The effect of short duration sprint interval exercise on plasma postprandial
triacylglycerol levels in young men
Allen, E., Gray, P., Kollias-Pearson, A., Oag, E., Pratt, K., Henderson, J., Gray S.R.
Musculoskeletal Research Programme, Institute of Medical Sciences, Aberdeen
University, Aberdeen, AB25 2ZD
Corresponding Author:
Dr Stuart R Gray
Institute of Medical Sciences
University of Aberdeen
AB25 2ZD
Tel: 01224 438026
Email: [email protected]
Running Title: High Intensity Exercise and Postprandial Lipaemia
Key Words: Lipids, Sprint, Exercise, Cardiovascular
It is well established that regular exercise can reduce the risk of cardiovascular
disease, although the most time efficient exercise protocol to confer benefits has yet
to be established. The aim of the current study was to determine the effects of short
duration sprint interval exercise on postprandial triacylglycerol. Fifteen healthy male
participants completed two 2 day trials. On day 1 participants rested (control) or
carried out twenty 6s sprints, interspersed with 24s recovery (sprint interval exercise
– 14 minutes for total exercise session). On day 2 participants consumed a high fat
meal for breakfast with blood samples collected at baseline, 2 and 4h. Gas exchange
was also measured at these time points. On day 2 of control and sprint interval
exercise trials there were no differences (P>0.05) between trials in plasma glucose,
triacylglycerol, insulin, or respiratory exchange ratio. The area under the curve for
plasma triacylglycerol was 7.67 ± 2.37 mmol/l/4h in the control trial and 7.26 ± 2.49
mmol/l/4h in the sprint interval exercise trial. Although the sprint exercise protocol
employed had no significant effect on postprandial triacylglycerol there was a clear
variability in responses that warrants further investigation.
Cardiovascular disease (CVD) is a major cause of mortality with the most common
form being coronary artery disease (CAD), a condition with atherosclerosis at the
centre of the pathology (Dahlof, 2010). Atherosclerosis, whilst being associated with
fasting low density lipoprotein levels, is not associated with fasting triacylglycerol
levels (Bansal et al., 2007). However as people spend the majority of the day in a
postprandial state it has been suggested that atherogenesis is a postprandial
phenomenon (Zilversmit, 1979), a thesis supported by several studies demonstrating
that postprandial triacylglycerol concentration is a strong independent risk factor for
cardiovascular disease (Bansal et al., 2007; Nordestgaard, Benn, Schnohr, &
Tybj+ªrg-Hansen, 2007). The precise link between postprandial triacylglycerol and
subsequent CVD is not entirely clear but both the generation of a state of oxidative
stress (Anderson et al., 2001) and activation of the immune system have been
implicated (Vogel, 1997; Hansson, 2001; Alipour et al., 2008; Friedman, Klatsky, &
Siegelaub, 1974).
It is well established that moderate intensity exercise can be a useful tool in reducing
postprandial triacylglycerol with several studies showing reductions after 30-120 min
of brisk walking (Miyashita, Burns, & Stensel, 2008; Gill, Herd, Vora, & Hardman,
2003; Gill et al., 2006; Gill et al., 2004). The effect of resistance exercise on
postprandial triacylglycerol is not as clear with some studies showing a benefit
(Burns, Miyashita, Ueda, & Stensel, 2007; Petitt, Arngr+¡msson, & Cureton, 2003)
with others finding no such effect (Burns, Corrie, Holder, Nightingale, & Stensel,
2005). These beneficial effects of exercise on postprandial triacylglycerol contribute
to the current recommendations for physical activity (Haskell et al., 2007). The
current number of people meeting these recommendations is low (British Heart
Foundation, 2012) with time being one of the major barriers to performing exercise to
be reported (Trost, Owen, Bauman, Sallis, & Brown, 2002). Short duration high
intensity exercise has, therefore, been proposed to be a time efficient method of
improving cardiovascular health.
Previous work from our lab has shown that five 30s maximal sprints which were
preceded, interspersed and followed by 4 mins of unloaded cycling can reduce
postprandial triacylglycerol (Gabriel, Ratkevicius, Gray, Frenneaux, & Gray, 2012).
However when rest periods are included the total time of this session is ~27 min and
so not actually reducing the time commitment further than those in the
recommendations. More recent work has used a 10 min exercise protocol which
when completed three times a week for 6 weeks can improve insulin sensitivity in
healthy but sedentary participants (Metcalfe, Babraj, Fawkner, & Vollaard, 2012).
This study involved 10 min of low intensity cycling exercise interspersed with two all
out sprints lasting 20 s (progressing from one 10 s sprint in the first week of training).
On the other hand a recent study found that two weeks of sprint interval exercise
training (6 sessions of 8-12 * 10 s sprints) has no effect on body composition or
insulin sensitivity (estimated by HOMA-IR) (Skleryk et al., 2013). There is no such
information, however, on the effect of shortened protocols on postprandial
triacylglycerol, although one recent study has shown that, alongside improvements in
insulin sensitivity, a single extended ‘sprint’ lasting 3.3 min can increase fat oxidation
(Whyte, Ferguson, Wilson, Scott, & Gill, 2013)
The aim of the present study, therefore, is to determine the effect of a short duration
sprint interval exercise on postprandial triacylglycerol in healthy young men. The
hypothesis was that the short duration sprint interval exercise protocol would
attenuate postprandial triacylglycerol response, in healthy young men, to a high fat
The study conformed to current local guidelines, the declaration of Helsinki and was
approved by the local ethics committee. Fifteen healthy male participants took part in
this study (age; 25±4 years, body fat %; 14±4, weight; 86±9 kg, height; 1.85±0.1 m).
All participants were regularly physically active but none were specifically trained.
Exclusion criteria for volunteers included a history of cardiovascular disease,
smokers, hypertension (systolic/diastolic blood pressure >140/90 mm Hg), diabetes,
obese (BMI >30 kg/m2) or participants with any form of musculoskeletal injury. All
participants were fully informed of the aims, risks and discomfort associated with the
investigation before providing written informed consent.
Anthropometric measurements
Height was measured to the nearest 0.5cm using a stadiometer (Holtain Ltd.,
Crymych, Dyfed, Wales, UK.). Weight was measured to the nearest 0.1 kg using a
weighing scale (Ohaus champ 2, Ohaus UK Ltd., Leicester, England). Skinfold
thickness was measured with calipers (Idass, Harpenden skinfold callipers, England,
UK.) at 4 sites (Bicep, triceps, sub scapula & supra iliac) to the nearest 0.1mm on
the right side of the body. Percentage body fat was calculated using standard
methods (Durnin & Womersley, 1973).
Experimental Protocol
Participants completed two 2 day trials in a randomised order. On day 1 at 2 p.m.
participants completed either a control trial or a high intensity exercise trial. On day 2
(beginning at 9 a.m.) Participants arrived after an overnight fast and consumed a
high fat meal for breakfast. Each trial was separated by at least 7 days. Participants
were instructed not to ingest alcohol or caffeine in the 24 h period prior to day 1 up
until the end of day 2. During this time they were also asked to refrain from exercise
or strenuous physical activity other than that of the trials. Participants were also
asked to record their diet on day 1 of the trial and replicate this during the
subsequent visit.
Day 1 Trials
Sprint Interval Exercise
The sprint interval exercise was performed on a friction braked cycle ergometer
(Monark 894, wingate bike, UK). Participants performed 2 mins warm-up of unloaded
cycling and then performed a 6 s maximal sprint against a load of 7.5 % body weight
followed by unloaded cycling/rest for 24s. This sprint exercise was repeated a further
19 times, with 24s unloaded cycling in between each sprint. A 2 min cool down of
unloaded cycling was then performed.
During the control trial participants sat and rested for 14 mins.
Day 2
Participants arrived at 8.45 am and rested for 15 mins before a resting blood sample
was collected from a vein in the antecubital fossa. A standardized high-fat meal was
then consumed for breakfast. This consisted of chocolate muffins, single cream,
strawberry milkshake flavouring and crisps. This meal provided approximately 5.34
MJ energy with 63.8% of energy from fat, 27.9% from carbohydrate and 7.7% from
protein. The meal contained 92.1 fat, 87.6g carbohydrate, 24.3g protein. The mean
time taken to consume the meal was 11.4 min.
Further blood samples were collected at 2 and 4 hours after the breakfast meal. A
four hour sample collection window was employed due to previous studies showing
little difference between this and longer protocols (Weiss, Fields, Mittendorfer,
Haverkort, & Klein, 2008) and also the finding that 4h post meal is the most
representative of the triacylglycerol response (Mihas et al., 2011). Water was
provided ad libitum throughout the day of the first trial and this volume of water was
consumed during subsequent trials.
Blood handling and analysis
Blood samples were collected with sterile 6 ml K+EDTA non-ridged vacutainers
(Vacuette, greiner bio-one, Kremsmunster, Austria) and were centrifuged (Eppendorf
Centrifuge 5702/R, UK.) at 2300g at 4˚C for 10 minutes. Then plasma was removed
and frozen at -20˚C until analysis. Blood triacylglycerol and glucose concentrations
were assessed using manual enzymatic colorometric assay kits (Randox,Crumlin,
Co. Antrim, UK) using a spectrophotometer (Camspec M330B, Leeds, UK). Insulin
was measured via Enzyme-Linked Immunosorbent Assay (ELISA) (Mercodia Insulin
ELISA, Mercodia AB, Syleveniusgatan, Sweden) using a spectrophotometric plate
reader (Synerg HT Multi-mode microplate reader, BioTek, Bedfordshire, UK).
Concentrations from the ELISA were calculated through the interpolation of sample
absorbance values compared to generated standard curves.
The coefficient of variation from duplicate samples for each assay was
Triacylglycerol; 1.5% glucose; 1.2%, insulin; 3.2%
Statistical Analysis
Data were analyzed with the use of Prism 5 software (GraphPad Software, La Jolla,
CA). Both total and incremental (taking into account changes in baseline
concentrations) areas under the curve for plasma triacylglycerol concentration were
calculated using the trapezium rule. The area under the curve values were
calculated to provide a summary of the triacylglycerol response during the 4 hour
test period. Calculated incremental and total area under the curve values were
compared between trials using paired t-tests. To compare differences between the
two trials over time a 2-way ANOVA with repeated measures was performed. Where
a significant effect was observed post-hoc Tukey’s tests were performed to locate
differences. Significance was taken at P<0.05. Data are presented as mean ±SD.
Insulin and Glucose
There was no difference (p>0.05) between the trials in either insulin or glucose
concentration in the plasma samples collected. The ANOVA did reveal a significant
effect of time for both insulin and glucose in response to the meals (p<0.05) (Figure
The ANOVA revealed no group or interaction effects when comparing plasma
triacylglycerol concentration. However there was with a significant effect of time in
response to the meal (p<0.05) (Figure 2). When the data were analyzed in the
form, area under the curve (AUC) no differences (p<0.05) were found between
groups for either total (Figure 3) or incremental AUC (not shown). As it is known that
there is inherent variability in the response to exercise (e.g. Bouchard et al., 2012)
the change in total triacylglycerol AUC is also shown in Figure 3.
The ANOVA revealed no group effect for RER but a time effect was observed. A
trend (P=0.09) for an interaction effect was found after analysis of variance, with
RER appearing to be lower (non-significant) in the Sprint interval exercise trial
(Figure 2).
The main finding of the current study is that a short duration sprint interval exercise
session, performed the day before a single high fat meal, has no effect on
postprandial triacylglycerol. This is in contrast to previous studies who have found
that high intensity interval exercise, employing 4-5 30s sprints, can reduce
postprandial triacylglycerol (Gabriel et al., 2012; Freese, Levine, Chapman,
Hausman, & Cureton, 2011). On the other hand, longer duration high intensity
interval exercise (4 min intervals at 85-95% HRmax) has been demonstrated to have
no effect on postprandial triacylglycerol, although flow mediated dilation was
improved (Tyldum et al., 2009). On top of these findings the current study found that
glucose and insulin responses to a single high fat meal are not altered by a prior
short duration sprint interval exercise session. This response was, perhaps, not
surprising given that previous studies using high intensity interval exercise which
have found reductions in postprandial triacylglycerol have found no differences in
plasma glucose and insulin responses to high fat feeding (e.g. Gabriel et al., 2012).
The reason for the lack of effect of this exercise protocol is not clear, although
several suggestions can be made. It has been hypothesised that high levels of
glycogen depletion associated with sprint exercise may be partly responsible for the
physiological effects, such as improved insulin sensitivity, observed after a bout of
high intensity exercise (Babraj et al., 2009; Whyte, Gill, & Cathcart, 2010), although
there is little evidence for this. It has been shown on several occasions that after a
longer duration 30s sprint muscle glycogen stores in the vastus lateralis are reduced
by ~25% (e.g. Gibala et al., 2009). Whilst glycogenolysis is activated in the first 15s
of a 30s sprint this is not the case for the final 15s where glycogenolysis is inhibited
(Parolin et al., 1999), and so we chose to utilise shorter sprints in the current study.
However, during the initial 6 s of an all out sprint against a load of 7.5% body weight
muscle glycogen is only reduced by around 10% (Gray, De Vito, Nimmo, Farina, &
Ferguson, 2006). It is therefore possible that this shorter duration exercise employed
in the current study is not sufficient to have beneficial effects, due to only small
decreases in glycogen, although this was not measured in the current study.
However, it is also possible that decreases in muscle glycogen may not be requisite
for a reduction in postprandial triacylglycerol after exercise. Indeed during light
physical activity, where muscle glycogen is unlikely to change, there is an increase in
lipoprotein lipase and a reduction in postprandial triacylglycerol (Gill et al., 2003).
Further work is clearly needed to identify the mechanisms underlying the beneficial
effects of sprint interval exercise to help in designing optimal exercise protocols.
As energy expenditure during exercise is an important determinant of the exercise
induced reduction in postprandial triacylglycerol (Gill & Hardman, 2000) it may be
possible that the energy expended during this exercise session was not sufficient.
Whilst, due to the nature of the exercise, it is problematic to measure energy
expenditure during sprint exercise this can be estimated using the power output
recorded during the sprints (e.g. Gabriel et al., 2012). In this study the energy
expenditure during the whole exercise session is likely to be approximately 120kcal.
Suggesting this level of energy expenditure is not sufficient to cause a reduction in
postprandial triacylglycerol would seem unlikely as the total exercise duration of
120s and estimated energy expenditure of exercise is similar to that employed in
previous studies (Freese et al., 2011; Gabriel et al., 2012), although there is the
possibility that the excess post-exercise oxygen consumption may be higher after the
30s sprint protocol. It may also be suggested that giving a fixed high fat meal, rather
than per kg body weight, may influence the response to exercise. Whilst this
suggestion would seem sensible several other studies have found decrease in
postprandial triacylglycerol after exercise using a fixed meals (e.g. Gill et al., 2004).
In summary it is not clear, at present, why such a protocol would, on average, fail to
reduce postprandial triacylglycerol and due to the need for time-efficient exercise
interventions (Trost et al., 2002) further work is required in this area.
Whilst the sprint interval exercise protocol employed in the current study did not
show, on average, a reduction in postprandial triacylglycerol Figure 3 shows that
there was a wide variation in response to this exercise. This variation in response
has been seen after aerobic exercise, although whilst the responses were variable
the majority of individuals clearly had reduced postprandial triacylglycerol (Arjunan,
Bishop, Reischak-Oliveira, & Stensel, 2013). In a more similar vein to the current
study whilst after multiple bouts of resistance exercise postprandial triacylglycerol
was reduced the response was very varied with 6/24 individuals actually increasing
postprandial triacylglycerol (Burns et al., 2007) compared to 6/15 individuals
increasing postprandial triacylglycerol, in response to sprint interval exercise, in the
current study. On top of the 6 participants who increased postprandial triacylglycerol
2/15 had no change giving a total of 8 participants who did not have a positive
response to such exercise. Similar observations to the current study have been
demonstrated after moderate intensity exercise in people with type 2 diabetes, where
no overall effect of exercise was observed but when looked at an individual level
wide variability in responses was observed (Gill et al., 2007). At this point it is also
prudent to point out that two participants who showed the largest increases in
postprandial triacylglycerol after high intensity exercise repeated all trials and the
same results were found, highlighting, albeit in a small number, that this was a
consistent response.
This highlights the general need to consider individual variations in response to
exercise rather than simply the mean of the group as whilst an intervention may be
found to have or not have a significant effect there may well be a wide variation in
this response. Indeed this variation in a variety of exercise, such as changes in
aerobic capacity, blood pressure and blood lipids, has been known for quite some
time (Bouchard et al., 1999). Further work in this area is therefore required to
determine underlying differences within the transcriptome/genome that can predict
an individual’s response to such exercise (Keller et al., 2011) and from a clinical
sense highlights the need to monitor patient responses to exercise training to ensure
no negative effects are occurring.
In summary the current study has shown that the short duration sprint exercise
protocol, 12 min total session time, employed in the current study had no effect on
postprandial triacylglycerol but that there was a very heterogeneous response when
individual data was examined.
Figure Legends
Figure 1
Plasma glucose (A) and insulin (B) concentrations in response to high intensity
exercise and control trials. Values are Mean±SD (n=15).
Figure 2
Plasma triacylglycerol concentration (A) and RER (B) in response to high intensity
exercise and control trials. Values are Mean±SD (n=15).
Figure 3
Triacylglycerol total (A) and incremental (B) area under the curve (AUC) over the 4
hour experimental period during high intensity exercise and control trials. Values are
Mean±SD (n=15).
Reference List
Alipour, A., van Oostrom, A. J., Izraeljan, A., Verseyden, C., Collins, J. M., Frayn, K.
N. et al. (2008). Leukocyte activation by triglyceride-rich lipoproteins. Arteriosclerosis,
Thrombosis, and Vascular Biology, 28, 792-797.
Anderson, R. A., Evans, M. L., Ellis, G. R., Graham, J., Morris, K., Jackson, S. K. et
al. (2001). The relationships between post-prandial lipaemia, endothelial function and
oxidative stress in healthy individuals and patients with type 2 diabetes. Atherosclerosis,
154, 475-483.
Arjunan, S. P., Bishop, N. C., Reischak-Oliveira, A., & Stensel, D. J. (2013). Exercise
and coronary heart disease risk markers in South asian and European men. Med Sci Sports
Exerc, 45, 1261-1268.
Babraj, J., Vollaard, N., Keast, C., Guppy, F., Cottrell, G., & Timmons, J. (2009).
Extremely short duration high intensity interval training substantially improves insulin action
in young healthy males. BMC Endocrine Disorders, 9, 3.
Bansal, S., Buring, J. E., Rifai, N., Mora, S., Sacks, F. M., & Ridker, P. M. (2007).
Fasting Compared With Nonfasting Triglycerides and Risk of Cardiovascular Events in
Women. JAMA: The Journal of the American Medical Association, 298, 309-316.
Bouchard, C., An, P., Rice, T., Skinner, J. S., Wilmore, J. H., Gagnon, J. et al.
(1999). Familial aggregation ofV-Öo 2 max response to exercise training: results from the
HERITAGE Family Study. Journal of Applied Physiology, 87, 1003-1008.
Bouchard, C., Blair, S. N., Church, T. S., Earnest, C. P., Hagberg, J. M., H+ñkkinen,
K. et al. (2012). Adverse Metabolic Response to Regular Exercise: Is It a Rare or Common
Occurrence? PLoS ONE, 7, e37887.
British Heart Foundation (2012). Physical activity statistics 2012.
Burns, S. F., Miyashita, M., Ueda, C., & Stensel, D. J. (2007). Multiple bouts of
resistance exercise and postprandial triacylglycerol and serum C-reactive-protein
concentrations. Int J Sport Nutr Exerc Metab, 17, 556-573.
Burns, S. F., Corrie, H., Holder, E., Nightingale, T., & Stensel, D. J. (2005). A single
session of resistance exercise does not reduce postprandial lipaemia. Journal of Sports
Sciences, 23, 251-260.
Dahlof, B. (2010). Cardiovascular Disease Risk Factors: Epidemiology and Risk
Assessment. The American Journal of Cardiology, 105, 3A-9A.
Durnin, J. V. & Womersley, J. (1973). Total body fat, calculated from body density,
and its relationship to skinfold thickness in 571 people aged 12-72 years. Proc Nutr Soc, 32,
Freese, E. C., Levine, A. S., Chapman, D. P., Hausman, D. B., & Cureton, K. J.
Friedman, G. D., Klatsky, A. L., & Siegelaub, A. B. (1974). The Leukocyte Count as a
Predictor of Myocardial Infarction. New England Journal of Medicine, 290, 1275-1278.
Gabriel, B., Ratkevicius, A., Gray, P., Frenneaux, M., & Gray, S. R. (2012). High
intensity exercise attenuates postprandial lipaemia and markers of oxidative stress. Clin Sci
(Lond), 123, 313-321.
Gibala, M. J., McGee, S. L., Garnham, A. P., Howlett, K. F., Snow, R. J., &
Hargreaves, M. (2009). Brief intense interval exercise activates AMPK and p38 MAPK
signaling and increases the expression of PGC-1{alpha} in human skeletal muscle. Journal
of Applied Physiology, 106, 929-934.
Gill, J. M. R., Al Mamari, A., Ferrell, W. R., Cleland, S. J., Packard, C. J., Sattar, N. et
al. (2004). Effects of prior moderate exercise on postprandial metabolism and vascular
function in lean and centrally obese men. Journal of the American College of Cardiology, 44,
Gill, J. M. R., Al Mamari, A., Ferrell, W. R., Cleland, S. J., Perry, C. G., Sattar, N. et
al. (2007). Effect of prior moderate exercise on postprandial metabolism in men with type 2
diabetes: Heterogeneity of responses. Atherosclerosis, 194, 134-143.
Gill, J. M. R., Al Mamari, A., Ferrell, W. R., Cleland, S. J., Sattar, N., Packard, C. J. et
al. (2006). Effects of a moderate exercise session on postprandial lipoproteins,
apolipoproteins and lipoprotein remnants in middle-aged men. Atherosclerosis, 185, 87-96.
Gill, J. M. R., Herd, S. L., Vora, V., & Hardman, A. E. (2003). Effects of a brisk walk
on lipoprotein lipase activity and plasma triglyceride concentrations in the fasted and
postprandial states. European Journal of Applied Physiology, 89, 184-190.
Gill, J. M. & Hardman, A. E. (2000). Postprandial lipemia: effects of exercise and
restriction of energy intake compared1. The American Journal of Clinical Nutrition, 71, 465471.
Gray, S. R., De Vito, G., Nimmo, M. A., Farina, D., & Ferguson, R. A. (2006).
Skeletal muscle ATP turnover and muscle fiber conduction velocity are elevated at higher
muscle temperatures during maximal power output development in humans. American
Journal of Physiology - Regulatory, Integrative and Comparative Physiology, 290, R376R382.
Hansson, G. K. (2001). Immune Mechanisms in Atherosclerosis. Arteriosclerosis,
Thrombosis, and Vascular Biology, 21, 1876-1890.
Haskell, W. L., Lee, I. M., Pate, R. R., Powell, K. E., Blair, S. N., Franklin, B. A. et al.
(2007). Physical activity and public health: updated recommendation for adults from the
American College of Sports Medicine and the American Heart Association. Med Sci Sports
Exerc, 39, 1423-1434.
Keller, P., Vollaard, N. B. J., Gustafsson, T., Gallagher, I. J., Sundberg, C. J.,
Rankinen, T. et al. (2011). A transcriptional map of the impact of endurance exercise training
on skeletal muscle phenotype. Journal of Applied Physiology, 110, 46-59.
Metcalfe, R., Babraj, J., Fawkner, S., & Vollaard, N. (2012). Towards the minimal
amount of exercise for improving metabolic health: beneficial effects of reduced-exertion
high-intensity interval training. Eur J Appl Physiol, 112, 2767-2775.
Mihas, C., Kolovou, G. D., Mikhailidis, D. P., Kovar, J., Lairon, D., Nordestgaard, B.
G. et al. (2011). Diagnostic value of postprandial triglyceride testing in healthy subjects: a
meta-analysis. Curr Vasc Pharmacol, 9, 271-280.
Miyashita, M., Burns, S. F., & Stensel, D. J. (2008). Accumulating short bouts of brisk
walking reduces postprandial plasma triacylglycerol concentrations and resting blood
pressure in healthy young men. The American Journal of Clinical Nutrition, 88, 1225-1231.
Nordestgaard, B. r. G., Benn, M., Schnohr, P., & Tybj+ªrg-Hansen, A. (2007).
Nonfasting Triglycerides and Risk of Myocardial Infarction, Ischemic Heart Disease, and
Death in Men and Women. JAMA: The Journal of the American Medical Association, 298,
Parolin, M. L., Chesley, A., Matsos, M. P., Spriet, L. L., Jones, N. L., &
Heigenhauser, G. J. F. (1999). Regulation of skeletal muscle glycogen phosphorylase and
PDH during maximal intermittent exercise. American Journal of Physiology - Endocrinology
And Metabolism, 277, E890-E900.
Petitt, D. S., Arngr+¡msson, S. +., & Cureton, K. J. (2003). Effect of resistance
exercise on postprandial lipemia. Journal of Applied Physiology, 94, 694-700.
Skleryk, J. R., Karagounis, L. G., Hawley, J. A., Sharman, M. J., Laursen, P. B., &
Watson, G. (2013). Two weeks of reduced-volume sprint interval or traditional exercise
training does not improve metabolic functioning in sedentary obese men. Diabetes, Obesity
and Metabolism, n/a.
Trost, S. G., Owen, N., Bauman, A. E., Sallis, J. F., & Brown, W. (2002). Correlates
of adults' participation in physical activity: review and update. Med Sci Sports Exerc, 34,
Tyldum, G. A., Schjerve, I. E., Tjonna, A. E., Kirkeby-Garstad, I., Stolen, T. O.,
Richardson, R. S. et al. (2009). Endothelial dysfunction induced by post-prandial lipemia:
complete protection afforded by high-intensity aerobic interval exercise. J Am Coll Cardiol,
53, 200-206.
Vogel, R. A. (1997). Coronary risk factors, endothelial function, and atherosclerosis:
a review. Clin Cardiol, 20, 426-432.
Weiss, E. P., Fields, D. A., Mittendorfer, B., Haverkort, M. A. D., & Klein, S. (2008).
Reproducibility of postprandial lipemia tests and validity of an abbreviated 4-hour test.
Metabolism, 57, 1479-1485.
Whyte, L. J., Ferguson, C., Wilson, J., Scott, R. A., & Gill, J. M. R. (2013). Effects of
single bout of very high-intensity exercise on metabolic health biomarkers in
overweight/obese sedentary men. Metabolism, 62, 212-219.
Whyte, L. J., Gill, J. M. R., & Cathcart, A. J. (2010). Effect of 2 weeks of sprint
interval training on health-related outcomes in sedentary overweight/obese men.
Metabolism, 59, 1421-1428.
Zilversmit, D. B. (1979). Atherogenesis: a postprandial phenomenon. Circulation, 60,

JSSRevisionSG - Aberdeen University Research Archive