Physical Activity and Obesity

Physical Activity and Obesity

Current modes of living in economically developed countries have created favourable conditions for excessive weight gain (Bleich, Cutler, Murray & Adams, 2008). Recent estimates suggest that 1.9 billion adults are overweight 650 million of which are obese (World Health Organisation, 2018). By 2030 the global overweight and obese population are projected to rise to 38% and 20%, respectively (Kelly, Yang, Chen, Reynolds & He, 2008). In the UK, 35.6% of adults are overweight and an additional 28.7% are obese (Health Survey for England, 2018). This could harm the youth population as obesogenic behaviours (e.g. poor food choices, low physical activity and high screen time) are intergenerationally transmittable (Næss et al., 2016). If no corrective action is taken 11 million more citizens will be diagnosed with obesity by 2030 (Wang, McPherson, Marsh, Gortmaker & Brown, 2011). This is of great concern as excess adiposity increases the risk of developing metabolic diseases, premature death and diminishes the quality of life (Saltiel & Olefsky, 2017). The comorbidities associated with the condition incur a tremendous financial burden, the NHS is estimated to have allocated £6.1 billion towards the treatment of illnesses associated with overweightness and obesity between 2014-15 (Public Health England, 2017). The growing prevalence of the condition will certainly demand greater expense (Wang et al., 2011).

Given the societal consequences associated with the current population with excess adiposity, it is pivotal to develop efficacious treatments that prevent and reduce the accumulation of body fat. Numerous studies have investigated the use of exercise as a viable treatment modality the findings indicate that increasing one’s physical activity level is an effective weight loss strategy (Schwingshackl, Dias & Hoffmann, 2014; Shaw, Gennat, O’Rourke & Del Mar, 2006; Littman, Kristal & White, 2005). As there is potential for it to be utilized as a medical intervention its use should be considered. The objective of this essay is to define the conditions, explain the physiological ramifications associated with the profusion of adipose tissue and discuss the role of physical activity and exercise as a treatment and preventative measure.

Humans possess a remarkable capacity for fat storage (Brown & Konner, 2006). Our ability to accumulate adipose tissue is an evolutionary function which serves to provide an alternative source of energy in times of food scarcity (Brown, 1991). While beneficial in an ecologically hostile environment this adaptation is ill-suited for modern environmental pressures. Innovations in agriculture and technology have made calorically dense foods easily accessible, affordable and highly palatable (Finkelstein, Ruhm & Kosa, 2005; Kopelman, 2000). These developments have reduced the time and effort required to produce food and facilitated the growth of sophisticated economic and labor systems which require little to no physical activity (Lakdawalla & Philipson, 2009). Also, modern conveniences (e.g. automated transport, elevators, etc) have substantially contributed to the reduction in the energy expenditure required for daily living (Lakdawalla & Philipson, 2009). Heredity is also an important factor in determining body composition as a segment of the global population are genetically predisposed for energy imbalance (Price, Cadoret, Stunkard & Troughton, 1987; (Stunkard et al., 1986)). The confluence of these factors has led to the majority of the population being in a consistent state of positive energy balance, consequently, this has given rise to an increase in the prevalence of overweight

and obese individuals in both developed and developing countries (Frayn, 2003; Bleich, Cutler, Murray & Adams, 2008).

Overweight and obesity is defined as a state of excess or abnormal adipose tissue accumulation to the point at which health is compromised (Haslam, Sattar & Lean, 2006). The criterion used to assess body composition is the body mass index (BMI) (kg/m²) (Aronne, 2002). According to this measure overweight and obesity is classified as a BMI of 25.0-29.9 kg/m² and >30 kg/m², respectively. There are subclasses of obesity which are categorized according to the severity of adiposity (see Table 1). The manner in which body fat is amassed is heterogeneous, accordingly, how it is distributed can have implications on one’s health status, hence the necessity for additional assessments (Foster & Pagliassotti, 2012). Waist circumference is an important measure as it directly assesses visceral fat which is a stronger predictor of metabolic diseases (Han, Sattar & Lean, 2006; Shuster, Patlas, Pinthus & Mourtzakis, 2012). Men with a waist circumference <40 in and Women <35 in are considered to be overweight any measure greater than these values would categorize them as obese (Ulijaszek, 2003).

A consistent energy surplus as insignificant as 220 kcal per day sustained for a year is adequate to cause a significant enlargement in fat mass (Hall et al., 2011; Hall et al., 2012). When the body’s nutritional requirements are met the excess energy is converted to triacylglyceride then stored in adipose tissue via de novo lipogenesis (Hellerstein, 1999).  During the development of obesity, the growth and proliferation of adipocytes induce changes in the phenotype of the cell which leads to deleterious functional outcomes (Rutkowski, Stern & Scherer, 2015). To increase lipid storage capacity, adipocytes undergo one of two processes; hyperplasia – the genesis of new cells, or hypertrophy – an increase in the size of the cell (Jo et al., 2009).

Hypertrophic adipocytes can increase in size up to 180 μm in diameter (Brook, Lloyd & Wolf, 1972). This is problematic as the diffusion distance limit for oxygen is 100 μm, inevitably, hypoperfusion will occur which leads to the development of necrotic adipose tissue (Helmlinger, Yuan, Dellian & Jain, 1997). This state of hypoxia is further exacerbated by the limited angiogenic capacity of the growing tissue mass (Sun, Kusminski & Scherer, 2011). The sheer size of the adipocyte incurs significant pressure from the surrounding cells and extracellular matrix proteins (Ghaben & Scherer, 2019). The combination of lipid engorgement and hypoxia is associated with changes in adipokine production notably a reduction in adiponectin secretion a crucial regulator of insulin sensitivity and tissue inflammation (Skurk, Alberti-Huber, Herder & Hauner, 2007). The oversecretion of leptin is also a side effect of adipocyte expansion (Coelho, Oliveira & Fernandes, 2013). Elevated circulating levels of this peptide encourages macrophage phagocytosis and the production of the following pro-inflammatory cytokines; IL-6, IL-12 and  TNF-α further exacerbating tissue inflammation (Kern et al., 2001). A suitable environment for the development of fibrosis spawned by an increase in the expression of pro-fibrotic genes (Buechler, Krautbauer & Eisinger, 2015) (figure 1).

Figure 1. When energy intake supersedes output the excess energy is converted to fat and stored in adipocytes. To sequester the lipids, adipocytes undergo hypertrophy. This enhances the pathogenic potential of adipocytes by altering its endocrine functions causing a decrease in adiponectin secretion and an increase in leptin production which initiates pathophysiological changes. (adapted from Ghaben and Scherer, 2019)

The aforementioned pathophysiological changes lead to a reduction in insulin sensitivity via enhanced ectopic lipid deposition and inflammation (Snel et al., 2012). This creates favourable conditions for a host of disease including but not limited to; dyslipidemia, type 2 diabetes mellitus, hypertension, atherosclerosis, coronary heart disease and certain types of cancers (endometrial, breast, colon, and prostate) (Alpert et al., 2014; Pi-Sunyer, 2002). The social and psychological toll is also great, the prejudice and contempt exhibited by some non-overweight/obese persons can lead to discrimination, binge eating, depression and anxiety amongst other difficulties (Fitzgibbon, Stolley & Kirschenbaum, 1993; Griffiths & Page, 2008; Friedman & Brownell, 1995).

There is plenty of evidence in support of the notion that frequent moderate to vigorous activity is a means of preventing and treating overweight and obesity. Littman et al (2005) concluded in their research of tracking activity levels in 15,000 adults aged 53-57 over the course of 10 years, that high levels of moderate activity are associated with lower weight gain by the age of 45.  This has provided practitioners and other researchers looking into adiposity avoidance, a clear idea on how individuals who may be under the impression that they are genetically predisposed to obesity or overweight, to inform their clients that the habits taken on while partaking in physical activity whether in the gym or daily life (e.g walking or cycling to work daily) can highly reduce the odds of obesity (Lahti-Koski et al,. 2002). With a multitude of studies making the point that frequent physical activity can lead to an avoidance of obesity and overweight, ensuring inactive individuals partake in exercise frequently and avoid apathy is one preventative method of adiposity. When it comes to a treatment for obesity, however, researchers have found it difficult to come to a general consensus on the matter.

The research that has looked into this issue has shown that exercise combined with dietary change can lead to weight loss. Shaw et al (2005) have provided evidence supporting the notion that exercise can only be a means of weight loss intervention when combined with dietary change. The findings indicate that even without seeing visible weight loss, the risk of cardiovascular disease or any other chronic illnesses is reduced. The physiological improvements have also been observed in the research of Thorogood et al (2011) who concluded that while physical activity has a positive impact on blood pressure and lipid levels, however, it was also noted isolated aerobic exercise is not a sufficient means for weight loss. Exercise solely is not conducive for weight loss because it keeps the weight away but it can not do the initial job of losing it. Exercise combined with healthier and lower food portions is what leads to visible weight loss.  To further validate this argument, a moderate-quality meta-analysis provided by Shwingshackl et al (2014) suggests that diet and exercise can be recommended for long term obesity management. This shows that diet and exercise combined has a greater impact on reducing adiposity.

Furthermore, the meta-analysis conducted by Franz et al (2007) with a large range of subjects who completed a 1-year weight management intervention showed that advice-only and exercise-alone groups experienced minimal weight loss, compared to weight loss interventions utilising a reduced energy diet and exercise where these groups experienced moderate weight loss. Collectively, this research is highly indicative of the notion that exercise alone does not result in weight loss. Physical activity combined with dietary change is a more practical approach to weight loss and the prevention of obesity and excessive weight load.

To conclude, the high prevalence of excess adiposity is an unintended consequence of modern developments. Should current trends persist a substantial portion of the global population will either be overweight or obese. Overnutrition enhances the pathogenic potential of adipocytes by altering its endocrine functions. This leads to conditions which affect most aspects of life. Treatments for these comorbidities demand a sizable portion of the government healthcare budget highlighting the need for effective low-cost treatment and preventative measures. Structured physical activity appears to be as such a remedy; however, research demonstrates its potency for reducing body fat is insubstantial. Nevertheless, the combination of exercise and changes in nutritional intake appears to be the most efficient means of reducing adiposity and should, therefore, be incorporated into medical practice.

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