Selección de estrategias

Not only does PA impact on energy balance directly by increasing EE, there is

accumulating evidence that PA also impacts on appetite control and EI (Blundell et al., 2015b). Acute studies (single day) demonstrate that exercise has a transient effect on appetite and there is no compensatory increase in EI to compensate for the energy expended through exercise. Broom et al. (2007) demonstrated that a single 60 minute bout of treadmill running at 72% ± 2.0 of maximal oxygen uptake suppressed acylated ghrelin and hunger during the exercise but did not differ significantly post exercise compared with the resting control condition. Similarly, King et al. (2010a) found that 90 minutes of treadmill running at 68.8% ± 0.3 of maximal oxygen uptake suppressed acylated ghrelin and hunger during and immediately after the exercise but did not differ compared with the resting control condition during the 22.5 hours after exercise. The suppression of hunger during and immediately after (15 minutes) acute exercise was reported in the early 1990s and was referred to as ‘exercise-induced anorexia’ (King et al., 1994). EI did not differ between conditions at any of the four ad libitum meals despite an energy deficit of 1273 ± 45 kcal. Brisk walking has also been shown to result in an energy deficit as there was no increase in EI to compensate for the energy expended through walking (King et al., 2010b). Pooled analysis of 17 studies also demonstrated acute exercise transiently supresses hunger and acylated ghrelin during exercise and has no effect on EI (King et al., 2017). There is some evidence that the

suppression of hunger and acylated ghrelin remains significant immediately post-exercise and persists for several hours post-post-exercise, but this requires further investigation (Broom et al., 2017, King et al., 2017, Broom et al., 2009). When the exercise is continued over several days, EI begins to rise to account for approximately 30% (on average) of the energy expended through exercise (Whybrow et al., 2008, Stubbs et al., 2002b).

Interestingly, medium-term exercise interventions have demonstrated large inter-individual differences in weight loss in response to increased exercise (King et al., 2008). Participants performed supervised exercise at 70% heart rate (HR) maximum, individually prescribed to expend 500 kcal per session five times per week for 12 weeks. Those who lost less weight than expected (compensators) showed an increase in EI (268.2 kcal/d ± 455) and hunger during post-intervention probe days, whereas those who achieved the expected weight loss (non compensators) showed a decrease in EI (130.0 kcal/d ± 485) and no change in subjective appetite sensations. In a similar study, King et al. (2009a) found that in response to the same 12 week exercise

regimen previously described, fasting hunger increased in those who experienced modest weight loss, but not in those who achieved expected weight loss. In addition the effect of a personalised fixed-breakfast on satiety was improved in both groups suggesting an enhancement of satiety signalling. This has been termed the ‘duel- process’ action of exercise on appetite control and is characterised by an increased overall drive to eat and a concomitant increase in the satiating efficiency of a fixed meal. These studies demonstrate the effect of exercise on weight loss varies

substantially between individuals. This variability is, in part, due to changes in the drive to eat and subsequent EI.

Observational studies have also examined the effects of habitual PA on appetite control. In line with the early work of Mayer et al. (1956) who demonstrated a

curvilinear relationship between EI and EE, more recent research has also identified an apparent uncoupling of EI to EE at low levels of PA. Harrington et al. (2013) reported differences in ad libitum EI at a buffet style meal for men (but not women) across tertiles of DLW measured PA EE. Men in the high, middle and low PA EE tertile consumed 1365 kcal ± 101, 866 kcal ± 104 and 1090 kcal ± 101, respectively. Only the difference between middle and high tertiles reached statistical significance, however, there was a trend towards significance between the middle and low tertiles.

Furthermore, men in the low PA EE tertile exhibited a significantly greater drive to eat in the fasted state (appetite sensations) compared to the high tertile, an effect which could be driving the uncoupling of EI and EE at low levels of PA. In a more recent study, Shook et al. (2015) grouped individuals by PA level on the basis of quintiles of MVPA measured using the SWA (mini). Twenty-four hour dietary recalls were

administered on three random occasion during a two week period, however, this data

was not used in analyses due to potential under reporting and instead EI was

estimated using an equation based on change in body composition over a three month period. The authors observed a ‘j-shaped’ relationship between PA group and EI; EI increased with increased PA with the exception of the least active group. The least active group had a higher EI than group two and three, however, these differences were not statistically significant. The Disinhibition factor of the Three Factor Eating Questionnaire (TFEQ) was significantly higher in the lowest activity group compared to all other groups. Furthermore, there was a negative linear relationship between activity category and body mass and FM with those in the lowest activity category exhibiting the highest body mass and FM. The greater FM in the lowest activity category could explain the significantly higher Disinhibition score compared with other activity categories since FM is positively associated with Disinhibition (Lawson et al., 1995, Hays et al., 2002). Finally, Long et al. (2002) examined the effects of PA status (self-report) on appetite sensations and EI following a dietary pre load. Physically active individuals (two or more >40 minute exercise sessions per week) had lower subjective hunger sensations compared with inactive males and were shown to have more sensitive appetite control. Following a high energy dense preload (600.2 kcal) physically inactive individuals (one or less >40 minute exercise session) failed to compensate by reducing their EI at a subsequent ad libitum buffet meal whereas those who were physically active reduced their EI to account for 90% of the preload. These studies suggest exercise and PA play an important role in appetite control and energy balance.

2.7 Individual variability in weight loss and compensatory responses to perturbation in energy balance

Body mass change is related to an imbalance between EI and EE. If EI exceeds EE, weight gain will occur and if EE exceeds EI, weight loss will occur. This equations appears very simple but is in fact complex (Hall et al., 2011). The depiction of energy balance as a set of kitchen scales is inaccurate and misleading. Perturbations in energy balance can be induced through dietary restriction (reduced EI) or an increase in PA (increased EE). Large individual variability and less than expected weight loss has been reported in response to both exercise (Thomas et al., 2012, King et al., 2008) and diet interventions (Camps et al., 2013). The effectiveness of a weight loss intervention is largely dependent on adherence to the diet or exercise regime.

However, even when compliance is accounted for weight loss is less than expected and highly variable between individuals. For example, King et al. (2008) reported weight change ranged from -14.7 to +1.7 kg in response to a 12 week supervised and monitored exercise intervention. This variability can be attributed to metabolic and behavioural compensatory responses that act to restore energy balance. It has been

noted that body mass regulation is asymmetrical; a positive energy balance and weight gain are permitted whilst a negative energy balance and weight loss are strongly defended against (Blundell and Gillett, 2001). The current obesity epidemic supports this notion. Compensatory responses that defend against a negative energy balance include increased EI and reduced NEPA (behavioural) and reduced FFM and RMR (metabolic) (King et al., 2007, Stiegler and Cunliffe, 2006). Behavioural

adaptations can be further categorised as either automatic (occur passively, without any deliberate intent; e.g. reduced spontaneous activity/increased sitting) or volitional (overt behaviour over which the individual can exert a choice; e.g. increased EI).

Together, the metabolic and behavioural compensatory responses compromise the effectiveness of weight loss interventions. The intensity of these compensatory responses vary between individuals and go some way to explaining why some individuals experience less than expected weight loss. Individualised interventions targeting these compensatory adaptations could lead to more successful weight loss outcomes.