Exercise and body weight

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The Effect of exercise on the production and maintenance of long-term reduction in body weight

Exercise intensity and duration on long-term weight loss

It is widely accepted that physical activity is related to a reduction in body weight however the optimal amount of exercise that will facilitate a long-term reduction in body weight is still debatable.

Recent randomized, controlled trials (RCTs) demonstrate slight weight loss with physical activity intervention alone and little increase in weight loss combining exercise and dietary restriction. Topical studies show that higher levels of exercise may result in greater weight loss.

The majority of recent studies show a reduction in body weight of 1-3kg over a time period of 4-16 months using exercise prescriptions of 60-180min per week. Jakicic et al. as well as other study groups, are interested in the effect of increased intensity (moderate vs. vigorous) and duration (moderate vs. high) of exercise on long-term weight loss. Individuals achieving and sustaining a weight loss of 10% or more of their initial body weight after 24 months carried out more physical activity compared with those maintaining a weight loss of less than 10%. This study demonstrates a correlation between increased leisure time activity and weight loss over time, concluding that 275min/wk (1500kcal/wk) is necessary to sustain weight loss. This suggests that increased exercise intensity and duration may create a large negative energy balance resulting in substantial weight loss.

Few studies that exceed a time period of 6-12 months, observing the amount and intensity of exercise required to augment long-term reduction in body weight have been carried out. This may be due to the challenging problems concerning overweight individuals in completing and adhering to increased levels of physical activity. In a study conducted by Donnelly et al. less than half the number of individuals engaging in physical activity completed the 16 month study despite being compensated.

Additional factors influencing results and energy balance may include compensation mechanisms such as resting metabolic rate (RMR) as well as increased energy intake due to long-term augmented energy expenditure which may attenuate weight loss. Difficulties in interpreting results may arise when calculating body weight, as adipose tissue lost due to exercise may be overshadowed by an increase in lean muscle mass. Studies that measure body composition compared to body weight solely, illustrate that exercise “reduces abdominal visceral fat” and “improves cardio metabolic risk factors”. Consequently body weight may not be the most favorable measure to evaluate the effects of physical activity on health.

The results mentioned above as well as being equivalent to results put forward by Schoeller et al., suggest that appropriate levels of exercise required to sustain weight loss is “approximately twice the public health recommendation,” a minimum of 150 minutes of moderate intensity activity per week.

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Maintenance of Long-Term Weight Loss

It has been shown in many studies that following weight loss, subjects often regain the lost weight, and sometimes even overshoot their original weight. Abderson et al , having analysed a large number and variety of weight loss studies carried out in the US that more than 35% of lost weight is regained within the first year, and the majority within five.(1) Metabolism plays a key role in this. Among other inputs, the reduction of leptin and insulin tell the brain that the body is energy-deficient, resulting in a drive to eat along with suppressed energy expenditure. The body’s choice of fuel also changes within the diurnal cycle and is affected by lifestyle. Therefore, to maintain their new weight, individuals need to limit their food intake to the same extent that expenditure is suppressed.

The role of exercise in this:

There is evidence to suggest that regular exercise prevents or counters these metabolic adaptations that lead to weight regain. Work done by MacLean et al (2) showed that not only that relapsing rats that exercised presented a reduction in weight in liver tissue and mesenteric fat pads compared to their sedentary counterparts, but did not succumb to the overeating normally seen after dramatic weight loss. The energy balance previously mentioned was delayed and much reduced (roughly 40%), therefore greatly reducing the rats’ desire to gorge themselves. Lean rats show a diurnal shift in fuel usage (favouring carbohydrates during the dark cycle and fat during the light). Obese rats did not present this shift. It however returned after weight loss. (see if can find more on this) In sedentary rats, carbohydrates were favoured regardless, while fat was stored and significant lipogenesis was observed.

AMPK is a hypothalamic nutrient sensor that responds to low nutrient availability. Signals from the periphery (leptin, insulin) were not increased by exercise regimes. The reception of these signals, however, seems to be more involved. Acute bouts of exercise have been shown in the study by MacLean et al to lessen the response of AMPK to peripheral deprivation signals, thereby reducing the drive to overfeed. Rats that had lost weight were observed to alternate massive overeating with periods of deprivation. Daily aerobic exercise reduced the extremes in fuel consumption that are associated with this phenomenon as well as the excessive desire to eat and/or hunger pains that are the downfall of many individuals after a calorie-restricted weight loss program.

The work done by MacLean et al suggested that preventing the typical increase in adipocytes may affect the ability to store excess calories, as the peripheries are wired so as to process and store any fuel excess rapidly and efficiently to promote regain and return to the defended body weight. The drive to physical activity is tightly regulated and has been shown to directly influence adiposity and body weight.

Contradictory evidence for the link between exercise and a reduction in body weight

More than half of British adults are overweight, and obesity among school children has increased by 70% in the past generation (Jeffery et al., 2004).

It is undisputed that if energy expenditure exceeds energy consumption, weight loss will be achieved. This is only maintained if energy expenditure and consumption are matched at this reduced body weight, in the long-term.

The correlation between increasingly sedentary lifestyles and the obesity epidemic has lead to a broad assumption that physical inactivity is to blame for the worldwide crisis. However, there is compelling evidence emerging to the contrary.

Perhaps the most reliable reports have been produced by the EarlyBird study, currently underway at the Universities of Exeter and Plymouth. This 12 year cohort study, to be completed in 2013, involves measuring the physical activity and body composition of 300 children from the age of 5. Unlike other trials, physical activity was measured using an impressively precise CSA accelerometer-based activity monitor. Similar previous trials have depended on unreliable qualitative reports from parents or children (Metacalf et al., 2001). One of their 56 peer reviewed articles finds no association between physical activity and BMI or body fat in either sex (Metcalf et al., 2008).

Gathering evidence suggests that children are intrinsically programmed to undertake a set level of activity per day, which is determined either genetically, or as a result of an early childhood experience. Hence, it would be incorrect to implicate TV watching in any resulting daily energy surplus (Sonneville et al., 2008). Adding further credence to this, results being published by EarlyBird in the near future suggest that it is obesity that makes children decreasingly active, and not inactivity that makes children obese.

A cluster randomised controlled trial was carried out in Glasgow, in which 545 pre-school children were subjected to a realistic level of enhanced activity per week, over the course of 24 weeks. It was similarly deduced from this study that physical activity does not reduce BMI in young children (Reilly et al., 2006).

The same conclusion was reached in a review published by Harris et al., in which 18 studies meeting inclusion criteria were scrutinised, exploring the effect of school-based physical activity interventions on BMI in children. (Harris et al., 2009).

Such findings have not been exclusive to children. Church randomized 411 sedentary women to either 1 of 3 exercise groups of varying energy expenditure, or a non-exercise control group. He found that the group assigned to no exercise lost a similar amount of weight to the exercisers (Church et al., 2009).

The explanation for this controversial evidence may depend on the observation that exercise increases appetite through orexigenic peptides such as NPY (Lewis et al., 1993). Caloric overcompensation is the result of our limited capacity to deal with excess calories, due to our minimal brown fat stores, the activation of orexigenic and reward pathways in the brain, and the tendency to underestimate calorie consumption. The frequent result is excessive dietary intake, resulting in an energy imbalance and net weight gain. This theory is supported by an 18-month study by Sonneville and Gortmaker involving 538 students who, on average, consumed 100 calories more than they had just expended following exercise (Sonneville et al., 2008).

Despite the link between exercise and weight loss becoming ever more tenuous, one must not underestimate the potential benefits of exercise in not only preventing numerous diseases, but also in enhancing mental health and cognitive ability.

These findings suggest that, in the absence of the will-power to override the desire to consume surplus calories post exercise, the key to achieving a net daily energy deficit is not to increase exercise, but to focus on limiting daily calorie consumption. 'Emily Moore 13:21, 25 October 2009 (UTC)'

References

http://www.earlybirddiabetes.org

The Times. ‘Exercise? A fat lot of good that is if you want to loose weight’. Times 2. Monday October 19th 2009.

Church T.S., Martin C.K., Thompson M.A., Earnest C.P., Mikusu C.R., Blair S.N. (2009) Changes in weight, waist circumference and compensatory responses with different doses of exercise among sedendary, overweight postmenopausal women. PLoS ONE. 4 (2): 1-11.

Harris K.C., Kuramoto L.K., Schulzer M., Retallack J.E. (2009) Effect of school-based physical activity interventions on body mass index in children: a meta-analysis. Candadian Medical Association Journal. 180 (7): 719-726.

Jeffery A.N., Voss L.D., Metcalf B.S., Alba S., Wilkin T.J. (2004) Parents’ awareness of overweight in themselves and their children: cross sectional study within a cohort (EarlyBird 21). BMJ.

Lewis D.E., Shellard L., Koeslag D.G., Boer D.E., McCarthy H.D., McKibbin P.E., Russell J.C., Williams G. (1993) Intense exercise and food restriction cause similar hypothalamic neuropeptide Y increases in rats. American Journal of Physiology – Endocrinology and Metabolism. 264 (2): 279-284. Metcalf B.S., Curnow J.S.H., Evans C., Voss L.D., Wilkin T.J. (2001) Technical reliability of the CSA activity monitor: The EarlyBird Study. Medicine & Science in Sports & Exercise. 1533-1537.

Metcalf B.S., Voss L.D., Hosking J., Jeffery A.N., Wilkin T.J. (2008) Physical activity at the government-recommended level and obesity-related health outcomes: a longitudinal study (Early Bird 37). Arch. Dis. Child. 93: 772-777.

Reilly J.J., Kelly L., Montgomery C., Williamson A., Fisher A., McColl J.H., Lo Conte R., Paton J.Y., Grant S. (2006) Physical activity to prevent obesity in young children: cluster randomised controlled trial. BMJ.

Sonneville K.R., Gortmaker S.L. (2008) Total energy intake, adolescent discretionary behaviours and the energy gap. International Journal of Obesity. 32: 19-27. 'Emily Moore 13:24, 25 October 2009 (UTC)'