Fast food increases postprandial cardiac workload in type 2 diabetes independent of pre-exercise: A pilot study

Siri Marte Hollekim-Strand, Vegard Malmo, Turid Follestad, Ulrik Wisløff, Charlotte Björk Ingul, Siri Marte Hollekim-Strand, Vegard Malmo, Turid Follestad, Ulrik Wisløff, Charlotte Björk Ingul

Abstract

Background: Type 2 diabetes aggravates the postprandial metabolic effects of food, which increase cardiovascular risk. We investigated the acute effects of fast food on postprandial left ventricular (LV) function and the potential effects of pre-exercise in type 2 diabetes individuals.

Methods: We used a cross-over study including 10 type 2 diabetes individuals (7 male and 3 females; 53.4 ± 8.1 years; 28.3 ± 3.8 kg/m(2); type 2 diabetes duration 3.1 ± 1.8 years) and 10 controls (7 male and 3 females; 52.8 ± 10.1 years; 28.5 ± 4.2 kg/m(2)) performing high intensity interval exercise (HIIE; 40 min, 4 × 4 min intervals, 90-95% HRmax), moderate intensity exercise (MIE; 47 min, 70% HRmax) and no exercise (NE) in a random order 16-18 hours prior to fast-food ingestion. Baseline echocardiography, blood pressure and biochemical measurements were recorded prior to and 16-18 hours after exercise, and 30 minutes, 2 hours and 4 hours after fast food ingestion.

Results: LV diastolic (peak early diastolic tissue velocity, peak early diastolic filling velocity), and systolic workload (global strain rate, peak systolic tissue velocity, rate pressure product) increased after consumption of fast food in both groups. In contrast to controls, the type 2 diabetes group had prolonged elevations in resting heart rate and indications of prolonged elevations in diastolic workload (peak early diastolic tissue velocity) as well as reduced systolic blood pressure after fast food consumption. No significant modifications due to exercise in the postprandial phase were seen in any group.

Conclusions: Our findings indicate that fast-food induces greater and sustained overall cardiac workload in type 2 diabetes individuals versus body mass index and age matched controls; exercise 16-18 hours pre-meal has no acute effects to the postprandial phase.

Trial registration: ClinicalTrials.gov: NCT01991769.

Figures

Fig. 1
Fig. 1
Effects of fast food (left panel; all trials combined) and exercise (right panel; high intensity interval exercise +moderate intensity exercise vs. no exercise) on left ventricular diastolic function. Abbreviations: BL, baseline; C, control group; e’, peak early diastolic tissue Doppler velocity; E/e’ , filling pressure; E, peak early filling velocity; HIIE, high intensity interval exercise; HIIE+MIE, exercise combined; IVRT, isovolumic relaxation time; MIE, moderate intensity exercise; NE, no exercise; T2D, type 2 diabetes group. Estimated means and 95 % CIs from LMMs with the factors time, group and their interaction (left panel, figures a-d), and with the factors time, group, trial and their interactions (right panel, figures E-H). In the left panel significant (p < 0.01) time differences are indicated by *(from BL1), † (from BL2), ‡ (from food +30 min) and § (from food +2 h). For peak early filling velocity (e) there is no significant time and group interaction, and the indicated significant time differences refer to the main effect of time for both groups
Fig. 2
Fig. 2
Effects of fast food (left panel; all trials combined) and exercise (right panel; high intensity interval exercise +moderate intensity exercise vs. no exercise) on left ventricular systolic function. Abbreviations: BL, baseline; C, control group; HIIE, high intensity exercise; HIIE+MIE, exercise combined; MIE, moderate intensity exercise; NE, no exercise; S' , peak systolic tissue Doppler velocity; T2D, type 2 diabetes group. Estimated means and 95 % CIs from LMMs with the factors time, group and their interaction (left panel, figures a-b), and with the factors time, group, trial and their interactions (right panel, figures c-d). In the left panel significant (p < 0.01) time differences are indicated by *(from BL1), † (from BL2), ‡ (from food +30 min) and § (from food +2 h). For S' and global strain rate there is no significant time and group interaction, and the indicated significant time differences refer to the main effect of time for both groups
Fig. 3
Fig. 3
Effects of fast food (left panel; all trials combined) and exercise (right panel; high intensity interval exercise+moderate intensity exercise vs. no exercise) on resting heart rate and blood pressure. Abbreviations: BL, baseline; BP, blood pressure; C, control group; HIIE, high intensity exercise; HIIE+MIE, exercise combined; HR, resting heart rate; MIE; moderate intensity exercise; NE, no exercise; RPP, rate pressure product; T2D, type 2 diabetes group. Estimated means and 95 % CIs from LMMs with the factors time, group and their interaction (left panel, figures a-d), and with the factors time, group, trial and their interactions (right panel, figures e-h). In the left panel significant (p < 0.01) time differences are indicated by *(from BL1), † (from BL2), ‡ (from food +30 min) and § (from food +2 h). For diastolic BP there is no significant time and group interaction, and the indicated significant time differences refer to the main effect of time for both groups. For RPP, the means and CIs are shown as back-transformed values, computed by direct exponentiation of the means and CIs from the LMM based on log-transformed data
Fig. 4
Fig. 4
Effects of fast food (left panel, trials combined) and exercise (right panel; high intensity interval exercise+moderate intensity exercise vs. no exercise) on blood glucose, C-peptide, triglycerides and total antioxidant status. Abbreviations: BL, baseline; C, control group; HIIE,  high intensity exercise; HIIE+MIE, exercise combined; MIE, moderate intensity exercise; NE, no exercise; TAS, total antioxidant status; T2D, type 2 diabetes group. Estimated means and 95 % CIs from LMMs with the factors time, group and their interaction (left panel, figures a-d), and with the factors time, group, trial and their interactions (right panel, figures e-h). In the left panel significant (p < 0.01) time differences are indicated by *(from BL1), † (from BL2), ‡ (from food +30 min) and § (from food +2 h). For triglycerides there is no significant time and group interaction, and the indicated significant time differences refer to the main effect of time for both groups. Except for TAS, the means and CIs are shown as back-transformed values, computed by direct exponentiation of the means and CIs from the LMMs based on log-transformed data

References

    1. Cavalot F, Pagliarino A, Valle M, Di Martino L, Bonomo K, Massucco P, Anfossi G, Trovati M. Postprandial blood glucose predicts cardiovascular events and all-cause mortality in type 2 diabetes in a 14-year follow-up: lessons from the San Luigi Gonzaga Diabetes Study. Diabetes Care. 2011;34:2237–2243. doi: 10.2337/dc10-2414.
    1. Pereira MA, Kartashov AI, Ebbeling CB, Van Horn L, Slattery ML, Jacobs DR, Jr, Ludwig DS. Fast-food habits, weight gain, and insulin resistance (the CARDIA study): 15-year prospective analysis. Lancet. 2005;365:36–42. doi: 10.1016/S0140-6736(04)17663-0.
    1. Eberly LE, Stamler J, Neaton JD, Multiple Risk Factor Intervention Trial Research G Relation of triglyceride levels, fasting and nonfasting, to fatal and nonfatal coronary heart disease. Arch Intern Med. 2003;163:1077–1083. doi: 10.1001/archinte.163.9.1077.
    1. Stephenson EJ, Smiles W, Hawley JA. The Relationship between Exercise, Nutrition and Type 2 Diabetes. Med Sport Sci. 2014;60:1–10. doi: 10.1159/000357331.
    1. de Simone G, Devereux RB, Chinali M, Lee ET, Galloway JM, Barac A, Panza JA, Howard BV. Diabetes and incident heart failure in hypertensive and normotensive participants of the Strong Heart Study. J Hypertens. 2010;28:353–360. doi: 10.1097/HJH.0b013e3283331169.
    1. Hollekim-Strand SM, Bjorgaas MR, Albrektsen G, Tjonna AE, Wisloff U, Ingul CB. High-intensity interval exercise effectively improves cardiac function in patients with type 2 diabetes mellitus and diastolic dysfunction: a randomized controlled trial. J Am Coll Cardiol. 2014;64:1758–1760. doi: 10.1016/j.jacc.2014.07.971.
    1. Ceriello A, Quagliaro L, Piconi L, Assaloni R, Da Ros R, Maier A, Esposito K, Giugliano D. Effect of postprandial hypertriglyceridemia and hyperglycemia on circulating adhesion molecules and oxidative stress generation and the possible role of simvastatin treatment. Diabetes. 2004;53:701–710. doi: 10.2337/diabetes.53.3.701.
    1. Tyldum GA, Schjerve IE, Tjonna AE, Kirkeby-Garstad I, Stolen TO, Richardson RS, Wisloff U. Endothelial dysfunction induced by post-prandial lipemia: complete protection afforded by high-intensity aerobic interval exercise. J Am Coll Cardiol. 2009;53:200–206. doi: 10.1016/j.jacc.2008.09.033.
    1. von Bibra H, St John Sutton M, Schuster T, Ceriello A, Siegmund T, Schumm-Draeger PM. Oxidative stress after a carbohydrate meal contributes to the deterioration of diastolic cardiac function in nonhypertensive insulin-treated patients with moderately well controlled type 2 diabetes. Horm Metab Res. 2013;45:449–455. doi: 10.1055/s-0033-1333752.
    1. Holland DJ, Erne D, Kostner K, Leano R, Haluska BA, Marwick TH, Sharman JE. Acute elevation of triglycerides increases left ventricular contractility and alters ventricular-vascular interaction. Am J Physiol Heart Circ Physiol. 2011;301:H123–128. doi: 10.1152/ajpheart.00102.2011.
    1. Gillen JB, Little JP, Punthakee Z, Tarnopolsky MA, Riddell MC, Gibala MJ. Acute high-intensity interval exercise reduces the postprandial glucose response and prevalence of hyperglycaemia in patients with type 2 diabetes. Diabetes Obes Metab. 2012;14:575–577. doi: 10.1111/j.1463-1326.2012.01564.x.
    1. Karstoft K, Christensen CS, Pedersen BK, Solomon TP. The acute effects of interval- Vs continuous-walking exercise on glycemic control in subjects with type 2 diabetes: a crossover, controlled study. J Clin Endocrinol Metab. 2014;99:3334–3342. doi: 10.1210/jc.2014-1837.
    1. International Diabetes Federation: Global Guideline for Type 2 Diabetes Available at: Accessed March 28, 20142012.
    1. Rognmo O, Hetland E, Helgerud J, Hoff J, Slordahl SA. High intensity aerobic interval exercise is superior to moderate intensity exercise for increasing aerobic capacity in patients with coronary artery disease. Eur J Cardiovasc Prev Rehabil. 2004;11:216–222. doi: 10.1097/01.hjr.0000131677.96762.0c.
    1. Thorstensen A, Dalen H, Amundsen BH, Aase SA, Stoylen A. Reproducibility in echocardiographic assessment of the left ventricular global and regional function, the HUNT study. Eur J Echocardiogr. 2010;11:149–156. doi: 10.1093/ejechocard/jep188.
    1. Ommen SR, Nishimura RA, Appleton CP, Miller FA, Oh JK, Redfield MM, Tajik AJ. Clinical utility of Doppler echocardiography and tissue Doppler imaging in the estimation of left ventricular filling pressures: A comparative simultaneous Doppler-catheterization study. Circulation. 2000;102:1788–1794. doi: 10.1161/01.CIR.102.15.1788.
    1. Reisner SA, Lysyansky P, Agmon Y, Mutlak D, Lessick J, Friedman Z. Global longitudinal strain: a novel index of left ventricular systolic function. J Am Soc Echocardiogr. 2004;17:630–633. doi: 10.1016/j.echo.2004.02.011.
    1. Lang RM, Bierig M, Devereux RB, Flachskampf FA, Foster E, Pellikka PA, Picard MH, Roman MJ, Seward J, Shanewise JS, et al. Recommendations for chamber quantification: a report from the American Society of Echocardiography's Guidelines and Standards Committee and the Chamber Quantification Writing Group, developed in conjunction with the European Association of Echocardiography, a branch of the European Society of Cardiology. J Am Soc Echocardiogr. 2005;18:1440–1463. doi: 10.1016/j.echo.2005.10.005.
    1. Wisloff U, Stoylen A, Loennechen JP, Bruvold M, Rognmo O, Haram PM, Tjonna AE, Helgerud J, Slordahl SA, Lee SJ, et al. Superior cardiovascular effect of aerobic interval training versus moderate continuous training in heart failure patients: a randomized study. Circulation. 2007;115:3086–3094. doi: 10.1161/CIRCULATIONAHA.106.675041.
    1. Fitzmaurice GM, Laird NM, Ware JH. Applied Longitudinal Analysis. New York: Wiley; 2004. pp. 126–132.
    1. Team RC . R: A Language and Environment for Statistical Computing. Vienna, Austria: R Foundation for Statistical Computing; 2014.
    1. Nielsen R, Norrelund H, Kampmann U, Botker HE, Moller N, Wiggers H. Effect of acute hyperglycemia on left ventricular contractile function in diabetic patients with and without heart failure: two randomized cross-over studies. PLoS One. 2013;8:e53247. doi: 10.1371/journal.pone.0053247.
    1. Valensi P, Chiheb S, Fysekidis M. Insulin- and glucagon-like peptide-1-induced changes in heart rate and vagosympathetic activity: why they matter. Diabetologia. 2013;56:1196–1200. doi: 10.1007/s00125-013-2909-x.
    1. Paolisso G, Manzella D, Rizzo MR, Barbieri M, Gambardella A, Varricchio M. Effects of glucose ingestion on cardiac autonomic nervous system in healthy centenarians: differences with aged subjects. Eur J Clin Invest. 2000;30:277–284. doi: 10.1046/j.1365-2362.2000.00626.x.
    1. Paolisso G, Manzella D, Rizzo MR, Ragno E, Barbieri M, Varricchio G, Varricchio M. Elevated plasma fatty acid concentrations stimulate the cardiac autonomic nervous system in healthy subjects. Am J Clin Nutr. 2000;72:723–730.
    1. Nielsen R, Norrelund H, Kampmann U, Kim WY, Ringgaard S, Schar M, Moller N, Botker HE, Wiggers H. Failing heart of patients with type 2 diabetes mellitus can adapt to extreme short-term increases in circulating lipids and does not display features of acute myocardial lipotoxicity. Circ Heart Fail. 2013;6:845–852. doi: 10.1161/CIRCHEARTFAILURE.113.000187.
    1. Jansen RW, Lipsitz LA. Postprandial hypotension: epidemiology, pathophysiology, and clinical management. Ann Intern Med. 1995;122:286–295. doi: 10.7326/0003-4819-122-4-199502150-00009.
    1. Tabara Y, Okada Y, Uetani E, Nagai T, Igase M, Kido T, Ochi N, Ohara M, Takita R, Kohara K, Miki T. Postprandial hypotension as a risk marker for asymptomatic lacunar infarction. J Hypertens. 2014;32:1084–1090. doi: 10.1097/HJH.0000000000000150.
    1. Lipsitz LA, Ryan SM, Parker JA, Freeman R, Wei JY, Goldberger AL. Hemodynamic and autonomic nervous system responses to mixed meal ingestion in healthy young and old subjects and dysautonomic patients with postprandial hypotension. Circulation. 1993;87:391–400. doi: 10.1161/01.CIR.87.2.391.
    1. Luciano GL, Brennan MJ, Rothberg MB. Postprandial hypotension. Am J Med. 2010;123:281 e281–286. doi: 10.1016/j.amjmed.2009.06.026.
    1. Parati G, Bilo G. Postprandial blood pressure fall: another dangerous face of blood pressure variability. J Hypertens. 2014;32:983–985. doi: 10.1097/HJH.0000000000000172.
    1. Gudmundsdottir FD: Effects of two different types of fast food on postprandial metabolism in normal- and overweight subjects. MSc thesis. University of Iceland Faculty of Food Science and Nutrition, School of Health Sciences 2012.
    1. Zhang JQ, Ji LL, Nunez G, Feathers S, Hart CL, Yao WX. Effect of exercise timing on postprandial lipemia in hypertriglyceridemic men. Can J Appl Physiol. 2004;29:590–603. doi: 10.1139/h04-038.
    1. Gill JM, Al-Mamari A, Ferrell WR, Cleland SJ, Packard CJ, Sattar N, Petrie JR, Caslake MJ. Effects of prior moderate exercise on postprandial metabolism and vascular function in lean and centrally obese men. J Am Coll Cardiol. 2004;44:2375–2382. doi: 10.1016/j.jacc.2004.09.035.
    1. van Dijk JW, Manders RJ, Tummers K, Bonomi AG, Stehouwer CD, Hartgens F, van Loon LJ. Both resistance- and endurance-type exercise reduce the prevalence of hyperglycaemia in individuals with impaired glucose tolerance and in insulin-treated and non-insulin-treated type 2 diabetic patients. Diabetologia. 2012;55:1273–1282. doi: 10.1007/s00125-011-2380-5.
    1. 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;51:11–22. doi: 10.1016/j.plipres.2011.11.002.
    1. Poirier P, Tremblay A, Catellier C, Tancrede G, Garneau C, Nadeau A. Impact of time interval from the last meal on glucose response to exercise in subjects with type 2 diabetes. J Clin Endocrinol Metab. 2000;85:2860–2864.
    1. Zhang JQ, Thomas TR, Ball SD. Effect of exercise timing on postprandial lipemia and HDL cholesterol subfractions. J Appl Physiol (1985) 1998;85:1516–1522.
    1. Mak GS, Sawaya H, Khan AM, Arora P, Martinez A, Ryan A, Ernande L, Newton-Cheh C, Wang TJ, Scherrer-Crosbie M. Effects of subacute dietary salt intake and acute volume expansion on diastolic function in young normotensive individuals. Eur Heart J Cardiovasc Imaging. 2013;14:1092–1098. doi: 10.1093/ehjci/jet036.
    1. Tzemos N, Lim PO, Wong S, Struthers AD, MacDonald TM. Adverse cardiovascular effects of acute salt loading in young normotensive individuals. Hypertension. 2008;51:1525–1530. doi: 10.1161/HYPERTENSIONAHA.108.109868.

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