‘Weight loss’ diets that rely on calorie restriction and aerobic exercise cause significant reductions in skeletal muscle mass. This skeletal muscle mass can make up to 50 % of the total weight loss on a such diet. This is detrimental to future health because the skeletal muscle mass of the individual is directly related to their resting metabolic weight. Reductions in skeletal muscle mass therefore reduce the requirement for energy and so when calorie restriction ends, resumption of a normal energy intake causes fat regain, almost always solely as fat. The reductions in skeletal muscle seen in such cases are almost never fully recovered unless intensive resistance training is performed. Successful long term fat loss necessitates that skeletal muscle mass in maintained because this reduces the risk of future weight gain. The amount of skeletal muscle loss seen during dieting is dependent largely on the circulating levels of thyroid hormones, and in particular the active thyroid hormone triiodothyronine (T3).
Studies have investigated the link between skeletal muscle loss and thyroid hormone levels. For example, in one such study1 six morbidly obese subjects were fed a low calorie diet for 64 days while they lived in a metabolic ward. In this tightly controlled study the subjects were provided with only 600 to 800 kcals per day and their presence in the ward prevented any deviation from this regimen. The protein level of the diet was set at 1.5 grams per kg of body weight per day for three of the subjects and the other three had half the protein intake replaced with carbohydrate. Safflower oil provided fat in the diet and vitamin and minerals at 100 % of the recommended intake were included in the liquid formula meals. The mean weight loss in the individuals was 174.3 grams per 1000 kcal of deficit. The composition of this weight loss was 36 % water, 58.9 % fat and 5.1 % protein. The fat loss between the subjects was fairly consistent, but wide variations in nitrogen balance and protein loss were seen in the individuals.
Overall, 37.5% of the weight loss occurred in the first 16 days of the study. Those on the lower protein diet lost more weight than those on the higher protein diet. As has been shown elsewhere the total protein losses in the first 16 days of the diet accounted for around 50 % of the weight lost. However, the mean nitrogen losses from those on the higher protein diet did not differ from those on the lower protein diet. Of course this could mean that both diets were insufficient to maintain correct nitrogen balance. Those subjects on the higher protein diet did lose more weight initially, but this weight was accounted for by water loss. The range of nitrogen losses from the subjects was between 90.5 and 278.7 grams, which means that inter-individual variation was large. This variation in nitrogen balance seen in the subjects is interesting because it gives a clue as to the reason for the loss of skeletal muscle during weight loss. This is particularly true if the levels of circulating thyroid hormones are taken into account.
The total nitrogen loss of the subjects correlated with the initial lean body mass of the subject, but correlated negatively with the fat cell size, but only for the first 16 days of the diet. Therefore those with more lean mass and smaller fats cells experienced less nitrogen loss. In addition the nitrogen loss was also negatively correlated to the size of the decrease in triiodothyronine from baseline to day 64 of the study. In other words those with the largest drop in the levels of circulating triiodothyronine experienced the lowest levels of nitrogen loss. The authors concluded that falls in the circulating levels of thyroid hormones may therefore be a protective effect to prevent excessive losses of skeletal muscle. This is not surprising as one of the mechanisms by which energy is produced is through stimulation of cellular activity by thyroid hormones. Higher levels of thyroid hormones are able to stimulate energy production some of which may be created through catabolic breakdown of skeletal muscle, and the formation of glucose through the alanine cycle.
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