Inactivity: The Chicken or the Egg?

Influence of Diet on Voluntary Physical Activity?

Explanations of how high glycemic foods as well as fiber deficiency can directly influence physical activity and exercise habits and lead to a vicious cycle of increased obesity and inactivity. 

 Physical activity is very important to health and longevity and to a certain extent exercise can help lose weight from fat stores but few of us have the time, dedication or body strength needed to lose weight by exercise alone: consider that an hour of fast running consumes around 1000 Calories and 10 kg of fat contains 90,000 Calories.  Nevertheless, many regard lack of exercise the main reason for rising obesity rates in children and adults alike but evidence suggests the type of foods we eat can suppress spontaneous activity and the natural desire for playful exercise.  These same foods fail to satisfy hunger and therefore lead to a vicious circle of overeating and inactivity.

In other pages of this blog we describe how high glycemic carbohydrates (sugar, flour, potatoes, rice, etc.) make up 60% or more of our staple foods and after every meal, day after day year after year, elevate blood glucose 2-3 fold and insulin levels more than 10 fold. There are numerous detrimental biological consequences of such changes and amongst them is an avoidance of physical activity.  This notion is supported by a recent study whereby laboratory animals were fed either a high glycemic or low glycemic diet.  Voluntary physical activity was 45% higher for the Low Glycemic fed mice after 38 weeks of feeding. The authors concluded that dietary composition can affect physical activity level (1) in addition body composition was changed by the type of food not energy intake and the high-GI diet caused a pre-diabetic condition which other studies suggest affect up to 30% of adolescents in the USA (2).

Basic science research has revealed some of  the biological mechanisms whereby physical activity can be suppressed by the type of food we eat:    Most people will be familiar with the overwhelming lack of energy and need for rest that occurs with illness for example a bout of “flu”.  Inflammatory cytokines, produced by activated immune cells, induce “sickness behaviour” (1) (3) which is essentially avoidance of physical activity.  Inflammation is associated with depressive symptoms, anxiety and invokes fatigue and reduced movement (3), anti-inflammatory compounds can block/reverse many of these changes (3).  A much milder form of sickness behavior may be brought about by low grade inflammation associated with high levels of blood glucose (and fructose) after meals containing large amounts of high glycemic starches and sugars documented by increased levels of markers of inflammation in these situations (5).  A more recent study has shown increased intestinal wall permeability in obese individuals associated with inflammation and its reversal with a low glycemic high fiber diet  (6).  Several other possible interactions exist such as the suppression of mitochondrial biosynthesis with high levels of insulin brought about by high glucose may directly decrease exercise tolerance.  High glucose also increases stress by increasing production of reactive oxygen molecules and widespread glycation of proteins results in serious impairment of cell function (7).

Although the science may seem complicated the take home message is simple: avoid high glycemic foods and eat much more fiber.  The sad reality is that trying to follow such a lifestyle choice is very difficult as just the opposite, high glycemic low fiber foods dominate our food culture and supermarkets.

1. Inflammatory modulation of exercise salience: using hormesis to return to a healthy lifestyle. Alistair V Nunn, Geoffrey W Guy, James S Brodie, Jimmy D Bell. s.l. : Nutrition & Metabolism , Vols. 2010, 7:87.

2. The Prevalence of the Metabolic Syndrome Among a Racially/Ethnically Diverse Group of U.S. Eighth-Grade Adolescents and Associations With Fasting Insulin and Homeostasis Model Assessment of Insulin Resistance Levels. R. Jago, T. Baranowski, J. Buse, S. Edelstein, P. Galassetti, J. Harrell, F. Kaufman, B. Linder, and T. Pham. s.l. : Diabetes Care, Vols. 31:2020–2025, 2008.

3. Inactivation of the cerebral NFkappaB pathway inhibits interleukin-1beta-induced sickness behavior and c-Fos expression in various brain nuclei. Nadjar A, Bluthe RM, May MJ, Dantzer R, Parnet P. s.l. : Neuropsychopharmacology , Vols. 2005, 30:1492-1499.

4. Inflammation and its discontents: the role of cytokines in the pathophysiology of major depression. Miller AH, Maletic V, Raison CL:. s.l. : Biol Psychiatry, Vols. 2009, 65:732-741.

5. High–glycemic index carbohydrate increases nuclear factor- B activation in mononuclear cells of young, lean healthy subjects. Scott Dickinson, Dale P Hancock, Peter Petocz, Antonio Ceriello and Jennie Brand-Miller. s.l. : Am J Clin Nutr, Vols. 2008;87:1188 –93. http://www.ajcn.org/cgi/content/full/87/5/1188.

6. Xiao, et al. A gut microbiota-targeted dietary intervention for amelioration of chronic inflammation underlying metabolic syndrome. s.l. : FEMS Microbiology Ecology, Volume 87, Issue 2, pages 357–367, February 2014.

7. Dicarbonyls linked to damage in the powerhouse: glycation of mitochondrial proteins and oxidative stress. N Rabbani, P Thornalley. s.l. : Biochem Soc Trans., Vols. 2008 October ; 36(Pt 5): 1045–1050. doi:10.1042/BST0361045.

 

 

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