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Journal of Sports Sciences Publication details, including instructions for authors and subscription information: http://www.tandfonline.com/loi/rjsp20
The effect of short-duration sprint interval exercise on plasma postprandial triacylglycerol levels in young men a
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Edward Allen , Partick Gray , Angeliki Kollias-Pearson , Erlend Oag , Katrina Pratt , Jennifer a
Henderson & Stuart Robert Gray
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Institute of Medical Sciences, University of Aberdeen, Foresterhill, Aberdeen, AB25 2ZD, UK Published online: 06 Feb 2014.
To cite this article: Edward Allen, Partick Gray, Angeliki Kollias-Pearson, Erlend Oag, Katrina Pratt, Jennifer Henderson & Stuart Robert Gray (2014) The effect of short-duration sprint interval exercise on plasma postprandial triacylglycerol levels in young men, Journal of Sports Sciences, 32:10, 911-916, DOI: 10.1080/02640414.2013.865254 To link to this article: http://dx.doi.org/10.1080/02640414.2013.865254
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Journal of Sports Sciences, 2014 Vol. 32, No. 10, 911–916, http://dx.doi.org/10.1080/02640414.2013.865254
The effect of short-duration sprint interval exercise on plasma postprandial triacylglycerol levels in young men
EDWARD ALLEN, PARTICK GRAY, ANGELIKI KOLLIAS-PEARSON, ERLEND OAG, KATRINA PRATT, JENNIFER HENDERSON, & STUART ROBERT GRAY Institute of Medical Sciences, University of Aberdeen, Foresterhill, Aberdeen, AB25 2ZD, UK
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(Accepted 10 November 2013)
Abstract 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 6 s sprints, interspersed with 24 s recovery (sprint interval exercise – 14 min for total exercise session). On day 2, participants consumed a high-fat meal for breakfast with blood samples collected at baseline, 2 h and 4 h. 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 (RER). The area under the curve for plasma triacylglycerol was 7.67 ± 2.37 mmol · l–1.4 h–1 in the control trial and 7.26 ± 2.49 mmol · l–1.4 h–1 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. Keywords: lipids, sprint, exercise, cardiovascular
Introduction 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 (Dahlöf, 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 CVD (Bansal et al., 2007; Nordestgaard, Benn, Schnohr, & Tybjarg-Hansen, 2007). The precise link between postprandial triacylglycerol and subsequent CVD is not entirely clear, but in both, the generation of a state of oxidative stress (Anderson et al., 2001) and activation of the immune system have been implicated (Alipour et al., 2008; Friedman, Klatsky, & Siegelaub, 1974; Hansson, 2001; Vogel, 1997).
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 (Gill et al., 2004, 2006; Gill, Herd, Vora, & Hardman, 2003; Miyashita, Burns, & Stensel, 2008). The effect of resistance exercise on postprandial triacylglycerol is not as clear with some studies showing a benefit (Burns, Miyashita, Ueda, & Stensel, 2007; Petitt, Arngrimsson, & Cureton, 2003) and 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 (Townsend et al., 2012), with time being reported as one of the major barriers to performing exercise (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.
Correspondence: Stuart Robert Gray, Institute of Medical Sciences, University of Aberdeen, Foresterhill, Aberdeen, AB25 2ZD, UK. E-mail: [email protected] © 2014 Taylor & Francis
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Previous work from our lab has shown that five 30 s maximal sprints which were preceded, interspersed and followed by 4 min 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 lowintensity 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 2 weeks of sprint interval exercise training (six sessions of 8–12 * 10 s sprints) has no effect on body composition or insulin sensitivity (estimated by homeostatic model assessment-insulin resistance (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 meal. Methods Participants 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 CVD, smokers, hypertension (systolic/diastolic blood pressure >140/ 90 mmHg), diabetes, obese (BMI > 30 kg.m–2) 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 0.5 cm 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 callipers (Idass, Harpenden skinfold callipers, England, UK) at four sites (Bicep, triceps, sub scapula and supra iliac) to the nearest 0.1 mm 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 pm, participants completed either a control trial or a high-intensity exercise trial. On day 2 (beginning at 9 am), 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 min 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 24 s. This sprint exercise was repeated a further 19 times, with 24 s unloaded cycling in between each sprint. A 2 min cool-down of unloaded cycling was then performed. Control. During the control trial, participants sat and rested for 14 min. Day 2 Participants arrived at 8.45 am and rested for 15 min before a resting blood sample was collected from a vein in the antecubital fossa. A standardised 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, 87.6 g carbohydrate and 24.3 g protein. The mean time taken to consume the meal was 11.4 min.
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Further blood samples were collected at 2 h and 4 h after the breakfast meal. A 4 h 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 4 h 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.
of the triacylglycerol response during the 4 h test period. Calculated incremental and total AUC values were compared between trials using paired t-tests. To compare differences between the two trials over time, a two-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 x– ± s.
Measurements
Results
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 2300 g at 4°C for 10 min. 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%.
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 1).
Triacylglycerol The ANOVA revealed no group or interaction effects when comparing plasma triacylglycerol concentration. However there was a significant effect of time in response to the meal (P < 0.05) (Figure 2). When the data were analysed in the form, 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.
Statistical analysis Data were analysed with the use of Prism 5 software (GraphPad Software, La Jolla, CA, USA). 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 (AUC) values were calculated to provide a summary
Respiratory exchange ratio (RER) 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).
Figure 1. Plasma glucose (A) and insulin (B) concentrations in response to high-intensity exercise and control trials. Values are x– ± s (n = 15).
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Figure 2. Plasma triacylglycerol concentration (A) and RER (B) in response to high intensity exercise and control trials. Values are x– ± s (n = 15).
Figure 3. Triacylglycerol total (A) and incremental (B) area under the curve (AUC) over the 4 h experimental period during high-intensity exercise and control trials. Values are x– ± s (n = 15).
Discussion The main finding of the current study is that a shortduration 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 which have found that highintensity interval exercise, employing four to five 30 s sprints, can reduce postprandial triacylglycerol (Freese, Levine, Chapman, Hausman, & Cureton, 2011; Gabriel et al., 2012). On the other hand, longer-duration high-intensity interval exercise (4 min intervals at 85–95% maximal heart rate (HRmax)) has been demonstrated to have no effect on postprandial triacylglycerol, although flowmediated dilation was improved (Tyldum et al., 2009). Furthermore, 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 highintensity 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 30 s 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 15 s of a 30 s sprint, this is not the case for the final 15 s 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
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High-intensity exercise and postprandial lipaemia 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 120 kcal. Suggesting that this level of energy expenditure is not sufficient to cause a reduction in postprandial triacylglycerol would seem unlikely as the total exercise duration of 120 s 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 30 s 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 a decrease in postprandial triacylglycerol after exercise using such 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 out of 24 individuals actually increasing postprandial triacylglycerol (Burns et al., 2007) compared to 6 out of 15 individuals increasing postprandial triacylglycerol, in response to sprint interval exercise, in the current study. Apart from the six participants who increased postprandial triacylglycerol, 2 out of 15 had no change, giving a total of eight participants who did not have a positive response to such exercise. Similar observations to those of the current study have been demonstrated after moderate-intensity exercise in
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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. Indeed the variation in the response of measures, such as aerobic capacity, blood pressure and blood lipids, after exercise training 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 were examined. References Alipour, A., van Oostrom, A. J., Izraeljan, A., Verseyden, C., Collins, J. M., Frayn, K. N., … Castro, C. M. (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., … Frenneaux, M. P. (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. Medicine & Science in Sports & Exercise, 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., … Rao, D. C. (1999). Familial aggregation of V-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., Häkkinen, K., … Rankinen, T. (2012). Adverse metabolic response to regular exercise: Is it a rare or common occurrence? PLoS ONE, 7, e37887.
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Journal of Sports Sciences Publication details, including instructions for authors and subscription information: http://www.tandfonline.com/loi/rjsp20
The effect of short-duration sprint interval exercise on plasma postprandial triacylglycerol levels in young men a
a
a
a
a
Edward Allen , Partick Gray , Angeliki Kollias-Pearson , Erlend Oag , Katrina Pratt , Jennifer a
Henderson & Stuart Robert Gray
a
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Institute of Medical Sciences, University of Aberdeen, Foresterhill, Aberdeen, AB25 2ZD, UK Published online: 06 Feb 2014.
To cite this article: Edward Allen, Partick Gray, Angeliki Kollias-Pearson, Erlend Oag, Katrina Pratt, Jennifer Henderson & Stuart Robert Gray (2014) The effect of short-duration sprint interval exercise on plasma postprandial triacylglycerol levels in young men, Journal of Sports Sciences, 32:10, 911-916, DOI: 10.1080/02640414.2013.865254 To link to this article: http://dx.doi.org/10.1080/02640414.2013.865254
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Journal of Sports Sciences, 2014 Vol. 32, No. 10, 911–916, http://dx.doi.org/10.1080/02640414.2013.865254
The effect of short-duration sprint interval exercise on plasma postprandial triacylglycerol levels in young men
EDWARD ALLEN, PARTICK GRAY, ANGELIKI KOLLIAS-PEARSON, ERLEND OAG, KATRINA PRATT, JENNIFER HENDERSON, & STUART ROBERT GRAY Institute of Medical Sciences, University of Aberdeen, Foresterhill, Aberdeen, AB25 2ZD, UK
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(Accepted 10 November 2013)
Abstract 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 6 s sprints, interspersed with 24 s recovery (sprint interval exercise – 14 min for total exercise session). On day 2, participants consumed a high-fat meal for breakfast with blood samples collected at baseline, 2 h and 4 h. 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 (RER). The area under the curve for plasma triacylglycerol was 7.67 ± 2.37 mmol · l–1.4 h–1 in the control trial and 7.26 ± 2.49 mmol · l–1.4 h–1 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. Keywords: lipids, sprint, exercise, cardiovascular
Introduction 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 (Dahlöf, 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 CVD (Bansal et al., 2007; Nordestgaard, Benn, Schnohr, & Tybjarg-Hansen, 2007). The precise link between postprandial triacylglycerol and subsequent CVD is not entirely clear, but in both, the generation of a state of oxidative stress (Anderson et al., 2001) and activation of the immune system have been implicated (Alipour et al., 2008; Friedman, Klatsky, & Siegelaub, 1974; Hansson, 2001; Vogel, 1997).
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 (Gill et al., 2004, 2006; Gill, Herd, Vora, & Hardman, 2003; Miyashita, Burns, & Stensel, 2008). The effect of resistance exercise on postprandial triacylglycerol is not as clear with some studies showing a benefit (Burns, Miyashita, Ueda, & Stensel, 2007; Petitt, Arngrimsson, & Cureton, 2003) and 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 (Townsend et al., 2012), with time being reported as one of the major barriers to performing exercise (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.
Correspondence: Stuart Robert Gray, Institute of Medical Sciences, University of Aberdeen, Foresterhill, Aberdeen, AB25 2ZD, UK. E-mail: [email protected] © 2014 Taylor & Francis
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Previous work from our lab has shown that five 30 s maximal sprints which were preceded, interspersed and followed by 4 min 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 lowintensity 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 2 weeks of sprint interval exercise training (six sessions of 8–12 * 10 s sprints) has no effect on body composition or insulin sensitivity (estimated by homeostatic model assessment-insulin resistance (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 meal. Methods Participants 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 CVD, smokers, hypertension (systolic/diastolic blood pressure >140/ 90 mmHg), diabetes, obese (BMI > 30 kg.m–2) 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 0.5 cm 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 callipers (Idass, Harpenden skinfold callipers, England, UK) at four sites (Bicep, triceps, sub scapula and supra iliac) to the nearest 0.1 mm 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 pm, participants completed either a control trial or a high-intensity exercise trial. On day 2 (beginning at 9 am), 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 min 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 24 s. This sprint exercise was repeated a further 19 times, with 24 s unloaded cycling in between each sprint. A 2 min cool-down of unloaded cycling was then performed. Control. During the control trial, participants sat and rested for 14 min. Day 2 Participants arrived at 8.45 am and rested for 15 min before a resting blood sample was collected from a vein in the antecubital fossa. A standardised 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, 87.6 g carbohydrate and 24.3 g protein. The mean time taken to consume the meal was 11.4 min.
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Further blood samples were collected at 2 h and 4 h after the breakfast meal. A 4 h 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 4 h 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.
of the triacylglycerol response during the 4 h test period. Calculated incremental and total AUC values were compared between trials using paired t-tests. To compare differences between the two trials over time, a two-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 x– ± s.
Measurements
Results
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 2300 g at 4°C for 10 min. 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%.
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 1).
Triacylglycerol The ANOVA revealed no group or interaction effects when comparing plasma triacylglycerol concentration. However there was a significant effect of time in response to the meal (P < 0.05) (Figure 2). When the data were analysed in the form, 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.
Statistical analysis Data were analysed with the use of Prism 5 software (GraphPad Software, La Jolla, CA, USA). 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 (AUC) values were calculated to provide a summary
Respiratory exchange ratio (RER) 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).
Figure 1. Plasma glucose (A) and insulin (B) concentrations in response to high-intensity exercise and control trials. Values are x– ± s (n = 15).
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Figure 2. Plasma triacylglycerol concentration (A) and RER (B) in response to high intensity exercise and control trials. Values are x– ± s (n = 15).
Figure 3. Triacylglycerol total (A) and incremental (B) area under the curve (AUC) over the 4 h experimental period during high-intensity exercise and control trials. Values are x– ± s (n = 15).
Discussion The main finding of the current study is that a shortduration 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 which have found that highintensity interval exercise, employing four to five 30 s sprints, can reduce postprandial triacylglycerol (Freese, Levine, Chapman, Hausman, & Cureton, 2011; Gabriel et al., 2012). On the other hand, longer-duration high-intensity interval exercise (4 min intervals at 85–95% maximal heart rate (HRmax)) has been demonstrated to have no effect on postprandial triacylglycerol, although flowmediated dilation was improved (Tyldum et al., 2009). Furthermore, 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 highintensity 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 30 s 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 15 s of a 30 s sprint, this is not the case for the final 15 s 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
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High-intensity exercise and postprandial lipaemia 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 120 kcal. Suggesting that this level of energy expenditure is not sufficient to cause a reduction in postprandial triacylglycerol would seem unlikely as the total exercise duration of 120 s 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 30 s 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 a decrease in postprandial triacylglycerol after exercise using such 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 out of 24 individuals actually increasing postprandial triacylglycerol (Burns et al., 2007) compared to 6 out of 15 individuals increasing postprandial triacylglycerol, in response to sprint interval exercise, in the current study. Apart from the six participants who increased postprandial triacylglycerol, 2 out of 15 had no change, giving a total of eight participants who did not have a positive response to such exercise. Similar observations to those of the current study have been demonstrated after moderate-intensity exercise in
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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. Indeed the variation in the response of measures, such as aerobic capacity, blood pressure and blood lipids, after exercise training 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 were examined. References Alipour, A., van Oostrom, A. J., Izraeljan, A., Verseyden, C., Collins, J. M., Frayn, K. N., … Castro, C. M. (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., … Frenneaux, M. P. (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. Medicine & Science in Sports & Exercise, 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., … Rao, D. C. (1999). Familial aggregation of V-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., Häkkinen, K., … Rankinen, T. (2012). Adverse metabolic response to regular exercise: Is it a rare or common occurrence? PLoS ONE, 7, e37887.
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