Compensatory mechanisms may be due to innate physiological and behavioural differences between individuals. A brief overview of the factors that may
contribute to exercise induced compensatory responses presented in figure 1.3.
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Figure 1.3 Behavioural, genetic and physiological factors that may influence individual exercise induced body mass reduction. (Diagram adapted from Boutcher and Dunn, 2009).
1.3.1.1 Behavioural
Changes in perceived appetite and desire for food have been identified in overweight and obese individuals who do not achieve predicted body mass reduction during a supervised 12 week exercise intervention. Emerging evidence indicates that even a single session of exercise may increase liking, wanting, and perceived reward value of food in some individuals (Finlayson et al, 2009 &
2011). This may be accompanied by an increased drive to eat and a greater satiety response to food ingestion (King et al, 2009). It has not yet been proven that these changes in appetite result in altered food consumption either; further investigation is required to quantify the contribution such a change may make to compensatory EI changes. Exact mechanisms driving these changes in appetite are yet to be identified; dopamine deficiency may be involved since this
neurotransmitter modulates the reward value of food (Wang et al, 2001). These changes could also be the result of behavioural influences such as dietary
restraint (Coletta et al, 2009). Some individuals seem to increase EI
post-exercise out of a desire to “reward” themselves for exercising (King et al, 2007).
Obese individuals are particularly prone to inaccurately estimating ExEE and EI (Lichtman et al, 1992); overestimating ExEE and thus the size of “reward” that has been earned may lead to overconsumption and a state of positive energy balance despite exercise participation.
Behavioural mechanisms may also drive compensatory reductions in non-exercise physical activity. Increased feelings of fatigue from participation in vigorous activity may result in increased sedentary behaviour outside of exercise sessions (Manthou et al, 2010). Sleep duration and ghrelin concentrations have been shown to be negatively correlated (Spiegel et al, 2004); an alteration in sleeping time, and thus total EE, could feasibly occur in response to increased exercise participation and influence appetite. Psychological stress could also play a role as it stimulated cortisol production, which in turn inhibits fat oxidation
(McMurray and Hackney, 2005), which may result in lower ExEE and body mass losses.
1.3.1.2 Physiological
Appetite regulating hormones, such as ghrelin and peptide YY, have been hypothesised to be involved in the exercise induced up-regulation of EI, and have been the subject of much research interest. Both of these hormones are secreted in the gut and have specific forms which are able to cross the blood-brain barrier and exert their influence via the hypothalamic circuits (figure 1.5).
Ghrelin is involved in initiating feelings of hunger (Lim et al, 2010), and is the only known orexigenic peptide at present. Peptide YY is one of many hormones which regulate satiety responses to food ingestion (le Roux and Bloom, 2005).
These hormones and their potential contribution to compensatory mechanisms in the short and long term will be explored in depth in section 1.4.
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Initial adiposity also plays a role as those with the highest BMI at baseline consistently experience the greatest body mass reductions (Hainer et al, 2005).
Fat cell numbers in adults are fixed and may partially dictate the magnitude of exercise-induced body fat mass reduction in the individual since it is only possible to reduce the size, but not the number, of these cells (Spalding et al, 2008). Size of the cells in the individual may be associated with exercise induced body fat reduction in males; those with the largest fat cells experienced the greatest body mass reduction during 20 weeks of exercise training (Despres et al, 1984). This effect was not seen in female participants indicating potential sex based differences in adipocyte adaptation to exercise training. Fat oxidation capacity also seems to play a role in females; changes in resting fat oxidation rate have been positively correlated with the magnitude of body mass reduction in response to exercise in overweight women (Barwell et al, 2009).
Reducing body mass often results in a reduction in resting metabolic rate, and hence total EE may decline and oppose further perturbations in energy balance (Elliot et al, 1989; Leibel et al, 1995; Doucet et al, 2003). Individuals who experience frequent fluctuations in body mass may be most prone to these metabolic adaptations. Such behaviour is associated with a relative decline in muscle mass and increase in fat mass, resulting in a significant decline in metabolic rate in some cases (Manore et al, 1991; Froidevaux et al, 1993).
Maintaining high levels of physical activity may minimise this compensatory decline (Gilliat-Wimberly et al, 2001).
1.3.1.3 Inherited (genetic) factors
Some factors which play a role in individual susceptibility to compensatory behaviours may be determined by genetics; these factors are not modifiable and will not be examined in any detail in this thesis except to note that they can affect the outcome of exercise participation. Gender has a profound influence on exercise induced body mass reduction due to inherent body composition and metabolic differences, enabling males to achieve higher ExEE for any given effort compared to women (Donnelly et al, 2003a). There are also inherent
differences in body composition, metabolic factors such as insulin resistance (Wulan et al, 2010), and levels of appetite regulatory peptides such as ghrelin (Kasa-Vubu et al, 2007) between different ethnic groups which may affect the extent of exercise induced body composition change.
There may be other physiological factors contributing to compensatory responses to exercise training but behavioural changes in EI and EE are of most interest in this thesis since these variables are modifiable and thus theoretically
preventable. Current evidence regarding the existence and magnitude of these changes are reviewed in this chapter.
1.3.1.4 Is energy intake matched to energy expenditure?
Preload studies have investigated the sensitivity of EI regulation; these studies involve the manipulation of the energy content of a preload, often in the form of a drink or milkshake, and subsequent monitoring of subsequent EI at a normal meal. Many such studies have found that lean habitual exercisers are able to regulate EI more sensitively than non exercisers in this case (Goldberg et al, 1998; Long et al, 2002; Martins et al, 2007a; Whybrow et al, 2008). This has led to speculation that regular exercise participation may increase sensitivity of energy balance regulation. Experimental evidence has supported this hypothesis;
both cross-sectional and intervention studies have observed that EI regulation in response to a high and low energy preloads is more sensitive in lean individuals who exercise regularly compared to their sedentary counterparts (Lluch et al, 2000; Martins et al, 2007a). However, it is difficult to determine if this effect is wholly attributable to exercise participation, and findings may not be applicable to overweight and obese. Thus exercise may improve EI regulation, a change which could theoretically decrease likelihood of compensatory behaviours.
Conversely, it has been put forward that chronic inactivity diminishes the ability to self regulate energy balance, leading to a state of positive energy balance resulting in a transition to overweight or obesity over time. Evidence has shown
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that a seven day regime of inactivity within a whole-body calorimeter does not result in a matching down-regulation of EI (Stubbs et al, 2004a), but in the longer term EI restriction gradually induces adaptations in EE level. A rather unique study observed eight healthy, lean and overweight men and women who resided in a biosphere for 2 years. Participants consumed a low energy diet for the first 6 months and after exiting the biosphere it was observed that their spontaneous PA levels were lower than control participants. Interestingly, this depression in activity levels persisted six months after their exit from the biosphere, despite regaining body mass to baseline levels (Weyer et al, 2000).
Regulatory systems seem sensitive to EI restriction, but not to forced inactivity.
Though this may seem contradictory initially, when we consider from an evolutionary perspective this inability to down-regulate EI to match EE makes perfect sense. Evolutionary and genetic research has shown that human-beings evolved as “hunter-gatherers” who endured periods of both feast and famine. To ensure survival in such an environment consuming a high EI whenever food was plentiful, regardless of EE, would have been a pivotal survival strategy
(Chakravarthy and Booth, 2004). Human-beings have thus evolved to be fuel-efficient but this has become a hindrance in the modern “obesogenic”
environment with constant, abundant fuel supply, and little requirement to be routinely active (Egger and Swinburn, 1997).