Skeletal muscle has a remarkable plasticity to adapt and remodel in response to environmental cues, such as physical exercise. Endurance exercise stimulates improvements in muscle oxidative capacity, while resistance exercise induces muscle growth. Here we show that the c-Jun N-terminal kinase (JNK) is a molecular switch that when active, stimulates muscle fibers to grow, resulting in increased muscle mass. Conversely, when muscle JNK activation is suppressed, an alternative remodeling program is initiated, resulting in smaller, more oxidative muscle fibers, and enhanced aerobic fitness. When muscle is exposed to mechanical stress, JNK initiates muscle growth via phosphorylation of the transcription factor, SMAD2, at specific linker region residues leading to inhibition of the growth suppressor, myostatin. In human skeletal muscle, this JNK/SMAD signaling axis is activated by resistance exercise, but not endurance exercise. We conclude that JNK acts as a key mediator of muscle remodeling during exercise via regulation of myostatin/SMAD signaling.

This review discusses the potential value of tracking interstitial glucose with continuous glucose monitors (CGMs) in athletes, highlighting possible applications and important considerations in the collection and interpretation of interstitial glucose data. CGMs are sensors that provide real time, longitudinal tracking of interstitial glucose with a range of commercial monitors currently available. Recent advancements in CGM technology have led to the development of athlete-specific devices targeting glucose monitoring in sport. Although largely untested, the capacity of CGMs to capture the duration, magnitude, and frequency of interstitial glucose fluctuations every 1–15 min may present a unique opportunity to monitor fueling adequacy around competitive events and training sessions, with applications for applied research and sports nutrition practice. Indeed, manufacturers of athlete-specific devices market these products as a “fueling gauge,” enabling athletes to “push their limits longer and get bigger gains.” However, as glucose homeostasis is a complex phenomenon, extensive research is required to ascertain whether systemic glucose availability (estimated by CGM-derived interstitial glucose) has any meaning in relation to the intended purposes in sport. Whether CGMs will provide reliable and accurate information and enhance sports nutrition knowledge and practice is currently untested. Caveats around the use of CGMs include technical issues (dislodging of sensors during periods of surveillance, loss of data due to synchronization issues), practical issues (potential bans on their use in some sporting scenarios, expense), and challenges to the underpinning principles of data interpretation, which highlight the role of sports nutrition professionals to provide context and interpretation.

The systematic review and meta-analysis evaluated the effect of aerobic, resistance and combined exercise on RMR (kCal·day^-1) and performed a methodological assessment of indirect calorimetry protocols within the included studies. Subgroup analyses included energy/diet restriction and body composition changes. Randomized control trials (RCTs), quasi – RCTs and cohort trials featuring a physical activity intervention of any form and duration excluding single exercise bouts were included. Participant exclusions included medical conditions impacting upon RMR, the elderly (≥65 years of age) or pregnant, lactating or post-menopausal women. The review was registered in the International Prospective Register of Systematic Reviews (CRD 42,017,058,503). 1669 articles were identified; 22 were included in the qualitative analysis and 18 were meta-analysed. Exercise interventions (aerobic and resistance exercise combined) did not increase resting metabolic rate (mean difference (MD): 74.6 kCal·day^-1[95% CI: −13.01, 161.33], P = 0.10). While there was no effect of aerobic exercise on RMR (MD: 81.65 kCal·day^-1[95% CI: −57.81, 221.10], P = 0.25), resistance exercise increased RMR compared to controls (MD: 96.17 kCal·day^-1[95% CI: 45.17, 147.16], P = 0.0002). This systematic review effectively synthesises the effect of exercise interventions on RMR in comparison to controls; despite heterogenous methodologies and high risk of bias within included studies.

Skeletal muscle unloading due to joint immobilization induces muscle atrophy, which has primarily been attributed to reductions in protein synthesis in humans. However, no study has evaluated the skeletal muscle proteome response to limb immobilization using SWATH proteomic methods. This study characterized the shifts in individual muscle protein abundance and corresponding gene sets after 3 and 14 d of unilateral lower limb immobilization in otherwise healthy young men. Eighteen male participants (25.4 ±5.5 y, 81.2 ±11.6 kg) underwent 14 d of unilateral knee-brace immobilization with dietary provision and following four-weeks of training to standardise acute training history. Participant phenotype was characterized before and after 14 days of immobilization, and muscle biopsies were obtained from thevastus lateralisat baseline (pre-immobilization) and at 3 and 14 d of immobilization for analysis by SWATH-MS and subsequent gene-set enrichment analysis (GSEA). Immobilization reduced vastus group cross sectional area (-9.6 ±4.6%, P <0.0001), immobilized leg lean mass (-3.3 ±3.9%, P = 0.002), unilateral 3-repetition maximum leg press (-15.6 ±9.2%, P <0.0001), and maximal oxygen uptake (-2.9 ±5.2%, P = 0.044). SWATH analyses consistently identified 2281 proteins. Compared to baseline, two and 99 proteins were differentially expressed (FDR <0.05) after 3 and 14 d of immobilization, respectively. After 14 d of immobilization, 322 biological processes were different to baseline (FDR <0.05, P<0.001). Most (77%) biological processes were positively enriched and characterized by cellular stress, targeted proteolysis, and protein-DNA complex modifications. In contrast, mitochondrial organization and energy metabolism were negatively enriched processes. This study is the first to use data independent proteomics and GSEA to show that unilateral lower limb immobilization evokes mitochondrial dysfunction, cellular stress, and proteolysis. Through GSEA and network mapping, we identify 27 hub proteins as potential protein/gene candidates for further exploration.

Salagaras, BS, Mackenzie-Shalders, KL, Nelson, MJ, Fraysse, F, Wycherley, TP, Slater, GJ, McLellan, C, Kumar, K, and Coffey, VG. Comparisons of daily energy intake vs. expenditure using the GeneActiv accelerometer in elite Australian Football athletes. J Strength Cond Res 35(5): 1273–1278, 2021—To assess validity of the GeneActiv accelerometer for use within an athlete population and compare energy expenditure (EE) with energy and macronutrient intake of elite Australian Football athletes during a competition week. The GeneActiv was first assessed for utility during high-intensity exercise with indirect calorimetry. Thereafter, 14 professional Australian Football athletes (age, 24 ± 4 [SD] y; height, 1.87 ± 0.08 m; body mass, 86 ± 10 kg) wore the accelerometer and had dietary intake assessed via dietitian-led 24-hour recalls throughout a continuous 7 days of competition period (including match day). There was a significant relationship between metabolic equivalents and GeneActiv g·min⁻¹ (SEE 1.77 METs; r ² = 0.64; p < 0.0001). Across the in-season week a significant difference only occurred on days 3 and 4 (day 3: energy intake [EI] EI 137 ± 31 kJ·kg⁻¹·d⁻¹; 11,763 ± 2,646 kJ·d⁻¹ and EE: 186 ± 14 kJ·kg⁻¹·d⁻¹; 16,018 ± 1973 kJ·d⁻¹; p < 0.05; d = −1.4; day 4: EI: 179 ± 44 kJ·kg⁻¹·d⁻¹, 15,413 ± 3,960 kJ·d⁻¹ and EE: 225 ± 42 kJ·kg⁻¹·d⁻¹; 19,313 ± 3,072 kJ·d⁻¹; d = −0.7). Carbohydrate intake (CI) was substantially below current sports nutrition recommendations on 6 of 7 days with deficits ranging from −1 to −7.2 g·kg⁻¹·d⁻¹ (p < 0.05), whereas daily protein and fat intake was adequate. In conclusion, the GeneActiv provides effective estimation of EE during weekly preparation for a professional team sport competition. Australian Footballers attempt to periodize dietary EI to varying daily training loads but fail to match expenditure on higher-training load days. Specific dietary strategies to increase CI may be beneficial to achieve appropriate energy balance and macronutrient distribution, particularly on days where athletes undertake multiple training sessions.