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Danielle T. Gescheit, Stuart J. Cormack, Machar Reid and Rob Duffield

Purpose:

To determine how consecutive days of prolonged tennis match play affect performance, physiological, and perceptual responses.

Methods:

Seven well-trained male tennis players completed 4-h tennis matches on 4 consecutive days. Pre- and postmatch measures involved tennis-specific (serve speed and accuracy), physical (20-m sprint, countermovement jump [CMJ], shoulder-rotation maximal voluntary contraction, isometric midthigh pull), perceptual (Training Distress Scale, soreness), and physiological (creatine kinase [CK]) responses. Activity profile was assessed by heart rate, 3D load (accumulated accelerations measured by triaxial accelerometers), and rating of perceived exertion (RPE). Statistical analysis compared within- and between-days values. Changes (± 90% confidence interval [CI]) ≥75% likely to exceed the smallest important effect size (0.2) were considered practically important.

Results:

3D load reduced on days 2 to 4 (mean effect size ± 90% CI –1.46 ± 0.40) and effective playing time reduced on days 3 to 4 (–0.37 ± 0.51) compared with day 1. RPE did not differ and total points played only declined on day 3 (–0.38 ± 1.02). Postmatch 20-m sprint (0.79 ± 0.77) and prematch CMJ (–0.43 ± 0.27) performance declined on days 2 to 4 compared with prematch day 1. Although serve velocity was maintained, compromised postmatch serve accuracy was evident compared with prematch day 1 (0.52 ± 0.58). CK increased each day, as did ratings of muscle soreness and fatigue.

Conclusions:

Players reduced external physical loads, through declines in movement, over 4 consecutive days of prolonged competitive tennis. This may be affected by tactical changes and pacing strategies. Alongside this, impairments in sprinting and jumping ability, perceptual and biochemical markers of muscle damage, and reduced mood states may be a function of neuromuscular and perceptual fatigue.

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Milou Beelen, Louise M. Burke, Martin J. Gibala and Luc J.C. van Loon

During postexercise recovery, optimal nutritional intake is important to replenish endogenous substrate stores and to facilitate muscle-damage repair and reconditioning. After exhaustive endurance-type exercise, muscle glycogen repletion forms the most important factor determining the time needed to recover. Postexercise carbohydrate (CHO) ingestion has been well established as the most important determinant of muscle glycogen synthesis. Coingestion of protein and/or amino acids does not seem to further increase muscle glycogensynthesis rates when CHO intake exceeds 1.2 g · kg−1 · hr−1. However, from a practical point of view it is not always feasible to ingest such large amounts of CHO. The combined ingestion of a small amount of protein (0.2–0.4 g · (0.2−0.4 g · kg−1 · hr−1) with less CHO (0.8 g · kg−1 · hr−1) stimulates endogenous insulin release and results in similar muscle glycogen-repletion rates as the ingestion of 1.2 g · kg−1 · hr−1 CHO. Furthermore, postexercise protein and/or amino acid administration is warranted to stimulate muscle protein synthesis, inhibit protein breakdown, and allow net muscle protein accretion. The consumption of ~20 g intact protein, or an equivalent of ~9 g essential amino acids, has been reported to maximize muscle protein-synthesis rates during the first hours of postexercise recovery. Ingestion of such small amounts of dietary protein 5 or 6 times daily might support maximal muscle protein-synthesis rates throughout the day. Consuming CHO and protein during the early phases of recovery has been shown to positively affect subsequent exercise performance and could be of specific benefit for athletes involved in multiple training or competition sessions on the same or consecutive days.

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Tiaki B. Smith, Will G. Hopkins and Tim E. Lowe

There is a need for markers that would help determine when an athlete’s training load is either insufficient or excessive. In this study we examined the relationship between changes in performance and changes in physiological and psychological markers during and following a period of overload training in 10 female and 10 male elite rowers. Change in performance during a 4-wk overload was determined with a weekly 30-min time-trial on a rowing ergometer, whereas an incremental test provided change in lactate-threshold power between the beginning of the study and following a 1-wk taper after the overload. Various psychometric, steroid-hormone, muscle-damage, and inflammatory markers were assayed throughout the overload. Plots of change in performance versus the 4-wk change in each marker were examined for evidence of an inverted-U relationship that would characterize undertraining and excessive training. Linear modeling was also used to estimate the effect of changes in the marker on changes in performance. There was a suggestion of an inverted U only for performance in the incremental test versus some inflammatory markers, due to the relative underperformance of one rower. There were some clear linear relationships between changes in markers and changes in performance, but relationships were inconsistent within classes of markers. For some markers, changes considered to predict excessive training (eg, creatine kinase, several proinflammatory cytokines) had small to large positive linear relationships with performance. In conclusion, some of the markers investigated in this study may be useful for adjusting the training load in individual elite rowers.

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Stephan R. Fisher, Justin H. Rigby, Joni A. Mettler and Kevin W. McCurdy

times and reducing muscle fatigue limiting postexercise strength losses. 1 After intense exercise, PBMT confines the degree of exercise-induced muscle damage, limiting the need for a large inflammatory process. 2 It also reduces patient-reported muscle soreness, modulates growth factors and myogenic

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Jeffrey R. Doeringer, Megan Colas, Corey Peacock and Dustin R. Gatens

would not change the muscle performance (flexibility, power, speed, and agility) 48 hr after intervention and would reduce the perceived pain/soreness at 24 hr and 48 hr after a muscle damage protocol when compared to a control group. Methods Participants Twenty-two healthy college athletes volunteered

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Brett S. Pexa, Eric D. Ryan, Elizabeth E. Hibberd, Elizabeth Teel, Terri Jo Rucinski and Joseph B. Myers

, leading to an influx of edema within the muscle tissue, 16 , 18 and this edema within the muscle is reflected by increased CSA. 26 Previous research indicates that eccentric muscle damaging protocols that mimic baseball pitching increases infraspinatus CSA when measured with ultrasound. 19 When

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Graeme L. Close, Craig Sale, Keith Baar and Stephane Bermon

Injuries There is limited direct research on nutrition to prevent/treat muscle injuries, with most research originating from laboratory-induced muscle damage to study delayed onset muscle soreness ( Owens et al., 2019 ). Although such studies provide insights into potential nutritional strategies, it must

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Kelly A. Brock, Lindsey E. Eberman, Richard H. Laird IV, David J. Elmer and Kenneth E. Games

Exercise-induced muscle damage (EIMD) is a consequence that occurs when an individual participates in an unfamiliar or eccentrically based activity. Such activities may result in delayed-onset muscle soreness (DOMS). The severity of muscle damage is dependent on the duration, intensity, and

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Dean Norris, David Joyce, Jason Siegler, James Clock and Ric Lovell

is a multifactorial construct, a variety of monitoring strategies are often employed within the professional setting, such as markers of muscle damage, neuromuscular function (NF), endocrine responses, immune status, and psychological well-being. 3 , 4 While informative, due to cost and time

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Stephen M. Cornish, Jeremie E. Chase, Eric M. Bugera and Gordon G. Giesbrecht

in skeletal muscle ( McKay et al., 2009 ). High-intensity exercise also increases blood myoglobin levels, indicating muscle damage, which can stimulate muscle growth in an untrained state, but muscle damage is likely not necessary in a trained state to induce muscle hypertrophy ( Damas et al., 2016