This study investigated the hypertrophic potential of load-matched blood-flow restricted resistance training (BFR) vs free-flow traditional resistance training (low-load TRT) performed to fatigue. Ten healthy young subjects performed unilateral BFR and contralateral low-load TRT elbow flexor dumbbell curl with 40% of one repetition maximum until volitional concentric failure 3 days per week for 6 weeks. Prior to and at 3 (post-3) and 10 (post-10) days post-training, magnetic resonance imaging (MRI) was used to estimate elbow flexor muscle volume and muscle water content accumulation through training. Acute changes in muscle thickness following an early vs a late exercise bout were measured with ultrasound to determine muscle swelling during the immediate 0-48 h post-exercise. Total work was threefold lower for BFR compared with low-load TRT (P < 0.001). Both BRF and low-load TRT increased muscle volume by approximately 12% at post-3 and post-10 (P < 0.01) with no changes in MRI-determined water content. Training increased muscle thickness during the immediate 48 h post-exercise (P < 0.001) and to greater extent with BRF (P < 0.05) in the early training phase. In conclusion, BFR and low-load TRT, when performed to fatigue, produce equal muscle hypertrophy, which may partly rely on transient exercise-induced increases in muscle water content.

Skeletal muscle satellite cells (SCs) are involved in remodeling and hypertrophy processes of skeletal muscle. However, little knowledge exists on extrinsic factors that influence the content of SCs in skeletal muscle. In a comparative human study, we investigated the muscle fiber type-specific association between emergence of satellite cells (SCs), muscle growth, and remodeling in response to 12 wk unilateral resistance training performed as eccentric (Ecc) or concentric (Conc) resistance training ± whey protein (Whey, 19.5 g protein + 19.5 g glucose) or placebo (Placebo, 39 g glucose) supplementation. Muscle biopsies (vastus lateralis) were analyzed for fiber type-specific SCs, myonuclei, and fiber cross-sectional area (CSA). Following training, SCs increased with Conc in both type I and type II fibers ( P < 0.01) and exhibited a group difference from Ecc ( P < 0.05), which did not increase. Myonuclei content in type I fibers increased in all groups ( P < 0.01), while a specific accretion of myonuclei in type II fibers was observed in the Whey-Conc ( P < 0.01) and Placebo-Ecc ( P < 0.01) groups. Similarly, whereas type I fiber CSA increased independently of intervention ( P < 0.001), type II fiber CSA increased exclusively with Whey-Conc ( P < 0.01) and type II fiber hypertrophy correlated with whole muscle hypertrophy exclusively following Conc training ( P < 0.01). In conclusion, isolated concentric knee extensor resistance training appears to constitute a stronger driver of SC content than eccentric resistance training while type II fiber hypertrophy was accentuated when combining concentric resistance training with whey protein supplementation.

Endurance exercise training induces adaptations in metabolically active organs, but adaptations in human subcutaneous adipose tissue (scAT) remains incompletely understood. On the basis of animal studies, we hypothesized that endurance exercise training would increase the expression of proteins involved in lipolysis and glucose uptake in scAT. To test these hypotheses, 19 young and healthy males were randomized to either endurance exercise training (TR; age 18–24 yr; BMI 19.0–25.4 kg/m2) or a nonexercising control group (CON; age 21–35 yr; BMI 20.5–28.8 kg/m2). Abdominal subcutaneous fat biopsies and blood were obtained at rest before and after intervention. By using Western blotting and PCR, we determined expression of lipid droplet-associated proteins, various proteins involved in substrate metabolism, and mRNA abundance of cell surface G protein-coupled receptors (GPCRs). Adipose tissue insulin sensitivity was determined from fasting plasma insulin and nonesterified fatty acids (adipose tissue insulin resistance index; Adipo-IR). Adipo-IR improved in TR compared with CON ( P = 0.03). This was accompanied by increased insulin receptor (IR) protein expression in scAT with a 1.54-fold (SD 0.79) change from baseline in TR vs. 0.85 (SD 0.30) in CON ( P = 0.007). Additionally, hexokinase II (HKII) and succinate dehydrogenase complex subunit A (SDHA) protein increased in TR compared with CON ( P = 0.006 and P = 0.04, respectively). We did not observe changes in lipid droplet-associated proteins or mRNA abundance of GPCRs. Collectively, 10 weeks of endurance exercise training improved adipose tissue insulin sensitivity, which was accompanied by increased IR, HKII, and SDHA protein expression in scAT. We suggest that these adaptations contribute to an improved metabolic flexibility. NEW & NOTEWORTHY This study is the first to investigate the molecular adaptations in human subcutaneous adipose tissue (scAT) after endurance exercise training compared with a nonexercising control group. We show that endurance exercise training improves insulin sensitivity in human scAT, and this is accompanied by increased expression of insulin receptor, hexokinase II, and succinate dehydrogenase complex subunit A. Collectively, our data suggest that endurance exercise training induces molecular adaptations in human scAT, which may contribute to an improved metabolic flexibility.

Repeated periodization of carbohydrate (CHO) intake using a diet‐exercise strategy called the sleep‐low model can potentially induce mitochondrial biogenesis and improve endurance performance in endurance‐trained individuals. However, more studies are needed to confirm the performance‐related effects and to investigate the sustained effects on maximal fat oxidation (MFO) rate and proteins involved in intramuscular lipid metabolism. Thirteen endurance‐trained males (age 23‐44 years; trueV˙O2‐max, 63.9 ± 4.6 mL·kg−1·min−1) were randomized into two groups: sleep‐low (LOW‐CHO) or high CHO availability (HIGH‐CHO) in three weekly training blocks over 4 weeks. The acute metabolic response was investigated during 60 minutes of exercise within the last 3 weeks of the intervention. Pre‐ and post‐intervention, 30‐minute time‐trial performance was investigated after a 90‐minute pre‐load, which as a novel approach included nine intense intervals (and estimation of MFO). Additionally, muscle biopsies (v. lateralis) were obtained to investigate expression of proteins involved in intramuscular lipid metabolism using Western blotting. During acute exercise, average fat oxidation rate was ~36% higher in LOW‐CHO compared to HIGH‐CHO (P = .03). This did not translate into sustained effects on MFO. Time‐trial performance increased equally in both groups (overall time effect: P = .005). We observed no effect on intramuscular proteins involved in lipolysis (ATGL, G0S2, CGI‐58, HSL) or fatty acid transport and β‐oxidation (CD‐36 and HAD, respectively). In conclusion, the sleep‐low model did not induce sustained effects on MFO, endurance performance, or proteins involved in intramuscular lipid metabolism when compared to HIGH‐CHO. Our study therefore questions the transferability of acute effects of the sleep‐low model to superior sustained adaptations.