Obesity is an excess of adipose tissue that results from a mixture of genetic predisposition, environmental influences (e.g., sedentary lifestyle), and behavioural components and it is a chronic, relapsing condition. The rapid increase in obesity prevalence is, however, not due to genetic changes but rather is a societal mismatch between physiology and environment, where food is abundant and exercise is unnecessary. Over the last decade, sedentary behaviour has emerged as a distinctive behavioural paradigm with detrimental effects on chronic disease risk (Ford et al., 2012; Harvey & Chastin, 2013; Matthew et al., 2008), and this is associated with reduced cardiorespiratory fitness, increased adiposity and elevated risk of metabolic syndrome (Despres et al., 2008; Rhodes et al., 2012).

 

Many surveys show that on average adults spend 6-10 h in sedentary behavior, e.g., sitting or reclining while expending ≤1.5 metabolic equivalents; (METs). METs are the energy cost of physical activity and are expressed as multiples of resting metabolic rate, where one MET (or 3.5 ml min-1 Kg -1) is equivalent to a typical metabolism at rest. Obesity is associated with many modifications of the heart structure, overall called obesity cardiomyopathy, observable even in the absence of others cardiovascular risk factors.

 

This condition tends to evolve in congestive heart failure, a leading cause of cardiovascular mortality and morbidity (Larsson et al., 1984; Poirier et al., 2006). From the pathophysiological point of view several mechanisms are involved (Van Gaal et al., 2006).