Exercise is Medicine

by Jade Teta ND, CSCS, and Keoni Teta, ND, LAc, CSCS

Weight Training for Insulin Management?

Issues of dysfunctional insulin metabolism continue to be a challenge for health-care practitioners. This month we look at the role that weight training can play in restoring insulin sensitivity.

Clarifying Insulin Resistance

Insulin resistance is often discussed in systemic terms, but the truth that is different tissues can be insulin resistant while others remain sensitive ⁽¹⁰⁾. The brain, muscle, liver, and fat can all remain independently sensitive or resistant to insulin depending on the person.

In the brain insulin suppresses hunger. In the liver, insulin turns off gluconeogenesis and increases glycogen synthesis. Insulin acts in muscle to shuttle glucose and amino acids into the cell. In adipose, insulin increases uptake of glucose and fat and suppresses its release. So, insulin resistance, depending on the tissue, would mean increased hunger (brain resistance), increased liver glucose production and release (liver resistance), decreased ability to burn sugar and build muscle (muscle resistance), and a decreased ability to store fat as well as increased fat release (fat resistance).

What may be most important is that insulin issues in one tissue do not necessarily mean insulin resistance systemically. ^(10-13) However, the development of insulin resistance in certain tissues, like the liver, may represent what we typically describe as “insulin resistance”. ⁽¹³⁾

Muscle Resistance

Muscle tissue may be the first tissue to begin to develop resistance to insulin^{. (7, 14-16)} Since muscle is responsible for 70% to 90% of glucose clearance and determines 40% of a person’s insulin sensitivity it makes sense to attack insulin resistance through movement. ^(7-8) Aerobic exercise has a large body of evidence for its benefits in preventing and treating insulin resistance, but weight-training studies have been harder to find.

Studies on Resistance Exercise and Insulin Resistance

Inactive adults lose roughly 5% of their lean body mass every decade and lean mass is inversely associated with body fat and insulin resistance ^(1-2,4-5). This can have a profound impact on functional strength and resting metabolic rate. Participation in weight training can restore much of this dysfunction. As little as 10-weeks of resistance training can increase lean mass by 3 pounds, reduce fat mass by close to 4 and, increase resting metabolic rate by 7%. ⁽¹⁾

A 2009 review by Tresierras et. al. looked at weight training studies over a 50 year period to ascertain associations related to insulin resistance ⁽⁶⁾. Training with weight was shown to positively correlate with increased muscle mass and reduced adiposity as well as decrease the risk of insulin resistance. This review also looked at adherence and safety profiles of weight lifting, as well as its comparisons to aerobic based approaches. Resistance training was able to generate similar or superior results to that of aerobic exercise at lower intensity levels and decreased exercise frequencies.

Resistance exercise has some interesting activity related to its impact on liver insulin resistance. A February 2000 study out of Cell Metabolism showed that growth of type IIb muscle fibers reversed insulin resistance induced on the liver by a high fat, high sugar diet. ⁽⁹⁾ The study looked at 1200 plus genes involved with insulin metabolism in the liver and showed two-thirds of these genes reverted to normal function. The authors were unable to define a mechanism but hypothesized that myokines might be playing a role.

Given weight trainings positive influence over insulin resistance, it would make sense it has similar preventive effects against diabetes compared to aerobic exercise, but this relationship had not been well quantified. An August 2012 study in JAMA looked at this question. Data were analyzed from information gathered in The Health Professionals Follow-up Study over a period from 1990 to 2008. This represented over 500,000 patient years. 150 minutes per week of either resistance training or aerobic exercise was shown to be protective against diabetes. The risk reduction was 34% and 52% respectively for resistance training and aerobic exercise. Those subjects participating in both modalities had even further risk reduction than either modality provided alone. ⁽³⁾

Prescribing Weight Lifting

We recommend full-body workouts done 2 to 3 times per week. A set to repetition range of 1 to 3 sets of 8 to 12 reps each works well. A simple push/pull program for upper body with the addition of leg training is easy to prescribe for the practitioner and simple to remember and execute for the patient. Bench press, back rows, shoulder press, barbell curls, and triceps extension for the upper body and squats, and or leg presses for the lower body is more than adequate. The weights should be heavy enough to induce failure at 8 to 12 repetitions.

Notes

1. Wescott, WL. Resistance training is medicine: effects of strength training on health. Current Sports Medicine Reports. July 2012;11(4):209-216

2. Srikanthan, et al. Relative muscle mass is inversely associated with insulin resistance and prediabetes. Findings from the third National Health and Nutrition Examination Survey. The Journal of Clinical Endocrinology & Metabolism. September 2011;96(9):2898-903.

3. Grontved, et al. A prospective study of weight training and risk of type 2 diabetes in men. Archives of Internal Medicine. August 6^th 2012;1-7 (published ahead of print)

4. Yki-Jarvinen, et. al. Effects of body composition on insulin sensitivity. Diabetes. 1983;32:965–969.

5. Takala, et. al. Insulin action on heart and skeletal muscle glucose uptake in weight lifters and endurance athletes. American Journal of Physiology. 1999;276:e706–e711.

6. Tresierras, et. al. Resistance training in the treatment of diabetes and obesity. Journal of Cardiopulmonary Rehabilitation and Prevention 2009;29:67–75

7. Nastala, Et. Al. Skeletal muscle insulin resistance is fundamental to the cardiometabolic syndrome. Journal of Cardiometabolic Syndrome. 2006;1(1):47-52.

8. Jens, Et. Al. A Muscle-Specific Insulin Receptor Knockout Exhibits Features of the Metabolic Syndrome of NIDDM without Altering Glucose Tolerance. 1998;2(5):559-569.

9. Izumiya, Et. Al. Fast/glycolytic muscle fiber growth reduces fat mass and improves metabolic parameters in obese mice. Cell Metabolism. 2000;7:159-172.

10. Unikrishnan, Et. Al. Tissue Specific Insulin Resistance. PMJ Online 2004;80:435.

11. Kim, Et. Al. Tissue-specific overexpression of lipoprotein lipase causes tissue-specific insulin resistance. PNAS. 2001;98(13):7522-7527.

12. Koopmans, Et. Al. Tissue-related changes in insulin receptor number and autophosphorylation induced by starvation and diabetes in rats. Metabolism. 1995;44(3):291-7.

13. Biddinger, Et. Al. FROM MICE TO MEN: Insights into the Insulin Resistance Syndromes Annu. Rev. Physiol. 2006. 68:123–58

14. Bruning, Et. Al. A Muscle-Specific Insulin Receptor Knockout Exhibits Features of the Metabolic Syndrome of NIDDM without Altering Glucose Tolerance Molecular Cell. 1998;2:559–569.

15. Petersen, Et. Al. The role of skeletal muscle insulin resistance in the pathogenesis of the metabolic syndrome. PNAS 2007;104(31):12587-12594.

16. Mohammed, Et. Al. Muscle and liver insulin resistance indexes derived from the oral glucose tolerance test. Diabetes Care. 2007;30:89-94.