DPT-402.2- Exercise Prescription: Special Considerations – Obesity

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In simple terms, obesity can be defined as ‘the excessive storage of body fat, frequently resulting in a significant impairment of health’ (Wallace, 1997). It used to be considered just a ‘condition’ that merely leads to associated and already declared diseases; however, the World Health Organisation (WHO, 1997) now recognises obesity as a disease in its own right, and one which is largely preventable through changes in lifestyle, especially diet. 

In the UK, 22.2% of men and 23% of women are classed as clinically obese, while 65.4% of males and 55.5% of females were considered either overweight or obese (National Health Survey England, 2003). The number of obese individuals in the UK has trebled since 1980. Since 1994, generalised obesity among both sexes has increased rapidly:

  • males            13.4% in 1994              22.9% in 2003
  • females         17.3% in 1994              23.4% in 2003

Adult obesity in England

The Health Survey for England 2017 estimates that 28.7% of adults in England are obese and a further 35.6% are overweight but not obese. Obesity is usually defined as having a body mass index (BMI) of 30 or above. BMI between 25 and 30 is classified as ‘overweight’.

Men are more likely than women to be overweight or obese (67.2% of men, 61.5% of women). People aged 65-74 are most likely to be overweight or obese.

BMI category by age in England

In the most deprived areas in England, prevalence of excess weight is 11 percentage points higher than the least deprived areas. 

Childhood obesity in England

9.5% of reception age children (age 4-5) are obese, with a further 12.8% overweight. At age 10-11 (year 6), 20.1% are obese and 14.2% overweight. This data is gathered as part of the National Child Measurement Programme.

Of every thousand 10 & 11 year olds in England...  201 are obese  142 are overweight  643 are of normal weight  14 are underweight

Trends in obesity amongst both males and females become more alarming with age. The above graphs show that for both sexes between the ages of 45 – 54 more than 1 in 4 individuals are considered clinically obese. Over 75% of males and nearly 60% of females in the same age category are overweight. The trend generally becomes worse as you move up each age category.

There may be many factors linked in with this rise in weight according to age, such as activity levels, affects of poor nutrition over time and stress. The type of employment that an individual has seems to have some influence on levels of body weight too. Males who are small employers or self employed seem to have a slightly higher prevalence of obesity, whilst females who work in semi-routine and lower supervisory roles have a higher prevalence of obesity

Children living in deprived areas are more likely to be obese. At age 4-5, 6.4% of those in the least deprived areas are obese, compared with 12.4% of those in the most deprived areas. At age 10-11, 13.3% of children in the least deprived areas are obese, compared with 26.7% in the most deprived areas. This gap has increased over the last decade.

To read the full study, please click HERE

As mentioned earlier, in the UK obesity has trebled in the last 20 years. We are quickly becoming the most overweight population in Europe with obesity rising faster in the UK than any other European community. Obesity accounts for 2-6% of total health care costs in several developed countries; some estimates put the figure as high as 7% (WHO, 2004). The true costs are undoubtedly much greater as not all obesity-related conditions are included in the calculations. Below is an illustration of many obesity-related conditions.

Physical Effects of Obesity

Obesity is either a cause of, or is linked with, many health problems.  These include diet-related non-communicable diseases, such as CHD, diabetes mellitus, hypertension, stroke, various forms of cancer (WHO, 2003), joint damage, gall bladder and respiratory problems as well as psychological problems (depression, low self-esteem). 

Obesity has a direct correlation to a condition known as metabolic syndrome. The medical profession had grouped several conditions together and in 1988 called it ‘syndrome X’. It has since been renamed metabolic syndrome with 6 specific health problems that tend to occur together, all of which significantly increase CHD risk. 

  • central adiposity
  • high cholesterol
  • hypertension
  • glucose intolerance
  • chronic inflammation
  • procoagulation

The true prevalence of metabolic syndrome is unknown but it has been estimated that 25% of the UK population show clear signs (British Nutrition Foundation, 2004).

Obesity is placing a strain upon the National Health Service with over £½ billion a year being directly spent on health related problems. The total cost to the economy is estimated at around £2 billion. Consequently, from a health and financial point of view, it is important to prevent where possible and treat obesity successfully.


There is not one single cause for obesity, but evidence suggests that there are many factors that lead to increased body fat. It is likely to be a number of factors that combine together rather than just one of the many factors exerting its effects.

Dietary habits (nutritional imbalance):

Dietary intake is central to weight management and therefore, will play a significant role in obesity. As the ACSM (2000) have stated, a key issue is energy balance. An excessive energy intake, in relation to energy expended, will lead to weight gain in the form of increased fat storage. This is irrespective of the type of excess energy, be it fat, carbohydrate or protein. Excess calories, regardless of the source, will ultimately be stored as fat (McArdle et al, 1996).

It is not always an excess of calories that may cause increased body fat. It is reasonably well documented that low calorie and very restrictive eating plans can initiate a starvation response in the body, which increases the body’s ability to store its best energy source, fat. So in the long term it can cause weight to cycle on and off through repeated dieting and often this causes stress and nutrient deficiency, which is also harmful to health.

Much of the highly processed food available to the public today has additives and chemicals added to increase the craving response for that product, which obviously leads to more food eaten and more money made in sales. This certainly plays a part in the huge increase in obesity. Many people are just falling foul of clever food science that encourages us to eat more. Some facts about processed foods are:

  • mono-sodium glutamate (MSG) and aspartame are some of the most common food additives. MSG has been widely used since the 1960’s and is present in most processed foods. Aspartame was sanctioned for use in 1981 and is now present in over 6000 food products. They have both been shown to cause lesions and damage to the hypothalamus which is directly responsible for the control of weight and appetite. 
obese women
  • if the body becomes overloaded with toxic substances, like harmful additives, it needs to protect itself and somehow safely store these toxins until the liver and kidneys are able to remove them from the body. Some experts believe that body fat can serve as this ‘safe’ store for toxic substances, and if more fat is needed to store these toxins prior to removal the body may well stimulate greater fat storage to provide for this need.
  • refined carbohydrates are often more appealing      visually, and in many cases geared up to be more palatable. These kinds of carbohydrates can have an addictive quality as they give the struggling blood glucose a quick kick. However, they have a higher glycaemic index and therefore, deliver glucose into the system quicker. This creates a glucose overload and strains the pancreas to produce sufficient levels of insulin. Ultimately, high insulin levels are directly linked to a fat storing environment in the body.

Physical inactivity (sedentary lifestyle):

Physical activity may be one of the most important factors in the maintenance of weight loss (Wallace, 1997). Exercise early in life has been shown in studies on rats (Oscai et al, 1972) to depress the development of fat cells. Thus for the same body mass, exercised rats had fewer adipocytes and less fat per cell. Exercise during calorie restriction diets will increase energy expenditure, slow or prevent the loss of fat-free tissue (muscle) and help maintain the resting metabolic rate (ACSM, 2000). Daily activity can account for as much as 40% of our daily calorie expenditure.



It is now well established that the development of obesity is linked to some extent by a variety of genetic factors (Wallace, 1997), the exact interaction of which is still the subject of continued research.  Some of the main genetic issues are:

  • metabolic rate – differences occur between individuals as regards their basal metabolic rate (BMR) or the number of calories needed to just ‘keep the engine ticking over’. 
  • linked closely to BMR is somatotype. Clearly those who are more naturally endomorphic are more likely to gain body fat.
  • leptin is a hormone-like protein produced by fat cells, and sends messages to the brain to blunt the urge to eat (McArdle et al, 1996). In normal situations, when the calorie intake is sufficient to maintain ideal fat stores, the drive, which would lead to overeating, is suppressed. A genetic defect in either leptin production or its receptor can lead to overeating and obesity. Leptin levels have been shown to be a significant predictor of obesity and developing metabolic syndrome (Franks et al, 2005).
  • ghrelin is another hormone-like substance that is regulated in relation to eating habits. During times of energy restriction or fasting, ghrelin levels increase, which in turn causes increased carbohydrate oxidation in preference to fat oxidation, a decrease in energy expenditure, and a general increase in fat stores. A genetic abnormality may also cause receptors and ghrelin response to be over-stimulated.
  • gene mutation is another area where science is suggesting that there may be people who are genetically predisposed to becoming obese. Scientists have located 5 genes in mice DNA that are directly linked to obesity in mice. Although versions of these genes have been found in humans, there has been no discovery of the gene mutations seen in mice that would increase the chances of obesity in humans. Research continues in this area.
  • ‘set point’ theory suggests that our brain continuously adjusts our metabolism and behaviour to maintain a target weight range. Although the set point may change with age it does so within a fixed genetic programme. The theory suggests that diet and exercise may move you away from set point for a time, but in the long run the body will draw you back (Gibbs, 2004).
  • ‘settling point’ theory suggests that we maintain our weight when our metabolic feedback systems, tuned by our genetic make up, settle into a state of equilibrium with our environment. The many changes of culture and environment today are upsetting these equilibriums and pushing us further towards obesity (Gibbs, 2004)

Smoking and alcohol:

Smoking and alcohol both have a significant influence on the body in relation to storing body fat. 

  • regular smoking has been shown to increase the likelihood of abdominal weight gain by 2 fold in men and 2½ fold in women (Ha Jee et al, 2002)
  • alcohol intake of over 4 units a day was associated with increased weight gain, particularly in women under the age of 35 years old (Wannamethee et al, 2004)


There are a number of assessment methods for body fat (such as skinfolds, bioelectrical impedance and underwater weighing), but there are insufficient trials on these and a lack of standardised equations. For these reasons, Body Mass Index (BMI) is the chosen form for most of the clinical standards, since it is easy to use and requires no specialist equipment.  Below is an adapted classification table taken from the National Institute of Health (NIH, 1998):

Classification of Overweight and Obesity by Body Mass Index (BMI)
 Obesity ClassBMI (kg/m2)
Underweight <18.5 
Normal                 Acceptable 18.5 – 24.9
Overweight          Special Attention 25 – 29.9 
Obesity                Medical ReferralI30 – 34.9
 II35 – 39.9
Extreme ObesityIII>40

Fat Distribution

Another factor to be considered is where the excess body fat is distributed. As Vega and Jimenez (2004), describe there are two types of fat distribution, android and gynoid obesity. Android obesity (apple-shaped)  denotes the excess fat being stored around the  abdomen. Gynoid obesity (pear-shaped) denotes the excess fat being stored on the hips and thighs. Excess fat stored near the viscera, as in android obesity, is an indicator on its own for Type II diabetes, CHD and hypertension (NIH, 2000).  Waist measurements can be used to evaluate those at high risk: 

High Risk
Men > 102 cm ( > 40 inches)
Women > 88cm ( > 35 inches)

Android fat distribution describes the distribution of human adipose tissue mainly around the trunk and upper body, in areas such as the abdomen, chest, shoulder and nape of the neck.[1] This pattern may lead to an “apple-shaped” body or central obesity, and is more common in males than in females. Thus, the android fat distribution of men is about 48.6%, which is 10.3% higher than that of premenopausal women.[2] In other cases, an ovoid shape forms which does not differentiate between men and women. Generally during early adulthood, females tend to have a more peripheral fat distribution such that their fat is evenly distributed over their body. However, it has been found that as females age, bear children and approach menopause, this distribution shifts towards the android pattern of fat distribution [3] resulting in a 42.1% increase in android body fat distribution in postmenstrual women.[2] This could potentially provide evolutionary advantages such as lowering a woman’s center of gravity making her more stable when carrying offspring.[1]

Android fat distribution is contrasted with gynoid fat distribution; fat around the hips, thighs and bottom, causing a “pear-shape”.

Jean Vague, a physician from Marseilles, was one of the first individuals to bring to attention the increased risk of developing certain diseases in individuals with an android distribution compared to a gynoid distribution.[4] For example, diabetes and gout. There are other health consequences beyond these, including psychological consequences.

Exercise Recommendations 

Prescribing exercise programmes for the obese client has to be approached with obvious caution and always with the written approval of their GP.  The list of disease complications and interrelated factors could be complex. The early stages of dealing with obesity would mostly involve dietary intervention until some successful weight reduction has been achieved (ACSM, 2000). The metabolic rate of a client who has lost 7 kg (15 lbs) will be reduced by about 120 kcal/day. To maintain weight loss it is necessary for the client to burn off any extra calories ingested with light aerobic exercise.

Clark (2004), identifies balance, stability and mobility as key areas for obese individuals. Clark quotes a study which proposed that obese individuals were at a greater risk of falls than non-obese individuals (Corbeil et al, 2001). This suggests that balance training (in and out of the swimming pool; with and without stability balls) and stability work, focusing on good posture, would be of tremendous benefit to this group too. ACSM recommendations for obesity are:

Additional recommendations would be:

  • some modifications to equipment may be required (e.g. wider seats for cycles or rowers)
  • use low impact modes of activity, because of the risk of musculoskeletal wear or trauma
Strength training may serve as a valuable companion to cardiovascular training when attempting to maintain or gain lean muscle tissue. As mentioned previously, resistance training should focus on core, hip, knee and ankle stability, good posture and balance training. 
Additional Lifestyle Recommendations 
  • the client will need to improve the quality of their food and ensure their body is receiving its vital nutrients
  • some mild calorie restriction may be employed in their diet to encourage the oxidation of body fat stores


Sproston, K., Primatesta, P (2003).  National Health Survey England, National Centre for Social Resources

Begley, C. E. (1991). Government should strengthen regulation in the weight loss industry. J. Am. Diet. Assoc., 91, 1255.

Clark, K. N. (2004). Balance and Strength Training for Obese Individuals. ACSM’s Health and Fitness Journal. 8, 14-20.

Corbeil, P., Simmoneau, M., Rancourt, D., Tremblay, A. and Teasdale, N. (2001). Increased risk for falling associated with obesity: mathematical modelling of postural control. IEEE Transactions on Neural Systems and Rehabilitation Engineering, 9 (2), 126-136.

McArdle, W. D., Katch, F. I. and Katch, V. L. (1996). Exercise Physiology. 4th Edition, Williams and Wilkins.

National Institutes of Health and National Heart, Lung and Blood Institute (2000). The Practical Guide: Identification, Evaluation, and Treatment of Overweight and Obesity in Adults. http://www.nhlbi.nih.gov.

Oscai, L. et al (1972) Effects of exercise on and of food restriction on adipose tissue cellularity. J. Lipid Res., 13, 588.

Sproston, K., Primatesta, P.  In a report from the Chief Medical Officer. (2004) At least five a week. Evidence on the impact of physical activity and its relationship to health. Department of Health.

Vega, C. L. and Jimenez, C. E. (2004). Clients with Nutritional and Metabolic Concerns. In (2000). In Essentials of Personal Training (Baechle, T. R. and Earle, R. W. eds.). pp. 483-518, Human Kinetics.

Wallce, J. P. (1997). Obesity. In ACSM’s Exercise Management for Persons with Chronic Diseases and Disabilities(Durstine, J. L., Ed.) pp. 106-111, Human Kinetics.

WHO (1997). Obesity epidemic puts millions at risk from related diseaseshttp://www.who.int/archives/inf-pr-1997/een/pr97-46.html

WHO (2003). Controlling the global obesity epidemic.


WHO (2004). Obesity and overweight.


Gibbs, W. W. (1996). Gaining on Fat, Scientific American

Franks, P W, Brage, S, Luan, J,  Ekelund, U, Rahman, M, Farooqi, S, Halsall, I, O’Rahilly, S, and Wareham, N J, (2005). Leptin Predicts a Worsening of the Features of the Metabolic Syndrome Independently of Obesity, The North American Association for the Study of Obesity.

Samuels, J L, (2004). The Obesity Epidemic: Should We Believe What We Read and Hear? The Weston A Price Foundation.

Ha Jee, S, Lee, S Y, Nam, C M, Kim, S Y, and Kim, M T, (2002). Effect of Smoking on the Paradox of High Waist to Hip Ratio and Low Body Mass Index,The North American Association for the Study of Obesity.

Wannamethee, S G, Field, A E, Colditz, G A, and Rimm E B, (2004). Alcohol Intake and 8-Year Weight Gain in Women: A Prospective Study, The North American Association for the Study of Obesity.

(2004). Getting Tough With Metabolic Syndrome, The McGraw-Hill Companies.

(2004). www.nutrition.org.ukThe Metabolic Syndrome, British Nutrition Foundation

(2003). National Health Survey England, Health and Safety Executive.

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