he resting metabolic rate (RMR) is the energy required when at rest. In other words, it is the energy required by the body for normal metabolic function, with no skeletal muscle work output. The RMR contributes the largest proportion of utilised energy and is therefore of interest in cases of obesity. Originally it was theorised that obese individuals may have lower RMRs compared to lean counterparts, but research has shown this to be false. Obese individuals have been shown to have RMRs higher compared to normal weight controls. Because skeletal muscle contributes the greatest proportion to RMR, the higher RMR in obese individuals is theorised to result from the increased fat free mass. Obese individuals may have increased fat free mass because of their increased body weight, which necessitates higher levels of structural support in the form of bone and muscle.
The contribution of RMR to obesity is therefore controversial because with increased energy needs at rest would suggest that obese people are less likely to gain weight than lean counterparts, given the same energy intake. However, this discrepancy may relate to the fact that obese individuals possess a lower thermic response to food (here). When the RMR is added to the thermic response to food, the total energy utilisation is lower in obese individuals, compared to lean controls. This suggests that obesity is a disorder that prevent the correct utilisation of ingested energy, and indeed this can be explained by the insulin resistance that is associated with abdominal adiposity. In obese individual, instead of being able to utilise glucose as a fuel, it is instead diverted to adipose tissue where it is converted to fatty acids and esterified to form triglycerides.
Forced energy restriction in those suffering from obesity results in an energy deficit as might be expected. This negative energy balance is supposed to force an increase reliance of fat oxidation by the body, thus reducing adipose tissue size. However, because obesity is characterised by insulin resistance, and because insulin resistance prevents the correct oxidation of lipids in muscle, the body is unable to oxidise fatty acids from adipose tissue efficiently. However, there is a desperate need for fuel, so instead, when faced with an energy deficit, the body uses gluconeogenic precursors to fuel its energy requirements. Alanine from muscle tissue is transported to the liver where it is converted to glucose via the gluconeogenic pathway. This catabolism of muscle decreases the muscle mass of the individual, causing weight loss, which explains some of the initial weigh loss seen on such regimens.
Repeated attempts at weight loss in obese individuals using forced energy restriction can therefore causes repeated reductions in muscle mass that reduces RMR. That obese individuals undergo these catabolic cycles during weight loss is evidence by studies investigating the RMR of individuals who were previously obese but have lost weight. For example, in a meta-analysis of the literature, researchers1 investigated the RMR of formerly obese individuals with body mass indexes of 27 kg/m2 or above. The 124 formerly obese subjects were compared to 121 controls of normal body weight. Adjusting RMR for fat free mass resulted in data showing that obese subjects had RMRs that were 2.9 % lower when compared to controls. While a lower than mean RMR was found in only 3.3 % of the control subjects, in formerly obese subjects the figure was 15.3 %.
The researchers also performed a second type of meta-analysis which confirmed the original findings. In the second analysis, formerly obese subjects had a 5.1 % lower RMR than control counterparts. These results confirm that formerly obese subjects have lower RMRs than lean controls. This supports the idea that forced energy restriction in obese individuals may cause muscle loss, which does not recover following cessation of the diet and necessitates a permanently lower intake of energy to prevent further weight gain. This explains the high failure rate in weight loss diets using the forced energy restriction model. It also supports the idea that fat free mass contributes a considerable amount of the weight lost during such diets. It cannot be argued that the obese subjects had lower RMRs before their weight loss, because studies show that such individuals actually have higher RMRs compared to normal weight individuals.
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