Medicine and Science in Sports and Exercise最新文献

Purpose: Ingestion of whey protein increases myofibrillar but not muscle connective protein synthesis rates. Recently, we defined a whey and collagen protein blend (5:1 ratio) to optimize post-prandial plasma amino acid availability. Here, we assessed the ability of this blend to increase myofibrillar and muscle connective protein synthesis rates at rest and during early recovery from exercise.

Methods: In a randomized, double-blind, parallel design, 28 men (age: 25 ± 5 yr; body mass index: 23.6 ± 2.3 kg·m -2 ) were randomly allocated to ingest either 30 g of protein (25 g whey/5 g collagen; BLEND, n = 14) or a noncaloric placebo (PLA, n = 14) following a single session of unilateral leg resistance-type exercise. Participants received primed continuous l -[ ring - 13 C 6 ]-phenylalanine infusions with blood and muscle biopsy samples collection for 5 h post-prandially to assess myofibrillar and muscle connective protein synthesis rates.

Results: Protein ingestion strongly increased plasma amino acid concentrations, including plasma leucine and glycine concentrations ( P < 0.001), with no changes following placebo ingestion ( P > 0.05). Post-prandial myofibrillar and muscle connective protein synthesis rates were higher in the exercised compared with the rested leg ( P < 0.001). In addition, myofibrillar protein synthesis rates were higher in BLEND compared with PLA in both the rested (0.038 ± 0.008 and 0.031 ± 0.006%·h -1 , respectively; P < 0.05) and exercised (0.052 ± 0.011 and 0.039 ± 0.009%·h -1 , respectively; P < 0.01) leg. Muscle connective protein synthesis rates were higher in BLEND compared with PLA in the rested (0.062 ± 0.013 and 0.051 ± 0.010%·h -1 , respectively; P < 0.05), but not the exercised (0.090 ± 0.021 and 0.079 ± 0.016%·h -1 , respectively; P = 0.11) leg.

Conclusions: Ingestion of a whey (25 g) plus collagen (5 g) protein blend increases both myofibrillar and muscle connective protein synthesis rates at rest and further increases myofibrillar but not muscle connective protein synthesis rates during recovery from exercise in recreationally active, young men.

Objective: Hamstring injuries are common in field-based sports and reinjury rates are high. Recent evidence suggests that hamstring injuries often occur during accelerative running, but investigations of hamstring mechanics have primarily considered constant-speed running. Thus, our objective was to compare hamstring lengths and velocities between accelerative running and constant-speed running.

Methods: We recorded videos of 10 participants during six accelerative running trials and six constant-speed running trials. We used OpenCap to estimate body segment kinematics and a three-dimensional musculoskeletal model to compute peak length and step-average lengthening velocity of the biceps femoris (long head) muscle-tendon unit. We compared running conditions using linear mixed models with running speed as the independent variable.

Results: At running speeds below 75% of top speed, accelerative running resulted in greater peak lengths than constant-speed running. For example, the peak hamstring muscle-tendon length when a person accelerated from running at only 50% of top speed was equivalent to running at a constant 88% of top speed. Lengthening velocities were greater during accelerative running at all running speeds. Differences in hip flexion kinematics drove the greater peak lengths and lengthening velocities observed in accelerative running.

Conclusions: Hamstrings are subjected to longer lengths and faster lengthening velocities in accelerative running than in constant-speed running. This provides a potential biomechanical perspective toward understanding the occurrence of hamstring injuries during acceleration. Our results suggest that coaches and sports medicine staff should consider the accelerative nature of running in addition to running speed to quantify exposure to high-risk circumstances with long lengths and fast lengthening velocities of the hamstrings.

Introduction: Female athletes are underrepresented in concussion research, and few studies have investigated associations of ovarian hormones with concussion outcomes. This study explored associations of concussion with levels and variability of progesterone, estradiol, and their ratio (P/E) and examined relationships of hormone levels with clinical measures and recovery after concussion in CARE Consortium female athletes and cadets.

Methods: Female participants enrolled ( n = 749) at pre-injury baseline. Participants with concussion (mean age, 19.34 yr; n = 130, 90 athletes, 40 nonathlete cadets) completed one or more visits at nonstandardized times of day: immediately post-injury, 24 h post-injury, upon initiating the return-to-play protocol (Init RTP), and 7 d following unrestricted return-to-play (PRTP). Controls (mean age, 19.85 yr; n = 67, 61 athletes, 6 nonathlete cadets) completed similar visits. Linear mixed models and general linear models tested associations of hormone levels and/or variation with concussion status, symptoms, and recovery, controlling for self-reported birth control use at pre-injury baseline.

Results: Female participants with concussion had higher progesterone levels relative to controls on average across all visits (mean difference (MD; ln ng·mL -1 ) (standard error) = 0.26 (0.08), t (193) = 3.03, P = 0.003). Those with concussion had elevated estradiol at 24 h (MD = 0.27 (0.09), t (506) = 3.04, P = 0.02), Init RTP (MD = 0.38 (0.09), t (508) = 4.29, P < 0.001), and PRTP (MD = 0.30 (0.09), t (515) = 3.25, P = 0.01) relative to pre-injury baseline and compared with controls at Init RTP (MD = 0.35 (0.12), t (429) = 2.78, P = 0.006). Concussed participants had a lower range of estradiol over 7-28 d than controls ( B (SE) = -0.24 (0.09), F (1,145) = 6.43, P = 0.01). Acutely after concussion, estradiol was positively associated with Brief Symptom Inventory Global Severity Index scores ( B (SE) = 0.29 (0.12), F (1,102) = 5.60, P = 0.02). No significant relationships were found between hormones and recovery.

Conclusions: These results, which warrant further research, suggest that ovarian hormones may be associated with concussion and psychological symptom severity post-concussion.

Purpose: Research on intermittent training has mainly focused on the effects of exercise intensity while overlooking the specific effect of the modulations associated with alternating exercise and recovery. This study investigated how the frequency of modulations during moderate-intensity exercise affects postexercise vagal reactivation.

Methods: Healthy, active females and males 18-39 yr old were recruited for the study. Participants completed three treadmill running sessions on separate days. Each moderate-intensity session accumulated 30 min at 90% of the intensity associated with the second ventilatory threshold and was performed as either high-frequency intermittent (HiFi; 15 × [2 min + 2 min recovery]), low-frequency intermittent (LoFi; 5 × [6 min + 2 min recovery]), or moderate-intensity continuous training (MICT; 1 × 30 min). Heart rate recovery (HR rec ) at 1 min and heart rate variability recovery (HRV rec ; lnRMSSD) were assessed in response to submaximal constant-speed tests performed before (CST1) and after (CST2) each of the exercise sessions. HR rec , HRV rec , blood lactate (BLa), and blood pressure were also collected during the exercise sessions.

Results: Twenty-one individuals (8 females, 13 males) participated in the study. HR rec from CST2 was faster in HiFi versus MICT ( P < 0.001), whereas HRV rec post-CST2 was higher after HiFi versus both LoFi ( P = 0.024) and MICT ( P < 0.001). BLa increased in all conditions ( P = 0.007) but remained lower during HiFi compared with LoFi and MICT (both P < 0.001). Diastolic blood pressure did not change during exercise with HiFi ( P = 0.939) but decreased during LoFi ( P = 0.006) and MICT ( P = 0.008).

Conclusions: Exercise pattern influences the physiologic response to exercise. Higher frequencies of modulations can preserve vagal activity and expedite postexercise recovery, suggesting moderate-intensity intermittent exercise as a potential strategy to mitigate autonomic impact and acute physiological stress while maintaining total work performed.

Purpose: To examine the relationship between menstrual cycle (MC) phase-dependent fluctuations of estrogen and progesterone and virtual cycling race performance, with a secondary aim of correlating perceived MC-related symptoms with performance.

Methods: In a novel observational study design, 37 female cyclists/triathletes not using any hormonal contraception completed one virtual cycling race (19.5-km time trial (TT)) per week across a 1-month period (totaling four races). Participants completed MC characterization and tracking, including urinary ovulation kits, across two complete MCs. Venous blood samples were collected within 21 h of racing to determine serum 17-β-estradiol and progesterone concentrations, as well as an assessment of self-reported, perceived race-day MC and gastrointestinal (GI) symptoms, which were all then correlated to race performance.

Results: There was no relationship between race completion time and individual estradiol ( r = -0.001, P = 0.992) or progesterone ( r = -0.023, P = 0.833) concentrations. There was no difference between race time between MC phases (follicular/luteal, P = 0.238), whether MC bleeding or not bleeding ( P = 0.619), and whether ovulating or not ovulating ( P = 0.423). The total number of perceived MC symptoms recorded on race day was positively correlated to increased race time ( r = 0.268 (95% confidence interval, 0.056-0.457), P = 0.014), as was the number of GI symptoms of at least "moderate" severity before the race ( r = 0.233 (95% confidence interval, 0.021-0.425), P = 0.031), but not post-race ( r = 0.022, P = 0.841).

Conclusions: When implementing a novel, virtual cycling race, fluctuations in ovarian hormone concentrations across the MC do not appear to affect real-world cycling performance among trained cyclists, whereas perceived negative MC and GI symptoms may relate to impaired performance. Therefore, the management of negative MC and GI symptoms appears important for athletic performance enhancement or to mitigate performance decline.

Purpose: The relationship between sedentary time, physical activity, and cardiometabolic risk factors during the transition from adolescence to adulthood remains uncertain. We examined the prospective associations of sedentary time and physical activity at age 15 yr with cardiometabolic risk markers at age 24 yr.

Methods: We used data from the Physical Activity among Norwegian Children Studies. Sedentary time, moderate-to-vigorous physical activity (MVPA), and vigorous physical activity (VPA) were measured by accelerometry. Outcomes included body mass index (BMI), waist circumference, visceral fat, maximal oxygen uptake (V̇O 2max ), systolic blood pressure, LDL-cholesterol, insulin, high-sensitivity C-reactive protein, and a clustered risk Z -score. The prospective associations were modeled through regression.

Results: A total of 731 boys and girls participated at ages 9 yr (2005-2006) and 15 yr (2011-2012), and 258 of these participated again at age 24 yr (2019-2021). Multiple imputation was performed for all eligible individuals ( n = 708). Each standard deviation increase (minutes per day) in sedentary time at age 15 yr was associated with lower V̇O 2max at age 24 yr ( β = -1.6 mL·kg -1 ·min -1 ; 95% confidence interval (CI), -2.8 to -0.5). Each standard deviation increase (minutes per day) in MVPA ( β = 1.6 mL·kg -1 ·min -1 ; 95% CI, 0.8 to 2.4) and VPA ( β = 1.6 mL·kg -1 ·min -1 ; 95% CI, 0.8 to 2.4) at age 15 yr were associated with higher V̇O 2max at age 24 yr. VPA in adolescence was further inversely associated with visceral fat mass ( β = -41 g; 95% CI, -78 to -3), insulin level ( β = -4.3 pmol·L -1 ; 95% CI, -8.2 to -0.4), and the clustered risk Z -score ( β = -0.09; 95% CI, -0.18 to -0.01) in young adulthood. Childhood BMI modified the association of both MVPA and VPA with clustered risk, with the greatest magnitude of association observed in the highest BMI tertile.

Conclusions: Physical activity, especially of vigorous intensity, during adolescence appears to beneficially affect cardiometabolic health in young adulthood. These health benefits may be most pronounced among overweight/obese youth.

Purpose: Obesity may blunt exercise responsiveness to improve muscular adaptations. The effect of resistance training (RT) targeting different body regions on muscle and inflammatory markers is unclear. This study aimed to investigate the impact of upper (upper body exercises), lower (lower body exercises), or combined (upper body + lower body exercises) RT on muscle and inflammatory markers, body composition, and performance in overweight and obese men.

Methods: Sixty overweight and obese men (age, 31 ± 4 yr) were randomly assigned to one of four groups: upper-body RT (UB; n = 15), lower-body RT (LB; n = 15), combined RT (UB + LB; n = 15), or control (C; n = 15). The training protocol consisted of three exercise sessions per week for 12 wk. Blood samples for measuring serum markers (follistatin, myostatin, C-reactive protein (CRP), adiponectin, tumor necrosis factor α (TNF-α), and irisin) were obtained at baseline and 48 h after the final training session. Fat mass (FM), body fat percentage, skeletal muscle mass (SMM), and fat-free mass were measured using bioelectrical impedance analysis (InBody 720).

Results: SMM, fat-free mass, UB and LB strength and power, follistatin, follistatin/myostatin ratio, adiponectin, and irisin significantly increased, whereas FM, body fat percentage, myostatin, CRP, and TNF-α significantly reduced from pre- to post-training in all training groups ( P < 0.05). Changes in LB muscle power ( r = 0.558), both UB ( r = 0.518) and LB ( r = 0.419) muscle strength, and follistatin ( r = 0.545) had moderate positive relationships with ΔSMM, whereas changes in myostatin ( r = -0.585) had a moderate negative relationship with ΔSMM. Also, changes in myostatin ( r = 0.825) and CRP ( r = 0.715) had a strong positive relationship with ΔFM, whereas TNF-α ( r = 0.467) had a moderate positive relationship with ΔFM. Follistatin ( r = -0.789) and adiponectin ( r = -0.713) had a strong negative relationship with ΔFM, whereas irisin ( r = -0.426) had a moderate negative relationship with ΔFM.

Conclusions: Combined RT elicits the greatest increases in follistatin, follistatin/myostatin ratio, and adiponectin, and decreases in myostatin and CRP compared with other training groups in overweight and obese men. However, systemic improvements may be achieved through performing UB or LB RT alone.

Introduction: The reduction in sex hormone production across the menopause transition is thought to accelerate age-related decline in muscle mass, strength, and stability, increasing the risk of falls and fractures. We aimed to investigate whether a novel low-impact resistance exercise program could improve strength, balance, and body composition and whether any improvement was affected by menopause status.

Methods: Seventy healthy, moderately active pre- (PRE; 46.7 ± (SD) 3.2 yr), peri- (PERI; 52.3 ± 2.2 yr), or post- (POST; 57.0 ± 2.5 yr) menopausal females, not taking hormone replacement therapy (HRT), were randomized to continue habitual physical activity (CON; n = 25) or complete a supervised resistance exercise program 4 d·wk -1 for 12 wk (EXC; n = 45). Strength at the hip and shoulder (isokinetic dynamometer), dynamic balance (Y-balance), flexibility (sit-and-reach and back-scratch), muscle thickness (rectus femoris, vastus intermedius (VI), and medial deltoid), and lean and % body fat (dual-energy x-ray absorptiometry) were measured before and after training.

Results: Hip abduction and flexion peak torque (19% ± 48% and 20% ± 17%, respectively; P < 0.05), posterolateral and posteromedial balance (12% ± 15% and 13% ± 15%, respectively; P < 0.001), flexibility (21% ± 36%, P < 0.001), VI thickness (12% ± 19%, P = 0.032), and lean mass (2% ± 2%, P = 0.007) all increased over 12 wk in EXC, but not CON, with no difference in response between PRE, PERI, and POST. The changes in shoulder strength and body mass over 12 wk were not different between CON and EXC.

Conclusions: This is the first study to demonstrate that the decline in sex hormones and an increase in age across the menopause transition do not affect the ability of lower limb (hip) strength and balance to adapt to a low-impact resistance exercise training program in females not taking HRT.

Introduction: Impaired physical fitness is a possible late effect among adult survivors of childhood cancer (ASCC). Our study describes lower body muscular strength and endurance among ASCC using the 1-min sit-to-stand (1-min STS) test, compares them with the general population, identifies risk factors, and describes changes over time.

Methods: In a prospective multicenter cohort study, we invited ASCC ≥18 yr of age at study who were diagnosed between ages 0 and 20 yr, treated in five pediatric oncology centers across Switzerland from 1976 to 2017, and survived ≥5 yr for a 1-min STS test. We collected information about lifestyle, medical history, and previous cancer treatment. Using population-based Swiss reference values, we calculated age- and sex-adjusted z -scores for 1-min STS performance and assessed the association between risk factors and 1-min STS test using multivariable linear regression. We fitted a multilevel linear model to describe the longitudinal course of 1-min STS performance.

Results: We included 338 CCS of 1048 invited ASCC (participation rate 32%) with a median age at study of 34 yr (interquartile range, 26-41 yr). Compared with the general population, mean 1-min STS z -score was half a standard deviation lower (-0.52; 95% confidence interval (CI), -0.64 to -0.40). Obesity ( B = -0.56; 95% CI, -0.97 to -0.16), cumulative cisplatin dose ( B = -0.12; 95% CI, -0.21 to -0.02), and cumulative cranial radiotherapy dose ( B = -0.10; 95% CI, -0.19 to -0.01) were associated with reduced 1-min STS performance. There was no change in 1-min STS z -scores over time ( B = 0.02; 95% CI, -0.05 to 0.09).

Conclusions: We found evidence for reduced lower body strength and endurance among ASCC, suggesting the need for counseling and effective training and rehabilitation programs for maintaining daily functioning, improving cardiovascular health, and reducing morbidity for ASCC.

Aims: Middle-aged and older male athletes have more coronary atherosclerosis than less active peers. We aimed to explore mechanisms that can contribute to this accelerated coronary atherosclerosis by comparing exercise-induced changes in hemodynamic factors, circulating hormones, electrolytes, and inflammatory markers across athletes with and without coronary atherosclerosis.

Methods: 59 male athletes recruited from the MARC-2 study were stratified as controls (coronary artery calcium score (CACS) = 0, n = 20), high CACS (≥300 Agatston Units or ≥ 75th MESA percentile, n = 20) or significant stenosis (≥50% in any coronary artery, n = 19). At rest, during an exhaustive endurance cycling test and following 3 hours of recovery, we measured blood pressure and blood concentrations of PTH, calcium, magnesium, phosphate, CRP, IL-6, IL-1RA, IL-10, ICAM-1, VCAM-1, and E-selectin.

Results: 58 participants completed the exercise test (76 ± 14 minutes). All biomarkers changed during exercise, except CRP, ICAM-1, and VCAM-1. Systolic blood pressure, PTH, calcium, phosphate, IL-6, IL-1RA and E-selectin concentrations increased during exercise. In contrast, diastolic blood pressure and magnesium concentrations decreased during exercise. The magnitude of exercise-induced responses of hemodynamic factors, circulating hormones, electrolytes, cytokine, and adhesion molecule concentrations did, however, not differ across groups.

Conclusions: Blood pressure, hormone, electrolyte, and cytokine concentrations changed following an exhaustive endurance exercise test, but the magnitude of these responses did not differ between athletes with versus without coronary atherosclerosis. These findings suggest that accelerated coronary atherosclerosis in endurance athletes may not be explained by differences in responses to exercise, but by differences in exercise exposure or other mechanisms not assessed in this study.