Periods of energy deficiency occur throughout the lifespan, from younger athletes within the relative energy deficiency in sport 1 or the female athlete triad 2 frameworks to older adults engaging in weight loss. Within these populations are a growing recognition that energy deficiency suppresses reproductive and metabolic hormones 3 leading to adverse health outcomes such as impaired bone health. 4,5 Despite a growing recognition of these important implications, limited knowledge of the training responses in an energy deficient state exists, particularly with respect to

Purpose Weight loss can result in the loss of muscle mass and bone mineral density. Resistance exercise is commonly prescribed to attenuate these effects. However, the anabolic endocrine response to resistance exercise during caloric restriction has not been characterized. Methods Participants underwent 3-day conditions of caloric restriction (15 kcal kg FFM−1) with post-exercise carbohydrate (CRC) and with post-exercise protein (CRP), and an energy balance control (40 kcal kg FFM−1) with post-exercise carbohydrate (CON). Serial blood draws were taken following five sets of five repetitions of the barbell back squat exercise on day 3 of each condition. Results In CRC and CRP, respectively, growth hormone peaked at 2.6 ± 0.4 and 2.5 ± 0.9 times the peak concentrations observed during CON. Despite this, insulin-like growth factor-1 concentrations declined 18.3 ± 3.4% in CRC and 27.2 ± 3.8% in CRP, which was greater than the 7.6 ± 3.6% decline in CON, over the subsequent 24 h. Sclerostin increased over the first 2 days of each intervention by 19.2 ± 5.6% in CRC, 21.8 ± 6.2% in CRP and 13.4 ± 5.9% in CON, but following the resistance exercise bout, these increases were attenuated and no longer significant. Conclusion During caloric restriction, there is considerable endocrine anabolic resistance to a single bout of resistance exercise which persists in the presence of post-exercise whey protein supplementation. Alternative strategies to restore the sensitivity of insulin-like growth factor-1 to growth hormone need to be explored.

Objective To characterize the contributions of the loss of energy-expending tissues and metabolic adaptations to the reduction in resting metabolic rate (RMR) following weight loss. Methods A secondary analysis was conducted on data from the Comprehensive Assessment of Long-term Effects of Reducing Intake of Energy study. Changes in RMR, body composition, and metabolic hormones were examined over 12 months of calorie restriction in 109 individuals. The contribution of tissue losses to the decline in RMR was determined by weighing changes in the size of energy-expending tissues and organs (skeletal muscle, adipose tissue, bone, brain, inner organs, residual mass) assessed by dual-energy X-ray absorptiometry with their tissue-specific metabolic rates. Metabolic adaptations were quantified as the remaining reduction in RMR. Results RMR was reduced by 101 ± 12 kcal/d as participants lost 7.3 ± 0.2 kg (both p < 0.001). On average, 60% of the total reduction in RMR were explained by energy-expending tissues losses, while 40% were attributed to metabolic adaptations. The loss of skeletal muscle mass (1.0 ± 0.7 kg) was not significantly related to RMR changes (r = 0.14, p = 0.16), whereas adipose tissue losses (7.2 ± 3.0 kg) were positively associated with the reduction in RMR (r = 0.42, p < 0.001) and metabolic adaptations (r = 0.31, p < 0.001). Metabolic adaptations were correlated with declines in leptin (r = 0.27, p < 0.01), triiodothyronine (r = 0.19, p < 0.05), and insulin (r = 0.25, p < 0.05). Conclusions During weight loss, tissue loss and metabolic adaptations both contribute to the reduction in RMR, albeit variably. Contrary to popularly belief, it is not skeletal muscle, but rather adipose tissue losses that seem to drive RMR reductions following weight loss. Future research should target personalized strategies addressing the predominant cause of RMR reduction for weight maintenance.

Suppression of insulin-like growth factor 1 (IGF-1) and leptin secondary to low energy availability (LEA) may contribute to adverse effects on bone health. Whether a high-protein diet attenuates these effects has not been tested. Seven men completed three five-day conditions operationally defined as LEA (15 kcal kg fat-free mass (FFM)-1 day-1) with low protein (LEA-LP; 0.8 g protein·kg body weight (BW)-1), LEA with high protein (LEA-HP; 1.7 g protein·kg BW-1) and control (CON; 40 kcal·kg FFM-1·day-1, 1.7 g protein·kg BW-1). In all conditions, participants expended 15 kcal·kg FFM-1·day-1 during supervised cycling sessions. Serum samples were analyzed for markers of bone turnover, IGF-1 and leptin. The decrease in leptin during LEA-LP (-65.6 ± 4.3%) and LEA-HP (-54.3 ± 16.7%) was greater than during CON (-25.4 ± 11.4%; p = 0.02). Decreases in P1NP (p = 0.04) and increases in CTX-I (p = 0.04) were greater in LEA than in CON, suggesting that LEA shifted bone turnover in favour of bone resorption. No differences were found between LEA-LP and LEA-HP. Thus, five days of LEA disrupted bone turnover, but these changes were not attenuated by a high-protein diet.