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Exercise as it relates to Disease/High Intensity interval training for Type 2 diabetics

This is an analysis of the journal article "Low-volume high-intensity interval training reduces hyperglycemia and increases muscle mitochondrial capacity in patients with type 2 diabetes" By Little et al (2011).[1]  

What is the Background to this Research?Edit

  Diabetes is the given name of metabolic chronic diseases in which the body cannot maintain healthy levels of glucose in the blood. The causation of diabetes is controlled by a hormone called insulin which is produced by the pancreas. When food is digested, and the macronutrients are transported into the bloodstream, insulin moves glucose out of the blood into the cells, where it is then broken down to produce energy.

However, patients with diabetes are unable to breakdown glucose into energy. Due to the fact that there is either not enough insulin to move the glucose via the bloodstream or the insulin produced does not work properly in order to achieve its purpose. Which further results in a accumulation of glucose in the blood resulting in high blood glucose levels.[2] These two conditions are generally termed type 1 or type 2 diabetes.

Type 2 diabetes develops over a prolonged number of years. During which the initial insulin response develops a resistance where the insulin present is increasingly ineffective at managing the blood glucose levels. As a result,the pancreas over produces greater amounts of insulin to compensate the levels that have not yet been achieved in managing blood glucose levels. As this over production of insulin occurs over time, the insulin producing cells within the pancreas eventually undergo cellular apoptosis losing 50-70% of cells.  Further resulting as a combination of ineffective insulin, and not enough insulin - which is why it is often termed as a progressive condition.[3]  

Where is the research from?Edit

  The study was carried out by researchers from the department of Kinesiology and of Pediatrics and Medicine, McMaster, Hamilton and Ontario University. The funding of this project was provided by the Canadian Diabetes Association.[1]

What kind of research was this ?Edit

 This was a meta- analysis controlled clinical trial where the primary purpose of this research was to examine the effects of low-volume HIT on glucose regulation and skeletal muscle metabolic capacity in individuals with T2D.  

What did the research involve?Edit

 The researchers ensured that all participants were diagnosed with T2D at least 3 months prior by a clinician according to standard criteria, including a fasting glucose ≥7.0 mmol/l , were not taking insulin, and had no history of end-stage liver or kidney disease. Participants were recruited through local diabetes clinics, community diabetes information sessions, and poster advertisement. Six participants were sedentary,two participants reported engaging in ∼30 min of low-intensity walking exercise on 3–5 days/wk. Six subjects were taking blood glucose lowering medications and were not on exogenous insulin therapy. Four patients were treated with metformin only, one patient with gliclazide only, and one patient with a combination.


The research consisted of a 4 stage experimental design:[1]


Stage 1 ) Medical Clearance and familiarization - Height and weight were recorded, alongside a maximal exercise test on a cycle ergometer, pre and post exercise 12-lead electrocardiogram (ECG) collection to confirm the absence of any underlying contraindications to vigorous exercise participation.  


Stage 2 ) Baseline Testing - Prior to training, participants performed a 15-min walking test to examine the cardiovascular response and ratings of perceived exertion (RPE) during exercise. Two days after the walk test participants reported back to the laboratory for continuous glucose monitoring (CGM) device insertions. Participants were further given instructions for calibration and capillary blood sampling and individualized control diets. Subjects then returned back to the laboratory 2 days later for the removal of CGM device and a collection of a resting skeletal muscle biopsy sample.  


Stage 3 ) The high intensity training protocol (HIT) involved a total of 6 supervised sessions over 2 weeks. Where each session consisted of 10 x 60 seconds cycling intervals intespersed with 60 seconds of recovery. The cycle ergometer is set to a constant watt mode at a pedal cadence of 80-100 revs/min  and for each working load heart rate was recorded. Each training session included a 3 min warm up and 2 min cool-down at 50W for a total of 25 mins.  


Stage 4)  Post testing protocol involved CGM data collection along with a recall of dietary intake, resting muscle biopsy samples, and similar procedures as baseline testing.     

What were the basic results ?Edit

Glucose
Pre Post
Average blood glucose conc. (24hrs 7.6mmol·l−1·day−1 6.6mmol·l−1·day−1
Post-prandial glucose conc. 965 mmol·l−1·9 h−1 670 mmol·l−1·9 h−1
Skeletal Muscle
Pre Post
Citrate synthase 2.7mmol/kg/hr 3.5mmol·kg/hr
ETC subunits protein conc. 1a.u. 2a.u.
GLUT4 conc. 1a.u. 3.9a.u.

Average blood glucose concentrations were recorded using the CGM data before and after training along with CGM manufacturers recommendations at four points during the day at a time where blood glucose would be expected to be stable, ( i.e., upon awakening, before lunch, before dinner, and before bed). [1]

  Muscle samples were taken to determine the maximal activity of citrate synthase , and the protein content of one subunit from each complex of the electron transport chain . These measurements were recorded by supplementing protease inhibitors to determine the protein concentration, along with the metabolic adaptations in skeletal muscle.

What conclusions can we make ? Edit

The study demonstrates that low volume HIT can rapidly reduce hyperglycemia and increase skeletal muscle oxidative capacity in patients with T2D.  A significant aspect in T2D treatment is the regulation of hyperglycaemia, where in this study implementation of low volume HIT training significantly lowered both fasting hyperglycaemia and lowered postprandial hyperglycaemia. The training-induced increase in GLUT4 protein content further plays a role in glucose regulation for it facilitates greater muscle glucose uptake and contribution to improve glycaemic regulation.   Furthermore, although it is currently unclear whether skeletal muscle mitochondrial impairment causes insulin resistance- it has been shown that individuals  with T2D do have reduced mitochondrial content, and/or reduced markers of mitochondrial biogenesis in skeletal muscle.[4] Low-volume HIT was a sufficient stimulus to increase mitochondrial capacity in the current study, as evidenced by increased enzyme activity of CS as well as elevated protein content of several subunits from complexes in the electron transport chain.  

Practical adviceEdit

This study implemented a protocol of two weeks of low-volume HIT, involving only 25 minuets of vigorous exercise within a total time commitment of 75 min/week. Indicating that low volume HIT represents a time-efficient exercise strategy for treatment of TD2 and for those looking to incorporate a more convenient exercise protocol rather than obliging to the recommended physical activity guidelines of 150 minutes of moderate to vigorous activity each week.[5] Alternatives to HIT training may be incorporated however advice should be sought from either a medical professional or exercise physiologist.

Further information/resourcesEdit

ReferencesEdit

  1. a b c d Jonathan P., Jenna B. et al (2011). 'Low-volume high-intensity interval training reduces hyperglycemia and increases muscle mitochondrial capacity in patients with type 2 diabetes', Journal of Applied Physiology 11(6),doi:10.1152/japplphysiol.00921.2011
  2. Health Direct (2016), ' What causes Diabetes', Retrieved from: https://www.healthdirect.gov.au/diabetes
  3. Diabetes Australia (2015), ' What happens with type 2 diabetics?', Retrieved from: https://www.diabetesaustralia.com.au/type-2-diabetes
  4. Holloszy JO (2009), Skeletal muscle “mitochondrial deficiency” does not mediate insulin resistance. Am J Clin Nutr 89: 463S–466S. Retrieved from: http://ajcn.nutrition.org/content/89/1/463S?ijkey=e4bbbe4c9d0f3c97b8d8ec0f27bf37e83da8e4ec&keytype2=tf_ipsecsha
  5. Colberg SR, Sigal RJ, et al (2010), 'Exercise and type 2 diabetes: 'The American College of Sports Medicine and the American Diabetes Association: Retrieved from: http://care.diabetesjournals.org/content/33/12/e147?ijkey=4d285d47521d39f7330ab3c98a4c0468458557aa&keytype2=tf_ipsecsha