Betaine supplementation enhances anabolic endocrine and Akt signaling in response to acute bouts of exercise.

Our aim was to examine the effect of betaine supplementation on selected circulating hormonal measures and Akt muscle signaling proteins after an acute exercise session. Twelve trained men (age 19.7 ± 1.23 years) underwent 2 weeks of supplementation with either betaine (B) (1.25 g BID) or placebo (P). Following a 2-week washout period, subjects underwent supplementation with the other treatment (B or P). Before and after each 2-week period, subjects performed an acute exercise session (AES). Circulating GH, IGF-1, cortisol, and insulin were measured. Vastus lateralis samples were analyzed for signaling proteins (Akt, p70 S6k, AMPK). B (vs. P) supplementation approached a significant increase in GH (mean ± SD (Area under the curve, AUC), B: 40.72 ± 6.14, P: 38.28 ± 5.54, p = 0.060) and significantly increased IGF-1 (mean ± SD (AUC), B: 106.19 ± 13.45, P: 95.10 ± 14.23, p = 0.010), but significantly decreased cortisol (mean ± SD (AUC), B: 1,079.18 ± 110.02, P: 1,228.53 ± 130.32, p = 0.007). There was no difference in insulin (AUC). B increased resting Total muscle Akt (p = 0.003). B potentiated phosphorylation (relative to P) of Akt (Ser(473)) and p70 S6 k (Thr(389)) (p = 0.016 and p = 0.005, respectively). Phosphorylation of AMPK (Thr(172)) decreased during both treatments (both p = 0.001). Betaine (vs. placebo) supplementation enhanced both the anabolic endocrine profile and the corresponding anabolic signaling environment, suggesting increased protein synthesis.

The influence of rehydration mode after exercise dehydration on cardiovascular function.

Our purpose was to compare the common modes of rehydration (REHY) on cardiovascular and fluid regulation recovery after exercise dehydration (EXDE). Twelve nonheat-acclimatized trained subjects (age: 23 ± 4 years, weight: 81.3 ± 3.7 kg, height: 180 ± 6 cm, V[Combining Dot Above]O2max: 56.9 ± 4.4 ml·min·kg , and body fat: 7.8 ± 3.0%) completed 20-hour fluid restriction and 2-hour EXDE to -4% body mass, and then were rehydrated to -2% body mass in a randomized, crossover design. The REHY methods included no fluid (NF), ad libitum, oral (OR), intravenous (IV), and a combination of IV and OR (IV + OR) of 1/2-normal saline (0.45% NaCl). The REHY occurred for 30 minutes, and the subjects were observed during rest for 30 minutes. Seated, standing, and mean arterial pressure (MAP) and blood pressure (BP) were measured every 15 minutes throughout REHY. Heart rate (HR), plasma arginine vasopressin concentration [AVP], and thirst perception were measured throughout REHY. The EXDE resulted in a body mass loss of 4.32 ± 0.22%. The REHY returned the subjects to -2.13 ± 0.47% body mass for controlled trials. Seated systolic BP was greater for IV + OR compared with that for OR (p = 0.015). Seated systolic BP and MAP during REHY showed that IV + OR was greater than OR, independent of time (p ≤ 0.011). Upon standing, IV + OR demonstrated a greater BP than both NF (p = 0.012) and OR (p = 0.031) did. The HR was reduced by IV and IV + OR to a greater extent than NF at REHY30 and REHY60 (p < 0.05). The IV + OR [AVP] demonstrated a strong trend for decreasing over time (p = 0.054) and was significantly less than NF at REHY60 (p = 0.003). Practical application seeking to restore cardiovascular function after EXDE, the combined use of IV + OR rather than a single REHY method seems to be most expedient.

Changes in creatine kinase and cortisol in National Collegiate Athletic Association Division I American football players during a season.

The purpose of this study was to track creatine kinase (CK) and serum cortisol over an American college football season starting with the preseason practice. A secondary purpose was to observe changes in basic clinical chemistries. Twenty-two National Collegiate Athletic Association Division I football players (age: 20.4 ± 1.1 years, height: 188.27 ± 8.3 cm, weight: 115.8 ± 29.7 kg) volunteered to participate in this study. Each of the players had participated in the summer strength and conditioning supervised program. Resting blood samples were obtained just before the start of preseason practice (T-1), 2 weeks later (T-2), and the day after game 2 (T-3), game 4 (T-4), game 6 (T-5), and game 9 (T-6) of a 12-game season. Creatine kinase, a panel of clinical chemistries, cortisol, and testosterone were assayed at each time point. No significant changes in CK concentrations were observed over the season with peak values of each range ≤1,070.0 IU·L(-1), but the largest range was observed at T-6 after game 9 (119-2,834 IU·L(-1). The analysis of covariance analysis demonstrated that the number of plays in the ninth game (T-6) explained the magnitude of the changes in CK. No changes in serum cortisol concentrations were observed yet, again large variations existed with peak values of each range ≤465.0 nmol·L(-1). Clinical chemistries showed various significant changes from T-1, but none were considered clinically relevant changes for any player over the time course of the study. In conclusion, the strength and conditioning program before preseason camp or the structure of summer camp practices and the in-season strength and conditioning appeared to mute muscle damage and the stress response of cortisol. Such data demonstrate that changes in muscle damage and adrenal cortical stress over the season are minimal, yet large individual variations can be observed. Management of these variables appears to be related to optimal strength and conditioning and sports medicine programs. Thus, the greater concerns for student-athlete safety in the sport of American football are related to preventing sudden death, traumatic injury, and managing concussion syndromes.

IGF-I measurement across blood, interstitial fluid, and muscle biocompartments following explosive, high-power exercise.

Insulin-like growth factor-I (IGF-I) resides across different biocompartments [blood, interstitial fluid (ISF), and muscle]. Whether circulating IGF-I responses to exercise reflect local events remains uncertain. We measured the IGF-I response to plyometric exercise across blood, ISF, and muscle biopsy from the vastus lateralis. Twenty volunteers (8 men, 12 women, 22 ± 1 yr) performed 10 sets of 10 plyometric jump repetitions at a 40% 1-repetition maximum. Blood, ISF, and muscle samples were taken pre- and postexercise. Circulating IGF-I increased postexercise: total IGF-I (preexercise = 546 ± 42, midexercise = 585 ± 43, postexercise = 597 ± 45, +30 = 557 ± 42, +60 = 536 ± 40, +120 = 567 ± 42 ng/ml; midexercise, postexercise, and +120 greater than preexercise, P < 0.05); Free IGF-I (preexercise = 0.83 ± 0.09, midexercise = 0.78 ± 0.10, postexercise = 0.79 ± 0.11, +30 = 0.93 ± 0.10, +60 = 0.88 ± 0.10, + 120 = 0.91 ± 0.11 ng/ml; +30 greater than all other preceding time points, P < 0.05). No exercise-induced changes were observed for ISF IGF-I (preexercise = 2.35 ± 0.29, postexercise = 2.46 ± 0.35 ng/ml). No changes were observed for skeletal muscle IGF-I protein, although IGF-I mRNA content increased ∼40% postexercise. The increase in circulating total and free IGF-I was not correlated with increases in ISF IGF-I or muscle IGF-I protein content. Our data indicate that exercise-induced increases in circulating IGF-I are not reflective of local IGF-I signaling.

Sex differences in creatine kinase after acute heavy resistance exercise on circulating granulocyte estradiol receptors.

Previous research has shown reduced tissue disruption and inflammatory responses in women as compared to men following acute strenuous exercise. While the mechanism of this action is not known, estrogen may reduce the inflammatory response through its interaction with granulocytes. The purpose of this study was to determine if estrogen receptor ß expression on granulocytes is related to sex differences in tissue disruption in response to an acute heavy resistance exercise protocol. Seven healthy, resistance-trained, eumenorrheic women (23 ± 3 years, 169 ± 9.1 cm, 66.4 ± 10.5 kg) and 8 healthy, resistance-trained men (25 ± 5 years, 178 ± 6.7 cm, 82.3 ± 9.33 kg) volunteered to participate in the study. Subjects performed an acute resistance exercise test consisting of six sets of five squats at 90% of the subject's one repetition maximum. Blood samples were obtained pre-, mid-, post-, and 1-, 6-, and 24-h postexercise. Blood samples were analyzed for 17-ß-estradiol by ELISA, creatine kinase by colorimetric enzyme immunoassay, and estradiol receptors on circulating granulocytes through flow cytometry. Men had higher CK concentrations than women at baseline/control. Men had significantly higher CK concentrations at 24-h postexercise than women. No significant changes in estradiol ß receptors were expressed on granulocytes after exercise or between sexes. While sex differences occur in CK activity in response to strenuous eccentric exercise, they may not be related to estradiol receptor ß expression on granulocytes. Thus, although there are sex differences in CK expression following acute resistance exercise, the differences may not be attributable to estrogen receptor ß expression on granulocytes.

Incidence of morphologic changes in asymptomatic Achilles tendons in an active young adult population.

CONTEXT: Achilles tendon rupture is often the result of a long-term degenerative process, frequently occurring asymptomatically. OBJECTIVE: To determine the prevalence of asymptomatic Achilles tendinopathy in an active, asymptomatic, young-adult population and to compare these findings across gender. DESIGN: Convenience sample, cohort study. SETTING: Research laboratory PARTICIPANTS: A sample of 52 (28 male, 24 female) healthy, active subjects were recruited from the student body at the University of Connecticut. Images of 104 Achilles tendons were made. INTERVENTION: Ultrasound images made with a Phillips HD11 with a 15-MHz real-time linear-array transducer were collected on both the longitudinal and transverse axes of the Achilles tendon. Activity level was measured with the International Physical Activity Questionnaire Short Form (IPAQ-SF). MAIN OUTCOME MEASURE: Presence of ultrasound evidence of Achilles tendinopathy as agreed on by 2 blinded assessors highly skilled in ultrasonography. RESULTS: More subjects were categorized as highly active (57.4%) on the IPAQ-SF than moderately active (42.6%). One female and one male subject were found to have ultrasound evidence of asymptomatic Achilles tendinopathy, equaling 3.8% prevalence in this study. CONCLUSION: We found a low prevalence of asymptomatic Achilles tendinopathy in an active, young-adult population. Further work is necessary to identify an optimal group warranting ultrasound screening for asymptomatic tendinopathy.

Glucocorticoid receptor expression on human B cells in response to acute heavy resistance exercise.

OBJECTIVE: To examine glucocorticoid receptor (GCR) expression on B lymphocytes in response to an acute bout of resistance exercise. METHODS: Using a within-subject design, resistance-trained women (n = 7; age: 22.13 ± 3.09 years; height: 1.69 ± 0.084 m; body weight: 65.60 ± 10.01 kg; body mass index: 22.63 ± 2.03 kg/m²; means ± SD) and men (n = 8; age: 23.28 ± 4.26 years; height: 1.73 ± 0.086 m; body weight: 73.93 ± 12.71 kg; body mass index: 24.51 ± 2.61 kg/m²; means ± SD) performed an acute resistance exercise protocol (6 sets of 5 repetition maximum heavy squats) and a control test in a balanced, randomized order. Blood samples were obtained before, during, and immediately after exercise, and after 1, 6, and 24 h of recovery. GCR expression on circulating B lymphocytes was evaluated with flow cytometry, and circulating cortisol was assayed. RESULTS: Resting GCR expression on B lymphocytes was similar between men and women. GCR expression was elevated in anticipation of exercise (p = 0.047), decreased during exercise (p = 0.049), and increased during recovery (p = 0.05 and p = 0.03 after 1 and 6 h of recovery, respectively). Trends for gender differences were apparent before and during exercise, and after 6 h of recovery. Men had significantly higher cortisol responses during (p = 0.002) and after exercise (p = 0.094) compared to before exercise. In women, however, circulating cortisol concentrations did not significantly increase in response to the squat exercise protocol. CONCLUSIONS: GCR expression on B lymphocytes decreased during resistance exercise and increased during recovery. Circulating cortisol increased during exercise in men only. Responses were attenuated in women compared to men. Our data provide insights into the temporal interactions between the endocrine and immune systems in response to acute heavy resistance exercise in men and women.

Effect of ambient temperature on caffeine ergogenicity during endurance exercise.

It is well established that caffeine ingestion during exercise enhances endurance performance. Conversely, the physiological and psychological strain that accompanies increased ambient temperature decreases endurance performance. Little is known about the interaction between environmental temperature and the effects of caffeine on performance. The purpose of this study was to compare the effects of ambient temperature (12 and 33°C) on caffeine ergogenicity during endurance cycling exercise. Eleven male cyclists (mean ± SD; age, 25 ± 6 years; [Formula: see text] 58.7 ± 2.9 ml kg(-1) min(-1)) completed four exercise trials in a randomized, double blind experimental design. After cycling continuously for 90 min (average 65 ± 7% [Formula: see text]) in either a warm (33 ± 1°C, 41 ± 5%rh) or cool (12 ± 1°C, 60 ± 7%rh) environment, subjects completed a 15-min performance trial (PT; based on total work accumulated). Subjects ingested 3 mg kg(-1) of encapsulated caffeine (CAF) or placebo (PLA) 60 min prior to and after 45 min of exercise. Throughout exercise, subjects ingested water so that at the end of exercise, independent of ambient temperature, their body mass was reduced 0.55 ± 0.67%. Two-way (temperature × treatment) repeated-measures ANOVA were conducted with alpha set at 0.05. Total work (kJ) during the PT was greater in 12°C than 33°C [P < 0.001, η(2) = 0.804, confidence interval (CI): 30.51-62.30]. When pooled, CAF increased performance versus PLA independent of temperature (P = 0.006, η(2) = 0.542 CI: 3.60-16.86). However, performance differences with CAF were not dependent on ambient temperature (i.e., non-significant interaction; P = 0.662). CAF versus PLA in 12 and 33°C resulted in few differences in other physiological variables. However, during exercise, rectal temperature (T (re)) increased in the warm environment (peak T (re); 33°C, 39.40 ± 0.45; 12°C, 38.79 ± 0.42°C; P < 0.05) but was not different in CAF versus PLA (P > 0.05). Increased ambient temperature had a detrimental effect on cycling performance in both the CAF and PLA conditions. CAF improved performance independent of environmental temperature. These findings suggest that caffeine at the dosage utilized (6 mg/kg body mass) is a, legal drug that provides an ergogenic benefit in 12 and 33°C.

Evaluating the athlete's claim of an unintentional positive urine drug test.

During a urine drug testing program, an athlete may make a claim that the results of a positive test have arisen from factors that were out of his or her control, and therefore, he or she should not be held responsible for the results. Some of these claims may include classic claims of passive inhalation of marijuana smoke or ingestion of poppy seeds leading to positive tests. In addition, with the proliferation of nutritional supplements on the market, many athletes claim that they accidentally ingested a banned substance contained in one of these. It is important that any sports medicine physician involved with sports drug testing be informed of the data that either support or refute these claims and that he or she contribute to a program wherein adequate education and policy establishment help to limit the likelihood of such claims. This article will review the data to help address these claims.

Acute energy deprivation affects skeletal muscle protein synthesis and associated intracellular signaling proteins in physically active adults.

To date, few studies have characterized the influence of energy deprivation on direct measures of skeletal muscle protein turnover. In this investigation, we characterized the effect of an acute, moderate energy deficit (10 d) on mixed muscle fractional synthetic rate (FSR) and associated intracellular signaling proteins in physically active adults. Eight men and 4 women participated in a 20-d, 2-phase diet intervention study: weight maintenance (WM) and energy deficient (ED; approximately 80% of estimated energy requirements). Dietary protein (1.5 g x kg(-1) x d(-1)) and fat (approximately 30% of total energy) were constant for WM and ED. FSR and intracellular signaling proteins were measured on d 10 of both interventions using a primed, constant infusion of [(2)H(5)]-phenylalanine and Western blotting techniques, respectively. Participants lost approximately 1 kg body weight during ED (P < 0.0001). FSR was reduced approximately 19% (P < 0.05) for ED (0.06 +/- 0.01%/h) compared with WM (0.074 +/- 0.01%/h). Protein kinase B and eukaryotic initiation factor 4E binding protein 1 phosphorylation were lower (P < 0.05) during ED compared with WM. AMP activated protein kinase phosphorylation decreased (P < 0.05) over time regardless of energy status. These findings show that FSR and associated synthetic intracellular signaling proteins are downregulated in response to an acute, moderate energy deficit in physically active adults and provide a basis for future studies assessing the impact of prolonged, and perhaps more severe, energy restriction on skeletal muscle protein turnover.

Influences of a dietary supplement in combination with an exercise and diet regimen on adipocytokines and adiposity in women who are overweight.

The influence of a proprietary blend of modified cellulose and cetylated fatty acids (Trisynextrade mark, Imagenetix, Inc., San Diego, CA 92127, USA) on adipocytokine and regional body composition responses to a weight loss program was examined. Twenty-two women (Supplement group (S) (n = 11): age = 36.8 +/- 7.2 years; weight = 87.1 +/- 6.2 kg; % body fat = 43.4 +/- 4.1; Placebo group (P) (n = 11): age = 38.3 +/- 6.8 years; weight = 86.9 +/- 4.7 kg; % body fat = 44.3 +/- 2.0) completed an 8-week placebo-controlled, double-blind study consisting of a caloric restricted diet and cardiovascular exercise. Body composition and serum insulin, leptin, and adiponectin were assessed at pre-, mid-, and post-intervention. From pre- to post-intervention, significant decreases (P < 0.05) were observed for body weight (S: 87.1 +/- 6.2-77.9 +/- 5.1 kg; P: 86.9 +/- 4.7-82.7 +/- 3.8 kg) (P < 0.05 S vs. P), % body fat (S: 43.4 +/- 4.1-36.1 +/- 3.6; P: 44.3 +/- 2.0-40.6 +/- 1.2) (P < 0.05 S vs. P), leptin (S: 28.3 +/- 3.5-16.2 +/- 2.6 ng ml(-1); P: 29.4 +/- 3.2-19.9 +/- 1.1 ng ml(-1)) (P < 0.05 S vs. P), and insulin (S: 7.3 +/- 0.8-5.1 +/- 0.2 mU l(-1); P: 7.7 +/- 0.9-5.1 +/- 0.3 mU l(-1)). Serum adiponectin increased (P < 0.05) (S: 12.2 +/- 2.4-26.3 +/- 3.0 microg ml(-1): 12.6 +/- 2.0-21.8 +/- 3.1 microg ml(-1)) (P < 0.05 for S vs. P). Supplementation with a proprietary blend of modified cellulose and cetylated fatty acids during an 8-week weight loss program exhibited favorable effects on adipocytokines and regional body composition.

Recovery from a national collegiate athletic association division I football game: muscle damage and hormonal status.

The purpose of this study was to examine markers of skeletal muscle tissue damage and circulating anabolic and catabolic hormones to gain insight into the recovery process from Friday until Monday, when a new practice week begins. Twenty-eight National Collegiate Athletic Association Division I football players gave consent to participate in the investigation in the ninth game of the season. Sixteen players started the game and played the entire game (PL), and 12 others did not play and were on the bench during the game (DNP). Each player had fasted blood samples obtained at the same time of day between 1000 and 1200 hours the day before the game (Friday; T1), 18-20 hours after the game (Sunday; T2), and then 42-44 hours after the game (Monday; T3). Blood samples were analyzed for concentrations of creatine kinase (CK), lactate dehydrogenase (LDH), myoglobin, testosterone, and cortisol. The PL players showed significantly (p T1 and T3), myoglobin (T2 > T1 and T3), and LDH (T2 > T1). In contrast, DNP players showed significant differences in cortisol (T3 < T1 and T2) and testosterone:cortisol (T3 > T1). Few changes were observed in testosterone and cortisol changes, indicating stability of the anabolic/catabolic hormones. In conclusion, these data indicate that participation in a college football game late in the season results in some degree of tissue damage but with minimal hormonal responses, which seem to have stabilized at resting concentrations without predominance of cortisol's catabolic presence. As previously noted in the literature, some type of "contact adaptation" to the season may have occurred with regard to tissue damage responses. However, by the ninth game of a season, players do carry soft tissue damage levels above resting ranges into subsequent games, indicating that recovery should be monitored, with coaches being careful with scheduling scrimmage and full-contact drills. How such data implicate overuse injuries remains unclear, considering that hormonal status in this study was highly stable, with catabolic influences minimized by the high level of athlete conditioning. These data again support that high-level conditioning can stabilize anabolic and catabolic hormonal signals and limit acute soft tissue injury, making cerebral concussion (acute and chronic) and traumatic injury the biggest threats to a student-athlete's health and well-being during an American football game.

Exacerbated heat strain during consecutive days of repeated exercise sessions in heat.

OBJECTIVES: An exercise session in a hot environment may increase thermal strain during subsequent exercise sessions on the same and consecutive days. Therefore, this study was conducted to determine lasting physiological strain from moderate-high intensity, intermittent exercise in heat on subsequent exercise. DESIGN: Repeated measures laboratory study. METHODS: Seventeen healthy, recreationally active men (age: 22±3 y, maximal oxygen consumption: 54.6±5.3mLkg-1min-1) underwent two intermittent moderate-high intensity aerobic exercise sessions separated by 2h of rest one day, followed by one session 24h later in a 40°C, 40% relative humidity environment. Heart rate, rectal temperature, heat stress perception, and environmental symptoms were assessed. RESULTS: 100%, 35%, and 71% of participants completed the full exercise protocol during the first exercise session, second exercise session, and the following day, respectively. Exercising heart rate and rectal temperature were greater during the second exercise session (189±11bpm, 38.80±0.47°C) than the first identical exercise session (180±17bpm, p=0.004; 38.41±0.52°C, p=0.001), respectively. Immediate post-exercise heart rate, rectal temperature, thirst, thermal sensation, fatigue, and perceived exertion were similar among exercise sessions despite a shorter exercise duration during the second exercise session (93±27min, p=0.001) and the following day (113±12min, p=0.032) than the first exercise session (120±0min). CONCLUSIONS: Moderate-high-intensity intermittent exercise in the heat resulted in greater heat strain during a second exercise session the same day, and exercise the subsequent day.

Intermittent exercise-heat exposures and intense physical activity sustain heat acclimation adaptations.

OBJECTIVES: To determine if intermittent exercise-heat exposures (IHE) every fifth day sustain heat acclimation (HA) adaptations 25 days after initial HA. DESIGN: Randomized control trial. METHODS: Sixteen non-heat acclimatized men heat acclimated during 10-11 days of exercise in the heat (40°C, 40% RH). A heat stress test (120min, 45% V˙O2peak) before (Pre HA) and after HA (Post HA) in similar hot conditions assessed HA status. Pair-matched participants were randomized into a control group (CON; n=7) that exercised in a temperate environment (24°C, 21%RH) or IHE group (n=9) that exercised in a hot environment (40°C, 40%RH) every fifth day for 25 days following HA (+25d) with out-of-laboratory exercise intensity and duration recorded. Both groups completed +25d in the hot condition. RESULTS: Both groups heat acclimated similarly (p>0.05) evidenced by lower heart rate (HR), thermoregulatory, physiological, and perceptual responses (perceived exertion, fatigue, thermal sensation) Pre HA vs. Post HA (p≤0.05). At +25d, post-exercise HR (p=0.01) and physiological strain index (p<0.05) but neither Tre (p=0.18) nor sweat rate (p=0.44) were lower in IHE vs. CON. In IHE only, post-exercise Tre and perceptual responses at Post HA and +25d were lower than Pre HA (p≤0.01). +25d post-exercise epinephrine was higher in CON vs. IHE (p=0.04). Exercise intensity during out-of-lab exercise and +25d post-exercise HR were correlated (r=-0.89, p=0.02) in IHE. CONCLUSIONS: Exercise-heat exposures every fifth day for 25 days and regular intense physical activity after HA sustained HR and Tre adaptations and reduced perceptual and physiological strain during exercise-heat stress ∼1 month later.

Effect of hydration state on resistance exercise-induced endocrine markers of anabolism, catabolism, and metabolism.

Hypohydration (decreased total body water) exacerbates the catabolic hormonal response to endurance exercise with unclear effects on anabolic hormones. Limited research exists that evaluates the effect of hypohydration on endocrine responses to resistance exercise; this work merits attention as the acute postexercise hormonal environment potently modulates resistance training adaptations. The purpose of this study was to examine the effect of hydration state on the endocrine and metabolic responses to resistance exercise. Seven healthy resistance-trained men (age = 23 +/- 4 yr, body mass = 87.8 +/- 6.8 kg, body fat = 11.5 +/- 5.2%) completed three identical resistance exercise bouts in different hydration states: euhydrated (EU), hypohydrated by approximately 2.5% body mass (HY25), and hypohydrated by approximately 5.0% body mass (HY50). Investigators manipulated hydration status via controlled water deprivation and exercise-heat stress. Cortisol, epinephrine, norepinephrine, testosterone, growth hormone, insulin-like growth factor-I, insulin, glucose, lactate, glycerol, and free fatty acids were measured during euhydrated rest, immediately preceding resistance exercise, immediately postexercise, and during 60 min of recovery. Body mass decreased 0.2 +/- 0.4, 2.4 +/- 0.4, and 4.8 +/- 0.4% during EU, HY25, and HY50, respectively, supported by humoral and urinary changes that clearly indicated subjects achieved three distinct hydration states. Hypohydration significantly 1) increased circulating concentrations of cortisol and norepinephrine, 2) attenuated the testosterone response to exercise, and 3) altered carbohydrate and lipid metabolism. These results suggest that hypohydration can modify the hormonal and metabolic response to resistance exercise, influencing the postexercise circulatory milieu.

Effect of resistance exercise on muscle steroidogenesis.

Circulating testosterone is elevated acutely following resistance exercise (RE) and is an important anabolic hormone for muscle adaptations to resistance training. The purpose of this study was to examine the acute effect of heavy RE on intracrine muscle testosterone production in young resistance-trained men and women. Fifteen young, highly resistance-trained men (n = 8; 21 +/- 1 yr, 175.3 +/- 6.7 cm, 90.8 +/- 11.6 kg) and women (n = 7; 24 +/- 5 yr, 164.6 +/- 6.7 cm, 76.4 +/- 15.6 kg) completed 6 sets of 10 repetitions of Smith machine squats with 80% of their 1-repetition maximum. Before RE and 10 and 70 min after RE, muscle biopsies were obtained from the vastus lateralis. Before RE, after 3 and 6 sets of squats, and 5, 15, 30, and 70 min into recovery from RE, blood samples were obtained using venipuncture from an antecubital vein. Muscle samples were analyzed for testosterone, 17beta-hydroxysteroid dehydrogenase (HSD) type 3, and 3beta-HSD type 1 and 2 content. Blood samples were analyzed for glucose and lactate concentrations. No changes were found for muscle testosterone, 3beta-HSD type 1 and 2, and 17beta-HSD type 3 concentrations. However, a change in protein migration in the Bis-Tris gel was observed for 17beta-HSD type 3 postexercise; this change in migration indicated an approximately 2.8 kDa increase in molecular mass. These findings indicate that species differences in muscle testosterone production may exist between rats and humans. In humans, muscle testosterone concentrations do not appear to be affected by RE. This study expands on the current knowledge obtained from animal studies by examining resting and postexercise concentrations of muscle testosterone and steroidogenic enzymes in humans.

Resistance exercise biology: manipulation of resistance exercise programme variables determines the responses of cellular and molecular signalling pathways.

Recent advances in molecular biology have elucidated some of the mechanisms that regulate skeletal muscle growth. Logically, muscle physiologists have applied these innovations to the study of resistance exercise (RE), as RE represents the most potent natural stimulus for growth in adult skeletal muscle. However, as this molecular-based line of research progresses to investigations in humans, scientists must appreciate the fundamental principles of RE to effectively design such experiments. Therefore, we present herein an updated paradigm of RE biology that integrates fundamental RE principles with the current knowledge of muscle cellular and molecular signalling. RE invokes a sequential cascade consisting of: (i) muscle activation; (ii) signalling events arising from mechanical deformation of muscle fibres, hormones, and immune/inflammatory responses; (iii) protein synthesis due to increased transcription and translation; and (iv) muscle fibre hypertrophy. In this paradigm, RE is considered an 'upstream' signal that determines specific downstream events. Therefore, manipulation of the acute RE programme variables (i.e. exercise choice, load, volume, rest period lengths, and exercise order) alters the unique 'fingerprint' of the RE stimulus and subsequently modifies the downstream cellular and molecular responses.

Effects of elevated circulating hormones on resistance exercise-induced Akt signaling.

PURPOSE: Hormones and muscle contraction alter protein kinase B (Akt) signaling via distinct mechanisms. Therefore, the purpose of this study was to determine whether physiologically elevated circulating hormones modulate resistance exercise (RE)-induced signaling of Akt and its downstream targets. We hypothesized that elevated circulating hormones would potentiate the signaling response. METHODS: Seven healthy men (mean +/- SD age, 27 +/- 4 yr; body mass, 79.1 +/- 13.6 kg; body fat, 16% +/- 7%) performed two identical lower-body RE protocols (five sets of five maximal repetitions of knee extensions) in a randomized order and separated by 1-3 wk: one protocol was preceded by rest [low-circulating hormonal concentration (LHC) trial], and the other was preceded by a bout of high-volume upper-body RE using short rest periods designed to elicit a large increase in circulating hormones [high-circulating hormonal concentration (HHC) trial]. RESULTS: The HHC trial invoked significantly (P < or = 0.05) greater growth hormone (GH) and cortisol concentrations compared with the LHC trial. There were minimal differences between trials in insulin and insulin-like growth factor-I (IGF-I) concentrations. Contrary to our hypothesis, 70-kDa ribosomal protein S6 kinase (p70 S6K) threonine (Thr) 389 phosphorylation within the vastus lateralis was attenuated at 180 min post-RE during the HHC trial. RE did not affect Akt or glycogen synthase kinase-3beta (GSK-3beta) phosphorylation nor were there differences between trials. Immediately post-RE, eukaryotic initiation factor (eIF) 4E binding protein-1 (4E-BP1) phosphorylation declined, and adenosine monophosphate-activated protein kinase (AMPK) phosphorylation increased; however, there were no differences between trials in these variables. CONCLUSION: p70 S6K Thr 389 phosphorylation was attenuated during the HHC trial despite dramatically greater (>2.5-fold) circulating GH concentrations; this was potentially due to cortisol-induced inhibition of p70 S6K Thr 389 phosphorylation.

Effects of stretching on upper-body muscular performance.

The purpose of this investigation was to examine the influence of upper-body static stretching and dynamic stretching on upper-body muscular performance. Eleven healthy men, who were National Collegiate Athletic Association Division I track and field athletes (age, 19.6 +/- 1.7 years; body mass, 93.7 +/- 13.8 kg; height, 183.6 +/- 4.6 cm; bench press 1 repetition maximum [1RM], 106.2 +/- 23.0 kg), participated in this study. Over 4 sessions, subjects participated in 4 different stretching protocols (i.e., no stretching, static stretching, dynamic stretching, and combined static and dynamic stretching) in a balanced randomized order followed by 4 tests: 30% of 1 RM bench throw, isometric bench press, overhead medicine ball throw, and lateral medicine ball throw. Depending on the exercise, test peak power (Pmax), peak force (Fmax), peak acceleration (Amax), peak velocity (Vmax), and peak displacement (Dmax) were measured. There were no differences among stretch trials for Pmax, Fmax, Amax, Vmax, or Dmax for the bench throw or for Fmax for the isometric bench press. For the overhead medicine ball throw, there were no differences among stretch trials for Vmax or Dmax. For the lateral medicine ball throw, there was no difference in Vmax among stretch trials; however, Dmax was significantly larger (p

National Athletic Trainers' Association Position Statement: Immediate Management of Appendicular Joint Dislocations.

OBJECTIVE: To provide certified athletic trainers (ATs) with recommendations and guidelines for the immediate management of patients with joint dislocations. BACKGROUND: One of the primary responsibilities of ATs is to provide immediate injury care for active individuals. Although ATs are confronted with managing patients who have many kinds of injuries, the onsite management of a joint dislocation presents challenges in evaluation and immediate treatment. The critical concern in managing a dislocation is deciding when a joint can be reduced onsite and when the patient should be splinted and transported for reduction to be performed in the hospital or medical setting. Factors that influence the decision-making process include the following: whether the AT possesses a documented protocol that is supported by his or her supervising physician(s), employer documents, and respective state regulations; the AT's qualifications and experience; the dislocated joint; whether the dislocation is first time or recurrent; the patient's age and general health; and whether associated injuries are present. RECOMMENDATIONS: These guidelines are intended to provide considerations for the initial care of specific joint dislocations. They are not intended to represent the standard of care and should not be interpreted as a standard of care for therapeutic or legal discussion.