Search Results (146)

According to the World Health Organization (WHO), a healthy lifestyle is defined as a way of living that lowers the risk of becoming seriously ill or dying prematurely. Physical activity, as a well-known contributor to overall health, plays a vital role in supporting such a lifestyle. Exercise induces complex molecular responses that mediate both acute metabolic stress and long-term physiological adaptations. FGF21 (fibroblast growth factor 21) and GDF15 (growth differentiation factor 15) are recognized as metabolic stress markers, while their receptors play critical roles in cellular signaling. However, the differential gene expression patterns of these molecules in trained and untrained individuals following exhaustive exercise remain poorly understood. This study aimed to examine the transcriptional and protein-level responses in trained and untrained individuals performed a treadmill maximal exercise test to voluntary exhaustion. Blood samples were collected at six time points (pre-exercise, immediately post-exercise, and 0.5 h, 6 h, 24 h, and 48 h post-exercise). Gene expression of FGF21, GDF15, FGFR1 (fibroblast growth factor receptors), FGFR3, FGFR4, KLB (β-klotho), and GFRAL (glial cell line-derived neurotrophic factor receptor alpha-like) was analyzed using RT-qPCR, while plasma protein levels of FGF21 and GDF15 were quantified via ELISA. The results obtained were statistically analyzed by using Shapiro–Wilk, Mann–Whitney U, and Wilcoxon tests in Statistica 13 software. Untrained individuals demonstrated significant post-exercise upregulation of FGFR3, FGFR4, KLB, and GFRAL. FGF21 and GDF15 protein levels were consistently lower in trained individuals (p < 0.01), with no significant correlations between gene and protein expression. Trained individuals showed more stable expression of genes, while untrained individuals exhibited transient upregulation of genes after exercise. Full article

Background: Aerobic exercise induces a range of complex molecular adaptations in skeletal muscle. However, a complete understanding of the specific transcriptional changes following exercise warrants further research. Methods: This study aimed to identify gene expression patterns following acute aerobic exercise by analyzing Gene Expression Omnibus (GEO) datasets. We performed a comparative analysis of transcriptional profiles of related genes in two independent studies, focusing on both established and novel genes involved in muscle physiology. Results: Our analysis revealed ten consistently upregulated and eight downregulated genes across both datasets. The upregulated genes were predominantly associated with mitochondrial function and cellular respiration, including MDH1, ATP5MC1, ATP5IB, and ATP5F1A. Conversely, downregulated genes such as YTHDC1, CDK5RAP2, and PALS2 were implicated in vascular structure and cellular organization. Importantly, our findings also revealed novel exercise-responsive genes not previously characterized in this context. Among these, MRPL41 and VEGF were significantly upregulated and are associated with p53-mediated apoptotic signaling and fatty acid metabolism, respectively. Novel downregulated genes included LIMCH1, CMYA5, and FOXJ3, which are putatively involved in cytoskeletal dynamics and muscle fiber type specification. Conclusions: These findings enhance our understanding of the transcriptional landscape of skeletal muscle following acute aerobic exercise and identify novel molecular targets for further investigation in the fields of exercise physiology and metabolic health. Full article

The ergogenic effects of music have been well described across various modes of exercise with widespread use across competitive athletes and recreational exercisers alike. Underlying the acute beneficial effects of music during exercise are profound physiological and psychological changes which involve an array of different organ systems, including but not limited to cardiovascular, endocrine, skeletal muscle, and nervous systems. While the use of music to enhance physical performance and improve associated mechanisms has been largely optimized in healthy individuals, the investigations of the translation to individuals with neurological conditions are still ongoing. Recently, it has been established that the personalization of music interventions greatly influences performance-enhancing benefits and aids in physical performance optimization in healthy individuals. Self-selected music (SSM) has been documented to impart ergogenic advantages over pre-determined or non-preferred music, including improved cardiorespiratory endurance, power development, and velocity of movement which are characterized by adaptative physiological and psychological changes. Evidence of the benefits of SSM has progressed to the degree to which the overlap of possible benefits between healthy and clinical populations is becoming more apparent. This aim of this theoretical review is to discuss how personalized music influences psychophysiological determinants of exercise ability in healthy individuals and consider how these findings may be applicable to neurological conditions to enhance exercise capacity. The current knowledge on the role of SSM in augmenting physiological and psychological responses to exercise in healthy individuals is presented along with how these mechanisms might be leveraged to overcome exercise limitations in neurological conditions. Overall, SSM appears to have theoretical support to be a promising therapeutic approach to improving exercise ability in neurological conditions through similar ergogenic mechanisms documented in healthy individuals, but further investigation is warranted. Full article

Background: Sarcopenia is a syndrome associated with aging, characterized by a progressive decline in skeletal muscle mass and function. Its onset compromises the health and longevity of older adults by increasing susceptibility to falls, fractures, and various comorbid conditions, thereby diminishing quality of life and capacity for independent living. Accumulating evidence indicates that moderate-intensity aerobic exercise is an effective strategy for promoting overall health in older adults and exerts a beneficial effect that mitigates age-related sarcopenia. However, the underlying molecular mechanisms through which exercise confers these protective effects remain incompletely understood. Methods: In this study, we established a naturally aging mouse model to investigate the effects of a 16-week treadmill-based aerobic exercise regimen on skeletal muscle physiology. Results: Results showed that aerobic exercise mitigated age-related declines in muscle mass and function, enhanced markers associated with protein synthesis, reduced oxidative stress, and modulated the expression of genes and proteins implicated in mitochondrial quality control. Notably, a single session of aerobic exercise acutely elevated circulating levels of β-hydroxybutyrate (β-HB) and upregulated the expression of BDH1, HCAR2, and PPARG in the skeletal muscle, suggesting a possible role of β-HB–related signaling in exercise-induced muscle adaptations. However, although these findings support the beneficial effects of aerobic exercise on skeletal muscle aging, further investigation is warranted to elucidate the causal relationships and to characterize the chronic signaling mechanisms involved. Conclusions: This study offers preliminary insights into how aerobic exercise may modulate mitochondrial quality control and β-HB–associated signaling pathways during aging. Full article

Exercise training in extreme temperatures concurrent with hypohydration status may potentiate the development of acute kidney injury (AKI) in young, healthy persons. Background/Objectives: It is unknown how repeated training bouts in ambient higher temperatures and humidity may influence measures of AKI. The purpose of this study was to investigate hydration status and renal biomarkers related to AKI in NCAA Division I female soccer athletes during preseason conditioning. Methods: A convenience sample of n = 21 athletes were recruited (mean ± SEM; age: 19.3 ± 0.25 y; height: 169.6 ± 1.36 cm; mass: 68.43 ± 2.46 kg; lean body mass: 45.91 ± 1.13 kg; fat mass: 22.51 ± 1.69 kg; body fat %: 32.22 ± 1.32%). The average temperature was 27.43 ± 0.19 °C, and the humidity was 71.69 ± 1.82%. Body composition, anthropometric, workload, and 14 urine samples were collected throughout the preseason training period for urine specific gravity (USG), creatinine (uCr), cystatin C (uCyst-C), and neutrophil gelatinase-associated lipocalin (uNGAL) analyses. Results: Our investigation showed that, when compared to baseline (D0), the athletes maintained a USG-average euhydrated status (1.019 ± 0.001) and were euhydrated prior to each exhibition game (D5-Pre: p = 0.03; 1.011 ± 0.001; D10-Pre: p = 0.0009; 1.009 ± 0.001); uCr was elevated on D8 (p = 0.001; 6.29 ± 0.44 mg·dL⁻¹·LBM⁻¹) and D10-Post (p = 0.02; 6.61 ± 0.44 mg·dL⁻¹·LBM⁻¹); uCyst-C was elevated on D6 through D10 (p = 0.001; ~0.42 ± 0.01 mg·dL⁻¹); no differences were found in uNGAL concentration. The highest distance (m) displaced was found during exhibition games (D5: p = <0.0001; ~8.6 km and D10: p = <0.0001; ~9.6 km). During the preseason conditioning, the athletes maintained a euhydrated status (~1.019) via USG, an increase in uCr that averaged within a normal range (208 mg·dL⁻¹), and an increase in uCyst-C to near AKI threshold levels (0.42 mg·L⁻¹) for several practice sessions, followed by an adaptive decline. No differences were found in uNGAL, which may be explained by athlete variation, chosen time sample collection, and variation in training and hydration status. Conclusions: The athletes maintained a euhydrated status, and this may help explain why urinary markers did not change or meet the reference threshold for AKI. Full article

Aim: To assess the acute effects of proprioceptive neuromuscular facilitation (PNF), stretching was applied to the hamstring muscles to evaluate deep cervical flexor endurance. Potential variables correlating with endurance adaptations were examined. Methods: This randomized controlled trial performed between September 2023 and June 2024 included healthy female university students aged 18–25 years. Participants were randomly assigned to either the control or the PNF group. Variables included age, height, weight, body mass index, Beighton score, hamstring flexibility, and deep cervical flexor muscle endurance; correlations between changes in hamstring flexibility and DCF endurance were explored. Hamstring flexibility was assessed using the Passive Knee Extension Test, and deep cervical flexor endurance was assessed using the Cranio-Cervical Flexion Test. The PNF group received hold–relax exercises while controls did not receive any intervention. Results: The study included 32 control participants and 32 individuals in the PNF group. The PNF group was marginally but significantly older than the control group [22 (21–23) vs. 21 (21–22); p = 0.038]. At baseline, the PNF group showed greater hamstring flexibility (p = 0.010). Both groups showed significant improvements in hamstring flexibility (p < 0.001 for both), but the improvement in the PNF recipients was far greater (p < 0.001). Regarding deep neck flexor endurance, no significant difference was observed between the groups at baseline (p = 0.958) or in final measurements (p = 0.244), although both groups showed significant improvements from baseline (p < 0.001 for both). There were no significant correlations between the change in deep neck flexor endurance and any of the examined variables. Conclusions: Our study found that a single session of PNF stretching significantly improved hamstring flexibility but did not immediately enhance deep neck flexor endurance. This emphasizes the need for further research into longer-term interventions to assess whether interventions on hamstring flexibility can improve cervical function. Full article

Background: This study aimed to investigate the acute changes in muscle and tendon viscoelastic properties in response to a progressive treadmill VO₂max test among professional male soccer players. Methods: Bilateral assessments at five sites—the Achilles tendon (AT), biceps femoris, semitendinosus, rectus femoris (RF), and sternocleidomastoid (SCM)—measured tone (oscillation frequency), dynamic stiffness, logarithmic decrement (elasticity), stress relaxation time, and creep. Each site was probed five times and values averaged. Repeated-measures ANOVA (Time × Side) with Bonferroni correction tested pre- to post-exercise changes; Pearson’s r examined associations with VO₂max. Results: Significant Time effects (all p < 0.05) were observed for RF frequency (η_p² = 0.226), RF creep (η_p² = 0.144), AT stiffness (η_p² ≈ 0.035), AT frequency (η_p² = 0.035), and SCM frequency (η_p² = 0.037). Post-exercise, right AT stiffness fell by 65 ± 14 N/m (p = 0.015), while left AT stiffness rose by 22 ± 9 N/m (p = 0.015). RF stiffness decreased by 28 ± 6 N/m (p < 0.001) and tone by 1.2 ± 0.3 Hz (p < 0.001), with creep (+0.08 ± 0.02; p < 0.001) and relaxation time (+1.5 ± 0.7 ms; p < 0.001) increasing. SCM tone declined by 0.8 ± 0.4 Hz (p = 0.010). Baseline RF properties—frequency (r = −0.597), stiffness (r = −0.59), relaxation time (r = 0.53), and creep (r = 0.48)—correlated moderately with VO₂max (all p < 0.05). Conclusions: These findings suggest that viscoelastic adaptations to exhaustive aerobic exercise are tissue- and side-specific, and that rectus femoris viscoelastic properties may serve as potential indicators of endurance readiness. Full article

Sclerostin (SOST) is a specific osteocyte protein. During the differentiation and proliferation of osteoblasts and osteoclasts, the high expression of SOST can inhibit bone formation and contribute to osteoporosis and the bone metastasis of malignant tumors. Most of the research on SOST has focused on bone cells, but studies have found that SOST is not a specific product of bone cells but that it is also expressed by articular chondrocytes. SOST can regulate the progression of osteoarthritis in bone and cartilage, promote subchondral bone sclerosis, and inhibit cartilage degeneration. A review of the literature found that SOST can not only regulate bone metabolism, but it is also expressed in cardiovascular, kidney, liver, and other tissues, influencing the occurrence and development of diseases in these organs and tissues. Studies have found that diseases of extra-bone organs, such as atherosclerosis, aneurysm, chronic kidney disease, and cirrhosis, may be related to the expression of SOST. Simultaneously, long-term exercise can reduce SOST levels, especially in areas of high bone strain. Prolonged exercise induces bone adaptation to mechanical stress, resulting in diminished responsiveness of bone cells to exercise and a reduction in serum SOST levels. Short-term acute exercise can elevate serum SOST levels, but these results are often limited by age, gender, and energy status. In general, serum SOST rises immediately after short-term acute exercise, returning to baseline or even decreasing after exercise. Full article

Objectives: The present study aimed to investigate changes in forearm muscle activity associated with short-term go-kart driving (680 m) and its potential effect on muscle activation patterns. Methods: Eleven male karting league drivers (mean age: 23.18 ± 1.40 years; body mass: 83.27 ± 10.98 kg; height: 182.73 ± 5.66 cm) volunteered to participate. Electromyographic (EMG) activity was recorded from four muscles: extensor carpi radialis (ECR), extensor carpi ulnaris (ECU), flexor carpi radialis (FCR), and flexor carpi ulnaris (FCU). Baseline EMG was measured before the intervention, followed by two consecutive kart-driving sessions on a 680 m closed track. Post-exercise EMG data were then collected. A repeated-measures analysis of covariance (ANCOVA) was used to analyze the effects of time (pre vs. post) while controlling for cumulative race time as a covariate. Results: A significant time effect with cumulative time as a covariate was observed, particularly in the ECR and ECU muscles on both the left and right sides. Notable findings include increases in maximum and mean activity of the left and right ECR (e.g., ECR right max: F = 51.57; p < 0.001; η² = 0.851) and ECU (e.g., ECU right max: F = 36.170; p < 0.001; η² = 0.801). Additionally, a significant increase was found in the maximum activation of the left FCR (F = 11.019; p = 0.009; η² = 0.550, which remained significant after controlling for total driving time. This heightened activation likely reflects an acute neuromuscular fatigue response to the demands of kart steering, rather than a long-term adaptation. Conclusions: The findings suggest that even short bouts of kart driving can induce measurable changes in neuromuscular activation of the forearm muscles, particularly in those involved in grip control and steering stability. This highlights the physical demands of karting and its potential impact on the upper limb muscle conditioning. Full article

The application of blood flow restriction (BFR) during resistance exercise enhances muscular adaptations under low-load conditions. However, its acute effects on explosive neuromuscular performance, particularly on kinetic variables such as the rate of force development (RFD), impulse, and peak force remain poorly understood in women. Twenty-five participants underwent randomized sessions under three occlusion conditions (0%, 40%, and 80% limb occlusion pressure), followed by isometric mid-thigh pull (IMTP) assessments at five time points (pre-exercise; post-exercise; and 5, 10, and 15 min post-exercise). Peak force, impulse, and RFD were analyzed across early (0–50 ms), mid (51–150 ms), and late (151–250 ms) time intervals. BFR did not result in statistically significant alterations in RFD or isometric force production at any time or pressure. These findings indicate that acute BFR application, even when volitional fatigue is induced, does not substantially impair neuromuscular function in isometric settings. These findings indicate that acute exposure to BFR, even under fatiguing conditions, does not substantially impair isometric force production or explosive performance in young physically active women. These results support the task-specific and temporally dependent nature of neuromuscular responses to BFR, highlighting the need for population-specific approaches in BFR programming. Full article

The surface properties of the running surface have an effect on physiological and biomechanical responses to exercise, but their influence on body composition, blood pressure, and knee joint kinetics during controlled sports loading is less researched. This study compared the effects of treadmill running (TR) and overground running (OR) on acute physiological and biomechanical adaptation in ten male athletes aged between 23 and 26 years old following a 30 min protocol at 75% VO₂max. Pre- and post-running body composition (fat volume, protein content, and fluid distribution), blood pressure, and knee joint kinetics (total work of muscle extensors—TWMEs) were assessed using bioelectrical impedance analysis, blood pressure monitor, and isokinetic dynamometry. The results indicated that TR led to highly significant reductions in protein content with a considerable accumulation of intracellular fluid. At the same time, TR reduced knee TWME by 27.4%, and OR elevated TWME by 5.6%. No significant differences in blood pressure were observed. These findings highlight surface-specific metabolic stress and biomechanical loading patterns and show that TR augments catabolic responses and knee joint strain despite equivalent external workloads. Full article

Cardiovascular complications are a hallmark of Post-Acute Sequelae of Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) infection (PASC), yet the mechanisms driving persistent cardiac dysfunction remain poorly understood. Emerging evidence implicates mitochondrial dysfunction in immune cells as a key contributor. This study investigated whether CD14⁺⁺ monocytes from long COVID patients exhibit bioenergetic impairment, mitochondrial DNA (mtDNA) damage, and defective oxidative stress adaptation, which may underlie cardiovascular symptoms in PASC. CD14⁺⁺ monocytes were isolated from 14 long COVID patients with cardiovascular symptoms (e.g., dyspnea, angina) and 10 age-matched controls with similar cardiovascular risk profiles. Mitochondrial function was assessed using a Seahorse Agilent Analyzer under basal conditions and after oxidative stress induction with buthionine sulfoximine (BSO). Mitochondrial membrane potential was measured via Tetramethylrhodamine Ethyl Ester (TMRE) assay, mtDNA integrity via qPCR, and reactive oxygen species (ROS) dynamics via Fluorescence-Activated Cell Sorting (FACS). Parallel experiments exposed healthy monocytes to SARS-CoV-2 spike protein to evaluate direct viral effects. CD14⁺⁺ monocytes from long COVID patients with cardiovascular symptoms (n = 14) exhibited profound mitochondrial dysfunction compared to age-matched controls (n = 10). Under oxidative stress induced by buthionine sulfoximine (BSO), long COVID monocytes failed to upregulate basal respiration (9.5 vs. 30.4 pmol/min in controls, p = 0.0043), showed a 65% reduction in maximal respiration (p = 0.4035, ns) and demonstrated a 70% loss of spare respiratory capacity (p = 0.4143, ns) with significantly impaired adaptation to BSO challenge (long COVID + BSO: 9.9 vs. control + BSO: 54 pmol/min, p = 0.0091). Proton leak, a protective mechanism against ROS overproduction, was blunted in long COVID monocytes (3-fold vs. 13-fold elevation in controls, p = 0.0294). Paradoxically, long COVID monocytes showed reduced ROS accumulation after BSO treatment (6% decrease vs. 1.2-fold increase in controls, p = 0.0015) and elevated mitochondrial membrane potential (157 vs. 113.7 TMRE fluorescence, p = 0.0179), which remained stable under oxidative stress. mtDNA analysis revealed severe depletion (80% reduction, p < 0.001) and region-specific damage, with 75% and 70% reductions in amplification efficiency for regions C and D (p < 0.05), respectively. In contrast, exposure of healthy monocytes to SARS-CoV-2 spike protein did not recapitulate these defects, with preserved basal respiration, ATP production, and spare respiratory capacity, though coupling efficiency under oxidative stress was reduced (p < 0.05). These findings suggest that mitochondrial dysfunction in long COVID syndrome arises from maladaptive host responses rather than direct viral toxicity, characterized by bioenergetic failure, impaired stress adaptation, and mitochondrial genomic instability. This study identifies persistent mitochondrial dysfunction in long COVID monocytes as a critical driver of cardiovascular complications in PASC. Key defects—bioenergetic failure, impaired stress adaptation and mtDNA damage—correlate with clinical symptoms like heart failure and exercise intolerance. The stable elevation of mitochondrial membrane potential and resistance to ROS induction suggest maladaptive remodeling of mitochondrial physiology. These findings position mitochondrial resilience as a therapeutic target, with potential strategies including antioxidants, mtDNA repair agents or metabolic modulators. The dissociation between spike protein exposure and mitochondrial dysfunction highlights the need to explore host-directed mechanisms in PASC pathophysiology. This work advances our understanding of long COVID cardiovascular sequelae and provides a foundation for biomarker development and targeted interventions to mitigate long-term morbidity. Full article

Background: Metabolic syndrome (MS) is a cluster of cardiovascular and metabolic risk factors that increase the likelihood of both acute events and chronic conditions. While exercise has been shown to improve individual risk factors associated with MS; research on its effects on MS as an integrated condition remains limited. This study aims to evaluate the effectiveness of a 6-month Adapted Personalized Motor Activity (AMPA) program for improving the health outcomes of individuals with MS. Methods: Seventy-one sedentary participants with MS (mean age: 63 ± 9.4 years, 46.5% female) completed a 6-month intervention, incorporating moderate-intensity aerobic and resistance training. Each participant received a personalized exercise plan prescribed by a sports medicine physician. The training was monitored via telemetry to ensure safety. No dietary recommendations were provided during the intervention. Baseline and post-intervention assessments included Cardiopulmonary Exercise Testing (CPET), anthropometric measurements, blood pressure, heart rate, lipid profile (total cholesterol, HDL, LDL, and triglycerides), fasting glucose, and HbA1c. Results: Significant improvements were observed in fasting glucose (−10.6%, p < 0.001), HbA1c (−3.88%, p < 0.001), HDL cholesterol (+20.8%, p < 0.001), LDL cholesterol (−25.1%, p < 0.001), and VO₂max (+8.6%, p < 0.001). Systolic and diastolic blood pressure also decreased significantly, with reductions of −12% (p < 0.001) and −5.9% (p < 0.001), respectively. Reductions in weight and waist circumference were statistically significant but modest and clinically irrelevant, showing no correlation with improvements in cardio-metabolic parameters. Logistic regression and correlation matrix analyses were performed to identify key predictors of changes in individual risk factors. Conclusions: While personalized exercise alone may not fully control individual risk factors of metabolic syndrome, its overall effect is comparable to low-intensity pharmacological polytherapy with minimal adverse effects. These benefits appear to be independent of dietary habits, gender, and both baseline and post-intervention physical performance and anthropometric measures. Full article

Background/objectives: The study aims to investigate potential differences in vertical jump performance between elite basketball and volleyball players before and after a standard training session, in comparison to a control group from the general population. The analysis focuses on the influence of selected gene polymorphisms that may contribute to variations in the assessed performance parameters. Aims: The aim was to investigate the influence of ACE (rs4646994), ACTN3 (rs1815739), PPARA rs4253778, HIF1A (rs11549465), and AMPD1 (rs17602729) genes polymorphisms on the combined effects of post-activation potentiation (PAP), post-activation performance enhancement (PAPE), and general adaptation syndrome (GAS), as reflected in vertical jump performance, in elite basketball and volleyball players compared to a control group from the general population. Methods: The effects of PAP at the beginning of the training load (acute exercise), and the combined influences of PAPE and GAS following the training load were evaluated using parameters measured by the OptoJump Next^® system (Microgate, Bolzano, Italy). Results: A statistically significant (h, p < 0.05) negative effect of the CT genotype of the AMPD1 gene on jump height was observed in the group of athletes. The CT genotype of the AMPD1 gene negatively impacted on PAPE and GAS adaptive responses (ΔP, Δh, p < 0.001) also in the control group. A positive effect on the power during the active phase of the vertical jump was identified for the II genotype of the ACE gene and the Pro/Ser genotype of the HIF1A gene, both exclusively in the control group (ΔP, p < 0.05). Conclusion: Our findings demonstrate that different gene polymorphisms exert variable influences on the combined effects of PAPE and GAS, as reflected in vertical jump parameters, depending on the participants’ level of training adaptation. Full article

Background: Breakfast is often termed the most important meal of the day. However, its importance to acute and chronic adaptations to exercise is currently not well summarized throughout the literature. Methods: A narrative review of the experimental literature regarding breakfast consumption’s impact on acute and chronic exercise performance and alterations in body composition prior to November 2024 was conducted. To be included in this review, the selected investigations needed to include some aspect of either endurance or resistance training performance and be conducted in humans. Results: These findings suggest that breakfast consumption may benefit acute long-duration (>60 min) but not short-duration (<60 min) morning endurance exercise. Evening time trial performance was consistently inhibited following breakfast omission despite the resumption of eating midday. No or minimal impact of breakfast consumption was found when examining acute morning or afternoon resistance training or the longitudinal adaptations to either resistance or endurance training. Favorable changes in body composition were often noted following the omission of breakfast. However, this was primarily driven by the concomitant reduced kilocalorie intake. Conclusions: Consuming breakfast may aid endurance athletes regularly performing exercise lasting >60 min in length. However, the morning meal’s impact on resistance training and changes in body composition appears to be minimal. Although, as the body of literature is limited, future investigations are needed to truly ascertain the dietary practice’s impact. Full article