The Role of Exercise and Nutrition in Lifestyle-Related Disease

Abstract

Daily energy intake per person in Japan reached a peak of 2,226 Kcal in 1975 and dropped dramatically to 1,902 Kcal in 2004, nearly identical to the value during the immediate post-World War II period. However, since 1975 obesity has sharply increased despite this dramatic decline in energy intake. This may be, in part, the result of a “relative energy surplus” caused by a decline in energy expenditure due to modern industrialization that far exceeds the decreased energy intake. Bray (J Nutr 121:1146–1162, 1991) has proposed the “MONA LISA” (Most Obesities kNown Are Low In Sympathetic Activity) hypothesis, suggesting that obesity is associated with a relative or absolute reduction in the activity of the thermogenic component of the sympathetic nervous system. It is now well recognized that “middle age obesity” is strongly associated with both aging and depressed autonomic nervous system (ANS) activity, particularly the sympathetic thermogenic responses to a high-fat diet and an irregular food intake pattern. Our series of studies have suggested the decline in ANS activity that regulates fat metabolism and appetite control is potentially reversible by regular exercise training in middle-aged individuals and obese children with depressed ANS activity. In other words, habitual exercise plays a vital role in enhancing not only fat and glucose metabolism, but also in preventing obesity and enhancing appetite control. Recent studies have clearly indicated that exercising obese individuals have a much lower mortality rate and incidence of disease than lean individuals with little or no exercise. A possible explanation could be that exercise effects immune functions and myocytokines, preventing and improving lifestyle-related diseases. Finally, our recent studies on the effect of functional muscle electrical stimulation on glucose utilization during hyperinsulinemic-euglycemic clamp will be discussed together with the most recent topics on brain derived neurotrophic factors (BDNFs) that appear to influence energy metabolism, appetite, and aspects of neurocognitive function. These data strongly suggest that a lack of exercise or a sedentary lifestyle combined with an unhealthy diet may lead to accelerated ageing, diseases of the body and brain, and an overall decline in the quality of life.

Keywords

Lifestyle-related disease Obesity Autonomic nervous system Brain-derived neurotrophic factor (BDNF) 

Supplementary material

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Copyright information

© Springer Japan 2015

Authors and Affiliations

  1. 1.Graduate School of Human and Environmental StudiesKyoto UniversityKyotoJapan

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