Abstract
PurposeWeight 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.MethodsParticipants 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.ResultsIn 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.ConclusionDuring 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.
Highlights
While weight loss is necessary to combat obesity and its associated comorbidities, it may negatively impact both the muscular (Weinheimer et al 2010) and skeletal (Ensrud et al 2018) systems
Though both aerobic and resistance exercise have been shown to preserve lean mass (Weiss et al 2017; Sardeli et al 2018) and bone mineral density (Armamento-Villareal et al 2012; Villareal et al 2006) during calorie-restricted weight loss, some evidence suggests that resistance training may be superior for preserving lean mass (Clark 2015; Villareal et al 2017) and bone mineral density
Previous research has demonstrated caloric restriction disrupts the growth hormone (GH):insulin-like growth factor-1 (IGF-1) axis, such that increasing GH secretion does not stimulate IGF-1 production and, in turn, there is no subsequent negative feedback to reduce GH production (Fazeli and Klibanski 2014). These alterations occur in a dose-dependent fashion, such that higher levels of caloric restriction produce greater increases in GH and reductions in IGF-1 compared to lower levels of caloric restriction and energy balance (Loucks and Thuma 2003)
Summary
While weight loss is necessary to combat obesity and its associated comorbidities, it may negatively impact both the muscular (Weinheimer et al 2010) and skeletal (Ensrud et al 2018) systems. Previous research has demonstrated caloric restriction disrupts the GH:IGF-1 axis, such that increasing GH secretion does not stimulate IGF-1 production and, in turn, there is no subsequent negative feedback to reduce GH production (Fazeli and Klibanski 2014) These alterations occur in a dose-dependent fashion, such that higher levels of caloric restriction produce greater increases in GH and reductions in IGF-1 compared to lower levels of caloric restriction and energy balance (Loucks and Thuma 2003). This dysregulated pairing of increased GH and decreased IGF-1 has been termed growth hormone resistance (Fazeli and Klibanski 2014) and represents a specific form of anabolic resistance. Whether this dysregulation persists in the face of a potent anabolic stimulus, such as resistance training, has not been investigated
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