6, and sICAM-1. Samples were collected at baseline (0 h) and at hourly intervals thereafter for 9 h. Additional samples were collected 15 and 30 min after each meal, i.e., at 0.25 and 0.50 h and at 4.25 and 4.5 h. Total cholesterol and HDL cholesterol were only measured from baseline samples; IL-6 and sICAM-1 concentrations were measured from samples collected at 0, 3, 6, and 9 h; glucose, insulin, and TAG were measured from all samples. Participants rested in a semisupine position during blood sampling. Venous blood samples were drawn into precooled 9-mL EDTA monovette tubes (Starstedt, Leicester, UK) and immediately centrifuged at 1500g (3000 rpm) for 10 min in a refrigerated centrifuge (Burkard, Hertfordshire, UK) at 4°C. The plasma supernatant was dispensed into Eppendorf tubes and stored at −80°C before analysis. After each blood sample collection, 10 mL of nonheparinized saline solution (0.9% (v/w) sodium chloride; Baxter Healthcare Ltd, Norfolk, United Kingdom) was flushed through the cannula to maintain cannula patency. Two milliliters of blood was drawn into a syringe and discarded at the start of each blood collection to prevent sample contamination from saline. Hemoglobin and hematocrit values were used to estimate changes in plasma volume across the 9-h main trial day (5).
Plasma total cholesterol, HDL cholesterol, TAG, and glucose concentrations were determined spectrophotometrically using commercially available kits and a bench top analyzer (Pentra 400; HORIBA ABX Diagnostics, Montpellier, France). Enzyme-linked immunosorbent assays were used to determine the concentrations of plasma insulin (Mercodia, Sylveniusgatan, Uppsala, Sweden), IL-6 (high sensitivity kit; Diaclone, Besançon, France), and sICAM-1 (Diaclone) with the aid of a plate reader (Expert Plus; ASYS, Eugendorf, Austria). To eliminate interassay variation, samples from each participant were analyzed in the same run. Coefficients of variation for each assay were as follows: 0.7% for total cholesterol, 0.7% for HDL cholesterol, 3.0% for TAG, 0.5% for glucose, 6.0% for insulin, 3.4% for IL-6, and 4.9% for sICAM-1.
Data lwere analyzed using Predictive Analytics Software version 18.0 for Windows (SPSS, Inc., Somers, NY). Physical characteristics and exercise responses were compared between South Asians and Europeans using the Student t-test. Three-way repeated-measures ANOVA with Bonferroni post hoc tests was used to examine differences between trials for plasma constituents (TAG, glucose, insulin, IL-6 and sICAM-1) with the three factors being (a) trial (exercise vs control), (b) ethnic group (South Asians vs Europeans), and (c) time (serial measurements over a 9 h period). Effect sizes (Cohen d) were also calculated for each of these variables by dividing the differences between the mean values (exercise vs control or South Asian vs European) with the SD (i.e., the average SD from both trials and ethnic groups combined). Area under the plasma concentration versus time curve (AUC) values were calculated for TAG, glucose, insulin, IL-6, and sICAM-1 using the trapezoidal method. These values were compared using two-way repeated-measures ANOVA with the two factors being trial (exercise vs control) and ethnic group (South Asian vs European). Two-way repeated-measures ANOVA was also used to assess between trial and ethnic group differences for fasting plasma concentrations. Statistical significance was accepted at the 5% level. Results are presented as mean ± SD in the text and tables and as mean ± SEM in figures.
The physical characteristics of the participants are displayed in Table 1. There were no significant differences between South Asian and European participants for age, height, weight, BMI, waist circumference, and resting diastolic blood pressure. Percentage body fat was higher in South Asians than Europeans, whereas resting systolic blood pressure and V˙O2max were lower in South Asians than in Europeans.
Responses to treadmill running
The European participants ran faster (9.6 ± 1.6 vs 7.6 ± 1.4 km·h−1, P < 0.008) and expended more energy during the run (3901 ± 473 vs 3313 ± 623 kJ, P < 0.029) than the South Asian participants. There were no significant differences between groups in the %V˙O2max, average heart rate or average RPE attained during the run (%V˙O2max: 71% ± 2% vs 74% ± 5%; heart rate: 172 ± 20 vs 172 ± 14 beats·min−1; RPE: 12 ± 1 vs 12 ± 2; for European and South Asian participants, respectively).
Fasting plasma concentrations
There were significant main effects of trial for fasting total cholesterol, TAG, and sICAM-1, indicating lower values on the exercise trial for fasting total cholesterol and TAG and higher values for fasting sICAM-1 (Table 2). There were significant main effects of group for fasting plasma insulin, HDL cholesterol, and the ratio of total cholesterol/HDL cholesterol, indicating higher insulin and total cholesterol/HDL cholesterol concentrations in the South Asian than the European participants and lower HDL cholesterol concentrations in the South Asian participants. There was a tendency (P = 0.074) for fasting TAG to be elevated in the South Asian participants.
Postprandial plasma concentrations
Three-way ANOVA revealed main effects of group for TAG (P < 0.001), insulin (P < 0.010), and glucose (P < 0.05), indicating higher postprandial TAG and insulin values in South Asian participants and higher postprandial glucose values in European participants (Fig. 1). The effect sizes for these ethnic group comparisons were all large: 1.22, 1.06, and 0.85, respectively. Body fat percentage was higher in the South Asian participants than the European participants, and this might confound the relation between ethnicity and plasma concentrations; therefore, three-way ANOVA was conducted a second time with body fat added as a covariate to remove its confounding influence. Between-group differences remained significant for TAG and glucose but were not significant for insulin after control for percentage body fat.
Three-way ANOVA revealed main effects of trial for TAG (P < 0.001), IL-6 (P < 0.003), and sICAM-1 (P < 0.001), indicating that TAG (Fig. 1) and IL-6 (Fig. 2) concentrations were lower on the exercise trial while sICAM-1 concentrations were higher on the exercise trial (Fig. 2). The effect size for these comparisons was medium for TAG (0.52) and IL-6 (0.55) and large for sICAM-1 (1.04).
Trial and ethnic group differences were confirmed when assessing AUC values using two-way ANOVA (Table 3). Again plasma TAG and insulin concentrations were higher in South Asian participants, whereas plasma glucose concentrations were higher in European participants. The TAG and IL-6 lowering effects of exercise were also confirmed as was the exercise-induced elevation in sICAM-1. Finally, a significant trial by group interaction effect was observed for TAG, indicating a greater decrease after exercise in the South Asian men than the European men (22% vs 10%).
Figure 3 displays the difference in the TAG AUC values between the exercise and the control trials for each participant. Negative values indicate a lowering of postprandial TAG concentration on the exercise trial. This figure demonstrates that postprandial TAG concentration was lower on the exercise trial in 9 of 10 South Asian participants and 8 of 10 European participants. It is also clear from the figure that the TAG lowering effect of exercise is greater in the South Asian than in the European participants.
The novel findings arising from this study are as follows: 1) postprandial plasma TAG concentrations were elevated to a much greater extent in the South Asian men than in the European men in response to high-fat meals; 2) exercise was equally effective if not more so for lowering postprandial plasma TAG concentrations in the South Asian men than in the European men. Another key finding arising from this study is that fasting and postprandial plasma insulin concentrations were higher in the South Asian men than in the European men. No ethnic group differences were apparent for IL-6 and sICAM-1, but postprandial plasma IL-6 concentrations were lower after exercise, whereas postprandial sICAM-1 concentrations were higher.
The most striking finding from this study is the clear elevation in postprandial TAG concentrations in response to high-fat meals in the South Asian participants compared with the European participants. Previous studies have observed higher fasting TAG concentrations in South Asians than in white people (1,28), but to our knowledge, the present study is the first to report a difference in postprandial TAG concentrations between these two ethnic groups. We are aware of only one other study that has compared postprandial lipemia in South Asians and Europeans, and this study did not observe a difference in the lipemic response to high-fat meals, although postprandial glucose and insulin concentrations were elevated in South Asians (3). A possible explanation for these different findings is that percentage body fat did not differ between ethnic groups in the study conducted by Cruz et al. (3), whereas body fat percentage was higher in the South Asian participants in the present study as is often the case (29). Nevertheless, between-group differences in postprandial lipemia remained significant in the present study even after controlling for differences in percentage body fat. Another possible explanation for the disparate findings is the test meals used. The percentage fat provided in the test meals was similar between studies (52% of energy from fat in the study by Cruz et al. (3) vs 57% of energy from fat in the present study), but the total amount of food consumed (which is not stated in the article by Cruz et al.) may have differed.
Another important finding from the present study is the effectiveness of running exercise for lowering postprandial TAG concentrations in the South Asian participants. The finding that postprandial TAG concentrations are lowered by a single session of prior exercise has been reported in many previous studies (for a review, see Katsanos ), but the present study is the first to report this in South Asians. Exercise was particularly effective in the South Asian group eliciting a 22% reduction in the TAG AUC values compared with only a 10% reduction in the European participants. This difference in the apparent effectiveness of exercise may have been due to the elevated TAG values in the South Asian participants, i.e., higher values may provide a greater potential for reductions. Despite the effectiveness of exercise in the South Asian participants, it is important to note that their TAG AUC values were still 33% higher after exercise than the control trial values exhibited by the European participants. If these findings are replicated in larger samples, they would suggest that South Asians are at a much higher risk of experiencing exaggerated postprandial lipemia in response to high-fat meals than Europeans, and this may be a contributing factor to their elevated risk of CHD. The reasons for the exaggerated postprandial lipemia in the South Asian participants are unclear. It is feasible that skeletal muscle and adipose tissue lipoprotein lipase activity is low in South Asians, hence reducing their capacity to clear TAG from plasma. It is also possible that hepatic secretion of TAG (in very low density lipoproteins) is increased in South Asians in the hours after dietary fat intake. Both of these possibilities are speculation, but they provide a clear avenue for future research.
In addition to elevated postprandial TAG concentrations, fasting insulin concentrations were nearly six times higher, and postprandial insulin concentrations were nearly three times higher in the South Asian versus the European participants. These differences suggest a degree of insulin resistance in the South Asian participants, and this is consistent with the findings of Cruz et al. (3). Insulin resistance is thought to be a major contributor to the increased risk of type 2 diabetes and CHD experienced by those of South Asian descent (23,28). Insulin resistance may also underlie the development of “early metabolic syndrome,” which has been noted in the South Asian pediatric population (7). Hyperinsulinemia resulting from insulin resistance is thought to decrease muscle lipoprotein lipase activity (19), and this would impair one of the major mechanisms for removal of TAG from blood. Thus, it is possible that the elevated postprandial lipemia exhibited by the South Asian participants in the present study is linked to their elevated plasma insulin concentrations.
Surprisingly, and in contrast to the differences noted for insulin, we observed a small but significant difference in postprandial plasma glucose concentrations between ethnic groups with higher values in the European participants. This finding conflicts with that of Cruz et al. (3) who observed higher postprandial glucose concentrations in South Asian participants and also with the finding that fasting glucose concentrations are elevated in those of South Asian descent (1). Aside from this finding, the other differences we observed between ethnic groups are consistent with previous research (1,28); i.e., South Asian participants in the present study had a tendency for higher fasting TAG concentrations, higher fasting total cholesterol to HDL cholesterol ratio values, and lower fasting HDL cholesterol concentrations. These findings indicate a higher risk of CHD in the South Asian participants (12).
IL-6 and sICAM-1 were assessed in the present study because both are indicative of chronic low-grade inflammation, which in turn is associated with an increased risk of type 2 diabetes and CHD (11,14,21). It has been suggested that an increased predisposition to chronic low-grade inflammation, due to higher visceral and overall adiposity, might explain the elevated CHD risk in South Asians, but the evidence to support this proposal is equivocal (28). We did not detect differences in IL-6 and sICAM-1 between the South Asian and European men in our study, but IL-6 concentrations were suppressed the day after exercise, whereas sICAM-1 concentrations were elevated. It is well documented that exercise causes a transient increase in the myokine IL-6, and this is known to stimulate an anti-inflammatory cascade involving increased concentrations of IL-10 and IL-1 receptor antagonist (10,18). The lower IL-6 concentrations we observed the day after exercise are possibly reflective of an anti-inflammatory effect of exercise after an initial increase in IL-6. The elevated sICAM-1 concentrations are probably related to an increased blood shear stress during exercise, and it is clear that this elevation lasts for at least 24 h, although the significance of this elevation is uncertain. Finally, we observed a small but significant reduction in fasting total cholesterol concentration the day after exercise. This is not a consistent finding in the literature, and hence, caution is warranted when interpreting this outcome.
This study had three notable limitations. First, the sample size is small, and hence, these findings require confirmation with a larger sample. Second, it is possible that the group differences observed here are confounded by the differences in percentage body fat, although South Asians are known to have a higher body fat percentage for a given BMI (29), and this may explain in part their elevated CHD risk. Third, most of the participants in the present study were Indian South Asians, and South Asians are a heterogeneous group, and hence, these findings require confirmation in other South Asian groups (e.g., Bangladeshis and Pakistanis) and also in South Asian females. Future work should examine whether exaggerated postprandial lipemia occurs in all South Asian subgroups and also the extent to which exercise is effective for lowering postprandial lipemia in each subgroup.
In conclusion; the findings of this study indicate striking elevations in postprandial lipemia in response to high-fat meals in South Asian men. This study also demonstrates that running exercise is effective for lowering postprandial lipemia in South Asian men. The relation between elevated postprandial lipemia and CHD risk in South Asians and the role of exercise in lowering postprandial lipemia and CHD risk in South Asians should be a priority for future research.
We would like to thank Miss Taru Saarinen and Miss Victoria Paley for help with data collection and Mr. Matt Sedgwick, Mr. Kevin Deighton, and Dr. James King for their assistance with blood biochemistry. We also extend our very sincere thanks to all of the participants for giving up their time so freely and cheerfully.
The research was supported by the National Institute for Health Research (NIHR) Diet, Lifestyle and Physical Activity Biomedical Research Unit based at the University Hospitals of Leicester and Loughborough University. Professor Reischak-Oliveira received funding from the Brazilian National Research Council (CNPq). The views expressed are those of the authors and not necessarily those of the NHS, the NIHR, or the Department of Health.
The authors have no financial, consultant, institutional, or other relations that might lead to bias or a conflict of interest.
The results of the present study do not constitute endorsement by the American College of Sports Medicine.
ACTR number: ACTRN12612000897864.
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