Exercise as it relates to Disease/Does incorporating more physical activity into everyday lifestyle improve body composition, thyroid function, and structure in obese children?

This article is a critical analysis of the paper:
“Effects of a short-term circuit weight training program on
glycaemic control in NIDDM” [1]

What is the background to this research?[edit | edit source]

Exercise has long been identified as an effective therapy for treating diabetes mellitus. Previous studies have utilised aerobic exercise as a means of improving/preventing Non-Insulin Dependent Diabetes Mellitus (NIDDM, type 2 diabetes-T2D). This study looks to identify the effect weight/strength training (specifically Circuit Weight Training – CWT) has on patients with NIDDM.[1] Evidence suggests weight training improves insulin sensitivity and glucose tolerance similarly to aerobic exercise.[2][3]

The table below presents background data from different exercise modality interventions examining similar diabetic indicators as those examined in this study.[4]

Diabetic indicators Aerobic Resistance Combined
Fasting glucose (mmol/L) -0.20 +- 0.15 (small) -0.10 +- 0.31 (unclear) 0.53 +- 0.31 (small)
Postprandial glucose (%) -0.44 +- 0.20 (small) -0.10 +- 0.53 (unclear) 0.28 +- 0.46 (small)
Insulin Sensitivity (%) 0.74 +- 0.47 (moderate) 0.34 +- 0.52 (small) 2.20 +- 1.85 (large)
Fasting insulin (%) 0.47 +- 0.63 (moderate) 0.78 +- 0.97 (moderate) 0.15 +- 1.89 (unclear)
  • Data: <0.20=trivial; 0.20–0.60=small; 0.60–1.20=moderate; >1.20=large. Small, moderate and large indicate magnitude of the benefit, ‘unclear’=evidence of a benefit is inconclusive.[4]

A more complex understanding of the characteristics of metabolic and physiological changes that occur from resistance/weight training, allows the most effective exercise treatment to be prescribed to type 2 diabetics.

Where is the research from?[edit | edit source]

The article was published in the Diabetes Research and Clinical Practice international journal. By authors that hold esteemed reputations, having published over 1500 documents between them investigating insulin sensitivity, diabetic and cardiometabolic markers response to exercise.[5][6][7] Such a wealth of knowledge is considered advantageous to a clinical health study.


  • K.G Stanton – Diabetes and Endocrinology department.
  • D.W Dunstan – International Diabetes Institute.
  • L.J. Beilin, V.Burke and I.B Puddey – Heart Research Institute.
  • A.R Morton – Human Movement Department.

Support from the National Health and Medical Research Council is acknowledged, and no obvious biases exist regarding the configuration of this original article.

What kind of research was this?[edit | edit source]

The study was a prospective Randomised Control Trial (RCT). One group (n 11) were randomly assigned to the CWT intervention, whilst 10 control subjects were assigned for later comparison. RCT’s are the most effective way of determining a cause and effect relation between the intervention (treatment) and the outcome (effect).[8]

What did the research involve?[edit | edit source]

  • 21 diagnosed NIDDM subjects assigned to the CWT or control group.
  • Medical screenings and physical examinations conducted.
  • 8-week full body CWT intervention, 3 days/week.
  • Intensity – 50-55% 1 RM, 10-15 reps, 2 sets. Additional set added after 2 weeks.
  • Program midpoint (4weeks) strength (1RM) reassessed, training load adjusted.
  • Fasting serum glucose and insulin measured following 12h fast (OGGT -75g) before and after 8 weeks.[1]

Critique of the methodology used[edit | edit source]

Firstly, of the 21 subjects involved in the study 15 were using oral hypoglycemic medication (sulfonylureas use reported). Sulfonylureas stimulates increased insulin secretion at all glucose concentration levels.[9] Therefore, despite the exclusion of participants taking insulin, pre- and post-intervention measures of glucose and insulin may be jeopardised. Population demographic applicability is also narrowed in this study. Firstly, 51 was the reported mean age, restricting younger and older population applicability. Furthermore, participants were only chosen for the study if they reported less than 60 mins/wk. of vigorous intensity exercise in the last 6 months. Despite diabetes being common in sedentary populations, the response to increased exercise stimulus may differ significantly in T2D patients.[10]

Perhaps most significant are the predictive claims made based on participants self-reported lowered blood glucose. Results were assumed to be caused by CWT and its effect on glycaemic control and insulin responsiveness, despite the collection and reporting methods being exposed to potential bias. A glucose clamp technique, for example, would have provided more accurate evidence and data.[11] Predictive claims based on self-reported evidence should be avoided, especially given the exact effects/mechanisms CWT has on glycaemic control and insulin responsiveness remains relatively unknown. Finally, the program’s length means the findings are acute and despite CWT potentially inducing chronic beneficial T2D adaptations, further research is needed to support this claim, especially given participant adherence may decline.

Despite the possible limitations of the study there are strengths. The exercises employed in this study are like previous resistance exercise intervention studies that have improved glucose tolerance.[12] Furthermore the OGGT (75gm) has been used previously to investigate the link between exercise and glucose tolerance/metabolism before and after exercise interventions.[12]

What were the basic results?[edit | edit source]

Most notable change from baseline to post intervention:

  • CWT reduced plasma insulin response to glucose ingestion.
What Were The Important Findings.[1]
Baseline Glucose (mmol/L-1) Post-Glucose (mmol/L-1) Baseline Insulin (pmol/L-1) Post Insulin
CWT 9.6 (+-0.9) 9.4 (+-0.8) 64.3 (+-12.7) 63.1 (+-12.6)
Control 9.9 (+-1.2) 9.8 (+-1.3) 82.6 (+-10.5) 93.8 (+-12.6)
  • Randomly allocated groups therefore, baseline measures differed between control and CWT group.

The implications drawn from study results is that a short-term CWT program improves glycaemic control in patients with NIDDM. However, despite potentially improving insulin sensitivity, plasma glucose response following glucose ingestion remained relatively unchanged. Authors comment on the potential mechanisms yet acknowledge the study doesn’t support those previously cited (decrease body fat, increase lean muscle mass).[13] The study measured skinfolds and BMI (relatively unchanged) however, measurements of lean muscle mass and body fat may have been more advantageous to investigate the potential mechanisms of adaptation.

What conclusions can we take from this research?[edit | edit source]

Short-term CWT improved insulin response to a glucose load, however, insignificant improvements in glucose tolerance suggest potential weaknesses in data collection. The study acknowledges findings are acute adaptations and longer-term exercise interventions are required to examine the underpinning mechanisms and chronic effects of CWT on NIDDM.

The implications of this research (1998) and more recent evidence suggest small physiological benefits to the lifestyle management of NIDDM despite the exercise mode (resistance, aerobic, combination).[4] Furthermore, recent evidence suggests exercise intensity has little influence on diabetic management, despite most physiological adaptations being intensity sensitive.[4] Therefore, exercise adherence, despite the modality and intensity is perhaps the most important factor responsible for inducing chronic beneficial adaptations in T2D patients.[4] Exercise programming should be individualised, as individuals who may benefit the most from aerobic exercise often have the greatest difficulty performing it.[14] Resistance training may be more achievable and therefore beneficial for individuals with severe obesity, arthritis and/or diabetic complications.[14]

Recommendations for exercise interventions:

  • Conduct risk assessments and pre-exercise screenings.(https://www.essa.org.au/Public/ABOUT_ESSA/Adult_Pre-Screening_Tool.aspx).
  • Conduct relevant physiological tests.
  • Progress intensities following at least 2 weeks of training (discretion).
  • Monitor technique, physiological/health responses (test, re-test).
  • Group training and encouragement (create/maintain active lifestyle).
  • Combining the effects of exercise, diet and drug therapy will help better manage type 2 diabetes.

Further information/resources[edit | edit source]

If this article is of interest to you as a health practitioner see further resources below:

If this article is of interest to you as a patient see further resources below:

  1. a b c d DW, Puddey IB, Beilin LJ, Burke V, Morton AR, Stanton K. Effects of a short-term circuit weight training program on glycaemic control in NIDDM. Diabetes research and clinical practice. 1998;40(1):53-61.
  2. Krotkiewski M, Lönnroth P, Mandroukas K, Wroblewski Z, Rebuffe-Scrive M, Holm G, et al. The effects of physical training on insulin secretion and effectiveness and on glucose metabolism in obesity and type 2 (non-insulin-dependent) diabetes mellitus. Diabetologia. 1985;28(12):881-90.
  3. Miller JP, Pratley RE, Goldberg AP, Gordon P, Rubin M, Treuth M, et al. Strength training increases insulin action in healthy 50-to 65-yr-old men. Journal of Applied Physiology. 1994;77(3):1122-7.
  4. a b c d e NJ, Hopkins WG. Effects of different modes of exercise training on glucose control and risk factors for complications in type 2 diabetic patients: a meta-analysis. Diabetes care. 2006;29(11):2518-27.
  5. Dunstan D, Zimmet P, Welborn T. The Australian diabetes obesity lifestyle study rising prevalence diabetes and impaired glucose tolerance. Diabetes Care. 2002;25:829-34.
  6. Healy GN, Matthews CE, Dunstan DW, Winkler EA, Owen N. Sedentary time and cardio-metabolic biomarkers in US adults: NHANES 2003–06. European heart journal. 2011;32(5):590-7.
  7. Kargotich S, Keast D, Goodman C, Bhagat C, Joske D, Dawson B, et al. Monitoring 6 weeks of progressive endurance training with plasma glutamine. International Journal of Sports Medicine. 2007;28(03):211-6.
  8. Kendall J. Designing a research project: randomised controlled trials and their principles. Emergency medicine journal: EMJ. 2003;20(2):164.
  9. Groop LC. Sulfonylureas in NIDDM. Diabetes care. 1992;15(6):737-54.
  10. Bassuk SS, Manson JE. Epidemiological evidence for the role of physical activity in reducing risk of type 2 diabetes and cardiovascular disease. Journal of applied physiology. 2005.
  11. Tessier D, Ménard J, Fülöp T, Ardilouze J-L, Roy M-A, Dubuc N, et al. Effects of aerobic physical exercise in the elderly with type 2 diabetes mellitus. Archives of gerontology and geriatrics. 2000;31(2):121-32.
  12. a b W, Sherman W, Ivy J. Effect of strength training on glucose tolerance and post-glucose insulin response. Medicine and science in sports and exercise. 1984;16(6):539.
  13. National Institutes of Health, Consensus developmentconference on diet and exercise in non-insulin-dependentdiabetes mellitus, Diabetes Care 10 (1987) 639 – 644
  14. a b ND, Plotnikoff RC. Resistance training and type 2 diabetes: considerations for implementation at the population level. Diabetes care. 2006;29(8):1933-41.

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