Elevated plasma triacylglycerol (TAG) concentrations, especially in the postprandial period, have been implicated in the development of atherosclerosis (42). Impaired clearance of postprandial TAG concentration is associated independently with an increased risk of future cardiovascular diseases (1,33), which remain the leading cause of death in the United Kingdom (36). Most people typically spend most of the daytime in a postprandial state; therefore, repeated daily exposure to elevated postprandial TAG concentration promotes the development of an atherogenic lipid profile of small, dense low-density lipoprotein, and low concentrations of high-density lipoprotein (7). Considering the process of atherosclerosis is initiated during childhood, lifestyle interventions that moderate postprandial lipemia by improving TAG metabolism may slow atherogenic progression, even during childhood and adolescence (32).
Acute moderate-intensity exercise (30 min to 3 h in duration) performed up to 16 h before a standardized meal reduces postprandial lipemia in adults (34), although this effect is short lived (19) and may be dependent on the exercise-induced energy expenditure (EE) (16). Similar postprandial studies with boys have also reported acute reductions in postprandial lipemia after a single moderate-intensity exercise session (2,29,39,41). Barrett et al. (2) suggested that the larger reduction in postprandial TAG concentration after intermittent games activity compared with continuous exercise may reflect the higher exercise EE. However, the evidence is limited by the between-measures design and the inability to estimate the exercise EE during the intermittent games activity (2). Subsequent studies suggest that a dose-dependent response is not supported in healthy young people (39,41).
Recent findings have suggested that low-volume, high-intensity interval training results in similar physiological and metabolic adaptations as higher volume, moderate- to vigorous-intensity continuous training (21,28). Furthermore, this type of training may also improve insulin sensitivity and glycemic control (28). Acute intermittent high-intensity exercise has also been shown to attenuate the postprandial lipemic response in healthy adult males (11,13,14). However, it is not known whether a single session of low-volume, high-intensity exercise attenuates the plasma TAG response to standardized meals in boys. Current international guidelines recommend that children and adolescents accumulate at least 60 min of moderate daily physical activity to promote and maintain health (9,23). Considering that many children and adolescents fail to meet these guidelines (35), low-volume, high-intensity exercise may represent a viable alternative to help improve health and to increase physical activity participation from a young age (4).
Therefore, the aim of the present study was to examine the effect of a single bout of low-volume, high-intensity interval running (HIIR) on postprandial lipemia in healthy, active 11- to 12-yr-old boys. It was hypothesized that acute HIIR would effectively reduce postprandial TAG concentration compared with a resting control despite the relatively low exercise EE.
After approval from the University Ethical Advisory Committee, 16 boys age 11.3 to 12.9 yr volunteered to participate in this study. Results are presented for 15 boys as one boy dropped out due to illness. Written assent was obtained from each participant and written informed consent by a parent or guardian. A health screen questionnaire revealed that all participants were in good general health, had no history of medical conditions that may compromise exercise participation, and were not taking any medications or dietary supplements known to influence lipid or carbohydrate metabolism. All participants indicated they were actively participating in sport but not specifically accustomed to high-intensity running. Physical and physiological characteristics of participants are presented in Table 1.
Anthropometry and physical maturation.
All anthropometric measurements were conducted with participants wearing shorts, T-shirt, and socks. Stature was measured to the nearest 0.01 m using a fixed stadiometer (Holtain, Crosswell, UK), and body mass was quantified to the nearest 0.1 kg using a balance beam scale (Avery, Birmingham, UK). Body mass index was calculated as body mass (kg) divided by stature (m) squared. Triceps and subscapular skinfold thickness were measured to the nearest 0.2 mm on the right-hand side of the body using Harpenden calipers (John Bull, St. Albans, UK). The median of three measurements at each site was used to estimate percent body fat (%BF) using the maturation, race, and sex-specific equations developed by Slaughter et al. (37). Lean body mass (LBM) was estimated as follows:
The level of physical maturity was estimated through the self-assessment of secondary sex characteristics. Participants were provided with drawings depicting the five stages of genital and pubic hair development (38), ranging from 1 indicating prepubescence to 5 indicating full sexual maturity, and were required to identify the stage reflecting their current level of sexual development.
Preliminary exercise measurements.
During the first visit to the laboratory, participants were familiarized with walking and running on the treadmill (Technogym Runrace, Gambettola, Italy) before completing an incremental speed-based treadmill protocol. This protocol was designed to determine peak oxygen uptake (V˙O2) and maximal aerobic speed (MAS), defined as the running speed eliciting the highest V˙O2 during an incremental test (27). The protocol started at an initial speed of 6.0 km·h−1 with 0.5 km·h−1 increments every 30 s until volitional exhaustion, with the treadmill gradient set at 1% throughout (25). Heart rate was monitored continuously via short-range telemetry (PE4000; Polar Electro Oy, Kempele, Finland), and RPE were recorded in the last 10 s of each 30-s stage (3). Expired air samples were monitored continuously using an online breath-by-breath gas analysis system (Metalyzer 3B; Cortex, Leipzig, Germany). The analyzer was calibrated before each test using a bottled gas mixture containing 5.01% CO2, 16.98% O2, and balance N2 (Cranlea and Company, Birmingham, UK) and a 3.0-L syringe (Hans Rudolf, Shawnee, KS). Participants wore an appropriate size facemask (Hans Rudolf), which was checked for leaks and connected to the online system via a flowmeter before the exercise began. All participants satisfied at least two of the following criteria to confirm attainment of maximal effort during the peak V˙O2 test: a plateau in V˙O2 (≤3%) with an increase in treadmill speed, a peak heart rate ≥95% of age-predicted maximum (220 − chronological age), and a respiratory exchange ratio ≥1.10. An average of the breath-by-breath V˙O2 data was taken every 10 s, and peak V˙O2 was defined as the highest 30-s rolling average; the treadmill speed corresponding to peak V˙O2 was recorded as MAS.
The experimental design was similar to previous studies with boys (2,39,41). Using a within-measures counterbalanced, crossover design, participants completed two 2-d experimental conditions: a resting control condition (CON) and a HIIR condition. The conditions were separated by a standardized period of 14 d. The study design is presented schematically in Figure 1.
On day 1 at 1530 h, participants arrived at the laboratory, and all measures were completed by 1630 h. Body mass was recorded at the start of each experimental condition to standardize the test meals provided on day 2. During HIIR, participants completed a 5-min warm-up at 60% MAS, followed immediately by the acute high-intensity running intervals, and concluding with a 3-min cool-down at 40% MAS. The high-intensity exercise session involved 10 × 1-min treadmill runs at 100% MAS with 1 min active recovery between each interval. Several recent studies adopting a low-volume, high-intensity exercise session (10 × 1-min high-intensity cycle sprints, 1-min recovery) reported that this protocol was well tolerated in patients with type 2 diabetes mellitus (21,28). After initial pilot work with 12- to 14-yr-old adolescents, this pattern of exercise on the treadmill was deemed suitable for this population. During the active recovery period, participants dismounted the treadmill and were encouraged to pace around the laboratory to avoid venous pooling and feeling light headed. Heart rate was monitored continuously, and the participants provided RPE in the last 10 s of each interval as described previously. During CON, participants rested in the laboratory to match the duration of HIIR.
On day 2 at approximately 0745 h, participants arrived at the laboratory after a 12-h overnight fast and provided a fasting capillary blood sample after 10 min seated rest. Participants then consumed a standardized test breakfast meal within 15 min, marking the start of the postprandial period (0800 h). Subsequent capillary blood samples were taken at 0.5, 1, 3, 4.5, 5, and 6.5 h in the postprandial period, with participants consuming a standardized test lunch meal within 20 min at 4 h (Fig. 1). To reduce the effect of any physical activity or postural variations on the postprandial measures, participants remained seated throughout the day and were able to read, watch DVDs, and play nonactive computer games. Participants consumed water ad libitum in the postprandial period of the first condition, and the ingested volume was replicated in the subsequent condition.
Standardization of diet and physical activity.
Participants recorded their dietary intake and all physical activity categorized according to intensity level during the 48-h period before day 2 of the first experimental condition. They were asked to minimize and record their physical activity in a diary during this period. The boys then replicated this diet and physical activity pattern before the second experimental condition—this was confirmed verbally by the lead investigator. The overnight fasting period was standardized by asking participants to consume a small carbohydrate-rich cereal snack bar at 1945 h on day 1 of each experimental condition. The macronutrient content of the cereal snack bar was 1.2 g fat, 16.1 g carbohydrate, and 1.0 g protein, which provided 334 kJ energy. After 2000 h, the participants were asked to only drink plain water before arriving at the laboratory on day 2. Two-day food records were analyzed using dietary analysis software (CompEat Pro Version 5.8.0; Nutrition Systems, Banbury, UK).
The test breakfast consisted of croissants, chocolate spread, whole milk, double cream, and milkshake powder. The meal quantity was prescribed relative to body mass and provided 1.5 g fat (60% of total energy), 1.8 g carbohydrate (33%), 0.4 g protein (7%), and 93 kJ energy per kilogram body mass. The test lunch consisted of white bread, mild cheddar cheese, butter, potato crisps, whole milk, and milkshake powder and provided 1.1 g fat (50%), 1.9 g carbohydrate (38%), 0.6 g protein (12%), and 86 kJ energy per kilogram of body mass. To ensure consistency across participants and experimental conditions, participants consumed either chocolate- or strawberry-flavored milkshake powder on both visits. The time taken to consume each meal during the first experimental condition was recorded and replicated in the remaining condition.
Capillary blood samples were taken after the hand was prewarmed in water heated to 40°C for 5 min. The fingertip was pierced (Unistick 3 Extra, Owen Mumford, UK), and 600 μL of whole capillary blood was collected into potassium–ethylenediaminetetraacetic acid-coated Microvette CB 300 tubes (Sarstedt Ltd., Leicester, UK). The whole blood samples were immediately centrifuged at 12,800g for 15 min (Eppendorf 5415c, Hamburg, Germany). An automatic pipette was used to dispense 200 μL of plasma into a 0.5-mL Eppendorf tube (Fisher Scientific Ltd., Loughborough, UK). The plasma samples were stored at −80°C for up to 2 months before subsequent analyses. Plasma TAG concentration and glucose concentration were analyzed by enzymatic, colorimetric methods (Randox Laboratories Ltd., Crumlin, UK) using a benchtop analyzer (Pentra 400; HORIBA ABX Diagnostics, Montpellier, France). Plasma insulin concentration was quantified using a commercially available enzyme-linked immunoassay (Mercodia Insulin ELISA; Mercodia AB, Uppsala, Sweden). The within-batch coefficients of variation for TAG concentration, glucose concentration, and insulin concentration were 1.0%, 0.4%, and 4.1%, respectively. Hemoglobin concentration and hematocrit were also quantified in duplicate in the fasting and final postprandial samples to estimate the acute change in plasma volume (10). Hemoglobin concentration was assessed using the cyanmethemoglobin method; a 20-μL whole blood sample was added to 5-mL Drabkin’s solution, and the absorbance was quantified photometrically at a wavelength of 546 nm (Cecil CE1011; Cecil Instruments, Cambridge, UK). Hematocrit was quantified using a microhematocrit centrifuge and reader (Hematospin 1300 Microcentrifuge; Hawksley and Sons Ltd., Sussex, UK).
Data were analyzed using the IBM Statistical Package for the Social Sciences for Windows (version 19; IBM Corporation, Armonk, NY). All results are expressed as mean ± SD. Descriptive statistics illustrating the physical and physiological characteristics of all participants and exercise responses were calculated (Table 1). Normality of the data was checked by Shapiro–Wilk tests. The homogeneity of variances was confirmed by Mauchly’s test of sphericity, and a Greenhouse–Geisser correction was applied to the degrees of freedom if the sphericity assumption was violated. The trapezium rule was used to calculate the total area under the plasma concentration versus time curves for TAG (TAUC-TAG), glucose (TAUC-glucose), and insulin (TAUC-insulin) (Table 2). The incremental areas under the plasma concentration versus time curves for TAG (iAUC-TAG), glucose (iAUC-glucose), and insulin (iAUC-insulin) were calculated using the same method after correcting for fasting concentrations. Energy and macronutrient intake along with TAUC and iAUC responses, fasting TAG concentration, glucose concentration, and insulin concentration and estimated changes in plasma volume were compared between each experimental condition using separate one-way within-measures ANOVA. Differences in TAG concentration, glucose concentration, and insulin concentration over for the total 6.5-h postprandial period were examined using separate 2 × 7 (condition × time) within-measures ANOVA. A 2 × 3 (condition × time) within-measures ANOVA was conducted and followed up with simple planned contrasts to identify differences in TAUC-TAG between CON and HIIR over subsections of the total postprandial period (0–1, 1–4.5, and 4.5–6.5 h). The 95% confidence intervals (CI) for mean absolute pairwise differences between experimental conditions were calculated using the t-distribution, and degrees of freedom (n − 1) and absolute standardized effect sizes (ES) are included to supplement important findings (12). In the absence of a clinical anchor, an ES of 0.2 was considered the minimum important difference for all outcome measures, 0.5 moderate and 0.8 large (6). Bivariate correlations identifying possible determinants of exercise-induced changes in TAUC-TAG were quantified using linear regression. Interpretation of the data will be based on the 95% CI and ES rather than more traditional dichotomous hypothesis testing.
Average energy intake was similar during the 48 h before day 2 of CON and HIIR (8.1 ± 1.6 vs 7.9 ± 1.6 MJ·d−1, respectively; 95% CI = −1.25 to 0.87). Average 2-d macronutrient intake did not differ between CON and HIIR for protein (69.0 ± 15.7 vs 68.8 ± 14.3 g·d−1, 95% CI = −8.4 to 8.1), carbohydrate (270.0 ± 48.4 vs 253.1 ± 55.4 g·d−1, 95% CI = −55.0 to 21.2), or fat (64.1 ± 20.8 vs 66.2 ± 20.1 g·d−1, 95% CI = −7.6 to 11.7), respectively.
Responses to HIIR.
The HIIR session was well tolerated by all participants and was performed at an average MAS of 12.5(1.6) km·h−1. Mean heart rate increased progressively from interval 1 to interval 10 (interval 1 = 184 ± 8 beats·min−1 vs interval 10 = 194 ± 8 beats·min−1, 95% CI = 7 to 13, ES = 1.29), which corresponded to 92% ± 3% and 97% ± 2% peak heart rate, respectively (95% CI = 4 to 6, ES = 1.88). The mean ± SD RPE during interval 1 was 10 ± 3 (between very light and fairly light on the scale) but increased to 19 ± 1 at the end of interval 10 (very, very hard) (95% CI = 7 to 11, ES = 3.97).
Plasma volume changes and fasting TAG concentration, glucose concentration, and insulin concentration.
Average changes in plasma volume between the fasting and the 6.5-h postprandial samples were small and did not differ significantly between the two conditions (CON = 0.46%, HIIR = 0.85%; 95% CI = −3.77 to 4.57). Therefore, the raw plasma TAG concentration, glucose concentration, and insulin concentration were used in all statistical analyses without adjustment. The fasting plasma TAG concentration, glucose concentration, and insulin concentration for each condition are shown in Table 2. Differences in fasting plasma TAG were small to moderate (95% CI = −0.11 to 0.01, ES = 0.40), with a slightly lower fasting TAG concentration evident after HIIR. There were no differences in fasting plasma glucose concentration (95% CI = −0.33 to 0.19) or insulin concentration (95% CI = −19.0 to 16.9) between CON and HIIR.
Plasma TAG, glucose, and insulin in the postprandial period.
Plasma TAG concentration responses over the postprandial period for the experimental conditions are shown in Figure 2. Postprandial plasma TAG concentration was lower during HIIR compared with CON (main effect condition 95% CI = −0.19 to −0.02, ES = 0.58; main effect time ES = 0.80; condition–time interaction ES = 0.15). The peak in plasma TAG concentration, occurring at 5 h in both conditions, was lower after HIIR compared with CON (95% CI = −0.36 to −0.06, ES = 0.70). In addition, TAUC-TAG was lower after HIIR compared with CON (95% CI = −1.18 to −0.12, ES = 0.50) (Table 2). Differences in subsections of the TAUC-TAG between CON and HIIR were moderate (main effect condition 95% CI = −0.40 to −0.04, ES = 0.57). Specifically, TAUC-TAG was lower after HIIR compared with CON between 1 and 4.5 h (95% CI = −0.50 to 0.02, ES = 0.47) and between 4.5 and 6.5 h (95% CI = −0.56 to −0.07, ES = 0.57). Individual changes (delta) in TAUC-TAG between CON and HIIR are shown in Figure 3. Ten boys responded to the interval running session (i.e., the reductions in TAUC-TAG after the HIIR exceeded the control). Percent peak heart rate during the interval runs was the only measured variable demonstrating a meaningful relationship with TAUC-TAG (r = −0.65; 95% CI = −0.87 to −0.20), explaining 42% of the variance (Fig. 4). Differences in iAUC-TAG between CON and HIIR were small to moderate (95% CI = −0.83 to 0.13, ES = 0.39) (Table 2).
Postprandial plasma glucose concentration did not differ meaningfully between CON and HIIR (main effect condition 95% CI = −0.30 to 0.15, ES = 0.19; main effect time ES = 0.43; condition–time interaction ES = 0.12). No meaningful difference in TAUC-glucose was evident between CON and HIIR (95% CI = −1.7 to 1.1) (Table 2). The iAUC-glucose did not differ meaningfully between CON and HIIR (95% CI = −1.76 to 1.94) (Table 2).
There was no meaningful difference in postprandial plasma insulin concentration between CON and HIIR (main effect condition 95% CI = −35 to 13, ES = 0.25; main effect time ES = 0.69; condition–time interaction ES = 0.11). In addition, TAUC-insulin was similar across the experimental conditions (95% CI = −210 to 90) (Table 2). No meaningful difference in iAUC-insulin was evident between CON and HIIR (95% CI = −149 to 41) (Table 2).
The main finding of the present study was that a single session of low-volume HIIR performed the day before standardized test meals attenuated postprandial plasma TAG concentration in healthy, active 11- to 12-yr-old boys. To our knowledge, this is the first study to investigate the effect of HIIR on postprandial lipemia in boys. The exercise protocol was well tolerated by all participants and therefore may have practical applications for health in similar populations.
Changes in fasting plasma TAG concentration were small to moderate after the exercise intervention, consistent with previous findings with young people involving moderate- and vigorous-intensity exercise (2,39,41). However, fasting TAG concentration is typically less predictive of cardiovascular disease risk than postprandial TAG concentration (1). In addition, substantial variation is evident in fasting TAG concentration in children (40), highlighting the importance of studying plasma TAG concentration in the postprandial period.
Along with the plethora of studies supporting the TAG-lowering effects of moderate-intensity exercise in adults (34), there is growing evidence that moderate- and vigorous-intensity exercise promote reductions in postprandial lipemia in healthy boys (2,29,39,41). The current study extends these findings by demonstrating for the first time that low-volume HIIR attenuates postprandial plasma TAG concentration in 11- to 12-yr-old boys. Several recent studies with adults also support the reduction in postprandial TAG concentration after intermittent high-intensity interval running (11) and all-out cycle sprints (13,14). Interestingly, a small to moderate reduction in iAUC-TAG was evident after HIIR, suggesting that the TAG-lowering effect of HIIR is influenced, in part, by the change in fasting TAG concentration (i.e., endogenous VLDL metabolism). Nevertheless, the iAUC-TAG was lower after HIIR compared with CON, indicating that differences in the metabolism of exogenous TAG may contribute somewhat to the lower postprandial TAG concentration evident after HIIR.
Currently, the change in postprandial lipemia after exercise in young people varies, with estimated ES ranging from 0.26 to 0.86 (2,29,39,41). However, on average, the changes are moderate and comparable with the attenuation evident after HIIR in our study. Although comparing different groups of boys indirectly may be confounded by differences in participant characteristics, it provides an important insight into the extent HIIR attenuates postprandial lipemia in this population. Previous studies with young boys demonstrate that the peak in postprandial TAG concentration occurs 2–4 h after the consumption of a single standardized meal (2,29,39,41). The later peak in the present study (∼5 h in both conditions) reflects the additional effect of the lunch meal on the postprandial lipemic response. Differences in postprandial TAG concentration between CON and HIIR emerged after 1 h up to the end of the postprandial period of 6.5 h. Although other studies with boys have not examined differences in TAUC-TAG over subsections of the total postprandial period, the TAG-lowering effect of moderate- and vigorous-intensity exercise seems to persist throughout the postprandial period (2,29,39,41).
The effect of exercise on postprandial TAG metabolism has traditionally been linked with the exercise EE in adults (16). A recent review suggests that an EE threshold of 2 MJ is required to elicit acute reductions in postprandial TAG concentration (31). However, the evidence of a dose-dependent response in young people is not supported (39,41). Although it was not possible to measure the exercise EE directly, it is reasonable to assume that the short duration of HIIR (10 min in total) would incur a lower EE than that reported in other studies investigating the effect of longer duration, moderate- or vigorous-intensity exercise on postprandial TAG concentration in boys (2,29,39,41), and below the 2-MJ threshold suggested in adults (31). Estimating EE during high-intensity exercise based on indirect calorimetry is limited by the disturbances in the bicarbonate pool that occur during non–steady-state exercise; therefore, the gas composition of expired air is unlikely to reflect tissue metabolism (24). Indeed, Gabriel et al. (14) reported that in adults, low-volume, sprint interval cycling attenuated postprandial lipemia, and yet no effect of brisk walking was observed on postprandial TAG concentration despite a 57% greater exercise EE estimated from the average power output and mechanical efficiency. Consequently, the capacity for high-intensity exercise to reduce postprandial TAG concentration suggests that the exercise-intensity is important in modifying the postprandial lipemic response.
Clear interindividual variability is evident in the exercise-induced changes in plasma TAG concentration, which is consistent with previous work in boys (39) and adults (15). Average percent peak heart rate during HIIR was the only physical or exercise response variable that demonstrated a significant correlation with exercise-induced TAUC-TAG, suggesting exercising at a higher relative intensity augments the attenuation in postprandial TAG concentration. Although V˙O2 was not measured during HIIR, oxygen uptake, substrate utilization, or exercise EE did not contribute meaningfully to the individual heterogeneity in postprandial lipemia after moderate-intensity exercise in adults and boys previously (15,39). Although most boys in the current study were classified as early pubescent, a range of self-assessed sexual maturity ratings was identified (pubic hair development stage 1: n = 2; stage 2: n = 11; stage 3: n = 2). Subsequent analyses revealed no discernible effect of maturity status on the postprandial TAG response (data not shown). However, the influence of maturity status on postprandial lipemia is limited by the relatively small sample size and therefore cannot be determined with confidence from our findings.
It is widely accepted that nonfasting TAG is an independent risk factor for future cardiovascular events (1,33), and efforts to reduce cardiovascular risk factors should begin from a young age (32). However, the clinical relevance of the exercise-induced reduction in postprandial TAG concentration cannot be determined from our findings. Currently, it has not been possible to identify a predefined postprandial lipemic response in young people or adults beyond which further reductions will confer improved health. Consequently, it is not possible to identify how many participants experienced meaningful reductions in postprandial TAG concentration after HIIR. Nevertheless, all participants in the present study demonstrated a healthy postprandial TAG concentration profile independent of the experimental condition and the time of TAG measurement; therefore, the potential for HIIR to elicit reductions in postprandial lipemia in individuals with normal postprandial TAG metabolism is encouraging.
The potential for low-volume HIIR to reduce the postprandial lipemic response is promising considering many young people fall short of the current physical activity recommendations (35). A perceived lack of time and enjoyment are highlighted frequently as barriers to exercise participation in adolescents (5). The total exercise time commitment (including warm-up, recovery, and cool-down) in the present study was 27 min, highlighting the time efficiency of our HIIR session. It has been found that combining moderate-intensity exercise with periods of high-intensity effort is associated with greater perceived enjoyment than performing a similar duration of continuous, moderate-intensity exercise alone in prepubertal boys (8). Moreover, children typically spend a lower percentage of time engaged in low-intensity activities and more time on high-intensity activities compared with adults (22). Consequently, HIIR may represent an effective strategy in boys to improve health that is practical, time-efficient and enjoyable, but further research is required to support this.
In the present study, no differences in the postprandial glucose or insulin response were evident and therefore are unlikely to contribute to the diminished postprandial plasma TAG concentration response after HIIR. The evidence for acute moderate-intensity exercise-induced changes in postprandial glucose concentration after high-fat meals are generally not well supported in young people (2,29,39,41). Furthermore, despite the paucity of research, no effect of moderate-intensity exercise was evident on the postprandial insulin profile (29). Insulin is known to play a pivotal role in TAG metabolism, regulating the uptake of TAG to skeletal muscle and adipose tissue, along with the release of VLDL from hepatic tissue. However, exercise-induced changes in postprandial lipemia seem independent of the postprandial insulin response (17).
The mechanism responsible for the acute attenuation in postprandial TAG concentration after exercise is not known currently in young people and cannot be elucidated from our findings. In adults, it is proposed that enhanced removal of TAG from the blood mediated by increased lipoprotein lipase activity in the plasma or muscle (18,20) and/or a reduction in hepatic VLDL-TAG synthesis and secretion (30) is responsible. However, it is likely that enhanced muscle lipoprotein lipase activity is mediated by a reduction in plasma insulin concentration (26), which was not observed in the present study. In support of the latter mechanism, Gill et al. (15) reported 3-hydroxybutyrate concentration, a marker of hepatic fatty acid oxidation, was associated with moderate-intensity exercise-induced changes in postprandial TAG concentration. However, no effect of high-intensity exercise was observed on plasma 3-hydroxybutyrate in adults (14).
A possible limitation of this study is the accuracy of physical activity replication between the experimental conditions. Participants were asked to subjectively record their physical activities 48 h before day 2 of the first experimental condition and then replicate this during the same period before the second condition. Although this procedure was verified verbally and by comparing the diaries, in the absence of an objective measure to quantify free-living physical activity, discrepancies between the conditions would introduce variability between the conditions that may influence the postprandial measures. A further limitation concerns the fact that participants did not complete a session of similar duration moderate-intensity exercise for comparison with HIIR.
In conclusion, the present study is the first to our knowledge to show that low-volume HIIR performed approximately 15.5 h before a standardized breakfast reduces postprandial TAG concentration in healthy, active 11- to 12-yr-old boys. Low-volume, high-intensity exercise may be a time-efficient strategy to improve health in boys, but further work is required to examine this chronically.
The authors thank Woodbrook Vale High School in Loughborough for their support and the participants and their parents for their commitment throughout this research. They also acknowledge Josh Hill and Natalie Wheat for their assistance in data collection.
No funding was received for this research, other than that available internally through Loughborough University.
The authors declare no conflict of interest.
The results of the present study do not constitute endorsement by the American College of Sports Medicine.
1. Bansal S, Buring JE, Rifai N, Mora S, Sacks FM, Ridker PM. Fasting compared with nonfasting triglycerides and risk of cardiovascular events in women. JAMA
. 2007; 298 (3): 309–16.
2. Barrett LA, Morris JG, Stensel DJ, Nevill ME. Exercise and postprandial plasma triacylglycerol concentrations in healthy adolescent boys. Med Sci Sports Exerc
. 2007; 39 (1): 116–22.
3. Borg GAV, Noble BJ. Perceived exertion. Exerc Sport Sci Rev
. 1974; 2 (1): 131–53.
4. Buchan DS, Ollis S, Young JD, et al. The effects of time and intensity of exercise on novel and established markers of CVD in adolescent youth. Am J Hum Biol
. 2011; 23 (4): 517–26.
5. Butt J, Weinberg RS, Breckon JD, Claytor RP. Adolescent physical activity participation and motivational determinants across gender, age, and race. J Phys Act Health
. 2011; 8 (8): 1074–83.
6. Cohen J. Statistical Power Analysis for the Behavioural Sciences
. 2nd ed. Hillsdale (NJ): Lawrence Erlbaum Associates; 1988. p. 23–4.
7. Cohn JS. Postprandial lipemia: emerging evidence for atherogenicity of remnant lipoproteins. Can J Cardiol
. 1998; 14: 18–27B.
8. Crisp NA, Fournier PA, Licari MK, Braham R, Guelfi KJ. Adding sprints to continuous exercise at the intensity that maximises fat oxidation: implications for acute energy balance and enjoyment. Metabolism
. 2012; 61 (9): 1280–8.
9. Department of Health, Physical Activity, Health Improvement and Protection. Start Active, Stay Active. A Report on Physical Activity for Health from the Four Home Countries’ Chief Medical Officers
. London: United Kingdom Department of Health, Physical Activity, Health Improvement and Protection; 2011. p. 26. Available from UK Department of Health.
10. Dill DB, Costill DL. Calculation of percentage changes in volumes of blood, plasma, and red cells in dehydration. J Appl Physiol
. 1974; 37 (2): 247–8.
11. Ferreira AP, Ferreira CB, Souza VC, et al. The influence of intense intermittent versus moderate continuous exercise on postprandial lipemia. Clinics
. 2011; 66 (4): 535–41.
12. Field A. Discovering Statistics Using SPSS for Windows
. London: Sage Publications; 2009. p. 332, 501.
13. Freese EC, Levine AS, Chapman DP, Hausman DB, Cureton KJ. Effects of acute sprint interval cycling and energy replacement on postprandial lipemia. J Appl Physiol
. 2011; 111 (6): 1584–9.
14. Gabriel B, Ratkevicius A, Gray P, Frenneaux MP, Gray SR. High-intensity exercise attenuates postprandial lipaemia and markers of oxidative stress. Clin Sci
. 2012; 123 (5): 313–21.
15. Gill JMR, Al-Mamari A, Ferrell WR, et al. Effect of prior moderate exercise on postprandial metabolism in men with type 2 diabetes: heterogeneity of responses. Atherosclerosis
. 2007; 194 (1): 134–43.
16. Gill JMR, Herd SL, Hardman AE. Moderate exercise and post-prandial metabolism: issues of dose-response. J Sports Sci
. 2002; 20 (12): 961–7.
17. Gill JMR, Herd SL, Tsetsonis NV, Hardman AE. Are the reductions in triacylglycerol and insulin levels after exercise related? Clin Sci
. 2002; 102 (2): 223–31.
18. Gill JMR, Herd SL, Vora V, Hardman AE. Effects of a brisk walk on lipoprotein lipase activity and plasma triglyceride concentrations in the fasted and postprandial states. Eur J Appl Physiol
. 2003; 89 (2): 184–90.
19. Herd SL, Hardman AE, Boobis LH, Cairns CJ. The effect of 13 weeks of running training followed by 9 d of detraining on postprandial lipaemia. Br J Nutr
. 1998; 80 (1): 57–66.
20. Herd SL, Kiens B, Boobis LH, Hardman AE. Moderate exercise, postprandial lipemia, and skeletal muscle lipoprotein lipase activity. Metabolism
. 2001; 50 (7): 756–62.
21. Hood MS, Little JP, Tarnopolsky MA, Myslik F, Gibala MJ. Low-volume interval training improves muscle oxidative capacity in sedentary adults. Med Sci Sports Exerc
. 2011; 58 (10): 1849–56.
22. Hoos MB, Kuipers H, Gerver WJ, Westerterp KR. Physical activity pattern of children assessed by triaxial accelerometry. Eur J Clin Nutr
. 2004; 58 (10): 1425–8.
23. Janssen I, LeBlanc AG. Systematic review of the health benefits of physical activity and fitness in school-aged children and youth. Int J Behav Nutr Phys Act
. 2010; 7: 40.
24. Jeukendrup AE, Wallis GA. Measurement of substrate oxidation during exercise by means of gas exchange measurements. Int J Sports Med
. 2005; 26(Suppl 1): S28–37.
25. Jones AM, Doust JH. A 1% treadmill grade most accurately reflects the energetic cost of outdoor running. J Sports Sci
. 1996; 14 (4): 321–7.
26. Kiens B, Lithell H, Mikines KJ, Richter EA. Effects of insulin and exercise on muscle lipoprotein lipase activity in man and its relation to insulin action. J Clin Invest
. 1989; 84 (4): 1124–9.
27. Lacour JR, Padilla-Magunacelaya S, Chatard JC, Arsac L, Barthélémy JC. Assessment of running velocity at maximal oxygen uptake. Eur J Appl Physiol
. 1991; 62 (2): 77–82.
28. Little JP, Gillen JB, Percival ME, et al. Low-volume high-intensity interval training reduces hyperglycemia and increases muscle mitochondrial capacity in patients with type 2 diabetes. J Appl Physiol
. 2011; 111 (6): 1554–60.
29. MacEneaney OJ, Harrison M, O’Gorman DJ, Pankratieva EV, O’Connor PL, Moyna NM. Effect of prior exercise on postprandial lipemia and markers of inflammation and endothelial activation in normal weight and overweight adolescent boys. Eur J Appl Physiol
. 2009; 106 (5): 721–9.
30. Magkos F. Basal very low-density lipoprotein metabolism in response to exercise: mechanisms of hypotriacylglycerolemia. Prog Lipid Res
. 2009; 48 (3–4): 171–90.
31. Maraki M, Sidossis LS. Effects of energy balance on postprandial triacylglycerol metabolism. Curr Opin Clin Nutr Metab Care
. 2010; 13 (6): 608–17.
32. McGill HC, McMahan CA, Herderick EE, Malcom GT, Tracy RE, Strong JP. Origin of atherosclerosis in childhood and adolescence. Am J Clin Nutr
. 2000; 72 (5): S1307–15.
33. Nordestgaard BG, Benn M, Schnohr P, Tybjærg-Hansen A. Nonfasting triglycerides and risk of myocardial infarction, ischemic heart disease, and death in men and women. JAMA
. 2007; 298 (3): 299–308.
34. Peddie MC, Rehrer NJ, Perry TL. Physical activity and postprandial lipidemia: are energy expenditure and lipoprotein lipase activity the real modulators of the positive effect? Prog Lipid Res
. 2012; 51 (1): 11–22.
35. Riddoch CJ, Mattocks C, Deere K, et al. Objective measurement of levels and patterns of physical activity. Arch Dis Child
. 2007; 92 (11): 963–9.
36. Scarborough P, Bhatnagar P, Wickramasinghe K, Smolina K, Mitchell C, Rayner M. Coronary Heart Disease Statistics
. London: British Heart Foundation; 2010. p. 14. Available from the British Heart Foundation.
37. Slaughter MH, Lohman TG, Boileau RA, et al. Skinfold equations for estimation of body fatness in children and youth. Hum Biol
. 1988; 60 (5): 709–23.
38. Tanner JM. Growth at Adolescence
. 2nd ed. Oxford (UK): Blackwell Scientific Publications; 1962. p. 28–39.
39. Tolfrey K, Bentley C, Goad M, Varley J, Willis S, Barrett L. Effect of energy expenditure on postprandial triacylglycerol in adolescent boys. Eur J Appl Physiol
. 2012; 112 (1): 23–31.
40. Tolfrey K, Campbell IG, Jones AM. Intra-individual variation of plasma lipids and lipoproteins in prepubescent children. Eur J Appl Physiol
. 1999; 79 (5): 449–56.
41. Tolfrey K, Doggett A, Boyd C, Pinner S, Sharples A, Barrett L. Postprandial triacylglycerol in adolescent boys: a case for moderate exercise. Med Sci Sports Exerc
. 2008; 40 (6): 1049–56.
42. Zilversmit DB. Atherogenesis: a postprandial phenomenon. Circulation
. 1979; 60 (3): 473–85.