Journal of Sport and Health Science最新文献

Background: Residual force enhancement (rFE), defined as increased isometric force following active lengthening compared to a fixed-end isometric contraction at the same muscle length and level of activation, is present across all scales of muscle. While rFE is always present at the cellular level, often rFE "non-responders" are observed during joint-level voluntary contractions.

Methods: We compared rFE between the joint level and single fiber level (vastus lateralis biopsies) in 16 young males. In vivo voluntary knee-extensor rFE was measured by comparing steady-state isometric torque between a stretch-hold (maximal activation at 150°, stretch to 70°, hold) and a fixed-end isometric contraction, with ultrasonographic recording of vastus lateralis fascicle length (FL). Fixed-end contractions were performed at 67.5°, 70.0°, 72.5°, and 75.0°; the joint angle that most closely matched FL of the stretch-hold contraction's isometric steady-state was used to calculate rFE. The starting and ending FLs of the stretch-hold contraction were expressed as % optimal FL, determined via torque-angle relationship.

Results: In single fiber experiments, the starting and ending fiber lengths were matched relative to optimal length determined from in vivo testing, yielding an average sarcomere excursion of ∼2.2-3.4 µm. There was a greater magnitude of rFE at the single fiber (∼20%) than joint level (∼5%) (p = 0.004), with "non-responders" only observed at the joint level.

Conclusion: By comparing rFE across scales within the same participants, we show the development of the rFE non-responder phenomenon is upstream of rFE's cellular mechanisms, with rFE only lost rather than gained when scaling from single fibers to the joint level.

Background: Fat loss mainly conveys the benefits of caloric restriction for people living with type 2 diabetes. The literature is equivocal regarding whether exercise facilitates fat loss during caloric restriction. This analysis aimed to assess the dose-response effects of exercise in combination with a caloric restriction on fat mass (FM) and FM percentage (FM %) in persons with diagnosed type 2 diabetes.

Methods: In this secondary analysis of a 4-armed randomized trial, 82 persons living with type 2 diabetes were randomly allocated to the control group (CON) (n = 21), diet control (DCON) (25 % caloric restriction; n = 20), diet control and exercise 3 times per wk (MED) (n = 20), or diet control and exercise 6 times per wk (HED) (n = 21) for 16 wk. The primary analysis was the change in FM% points. Secondary analyses included fat-free mass and visceral adipose tissue (VAT) volume (cm³).

Results: FM% decreased compared to CON by a mean difference of -3.5% (95% confidence interval (95%CI): -5.6% to -1.4%), -6.3% (95%CI: -8.4% to -4.1%), and -8.0% (95%CI: -10.2% to -5.8%) for DCON, MED, and HED, respectively. Compared to DCON, MED and HED decreased FM% by -2.8% (95%CI: -4.9% to -0.7%) and -4.5% (95%CI: -6.6% to -2.4%), respectively. The difference in FM% between HED and MED was -1.8% (95%CI: -3.9% to 0.4%). DCON and MED decreased fat-free mass compared to CON, whereas HED preserved fat-free mass (-0.2% (95%CI: -2.0% to 1.7%)). Compared to CON, VAT volume decreased by -666.0 cm³ (95%CI: -912.8 cm³ to -385.1 cm³), -1264.0 (95%CI: -1679.6 cm³ to -655.9 cm³), and -1786.4 cm³ (95%CI: -2264.6 cm³ to -1321.2 cm³) more for DCON, MED, and HED, respectively. HED decreased VAT volume more than DCON (-1120.4 cm³ (95%CI: -1746.6 cm³ to -639.4 cm³)) while the remaining comparisons did not reveal any differences.

Conclusion: All interventions were superior in reducing FM% compared to standard care. Adding exercise to a caloric restriction was superior in reducing FM% compared to a caloric restriction alone.

Exercise is a therapeutic approach in cancer treatment, providing several benefits. Moreover, exercise is associated with a reduced risk for developing a range of cancers and for their recurrence, as well as with improving survival, even though the underlying mechanisms remain unclear. Preclinical and clinical evidence shows that the acute effects of a single exercise session can suppress the growth of various cancer cell lines in vitro. This suppression is potentially due to altered concentrations of hormones (e.g., insulin) and cytokines (e.g., tumor necrosis factor alpha and interleukin 6) after exercise. These factors, known to be involved in tumorigenesis, may explain why exercise is associated with reduced cancer incidence, recurrence, and mortality. However, the effects of short- (<8 weeks) and long-term (≥8 weeks) exercise programs on cancer cells have been reported with mixed results. Although more research is needed, it appears that interventions incorporating both exercise and diet seem to have greater inhibitory effects on cancer cell growth in both apparently healthy subjects as well as in cancer patients. Although speculative, these suppressive effects on cancer cells may be driven by changes in body weight and composition as well as by a reduction in low-grade inflammation often associated with sedentary behavior, low muscle mass, and excess fat mass in cancer patients. Taken together, such interventions could alter the systemic levels of suppressive circulating factors, leading to a less favorable environment for tumorigenesis. While regular exercise and a healthy diet may establish a more cancer-suppressive environment, each acute bout of exercise provides a further "dose" of anticancer medicine. Therefore, integrating regular exercise could potentially play a significant role in cancer management, highlighting the need for future investigations in this promising area of research.

Purpose: This study aimed to assess the influence of older vs. younger age and previous anterior cruciate ligament (ACL) injury on resting serum cartilage oligomeric matrix protein (sCOMP(t_pre)) concentration, on immediate load-induced sCOMP kinetics after a 30-min treadmill walking stress (∆_sCOMP(t_post)), and on the dose-response relationship between ambulatory load magnitude and ∆_sCOMP(t_post).

Methods: A total of 85 participants were recruited in 4 groups (20-30 years: 24 healthy, 23 ACL-injured; 40-60 years: 23 healthy, 15 ACL-injured). Blood samples were collected immediately before and after a walking stress at 80%, 100%, or 120% bodyweight (BW) on 3 test days and analyzed for sCOMP concentration. Linear models were used to estimate the effect of age, knee status (unilateral ACL injury, 2-10 years prior), and sex on sCOMP(t_pre), ∆_sCOMP(t_post), and the dose-response between ambulatory load magnitude and ∆_sCOMP(t_post).

Results: We found that sCOMP(t_pre) was 21% higher in older than younger participants (p < 0.001) but did not differ between ACL-injured and healthy participants (p = 0.632). Also, ∆_sCOMP(t_post) was 19% lower in older than younger participants (p = 0.030) and increased with body mass index (p < 0.001), sCOMP(t_pre) (p = 0.008), and with 120%BW (p < 0.001), independent of age, ACL injury, or sex.

Conclusion: Age but not prior ACL injury influences resting sCOMP and load-induced sCOMP. The dose-response relationship between ambulatory load magnitude and load-induced sCOMP changes is not affected by age, ACL injury, or sex. A better understanding of systemic sCOMP and the role of its mechanoresponse for the understanding of osteoarthritis pathophysiology and monitoring intervention efficacy may require knowledge of individual cartilage composition and tissue-level loading parameters.

Background: Physical activity can regulate and affect gene expression in multiple tissues and cells. Recently, with the development of next-generation sequencing, a large number of RNA-sequencing (RNA-seq)-based gene expression profiles about physical activity have been shared in public resources; however, they are poorly curated and underutilized. To tackle this problem, we developed a data atlas of such data through comprehensive data collection, curation, and organization.

Methods: The data atlas, termed gene expression profiles of RNA-seq-based exercise responses (GEPREP), was built on a comprehensive collection of high-quality RNA-seq data on exercise responses. The metadata of each sample were manually curated. Data were uniformly processed and batch effects corrected. All the information was well organized in an easy-to-use website for free search, visualization, and download.

Results: GEPREP now includes 69 RNA-seq datasets of pre- and post-exercise, comprising 26 human datasets (1120 samples) and 43 mouse datasets (1006 samples). Specifically, there were 977 (87.2 %) human samples of skeletal muscle and 143 (12.8 %) human samples of blood. There were also samples across 9 mice tissues with skeletal muscle (359, 35.7 %) and brain (280, 27.8 %) accounting for the main fractions. Metadata-including subject, exercise interventions, sampling sites, and post-processing methods-are also included. The metadata and gene expression profiles are freely accessible at http://www.geprep.org.cn/.

Conclusion: GEPREP is a comprehensive data atlas of RNA-seq-based gene expression profiles responding to exercise. With its reliable annotations and user-friendly interfaces, it has the potential to deepen our understanding of exercise physiology.