The Effect of a Detraining Period after Two Type Concurrent Training on the Exercise ‎Performance and HbA1c in Women with Type II Diabetes

Document Type : Original Article

Authors

Department of Exercise Physiology, Faculty of Psychology and Educational Sciences, Shiraz University, Shiraz, Iran

Abstract

Purpose:
The purpose of this study was to investigate the effect of a period of detraining following two types of concurrent training on glycosylated hemoglobin and exercise performance in women with type 2 diabetes.
Methods:
Twenty-three women with type II diabetes mellitus in Shiraz, randomly were divided into three groups: control group that performed one day endurance training and one day resistance training (Different Day), and a group that performed endurance and resistance exercises in one day (Same Day). Before and after 8 weeks of concurrent training and after four weeks of detraining, glycosylated hemoglobin (Hb A1c) measured after 12 hours of fasting. Maximum oxygen consumption (VO2max) and Time to Exhaustion (TTE) was also calculated through the implementation of the Balkan test on the treadmill.
Results:
Two months of concurrent training in both groups of training significantly decreased Hb A1c, a significantly increased in VO2max and TTE in women with type II diabetes (p≤0.05). One month after the concurrent training in SD group resulted in a significant decrease in VO2max and TTE (p ≥0.05), but this decrease was not statistically significant in the DD group. Increase in Hb A1c after detraining was not statistically significant in both training groups (p ≥0.05).
Conclusions:
The findings indicate that concurrent training improves glycemic control and increases exercise performance (VO2max and TTE) in women with type II diabetes, but doing DD concurrent training results to keep longer outcomes of training in the detraining periods.

Keywords


  1. Bhaskarabhatla KV, Birrer R. Physical activity and type 2 diabetes: tailoring exercise to optimize fitness and glycemic control. Phys Sportsmed 2004; 32(1): 13-17.
  2. Schleicher E, Wieland O. Protein glycation: measurement and clinical relevance. J Clin Chem Clin Biochem 1989; 27(9): 577-587.
  3. Sigal RJ, Kenny GP, Boulé NG, Wells GA, et al. Effects of aerobic training, resistance training, or both on glycemic control in type 2 diabetes: a randomized trial. Annals of internal medicine 2007; 147(6): 357-369. 
  4. Colberg SR, Sigal RJ, Fernhall B, Regensteiner JG, et al. Exercise and type 2 diabetes: the American College of Sports Medicine and the American Diabetes Association: joint position statement. Diabetes care 2010; 33(12): e147-e67.
  5. Albright A, Franz M, Hornsby G, Kriska A, et al. American College of Sports Medicine position stand. Exercise and type 2 diabetes. Medicine and science in sports and exercise 2000; 32(7): 1345-1360.
  6. Wilmore JH, Costill DL, Kenney WL. Physiology of sport and exercise: Human kinetics Champaign, IL; 1994.
  7. Higgins PJ, Bunn HF. Kinetic analysis of the nonenzymatic glycosylation of hemoglobin. Journal of Biological Chemistry 1981; 256(10): 5204-5208.
  8. Gochman DS. Provider determinants of health behavior.  Handbook of Health Behavior Research II: Springer; 1997: 397-417.
  9. Larose J. The effect of exercise training on physical fitness in type 2 diabetes mellitus: University of Ottawa (Canada); 2009.
  10. Karstoft K, Pedersen BK. Exercise and type 2 diabetes: focus on metabolism and inflammation. Immunology and cell biology 2016; 94(2): 146-150.
  11. Eklund D, Häkkinen A, Laukkanen JA, Balandzic M, et al. Fitness, body composition and blood lipids following 3 concurrent strength and endurance training modes. Applied Physiology, Nutrition, and Metabolism 2016; 41(7): 767-774.
  12. Cadore EL, Izquierdo M, Pinto SS, Alberton CL, Pinto RS, Baroni BM, et al. Neuromuscular adaptations to concurrent training in the elderly: effects of intrasession exercise sequence. Age 2013; 35(3): 891-903.
  13. Hawley J, Burke L. Peak performance: training and nutritional strategies for sport. Sydney: Allen and Unwinoxidation in the intracellular lactate shuttle. Proc Natl Acad Sci 1999; 96: 1129-1134.
  14. Friman G. Effect of clinical bed rest for seven days on physical performance. Acta Medica Scandinavica 1979; 205(1‐6): 389-393.
  15. Tokmakidis S, Touvra A-M, Douda H, Smilios I, Kotsa K, Volaklis K. Training, detraining, and retraining effects on glycemic control and physical fitness in women with type 2 diabetes. Hormone and Metabolic Research 2014; 46(13): 974-979.
  16. Colberg SR, Sigal RJ, Yardley JE, Riddell MC, et al. Physical activity/exercise and diabetes: a position statement of the American Diabetes Association. Diabetes care 2016; 39(11): 2065-2079.
  17. Little JP, Gillen JB, Percival ME, Safdar A, et al. Low-volume high-intensity interval training reduces hyperglycemia and increases muscle mitochondrial capacity in patients with type 2 diabetes. Journal of applied physiology 2011; 111(6): 1554-1560.
  18. Mujika I, Padilla S. Detraining: loss of training-induced physiological and performance adaptations. Part I. Sports Medicine 2000; 3(2): 79-87.
  19. Röhling M, Herder C, Stemper T, Müssig K. Influence of acute and chronic exercise on glucose uptake. Journal of diabetes research 2016; 2016.
  20. Marcus RL, Smith S, Morrell G, Addison O, et al. Comparison of combined aerobic and high-force eccentric resistance exercise with aerobic exercise only for people with type 2 diabetes mellitus. Physical therapy 2008; 88(11): 1345-1354.
  21. Cauza E, Hanusch‐Enserer U, Strasser B, Kostner K, et al. Strength and endurance training lead to different post exercise glucose profiles in diabetic participants using a continuous subcutaneous glucose monitoring system. European journal of clinical investigation 2005; 35(12): 745-751.
  22. Ritov VB, Menshikova EV, Azuma K, Wood R, et al. Deficiency of electron transport chain in human skeletal muscle mitochondria in type 2 diabetes mellitus and obesity. American Journal of Physiology-Endocrinology and Metabolism 2010 ; 298(1): E49-E58.
  23. Schrauwen-Hinderling V, Kooi M, Hesselink M, Jeneson J, et al. Impaired in vivo mitochondrial function but similar intramyocellular lipid content in patients with type 2 diabetes mellitus and BMI-matched control subjects. Diabetologia 2007; 50(1): 113-120.
  24. Bruce CR, Anderson MJ, Carey AL, Newman DG, et al. Muscle oxidative capacity is a better predictor of insulin sensitivity than lipid status. The Journal of Clinical Endocrinology & Metabolism 2003; 88(11): 5444-5451.
  25. Methenitis S. A brief review on concurrent training: from laboratory to the field. Sports 2018; 6(4): 127.
  26. Byrkjeland R, Njerve IU, Anderssen S, Arnesen H, Set al. Effects of exercise training on HbA1c and VO2peak in patients with type 2 diabetes and coronary artery disease: a randomised clinical trial. Diabetes and Vascular Disease Research 2015; 12(5): 325-333.
  27. Park S-Y, Lee I-H. Effects on training and detraining on physical function, control of diabetes and anthropometrics in type 2 diabetes; a randomized controlled trial. Physiotherapy Theory and Practice 2015; 31(2): 83-88.
  28. Kemi OJ, Haram PM, Wisløff U, Ellingsen Ø. Aerobic fitness is associated with cardiomyocyte contractile capacity and endothelial function in exercise training and detraining. Circulation 2004; 109(23): 2897-2904.
  29. Gettman LR, Pollock ML. Circuit weight training: a critical review of its physiological benefits. The Physician and Sportsmedicine 1981; 9(1): 44-60.
  30. Houmard J, Hortobagyi T, Johns R, Bruno N, et al. Effect of short-term training cessation on performance measures in distance runners. International journal of sports medicine 1992; 13(08): 572-576.
  31. Allen G. Physiological and metabolic changes with six weeks detraining. Aust J Sci Med Sport 1989 ;21(1): 4-9.
  32. LeMura LM, von Duvillard SP, Andreacci J, Klebez JM, et al. Lipid and lipoprotein profiles, cardiovascular fitness, body composition, and diet during and after resistance, aerobic and combination training in young women. European journal of applied physiology 2000; 82(5-6): 451-458.