Acetaminophen influences musculoskeletal signaling but not adaptations to endurance exercise training.

Acetaminophen (ACE) is a widely used analgesic and antipyretic drug with various applications, from pain relief to fever reduction. Recent studies have reported equivocal effects of habitual ACE intake on exercise performance, muscle growth, and risks to bone health. Thus, this study aimed to assess the impact of a 6-week, low-dose ACE regimen on muscle and bone adaptations in exercising and non-exercising rats. Nine-week-old Wistar rats (n = 40) were randomized to an exercise or control (no exercise) condition with ACE or without (placebo). For the exercise condition, rats ran 5 days per week for 6 weeks at a 5% incline for 2 min at 15 cm/s, 2 min at 20 cm/s, and 26 min at 25 cm/s. A human equivalent dose of ACE was administered (379 mg/kg body weight) in drinking water and adjusted each week based on body weight. Food, water intake, and body weight were measured daily. At the beginning of week 6, animals in the exercise group completed a maximal treadmill test. At the end of week 6, rats were euthanized, and muscle cross-sectional area (CSA), fiber type, and signaling pathways were measured. Additionally, three-point bending and microcomputer tomography were measured in the femur. Follow-up experiments in human primary muscle cells were used to explore supra-physiological effects of ACE. Data were analyzed using a two-way ANOVA for treatment (ACE or placebo) and condition (exercise or non-exercise) for all animal outcomes. Data for cell culture experiments were analyzed via ANOVA. If omnibus significance was found in either ANOVA, a post hoc analysis was completed, and a Tukey's adjustment was used. ACE did not alter body weight, water intake, food intake, or treadmill performance (p > .05). There was a treatment-by-condition effect for Young's Modulus where placebo exercise was significantly lower than placebo control (p < .05). There was no treatment by condition effects for microCT measures, muscle CSA, fiber type, or mRNA expression. Phosphorylated-AMPK was significantly increased with exercise (p < .05) and this was attenuated with ACE treatment. Furthermore, phospho-4EBP1 was depressed in the exercise group compared to the control (p < .05) and increased in the ACE control and ACE exercise group compared to placebo exercise (p < .05). A low dose of ACE did not influence chronic musculoskeletal adaptations in exercising rodents but acutely attenuated AMPK phosphorylation and 4EBP1 dephosphorylation post-exercise.

The dose-response effects of arachidonic acid on primary human skeletal myoblasts and myotubes.

Background: Cellular inflammatory response, mediated by arachidonic acid (AA) and cyclooxygenase, is a highly regulated process that leads to the repair of damaged tissue. Recent studies on murine C2C12 cells have demonstrated that AA supplementation leads to myotube hypertrophy. However, AA has not been tested on primary human muscle cells. Therefore, the purpose of this study was to determine whether AA supplementation has similar effects on human muscle cells. Methods: Proliferating and differentiating human myoblasts were exposed to AA in a dose-dependent manner (50-0.80 µM) for 48 (myoblasts) or 72 (myotubes) hours. Cell viability was tested using a 3-(4,5-Dimethylthiazol-2-Yl)-2,5-Diphenyltetrazolium Bromide (MTT) assay and cell counting; myotube area was determined by immunocytochemistry and confocal microscopy; and anabolic signaling pathways were evaluated by western blot and RT-PCR. Results: Our data show that the treatment of primary human myoblasts treated with 50 µM and 25 µM of AA led to the release of PGE2 and PGF2α at levels higher than those of control-treated cells (p < 0.001 for all concentrations). Additionally, 50 µM and 25 µM of AA suppressed myoblast proliferation, myotube area, and myotube fusion. Anabolic signaling indicated reductions in total and phosphorylated TSC2, AKT, S6, and 4EBP1 in myoblasts at 50 µM of AA (p < 0.01 for all), but not in myotubes. These changes were not affected by COX-2 inhibition with celecoxib. Conclusion: Together, our data demonstrate that high concentrations of AA inhibit myoblast proliferation, myotube fusion, and myotube hypertrophy, thus revealing potential deleterious effects of AA on human skeletal muscle cell health and viability.

The Relationship between Resistance Training Frequency and Muscle Quality in Adolescents.

Previous research has established the role of resistance training (RT) on muscle function in adolescents, but a lack of evidence to optimize RT for enhancing muscle quality (MQ) exists. This study examined whether RT frequency is associated with MQ in a nationally representative adolescent cohort. A total of 605 adolescents (12−15 year) in NHANES were stratified based on RT frequency. MQ was calculated as combined handgrip strength divided by arm lean mass (via dual-energy X-ray absorptiometry). Analysis of covariance was adjusted for sex, race/ethnicity, and arm fat percentage; p < 0.05 was considered significant. RT frequency was associated with MQ for 2−7 day/week but not 1 day/week. When no RT was compared to 1−2 and 3−7 day/week, associations were present for 3−7 day/week but not 1−2 day/week. When comparing no RT to 1−4 and 5−7 day/week, associations existed for 5−7 day/week but not 1−4 day/week. Next, no RT was compared to 1, 2−3, and 4−7 day/week; associations were found for 4−7 day/week, while 2−3 day/week had a borderline association (p = 0.06); there were no associations for 1 day/week. Finally, no RT was compared to 1, 2, 3, 4, and 5−7 day/week; associations were present for all except 1 and 3 day/week. These prospective data suggest a minimum RT frequency of 2 day/week is associated with MQ in adolescents as indicated by the lack of differences in MQ between 1 day/week RT versus no RT.

Improved impedance to maladaptation and enhanced VCAM-1 upregulation with resistance-type training in the long-lived Snell dwarf (Pit1dw/dw) mouse.

Snell dwarf mice with the Pit1dw/dw mutation are deficient in growth hormone, prolactin, and thyroid stimulating hormone and exhibit >40% lifespan extension. This longevity is accompanied by compromised muscular performance. However, research regarding young (3-month-old) Snell dwarf mice demonstrate exceptional responsivity to resistance-type training especially in terms of a shifted fiber type distribution and increased protein levels of vascular cell adhesion molecule-1 (VCAM-1), a possible mediator of such remodeling. In the present study, we investigated whether this responsiveness persists at 12 months of age. Unlike 12-month-old control mice, age-matched Snell dwarf mice remained resistant to training-induced maladaptive decreases in performance and muscle mass. This was accompanied by retainment of the remodeling capacity in muscles of Snell dwarf mice to increase VCAM-1 protein levels and a shift in myosin heavy chain (MHC) isoform distribution with training. Even decreasing training frequency for control mice, an alteration which protected muscles from maladaptation at 12 months of age, did not result in the overt remodeling observed for Snell dwarf mice. The results demonstrate a distinct remodeling response to resistance-type exercise operative in the context of the Pit1dw/dw mutation of long-lived Snell dwarf mice.

Skeletal Muscle Quality: A Biomarker for Assessing Physical Performance Capabilities in Young Populations.

Muscle quality (MQ), defined as the amount of strength and/or power per unit of muscle mass, is a novel index of functional capacity that is increasingly relied upon as a critical biomarker of muscle health in low functioning aging and pathophysiological adult populations. Understanding the phenotypical attributes of MQ and how to use it as an assessment tool to explore the efficacy of resistance exercise training interventions that prioritize functional enhancement over increases in muscle size may have implications for populations beyond compromised adults, including healthy young adults who routinely perform physically demanding tasks for competitive or occupational purposes. However, MQ has received far less attention in healthy young populations than it has in compromised adults. Researchers and practitioners continue to rely upon static measures of lean mass or isolated measures of strength and power, rather than using MQ, to assess integrated functional responses to resistance exercise training and physical stress. Therefore, this review will critically examine MQ and the evidence base to establish this metric as a practical and important biomarker for functional capacity and performance in healthy, young populations. Interventions that enhance MQ, such as high-intensity stretch shortening contraction resistance exercise training, will be highlighted. Finally, we will explore the potential to leverage MQ as a practical assessment tool to evaluate function and enhance performance in young populations in non-traditional research settings.

Reduced frequency of resistance-type exercise training promotes adaptation of the aged skeletal muscle microenvironment.

The purpose of this study was to characterize the growth and remodeling molecular signaling response in aged skeletal muscle following 1 mo of "resistance-type exercise" training. Male Fischer 344 × Brown Norway hybrid rats aged 3 (young) and 30 mo (old) underwent stretch-shortening contraction (SSC) loading 2 or 3 days/wk; muscles were removed 72 h posttraining. Young rats SSC loaded 3 (Y3x) or 2 days/wk (Y2x) adapted via increased work performance. Old rats SSC loaded 3 days/wk (O3x) maladapted via decreased negative work; however, old rats SSC loaded 2 days/wk (O2x) adapted through improved negative and positive work. Y3x, Y2x, and O2x, but not O3x, displayed hypertrophy via larger fiber area and myonuclear domains. Y3x, Y2x, and O2x differentially expressed 19, 30, and 8 phosphatidylinositol 3-kinase-Akt genes, respectively, whereas O3x only expressed 2. Bioinformatics analysis revealed that rats in the adapting groups presented growth and remodeling processes (i.e., increased protein synthesis), whereas O3x demonstrated inflammatory signaling. In conclusion, reducing SSC-loading frequency in aged rodents positively influences the molecular signaling microenvironment, promoting muscle adaptation. NEW & NOTEWORTHY Decreasing resistance-type exercise training frequency in old rodents led to adaptation through enhancements in performance, fiber areas, and myonuclear domains. Modifying frequency influenced the molecular environment through improvements in phosphatidylinositol 3-kinase-Akt pathway-specific expression and bioinformatics indicating increased protein synthesis. Reducing training frequency may be appropriate in older individuals who respond unfavorably to higher frequencies (i.e., maladaptation); overall, modifying the parameters of the exercise prescription can affect the cellular environment, ultimately leading to adaptive or maladaptive outcomes.

VCAM-1 upregulation accompanies muscle remodeling following resistance-type exercise in Snell dwarf (Pit1dw/dw ) mice.

Snell dwarf mice (Pit1dw/dw ) exhibit deficiencies in growth hormone, prolactin, and thyroid stimulating hormone. Besides being an experimental model of hypopituitarism, these mice are long-lived (>40% lifespan extension) and utilized as a model of slowed/delayed aging. Whether this longevity is accompanied by a compromised quality of life in terms of muscular performance has not yet been characterized. In this study, we investigated nontrained and trained muscles 1 month following a general validated resistance-type exercise protocol in 3-month-old Snell dwarf mice and control littermates. Nontrained Snell dwarf gastrocnemius muscles exhibited a 1.3-fold greater muscle mass to body weight ratio than control values although muscle quality, maximum isometric torque normalized to muscle mass, and fatigue recovery were compromised. For control mice, training increased isometric torque (17%) without altering muscle mass. For Snell dwarf mice, isometric torque was unaltered by training despite decreased muscle mass that rendered muscle mass to body weight ratio comparable to control values. Muscle quality and fatigue recovery improved twofold and threefold, respectively, for Snell dwarf mice. This accompanied a fourfold increase in levels of vascular cell adhesion molecule-1 (VCAM-1), a mediator of progenitor cell recruitment, and muscle remodeling in the form of increased number of central nuclei, additional muscle fibers per unit area, and altered fiber type distribution. These results reveal a trade-off between muscle quality and longevity in the context of anterior pituitary hormone deficiency and that resistance-type training can diminish this trade-off by improving muscle quality concomitant with VCAM-1 upregulation and muscle remodeling.

High-intensity stretch-shortening contraction training modifies responsivity of skeletal muscle in old male rats.

Utilization of high-intensity resistance training to counter age-related sarcopenia is currently debated because of the potential for maladaptation when training design is inappropriate. Training design is problematic because the influence of various loading variables (e.g. contraction mode, repetition number, and training frequency) is still not well characterized at old age. To address this in a precisely controlled manner, we developed a rodent model of high-intensity training consisting of maximally-activated stretch-shortening contractions (SSCs), contractions typical during resistance training. With this model, we determined that at old age, high-repetition SSC training (80 SSCs: 8 sets of 10 repetitions) performed frequently (i.e. 3 days per week) for 4.5 weeks induced strength deficits with no muscle mass gain while decreasing frequency to 2 days per week promoted increases in muscle mass and muscle quality (i.e. performance normalized to muscle mass). This finding confirmed the popular notion that decreasing training frequency has a robust effect with age. Meanwhile, the influence of other loading variables remains contentious. The aim of the present study was to assess muscle adaptation following modulation of contraction mode and repetition number during high-intensity SSC training. Muscles of young (3 month old) and old (30 month old) male rats were exposed to 4.5 weeks of low-repetition static training of 4 (i.e. 4 sets of one repetition) isometric (ISO) contractions 3 days per week or a more moderate-repetition dynamic training of 40 SSCs (i.e. 4 sets of 10 repetitions) 3 days per week. For young rats, performance and muscle mass increased regardless of training protocol. For old rats, no muscle mass adaptation was observed for 4 ISO training while 40 SSC training induced muscle mass gain without improvement in muscle quality, an outcome distinct from modulating training frequency. Muscle mass gain for old rats was accompanied by decreased protein levels of tumor necrosis factor alpha, a mediator of age-related chronic inflammatory signaling, to young levels. These findings suggest that while dynamic high-intensity training with a moderate number of repetitions has a limited capacity for altering muscle quality, such training is a viable strategy for countering age-related inflammatory signaling and modifying muscle mass.

Agonist muscle adaptation accompanied by antagonist muscle atrophy in the hindlimb of mice following stretch-shortening contraction training.

BACKGROUND: The vast majority of dynamometer-based animal models for investigation of the response to chronic muscle contraction exposure has been limited to analysis of isometric, lengthening, or shortening contractions in isolation. An exception to this has been the utilization of a rat model to study stretch-shortening contractions (SSCs), a sequence of consecutive isometric, lengthening, and shortening contractions common during daily activity and resistance-type exercise. However, the availability of diverse genetic strains of rats is limited. Therefore, the purpose of the present study was to develop a dynamometer-based SSC training protocol to induce increased muscle mass and performance in plantarflexor muscles of mice. METHODS: Young (3 months old) C57BL/6 mice were subjected to 1 month of plantarflexion SSC training. Hindlimb muscles were analyzed for muscle mass, quantitative morphology, myogenesis/myopathy relevant gene expression, and fiber type distribution. RESULTS: The main aim of the research was achieved when training induced a 2-fold increase in plantarflexion peak torque output and a 19% increase in muscle mass for the agonist plantaris (PLT) muscle. In establishing this model, several outcomes emerged which raised the value of the model past that of being a mere recapitulation of the rat model. An increase in the number of muscle fibers per transverse muscle section accounted for the PLT muscle mass gain while the antagonist tibialis anterior (TA) muscle atrophied by 30% with preferential atrophy of type IIb and IIx fibers. These alterations were accompanied by distinct gene expression profiles. CONCLUSIONS: The findings confirm the development of a stretch-shortening contraction training model for the PLT muscle of mice and demonstrate that increased cross-sectional fiber number can occur following high-intensity SSC training. Furthermore, the TA muscle atrophy provides direct evidence for the concept of muscle imbalance in phasic non-weight bearing muscles, a concept largely characterized based on clinical observation of patients. The susceptibility to this imbalance is demonstrated to be selective for the type IIb and IIx muscle fiber types. Overall, the study highlights the importance of considering muscle fiber number modulation and the effect of training on surrounding muscles in exercise comprised of SSCs.

Enhancement of Skeletal Muscle in Aged Rats Following High-Intensity Stretch-Shortening Contraction Training.

Exercise is the most accessible, efficacious, and multifactorial intervention to improve health and treat chronic disease. High-intensity resistance exercise, in particular, also maximizes skeletal muscle size and strength-outcomes crucial at advanced age. However, such training is capable of inducing muscle maladaptation when misapplied at old age. Therefore, characterization of parameters (e.g., mode and frequency) that foster adaptation is an active research area. To address this issue, we utilized a rodent model that allowed training at maximal intensity in terms of muscle activation and tested the hypothesis that muscles of old rats adapt to stretch-shortening contraction (SSC) training, provided the training frequency is sufficiently low. At termination of training, normalized muscle mass (i.e., muscle mass divided by tibia length) and muscle quality (isometric force divided by normalized muscle mass) were determined. For young rats, normalized muscle mass increased by ∼20% regardless of training frequency. No difference was observed for muscle quality values after 2 days versus 3 days per week training (0.65 ± 0.09 N/mg/mm vs. 0.59 ± 0.05 N/mg/mm, respectively). For old rats following 3 days per week training, normalized muscle mass was unaltered and muscle quality was 30% lower than young levels. Following 2 days per week training at old age, normalized muscle mass increased by 17% and muscle quality was restored to young levels. To investigate this enhanced response, oxidative stress was assessed by lipid peroxidation quantification. For young rats, lipid peroxidation levels were unaltered by training. With aging, baseline levels of lipid peroxidation increased by 1.5-fold. For old rats, only 2 days per week training decreased lipid peroxidation to levels indistinguishable from young values. These results imply that, appropriately scheduled high-intensity SSC training at old age is capable of restoring muscle to a younger phenotype in terms of lipid peroxidation levels and muscle quality.

The effects of 12 weeks of beta-hydroxy-beta-methylbutyrate free acid supplementation on muscle mass, strength, and power in resistance-trained individuals: a randomized, double-blind, placebo-controlled study.

INTRODUCTION: Studies utilizing beta-hydroxy-beta-methylbutyrate (HMB) supplementation in trained populations are limited. No long-term studies utilizing HMB free acid (HMB-FA) have been conducted. Therefore, we investigated the effects of 12 weeks of HMB-FA supplementation on skeletal muscle hypertrophy, body composition, strength, and power in trained individuals. We also determined the effects of HMB-FA on muscle damage and performance during an overreaching cycle. METHODS: A three-phase double-blind, placebo- and diet-controlled randomized intervention study was conducted. Phase 1 was an 8-week-periodized resistance-training program; Phase 2 was a 2-week overreaching cycle; and Phase 3 was a 2-week taper. Muscle mass, strength, and power were examined at weeks 0, 4, 8, and 12 to assess the chronic effects of HMB-FA; and assessment of these, as well as cortisol, testosterone, and creatine kinase (CK) was performed at weeks 9 and 10 of the overreaching cycle. RESULTS: HMB-FA resulted in increased total strength (bench press, squat, and deadlift combined) over the 12-week training (77.1 ± 18.4 vs. 25.3 ± 22.0 kg, p < 0.001); a greater increase in vertical jump power (991 ± 168 vs. 630 ± 167 W, p < 0.001); and increased lean body mass gain (7.4 ± 4.2 vs. 2.1 ± 6.1 kg, p < 0.001) in HMB-FA- and placebo-supplemented groups, respectively. During the overreaching cycle, HMB-FA attenuated increases in CK (-6 ± 91 vs. 277 ± 229 IU/l, p < 0.001) and cortisol (-0.2 ± 2.9 vs. 4.5 ± 1.7 µg/dl, p < 0.003) in the HMB-FA- and placebo-supplemented groups, respectively. CONCLUSIONS: These results suggest that HMB-FA enhances hypertrophy, strength, and power following chronic resistance training, and prevents decrements in performance following the overreaching.

Effects of static stretching on 1-mile uphill run performance.

It is previously demonstrated that static stretching was associated with a decrease in running economy and distance run during a 30-minute time trial in trained runners. Recently, the detrimental effects of static stretching on economy were found to be limited to the first few minutes of an endurance bout. However, economy remains to be studied for its direct effects on performance during shorter endurance events. The aim of this study was to investigate the effects of static stretching on 1-mile uphill run performance, electromyography (EMG), ground contact time (GCT), and flexibility. Ten trained male distance runners aged 24 ± 5 years with an average VO2max of 64.9 ± 6.5 mL·kg-1·min-1 were recruited. Subjects reported to the laboratory on 3 separate days interspersed by 72 hours. On day 1, anthropometrics and V[Combining Dot Above]O2max were determined on a motor-driven treadmill. On days 2 and 3, subjects performed a 5-minute treadmill warm-up and either performed a series of 6 lower-body stretches for three 30-second repetitions or sat still for 10 minutes. Time to complete a 1-mile run under stretching and nonstretching conditions took place in randomized order. For the performance run, subjects were instructed to run as fast as possible at a set incline of 5% until a distance of 1 mile was completed. Flexibility from the sit and reach test, EMG, GCT, and performance, determined by time to complete the 1-mile run, were recorded after each condition. Time to complete the run was significantly less (6:51 ± 0:28 minutes) in the nonstretching condition as compared with the stretching condition (7:04 ± 0:32 minutes). A significant condition-by-time interaction for muscle activation existed, with no change in the nonstretching condition (pre 91.3 ± 11.6 mV to post 92.2 ± 12.9 mV) but increased in the stretching condition (pre 91.0 ± 11.6 mV to post 105.3 ± 12.9 mV). A significant condition-by-time interaction for GCT was also present, with no changes in the nonstretching condition (pre 211.4 ± 20.8 ms to post 212.5 ± 21.7 ms) but increased in the stretching trial (pre 210.7 ± 19.6 ms to post 237.21 ± 22.4 ms). A significant condition-by-time interaction for flexibility was found, which was increased in the stretching condition (pre 33.1 ± 2 to post 38.8 ± 2) but unchanged in the nonstretching condition (pre 33.5 ± 2 to post 35.2 ± 2). Study findings indicate that static stretching decreases performance in short endurance bouts (∼8%) while increasing GCT and muscle activation. Coaches and athletes may be at risk for decreased performance after a static stretching bout. Therefore, static stretching should be avoided before a short endurance bout.

Contextual interference effects on the acquisition of skill and strength of the bench press.

The purpose of this study was to investigate contextual interference effects on skill acquisition and strength gains during the learning of the bench press movement. Twenty-four healthy, college-aged males and females were stratified to control, high contextual interference (HCI), and low contextual interference (LCI) groups. Treatment groups were provided with written and visual instruction on proper bench press form and practiced the bench press and dart throwing for four weeks. Within each session, LCI performed all bench press sets before undertaking dart-throws. HCI undertook dart-throws immediately following each set of bench press. Control only did testing. Measurements, including one repetition maximum (1RM), checklist scores based on video recordings of participants' 1RM's, and dart-throw test scores were taken at pre-test, 1 week, 2 week, post-test, and retention test. Results were consistent with the basic premise of the contextual interference effect. LCI had significant improvements in percent 1RM and checklist scores during training, but were mostly absent after training (post-test and retention test). HCI had significant improvements in percent 1RM and checklist scores both during and after training. Thus, HCI may augment strength and movement skill on the bench press since proper technique is an important component of resistance exercise movements.

Practical blood flow restriction training increases acute determinants of hypertrophy without increasing indices of muscle damage.

Vascular blood flow restriction (BFR) training stimulates muscle hypertrophy by increasing muscle activation and muscle swelling. Previous studies used expensive pneumatic cuffs, which may not be practical for regular use. The aim was to investigate the acute effects of low-intensity practical BFR (LI-pBFR) on muscle activation, muscle swelling, and damage. Twelve trained male participants completed a 30-, 15-, 15-, 15-repetition scheme at 30% of their leg press 1-repetition maximum under control and LI-BFR conditions. Under the LI-BFR trial, knee wraps were applied to the thighs at a pressure that resulted in venous, not arterial, occlusion. In the control trial, wraps were applied with zero pressure. Ultrasound-determined muscle thickness was recorded at baseline; 0 minutes post with wraps; 0, 5, and 10 minutes post without wraps. Muscle activation was recorded during warm-ups and on the final set of 15 repetitions. Indices of muscle damage (soreness, power, and muscle swelling) were also recorded. There was a condition by time effect for muscle thickness (p < 0.0001, effect size [ES] = 0.5), in which muscle thickness increased in the LI-pBFR condition 0 minutes post with wraps and through 5 minutes post without wraps. No changes occurred in the control. There was a condition by time effect for muscle activation (p < 0.05, ES = 0.2). The LI-pBFR had greater activation than the control did. There were no condition by time effects on indices of muscle damage. Our data indicate that practical BFR significantly increases muscle activation and muscle thickness without increasing indices of damage.

Changes in perceived recovery status scale following high-volume muscle damaging resistance exercise.

Currently no research has investigated the relationship between muscle damage, hormonal status, and perceived recovery scale (PRS). Therefore, the purpose of this study was to determine the effects of a high-volume training session on PRS and to determine the relationship between levels of testosterone, cortisol, and creatine kinase (CK) and PRS. Thirty-five trained subjects (21.3 ± 1.9 years) were recruited. All subjects participated in a high-volume resistance training session consisting of 3 sets of full squats, bench press, deadlifts, pullups, dips, bent over rows, shoulder press, and barbell curls and extensions. Pre-PRS and post-PRS measurements (0-10), soreness, CK, cortisol, and testosterone were measured before and 48 hours after training. Perceived recovery scale declined from 8.6 ± 2.3 to 4.2 ± 1.85 (p < 0.05). Leg, chest, and arm soreness increased from pre- to postexercise. Creatine kinase significantly increased from pre- to postworkout (189.4 ± 100.2 to 512 ± 222.7 U/L). Cortisol, testosterone, and free testosterone did not change. There was an inverse relationship between CK and PRS (r = 0.58, p < 0.05). When muscle damage was low before training, cortisol and free and total testosterone were not correlated to PRS. However, when damage peaked at 48 hours postexercise, free, but not total, testosterone showed a low direct relationship with PRS (r = 0.2, p < 0.05). High-volume resistance exercise lowers PRS scores. These changes are partly explained by a rise in serum indices of muscle damage. Moreover, free testosterone seems to have a positive relationship with PRS.

The effects of potentiating stimuli intensity under varying rest periods on vertical jump performance and power.

Previous research has demonstrated that post-activation potentiation (PAP) increases in an intensity-dependent manner. However, these studies did not control for volume loads. The purpose of this study was to investigate the effects of varying intensities and rest period lengths, while controlling for volume load, on vertical jump (VJ) performance. Thirteen men, aged 21 ± 3 years with an average relative full squat of 1.7 ± 2 times their body weight, were recruited for this study. Participants were assigned to 3 different experimental sessions that required them to perform the back squat at 56% (low intensity), 70% (moderate intensity), and 93% (high intensity) of their 1 repetition maximums. Vertical jump height and power were recorded at 0, 2, 4, 8, and 12 minutes after squat. There was a significant condition by time interaction for VJ height and power, in which both variables did not change in the low-intensity condition, whereas decreasing immediately after squat for both the moderate- and high-intensity conditions. In the moderate- and high-intensity conditions, VJ height and power increased and peaked at minute 4 and returned to baseline by minutes 8 and 12. These results indicate that when controlling for total work, jump performance and power are enhanced similarly by moderate and high squat intensities. However, high-intensity workloads may prolong the duration of PAP. Therefore, athletes may use moderate- and high-intensity loads during warm-ups to improve jump performance and power.