Abstract
Beta-hydroxy-beta-methylbutyrate (HMB), a leucine metabolite, enhances the gain of skeletal muscle mass by increasing protein synthesis or attenuating protein degradation or both. The aims of this study were to investigate the effect of HMB on molecular factors controlling skeletal muscle protein synthesis and degradation, as well as muscle contractile function, in fed and fasted conditions. Wistar rats were supplied daily with HMB (320mg/kg body weight diluted in NaCl-0.9%) or vehicle only (control) by gavage for 28days. After this period, some of the animals were subjected to a 24-h fasting, while others remained in the fed condition. The EDL muscle was then removed, weighed and used to evaluate the genes and proteins involved in protein synthesis (AKT/4E-BP1/S6) and degradation (Fbxo32 and Trim63). A sub-set of rats were used to measure in vivo muscle contractile function. HMB supplementation increased AKT phosphorylation during fasting (three-fold). In the fed condition, no differences were detected in atrogenes expression between control and HMB supplemented group; however, HMB supplementation did attenuate the fasting-induced increase in their expression levels. Fasting animals receiving HMB showed improved sustained tetanic contraction times (one-fold) and an increased muscle to tibia length ratio (1.3-fold), without any cross-sectional area changes. These results suggest that HMB supplementation under fasting conditions increases AKT phosphorylation and attenuates the increased of atrogenes expression, followed by a functional improvement and gain of skeletal muscle weight, suggesting that HMB protects skeletal muscle against the deleterious effects of fasting.
Highlights
Among nutritional strategies aiming to preserve skeletal muscle mass and contractile function, hydroxy-betamethylbutyrate (HMB), a leucine derivative metabolite, is recognized as a compound that prevents skeletal muscle atrophy [1,2,3] and improves muscle function [4]
The present study aimed to investigate the effect of a 29-day HMB supplementation on the molecular mechanisms involved in muscle protein synthesis and degradation and associated contractile function in fed and fasted rats
Skeletal muscle hypertrophy occurs when the rate of protein synthesis exceeds the rate of protein degradation, whereas skeletal muscle atrophy occurs when protein degradation exceeds synthesis
Summary
Among nutritional strategies aiming to preserve skeletal muscle mass and contractile function, hydroxy-betamethylbutyrate (HMB), a leucine derivative metabolite, is recognized as a compound that prevents skeletal muscle atrophy [1,2,3] and improves muscle function [4]. HMB supplementation in different models of skeletal muscle atrophy prevents proteolysis, mainly through inhibition of catabolic pathways [5, 6]. It improves sports performance [7, 8]. Understanding the mechanisms maintaining skeletal muscle mass and contractile function is important in developing effective strategies to combat and prevent skeletal muscle wasting. These strategies will ameliorate the well being of many patients with chronic diseases as well as improve rehabilitation and training strategies for athletes [3, 5, 8, 12,13,14]
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