Medicine and Science in Sports and Exercise最新文献

Background: Protein ingestion stimulates muscle protein synthesis (MPS) rates to support the turnover of skeletal muscle protein mass. However, dietary patterns consist of a variety of protein foods with different amino acid compositions consumed at multiple meal times throughout the day. Omnivorous (OMN) and vegan (VGN) dietary patterns may differentially stimulate MPS. Moreover, the distribution and frequency of protein intake may also play an important anabolic regulatory role.

Objective: We aimed to determine the effect of OMN and VGN dietary patterns and protein distribution (balanced (B) and unbalanced (UB)) in regulating changes in daily myofibrillar protein synthesis rates during a 9-d resistance training intervention.

Design: Forty healthy, physically active males and females (28 males, 12 females; 25 ± 4 yr; body mass index, 24.1 ± 2.1 kg·m -2 ) consumed a weight-maintenance diet providing 1.1-1.2 g·kg -1 ·d -1 of dietary protein from an OMN or VGN dietary pattern with UB (10%, 30%, and 60% of daily protein at meals 1, 2, and 3, respectively) or B (20% of daily protein at five eating occasions) distribution. Participants completed whole-body resistance exercise three times during the controlled feeding trial while consuming deuterated water (D 2 O) for the measurement of daily myofibrillar protein synthesis rates.

Results: The percent kilocalories from carbohydrate was higher ( P = 0.045) in the OMN compared with VGN groups, but no other differences in dietary intakes were observed. Myofibrillar protein synthesis rates did not differ between the OMN-UB (3.04% ± 1.85%·d -1 ), OMN-B (2.43% ± 1.21%·d -1 ), VGN-UB (2.52% ± 1.77%·d -1 ), and VGN-B (2.49% ± 1.56%·d -1 ) groups (all P > 0.05).

Conclusions: Our results demonstrated that the anabolic action of animal versus vegan dietary patterns is similar. Moreover, there is no regulatory influence of distribution between the two dietary patterns on the stimulation of myofibrillar protein synthesis rates in young adults.This trial was registered with ClinicalTrials.gov (NCT04232254).

Objective: This study aimed to investigate the molecular mechanisms underlying the improvement of aged skeletal muscle atrophy by high-intensity interval training (HIIT) combined with glycine supplementation.

Methods: Male C57BL/6J mice aged 19 months ( n = 16) were randomly assigned to old sedentary (OSED), HIIT, OSED + glycine, and HIIT + glycine (H-Gly) groups for an 8-wk intervention. Maximum grip strength and running speed were assessed. Myocyte apoptosis was detected by TUNEL staining; myofiber cross-sectional area was measured by laminin staining; reactive oxygen species in myocytes were detected by dihydroethidium staining. Western blot and RT-qPCR were used to measure protein and gene expression levels related to senescence, apoptosis, and ferroptosis in myocytes. Chemical methods were employed to detect changes in malondialdehyde, lipid peroxide, glutathione, glutathione-oxidized, and total glutathione contents. RNA-seq technology was utilized to screen for key differentially expressed genes. AutoDockTools software was used for molecular docking predictions between glycine and key differential proteins.

Results: H-Gly group mice showed an improved maximum grip strength and muscle fiber cross-sectional area, with a significant reduction in TUNEL-positive cells. RNA-seq analysis revealed a high correlation between ferroptosis pathway genes and Slc25a25 ion transport-related genes, which was further validated by the detection of ferroptosis-related markers. Molecular docking indicated that glycine has binding sites with Slc25a25, with the highest binding energy of -3.7 kcal·mol -1 .

Conclusions: Glycine supplementation has a significant synergistic effect with HIIT in increasing muscle mass and grip strength in aged muscle. The mechanism might be associated with the decrease of Slc25a25-mediated ferroptosis.

Introduction: Exercise interventions are less effective in generating weight loss in females compared to males suggesting that the menstrual cycle may be important. Fluctuations in ovarian hormones are proposed to alter the appetite-regulatory response to exercise across the menstrual cycle and no study has assessed the response in all distinct hormonal phases.

Purpose: To compare post-exercise appetite-regulating parameters following a single bout of MICT across three distinct menstrual phases.

Methods: Thirteen females (24 ± 4 y; 24.8 ± 5.4 kg·m-2) completed 30 min of moderate-intensity continuous training (MICT) running in the follicular phase (FP), ovulatory phase (OP), and luteal phase (LP). Acylated ghrelin, active glucagon-like peptide-1 (GLP-1), plasma glucose, insulin, blood lactate, and appetite perceptions were measured pre-exercise, 0 min, 30 min, 60 min, and 120 min post-exercise. Energy intake was recorded for a 3-day period (day before, of, and after each session).

Results: Acylated ghrelin was not different across phases (p = 0.672, ηp2 = 0.032) and only showed a main effect of time (p = 0.006, ηp2 = 0.757) increasing with time. Active GLP-1 was not different across phases (p = 0.735, ηp2 = 0.025) and had a main effect of time (p < 0.001, ηp2 = 0.569) decreasing with time. Appetite perceptions were not different across phases (p = 0.577, ηp2 = 0.045) and exhibited a main effect of time (p < 0.001, ηp2 = 0.786) increasing with time. There was no effect of phase for energy intake (p = 0.544, ηp2 = 0.065). Finally, there were no differences in plasma glucose, insulin, or blood lactate across phases (p > 0.421, ηp2 < 0.070).

Conclusions: There were no divergent appetite responses following MICT running across three hormonally distinct phases (mid-FP, OP, mid-LP) of the menstrual cycle in young eumenorrheic females not using oral contraceptives.

Purpose: Cardiorespiratory fitness (CRF) and muscle strength are associated with cancer risk/mortality in adults. However, there is yet no evidence for pediatric tumors. This study investigated the association of CRF and muscle strength with several tumor-related phenotypes in an aggressive childhood malignancy, high-risk neuroblastoma (HR-NB).

Methods: Twelve mice bearing orthotopic HR-NB were studied. CRF and muscle strength were assessed using treadmill and grip strength testing, respectively. The following tumor-related outcomes were studied: survival, clinical severity, tumor weight/volume, metastasis, and intratumor immune infiltrates. Additionally, tumor samples underwent quantitative proteomic analysis via liquid chromatography-tandem mass spectrometry. Spearman correlations (or logistic regression) were performed between CRF/muscle strength and the abovementioned variables. Proteins significantly correlated with CRF or muscle strength were mapped into protein-protein interaction (PPI) networks using the Search Tool for the Retrieval of Interacting Genes/Proteins (STRING) database.

Results: CRF was inversely correlated with clinical severity score (r = -0.657, p = 0.020). Of 6,840 identified tumor proteins, 76 correlated significantly with CRF (19 positively, 57 negatively), whereas 194 correlated with muscle strength (97 positively, 97 negatively). Proteins correlated with CRF were primarily involved in metabolic and structural pathways, including angiotensinogen and elastin. In turn, muscle strength-associated proteins were more abundant, and included keratin family proteins (e.g., keratin, type I cytoskeletal 14 and type II cytoskeletal 5), proteins involved in cell adhesion (e.g., desmoglein-1-alpha), and translational regulators (e.g., eukaryotic initiation factor 4A). Network analysis revealed significant enrichment in structural organization and cellular adhesion pathways.

Conclusions: Besides the association of CRF with clinical severity of the tumor, distinct novel tumor proteomic signatures associated with CRF and muscle strength were identified, highlighting potential mechanisms linking physical fitness with childhood cancer biology.

Purpose: Previous work showed altered mechanical properties of the Achilles tendon in the presence of tendinopathy, considering the Achilles tendon as a homogeneous structure with the gastrocnemius medialis (GM) subtendon representative of it. However, the Achilles tendon consists of three semi-independent structures: the GM, gastrocnemius lateralis (GL), and soleus (SOL) subtendons, each independently pulled by their respective muscle. The aim of this study was (i) to compare the mechanical properties of the different Achilles subtendons in humans in vivo by considering the force of each muscle within the triceps surae group and (ii) to determine whether the loss of stiffness in the presence of tendinopathy is specific to individual subtendons. We hypothesized that (i) stiffness would differ between subtendons in healthy participants and that (ii) the loss of stiffness in people with Achilles tendinopathy compared with healthy controls would not affect the three subtendons identically.

Methods: Fourteen participants with tendinopathy and 14 controls performed ramped isometric plantarflexions. Simultaneously, the elongation of the three subtendons was recorded, and an estimate of the force pulling on each was made (from muscle activation and volume). Stiffness was calculated from the individual muscle index of force-subtendon elongation relationships.

Results: Results showed that regardless of the group, SOL stiffness was significantly higher than stiffness of both gastrocnemii (muscle effect: P < 0.001). A muscle-group interaction showed specific loss of stiffness of GL in Achilles tendinopathy compared with controls ( P = 0.029, d = 1.3), with no between-group difference for GM or SOL (both P > 0.925, d = 0.3).

Conclusions: This study supports the hypothesis that the biomechanical properties of the Achilles tendon differ between subtendons and further shows that the loss of stiffness in Achilles tendinopathy is specific to the GL subtendon.

Background/purpose: Adjusting running style can influence musculoskeletal loading, thereby altering injury risk. Duty factor, defined as the ratio of contact time to stride time, along with stride frequency, have been linked to peak loading in previous studies, although their specific influences remain unclear. This study elucidates how duty factor and stride frequency, both individually and in tandem, affect peak loading at an individualized constant speed, enhancing our understanding of how changes in running pattern affect musculoskeletal loading.

Methods: Nineteen female novice runners ran on treadmill at 90% of their individually preferred running speed. Subjects were instructed to adjust duty factor and/or stride frequency according to a specific protocol. Ground reaction forces and motion capture data were recorded. Peak loading was assessed through maximal vertical ground reaction force, maximal resultant joint reaction forces, and maximal extensor and flexor moments of the lower limb joints using an inverse dynamics approach. Mixed-effects models were utilized to analyze the individual and combined effects of duty factor and stride frequency on peak loading.

Results and discussion: Increasing duty factor consistently reduced peak loading across all metrics except hip extensor and flexor moments, which showed an increase. In contrast, the relationship between stride frequency and peak loading varied across loading metrics. Increasing stride frequency reduced peak knee and hip extensor moments and had no effect on maximal vertical ground reaction force or peak joint reaction forces, but increased peak hip flexor moment. Surprisingly, when controlled for duty factor, stride frequency also became a determinant of maximal vertical ground reaction force and peak joint reaction forces, leading to unexpected increases in peak loading as stride frequency increased.

Conclusions: This study establishes duty factor as the primary factor in modulating peak loading in running. Stride frequency may also affect peak loading, but its effect varies based on individual characteristics and the metric considered.

Purpose: To examine the effects of voluntary wheel running on tumor growth and explore potential intratumoral molecular pathways responsible for the beneficial effects of voluntary wheel running on tumor formation and progression in a mouse model of castration-resistant prostate cancer (CRPC).

Methods: Male immunodeficient mice (SCID) were castrated and subcutaneously inoculated with human CWR-22RV1 cancer cells to construct CRPC xenograft model before assigned to either voluntary wheel running (VWR) or sedentary (SED) group ( n = 6/group). Tumor size was measured and calculated throughout the study. After 3 wk, tumor tissues were collected. mRNA expression of markers of DNA replication, androgen receptor (AR) signaling, and mitochondrial dynamics was determined by quantitative real-time polymerase chain reaction. Protein expression of mitochondrial dynamics was determined by Western blotting. Finally, transcriptomics analysis was performed using the tumor tissues.

Results: Voluntary wheel running resulted in smaller tumor volume at the initial stage and attenuated tumor progression throughout the time course ( P < 0.05). The reduction of tumor volume in the VWR group coincided with lower mRNA expression of DNA replication markers ( MCM2 , MCM6 , and MCM7 ), AR signaling ( ELOVL5 and FKBP5 ), and regulatory proteins of mitochondrial fission (Drp1 and Fis1) and fusion (MFN1 and OPA1) when compared with the SED group ( P < 0.05). RNA sequencing data further revealed that pathways related to angiogenesis, extracellular matrix formation, and endothelial cell proliferation were downregulated.

Conclusions: Three weeks of voluntary wheel running was effective in delaying tumor formation and progression, which coincided with reduced transcription of DNA replication, AR signaling targets, and mitochondrial dynamics. We further identified a downregulation in molecular pathways related to angiogenesis that may be responsible for the delayed tumor formation and progression by voluntary wheel running.

Purpose: Non-Hispanic Black (NHB) women in the United States exhibit higher prevalence and mortality rates from cardiovascular diseases compared with non-Hispanic White (NHW) women. Previous studies in NHB men have demonstrated impaired vascular function at rest and during exercise; however, to date, no studies have investigated the hyperemic responses during exercise in NHB women. Therefore, we tested the hypothesis that, compared with NHW women, NHB women would present an attenuated increase in forearm blood flow (FBF) and forearm vascular conductance (FVC) during steady-state rhythmic handgrip exercise.

Methods: FBF (duplex Doppler ultrasound) and central hemodynamics including mean arterial pressure (MAP; finger photoplethysmography) were measured in healthy young NHW ( n = 16) and NHB ( n = 14) women during rhythmic handgrip exercise performed at 15%, 30%, and 45% of maximal voluntary contraction (MVC).

Results: FVC (calculated as FBF/MAP), FBF, and MAP were not different between groups at rest (FVC: 52 ± 13 mL·min -1 ·100 mm Hg -1 in NHW women vs 56 ± 14 mL·min -1 ·100 mm Hg -1 in NHB women; P = 0.43). There was an intensity-dependent increase in FBF and FVC during exercise in both groups, but there was no difference between the groups (e.g., FVC at 45% MVC; NHW: 304 ± 55 mL·min -1 ·100 mm Hg -1 , NHB: 351 ± 121 mL·min -1 ·100 mm Hg -1 , interaction P = 0.257). MAP responses during exercise were also not different between groups (e.g., ΔMAP at 45% MVC; NHW: 7 ± 6 mm Hg, NHB:8 ± 6 mm Hg, P = 0.553). In addition, all central hemodynamics during exercise and flow-mediated dilation were comparable between the groups.

Conclusions: Collectively, these findings indicate that the hyperemic responses to rhythmic handgrip exercise are not different between young, healthy NHB and NHW women.

Purpose: This study aimed to examine central and peripheral physiological adaptations contributing to increases in maximal oxygen uptake (V̇O 2max ) following a 12-wk vigorous endurance exercise program in healthy, older and young adults.

Methods: Fourteen participants (7 older: 68 ± 7 yr and 7 young: 26 ± 7 yr; 9 males and 5 females) engaged in a cycling training program three times a week for 45 min at ~70%V̇O 2max . Changes in V̇O 2max , cardiac function, V̇O 2 extraction, muscle capillarization, and mitochondrial content from pre- to post-training were examined.

Results: The increase in V̇O 2max from pre- to post-training for all participants (20% ± 8%) was accompanied by increases in maximal cardiac output (Q˙ max ; 15% ± 11%), maximal stroke volume (SVmax; 14% ± 12%), muscle fiber cross-sectional area (CSA; 17% ± 21%) and perimeter (P; 7% ± 9%), citrate synthase (CS) activity (144% ± 175%), individual capillary-to-fiber ratio (C:Fi; 32% ± 17%), capillary-to-fiber perimeter exchange index (CPFE: 30% ± 15%), capillary contact (CC; 38% ± 20%), capillary density (CD; 22% ± 17%), and arteriovenous O 2 difference (a-vO 2 diff; 4% ± 6%) ( P < 0.05 for all). No training-related variation existed for maximal heart rate (HRmax; -1% ± 4%; P = 0.448). Changes in V̇O 2max were positively correlated with Q˙ max ( r = 0.830: P < 0.001), SVmax ( r = 0.655; P = 0.011), CD ( r = 0.546; P = 0.043), and CS activity ( r = 0.630; P = 0.021). No significant correlations were found for changes in V̇O 2max and changes in HRmax, a-vO 2 diff, muscle fiber CSA and P, CC, C:Fi, and CPFE ( P > 0.05 for all).

Conclusions: Cardiorespiratory fitness improvements were primarily determined by enhancement in central (i.e., cardiac function) and peripheral (i.e., vascularization) adaptations within the V̇O 2 transport system as well as the upregulation of mitochondrial aerobic enzymatic activity (i.e., CS activity) at the intracellular level.