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Clinical Trial
. 2015 Mar 1;118(5):624-34.
doi: 10.1152/japplphysiol.00917.2014. Epub 2014 Dec 24.

Postdinner resistance exercise improves postprandial risk factors more effectively than predinner resistance exercise in patients with type 2 diabetes

Affiliations
Clinical Trial

Postdinner resistance exercise improves postprandial risk factors more effectively than predinner resistance exercise in patients with type 2 diabetes

Timothy D Heden et al. J Appl Physiol (1985). .

Abstract

Abnormally elevated postprandial glucose and triacylglycerol (TAG) concentrations are risk factors for cardiovascular disease in type 2 diabetes. The most effective time to exercise to lower postprandial glucose and TAG concentrations is unknown. Thus the aim of this study was to determine what time is more effective, either pre- or postdinner resistance exercise (RE), at improving postprandial risk factors in patients with type 2 diabetes. Thirteen obese patients with type 2 diabetes completed three trials in a random order in which they consumed a dinner meal with 1) no RE (NoRE), 2) predinner RE (RE → M), and 3) postdinner RE beginning 45 min after dinner (M → RE). Clinical outcome measures included postprandial glucose and TAG concentrations. In addition, postprandial acetaminophen (gastric emptying), endocrine responses, free fatty acids, and β-cell function (mathematical modeling) were measured to determine whether these factors were related to changes in glucose and TAG. The TAG incremental area under the curve (iAUC) was ∼92% lower (P ≤ 0.02) during M → RE compared with NoRE and RE → M, an effect due in part to lower very-low-density lipoprotein-1 TAG concentrations. The glucose iAUC was reduced (P = 0.02) by ∼18 and 30% during the RE → M and M → RE trials, respectively, compared with NoRE, with no difference between RE trials. RE → M and M → RE reduced the insulin iAUC by 35 and 48%, respectively, compared with NoRE (P < 0.01). The glucagon-like peptide-1 iAUC was ∼50% lower (P ≤ 0.02) during M → RE compared with NoRE and RE → M. Given that predinner RE only improves postprandial glucose concentrations, whereas postdinner RE improves both postprandial glucose and TAG concentrations, postdinner RE may lower the risk of cardiovascular disease more effectively.

Keywords: exercise timing; glucose metabolism; glycemic control; lipid metabolism; obesity; weight training.

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Figures

Fig. 1.
Fig. 1.
Total, exogenous, and endogenous triacylglycerol (TAG) responses to the dinner meal with pre- or postdinner resistance exercise or no exercise. A, C, E, G: total, chylomicron, very-low-density lipoprotein (VLDL)-1, and VLDL-2 TAG time course, respectively. In the time course figures, the space in between the vertical dashed lines represents the time frame when resistance exercise was performed during the indicated trial. B, D, F, H: total, chylomicron, VLDL-1, and VLDL-2 TAG incremental area under the curve (iAUC), respectively. NoRE, no resistance exercise; RE → M, resistance exercise performed before dinner consumption; M → RE, dinner consumption before resistance exercise. Values are means ± SE; n = 13 subjects.
Fig. 2.
Fig. 2.
Glucose and insulin responses to the dinner meal with pre- or postdinner resistance exercise or no exercise. A and D: glucose and insulin time course, respectively. In the time course figures, the space in between the vertical dashed lines represents the time frame when resistance exercise was performed during the indicated trial. B and E: premeal glucose and insulin iAUC, respectively. C and F: postmeal glucose and insulin iAUC, respectively. Values are means ± SE; n = 13 subjects.
Fig. 3.
Fig. 3.
Insulin secretion or clearance responses to the dinner meal with pre- or postdinner resistance exercise or no exercise. A and C: insulin secretion response (ISR) and insulin clearance time course, respectively. In the time course figures, the space in between the vertical dashed lines represents the time frame when resistance exercise was performed during the indicated trial. B and D: postmeal ISR and insulin clearance iAUC, respectively. Values are means ± SE; n = 13 subjects.
Fig. 4.
Fig. 4.
Gut hormone and free fatty acid responses to the dinner meal with pre- or postdinner resistance exercise or no exercise. A, D, and G: glucose-dependent insulinotropic polypeptide (GIP), glucagon-like peptide-1 (GLP-1), and free fatty acid (FFA) time course, respectively. In the time course figures, the space in between the vertical dashed lines represents the time frame when resistance exercise was performed during the indicated trial. B, E, and H: premeal GIP, GLP-1, and FFA iAUC, respectively. C, F, and I: postmeal GIP, GLP-1, and FFA iAUC, respectively. Values are means ± SE; n = 13 subjects.
Fig. 5.
Fig. 5.
C-peptide and glucagon responses to the dinner meal with pre- or postdinner resistance exercise or no exercise. A and D: C-peptide and glucagon time course, respectively. In the time course figures, the space in between the vertical dashed lines represents the time frame when resistance exercise was performed during the indicated trial. B and E: premeal C-peptide and glucagon iAUC, respectively. C and F: postmeal C-peptide and glucagon iAUC, respectively. Values are means ± SE; n = 13 subjects.
Fig. 6.
Fig. 6.
Subjective well-being responses to the dinner meal with pre- or postdinner resistance exercise or no exercise. A and C: premeal and postmeal change in well-being, respectively. In the time course figures, the space in between the vertical dashed lines represents the time frame when resistance exercise was performed during the indicated trial. B and D: premeal and postmeal well-being iAUC, respectively. Values are means ± SE; n = 13 subjects.

Comment in

  • Exercising tactically for metabolic control.
    Chacko E. Chacko E. J Appl Physiol (1985). 2015 Apr 15;118(8):1088. doi: 10.1152/japplphysiol.00050.2015. J Appl Physiol (1985). 2015. PMID: 25878222 No abstract available.
  • Reply to Dr. Chacko.
    Heden TD, Kanaley JA. Heden TD, et al. J Appl Physiol (1985). 2015 Apr 15;118(8):1089. doi: 10.1152/japplphysiol.00081.2015. J Appl Physiol (1985). 2015. PMID: 25878223 Free PMC article. No abstract available.
  • Clarifications.
    Chacko E. Chacko E. J Appl Physiol (1985). 2015 Jul 15;119(2):159. doi: 10.1152/japplphysiol.00351.2015. J Appl Physiol (1985). 2015. PMID: 26177973 No abstract available.
  • Reply to Dr. Chacko.
    Heden TD, Kanaley JA. Heden TD, et al. J Appl Physiol (1985). 2015 Jul 15;119(2):160. doi: 10.1152/japplphysiol.00372.2015. J Appl Physiol (1985). 2015. PMID: 26177974 No abstract available.

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