Intermittent Dieting: Theoretical Considerations for the Athlete

Abstract

Athletes utilise numerous strategies to reduce body weight or body fat prior to competition. The traditional approach requires continuous energy restriction (CER) for the entire weight loss phase (typically days to weeks). However, there is some suggestion that intermittent energy restriction (IER), which involves alternating periods of energy restriction with periods of greater energy intake (referred to as 'refeeds' or 'diet breaks') may result in superior weight loss outcomes than CER. This may be due to refeed periods causing transitory restoration of energy balance. Some studies indicate that intermittent periods of energy balance during energy restriction attenuate some of the adaptive responses that resist the continuation of weight and fat loss. While IER-like CER-is known to effectively reduce body fat in non-athletes, evidence for effectiveness of IER in athletic populations is lacking. This review provides theoretical considerations for successful body composition adjustment using IER, with discussion of how the limited existing evidence can be cautiously applied in athlete practice.

Keywords: adaptive thermogenesis; body weight maintenance; caloric restriction; composition—body; diet—reducing; intermittent energy restriction; weight loss.

Figure 1

Adaptive responses in energy expenditure during energy restriction (ER). Over the course of a weight loss phase, total daily energy expenditure will decrease as a consequence of declines in resting energy expenditure (REE), non-exercise (NEAT) and exercise activity thermogenesis (EAT), and the thermic effect of feeding (TEF). This results in a lessening of the energy deficit, which can cause plateaus in weight loss if energy intake matches the new level of energy output. Plateaus may only be overcome by a further reduction in energy intake or an increase in activity levels.

Figure 2

Adaptive responses in the endocrine system during energy restriction (ER). In response to ER, the resulting energy deficit and corresponding weight loss causes an increase in the drive to eat and reduced energy expenditure, collectively making the continuation of weight loss more challenging. Changes in circulating levels of orexigenic and anorexigenic hormones communicate a nutrient deprivation signal to the brain, causing stimulation of appetite, and a decrease in feelings of satiation. Furthermore, ER causes a shift in circulating levels of hormones involved with the regulation of thermogenesis and energy expenditure. Changes in these hormones indicate a physiological shift directed at correcting the state of energy deprivation and favouring weight regain. EAT: exercise activity thermogenesis; FFM: fat free mass; NEAT: non-exercise activity thermogenesis; PYY: peptide YY; REE: resting energy expenditure.

Figure 3

Adaptive responses in adipose tissues during energy restriction (ER). ER causes a decrease in the size of adipocytes, with no discernible change in adipocyte number in the adipose depot. Due to the modification of the metabolic profile of these smaller adipocytes, the potential for storage of triglyceride increases, subsequently making the maintenance of lost weight more challenging. The possibility of adipocyte hyperplasia early in the weight regain period may also increase the likelihood of weight-reduced individuals surpassing their pre-energy-restriction body weight.

Figure 4

Long-form IER protocol designed by Peos and colleagues. (A) Fat mass, fat free mass, and body weight measured at 0 weeks, 15 weeks, and at 6 months in the moderate intermittent energy restriction group (mIER); (B) muscle performance, resting energy expenditure, a drive to eat, and levels of appetite-regulating hormones measured at 0 weeks, 15 weeks, and 16 weeks; (C) mood states, diet acceptability, physical activity, and sleep quality measured at 0 weeks, 7 weeks, and 15 weeks.