Liver L-glutamine is an important vehicle for the transport of ammonia and intermediary metabolism of amino acids between tissues, particularly under catabolic situations, such as high-intensity exercise. Hence, the aim of this study was to investigate the effects of oral supplementations with L-glutamine in its free or dipeptide forms (with L-alanine) on liver glutamine-glutathione (GSH) axis, and 70 kDa heat shock proteins (HSP70)/heat shock transcription factor 1 (HSF1) expressions. Adult male Wistar rats were 8-week trained (60 min/day, 5 days/week) on a treadmill. During the last 21 days, the animals were daily supplemented with 1 g of L-glutamine/kg body weight per day in either l-alanyl-L-glutamine dipeptide (DIP) form or a solution containing L-glutamine and l-alanine in their free forms (GLN+ALA) or water (controls). Exercise training increased cytosolic and nuclear HSF1 and HSP70 expression, as compared with sedentary animals. However, both DIP and GLN+ALA supplements enhanced HSF1 expression (in both cytosolic and nuclear fractions) in relation to exercised controls. Interestingly, HSF1 rises were not followed by enhanced HSP70 expression. DIP and GLN+ALA supplements increased plasma glutamine concentrations (by 62% and 59%, respectively) and glutamine to glutamate plasma ratio in relation to trained controls. This was in parallel with a decrease in plasma ammonium levels. Supplementations increased liver GSH (by 90%), attenuating the glutathione disulfide (GSSG) to GSH ratio, suggesting a redox state protection. In conclusion, oral administration with DIP and GLN+ALA supplements in endurance-trained rats improve liver glutamine-GSH axis and modulate HSF1 pathway.
Éder Ricardo Petry, Vinicius Fernandes Cruzat, Thiago Gomes Heck, Paulo Ivo Homem de Bittencourt Jr. and Julio Tirapegui
Martin J. Turner and Alberto P. Avolio
International guidelines suggest limiting sodium intake to 86–100 mmol/day, but average intake exceeds 150 mmol/day. Participants in physical activities are, however, advised to increase sodium intake before, during and after exercise to ensure euhydration, replace sodium lost in sweat, speed rehydration and maintain performance. A similar range of health benefits is attributable to exercise and to reduction in sodium intake, including reductions in blood pressure (BP) and the increase of BP with age, reduced risk of stroke and other cardiovascular diseases, and reduced risk of osteoporosis and dementia. Sweat typically contains 40–60 mmol/L of sodium, leading to approximately 20–90 mmol of sodium lost in one exercise session with sweat rates of 0.5–1.5 L/h. Reductions in sodium intake of 20–90 mmol/day have been associated with substantial health benefits. Homeostatic systems reduce sweat sodium as low as 3–10 mmol/L to prevent excessive sodium loss. “Salty sweaters” may be individuals with high sodium intake who perpetuate their “salty sweat” condition by continual replacement of sodium excreted in sweat. Studies of prolonged high intensity exercise in hot environments suggest that sodium supplementation is not necessary to prevent hyponatremia during exercise lasting up to 6 hr. We examine the novel hypothesis that sodium excreted in sweat during physical activity offsets a significant fraction of excess dietary sodium, and hence may contribute part of the health benefits of exercise. Replacing sodium lost in sweat during exercise may improve physical performance, but may attenuate the long-term health benefits of exercise.
Tanja Oosthuyse, Matthew Carstens and Aletta M.E. Millen
Certain commercial carbohydrate replacement products include slowly absorbed carbohydrates such as isomaltulose. Few studies have investigated the metabolic effects of ingesting isomaltulose during exercise and none have evaluated exercise performance and gastrointestinal comfort. Nine male cyclists participated postprandially during three trials of 2-h steady-state (S-S) exercise (60% W max) followed by a 16 km time trial (TT) while ingesting 63 g∙h-1 of either, 0.8:1 fructose: maltodextrin (F:M) or isomaltulose (ISO) or placebo-flavored water (PL). Data were analyzed by magnitude-based inferences. During S-S exercise, ISO and PL similarly increased plasma nonesterified fatty acid (NEFA) concentration (mean change ISO versus F:M: 0.18, 90%CI ± 0.21 mmol∙L-1, 88% likelihood) and fat oxidation (10, 90%CI ± 9 g, 89% likelihood) while decreasing carbohydrate oxidation (-36, 90%CI ± 30.2 g, 91% likelihood) compared with F:M, despite equal elevations in blood glucose concentration with ISO and F:M. Rating of stomach cramps and bloating increased progressively with ISO (rating: 0-90 min S-S, weak; 120 min S-S, moderate; TT, strong) compared with F:M and PL (0-120 min S-S and TT, very weak). TT performance was substantially slower with ISO (mean change: 1.5, 90%CI ± 1.4 min, 94% likely harmful) compared with F:M. The metabolic response of ISO ingestion during moderate exercise to increase NEFA availability and fat oxidation despite elevating blood glucose concentration is anomalous for a carbohydrate supplement. However, ingesting isomaltulose at a continuous high frequency to meet the recommended carbohydrate replacement dose, results in severe gastrointestinal symptoms during prolonged or high intensity exercise and negatively affects exercise performance compared with fructose-maltodextrin supplementation.
Dawn M. Maffucci and Robert G. McMurray
The purpose of this study was to compare the effect a 6-hr versus 3-hr prefeeding regimen on exercise performance. The subjects were 8 active women (21.4 ± 0.9 years, 60.4±2.4 kg, 19.9 ± 1.3% body fat. and 165.6±2.1 cm). All women completed 2 exercise trials (separated by 3—6d) on a treadmill where they ran at moderate intensity for 30 min with 30-s sprints at 5-min intervals, followed directly by increasing incrementally the grade until volitional fatigue was achieved. The exercise trials were performed 3 hr and 6 hr after consuming 40 ± 3 kJ/kg meal. Time to exhaustion was 0.75 min shorter (p = .0001) for the 6-H trials compared to the 3-H trials. There were no significant differences in submaximal or peak oxygen uptake, heart rate, or rating of perceived exertion (p > .05). The 6-H trials compared to the 3-H trials resulted in .05 lower RERs (p = .0002), and a 2 mmol lower blood lactate at exhaustion (p = .012). Blood glucose levels and cortisol responses to exercise were similar between trials (p > .05). However, both resting and post exercise insulin levels were lower during 6-H trials. It was concluded that performance of moderate- to high-intensity exercise lasting 35—40 min is improved by consuming a moderately-high carbohydrate. low fat, low protein meal 3-hr before exercise compared to a similar meal consumed 6 hr prior to exercise. Thus, athletes should not skip meals before competition or training sessions.
Deborah K. Fletcher and Nicolette C. Bishop
This study investigated the effect of a high and low dose of caffeine on antigen-stimulated natural killer (NK) cell (CD3−CD56+) activation after prolonged, strenuous cycling, as assessed by the early-activation molecule CD69. In a randomized crossover design, 12 healthy male endurance-trained cyclists cycled for 90 min at 70% VO2peak 60 min after ingesting either 0 (PLA), 2 (2CAF), or 6 (6CAF) mg/kg body mass of caffeine. Whole blood was stimulated with Pediacel (5 in 1) vaccine. A high dose of caffeine (6CAF) increased the number of CD3−CD56+ cells in the circulation immediately postexercise compared with PLA (p < .05). For both 2CAF and 6CAF, the geometric mean fluorescence intensity (GMFI) of CD69+ expression on unstimulated CD3−CD56+ cells was significantly higher than with PLA (both p < .05). When cells were stimulated with antigen, the GMFI of CD69 expression remained significantly higher with 2CAF than with PLA 1 hr postexercise (p < .05). Although not achieving statistical significance, 6CAF also followed a similar trend when stimulated (p = .09). There were no differences in GMFI of CD69 expression between 2CAF and 6CAF. These results suggest that a high (6 mg/kg) dose of caffeine was associated with the recruitment of NK cells into the circulation and that both a high and low (2 mg/kg) dose of caffeine increased unstimulated and antigen-stimulated NK-cell activation 1 hr after high-intensity exercise. Furthermore, there does not appear to be a dose-dependent effect of caffeine on NK-cell activation 1 hr after prolonged intensive cycling.
Rob Duffield, Johann Edge, Robert Merrells, Emma Hawke, Matt Barnes, David Simcock and Nicholas Gill
The aim of this study was to determine whether compression garments improve intermittent-sprint performance and aid performance or self-reported recovery from high-intensity efforts on consecutive days.
Following familiarization, 14 male rugby players performed two randomized testing conditions (with or without garments) involving consecutive days of a simulated team sport exercise protocol, separated by 24 h of recovery within each condition and 2 weeks between conditions. Each day involved an 80-min high-intensity exercise circuit, with exercise performance determined by repeated 20-m sprints and peak power on a cart dynamometer (single-man scrum machine). Measures of nude mass, heart rate, skin and tympanic temperature, and blood lactate (La−) were recorded throughout each day; also, creatine kinase (CK) and muscle soreness were recorded each day and 48 h following exercise.
No differences (P = .20 to 0.40) were present between conditions on either day of the exercise protocol for repeated 20-m sprint efforts or peak power on a cart dynamometer. Heart rate, tympanic temperature, and body mass did not significantly differ between conditions; however, skin temperature was higher under the compression garments. Although no differences (P = .50) in La− or CK were present, participants felt reduced levels of perceived muscle soreness in the ensuing 48 h postexercise when wearing the garments (2.5 ± 1.7 vs 3.5 ± 2.1 for garment and control; P = .01).
The use of compression garments did not improve or hamper simulated team-sport activity on consecutive days. Despite benefits of reduced self-reported muscle soreness when wearing garments during and following exercise each day, no improvements in performance or recovery were apparent.
Peter Peeling, Brian Dawson, Carmel Goodman, Grant Landers, Erwin T. Wiegerinck, Dorine W. Swinkels and Debbie Trinder
Urinary hepcidin, inflammation, and iron metabolism were examined during the 24 hr after exercise. Eight moderately trained athletes (6 men, 2 women) completed a 60-min running trial (15-min warm-up at 75–80% HRpeak + 45 min at 85–90% HRpeak) and a 60-min trial of seated rest in a randomized, crossover design. Venous blood and urine samples were collected pretrial, immediately posttrial, and at 3, 6, and 24 hr posttrial. Samples were analyzed for interleukin-6 (IL-6), C-reactive protein (CRP), serum iron, serum ferritin, and urinary hepcidin. The immediate postrun levels of IL-6 and 24-hr postrun levels of CRP were significantly increased from baseline (6.9 and 2.6 times greater, respectively) and when compared with the rest trial (p ≤ .05). Hepcidin levels in the run trial after 3, 6, and 24 hr of recovery were significantly greater (1.7–3.1 times) than the pre- and immediate postrun levels (p ≤ .05). This outcome was consistent in all participants, despite marked variation in the magnitude of rise. In addition, the 3-hr postrun levels of hepcidin were significantly greater than at 3 hr in the rest trial (3.0 times greater, p ≤ .05). Hepcidin levels continued to increase at 6 hr postrun but failed to significantly differ from the rest trial (p = .071), possibly because of diurnal influence. Finally, serum iron levels were significantly increased immediately postrun (1.3 times, p ≤ .05). The authors concluded that high-intensity exercise was responsible for a significant increase in hepcidin levels subsequent to a significant increase in IL-6 and serum iron.
Samuel T. Howe, Phillip M. Bellinger, Matthew W. Driller, Cecilia M. Shing and James W. Fell
Beta-alanine may benefit short-duration, high-intensity exercise performance. The aim of this randomized double-blind placebo-controlled study was to examine the effects of beta-alanine supplementation on aspects of muscular performance in highly trained cyclists. Sixteen highly trained cyclists (mean ± SD; age = 24 ± 7 yr; mass = 70 ± 7kg; VO2max = 67 ± 4ml·kg−1·min–1) supplemented with either beta-alanine (n = 8, 65 mg·kg−1BM) or a placebo (n = 8; dextrose monohydrate) over 4 weeks. Pre- and postsupplementation cyclists performed a 4-minute maximal cycling test to measure average power and 30 reciprocal maximal isokinetic knee contractions at a fixed angular velocity of 180°·sec−1 to measure average power/repetition, total work done (TWD), and fatigue index (%). Blood pH, lactate (La−) and bicarbonate (HCO3 -) concentrations were measured preand postisokinetic testing at baseline and following the supplementation period. Beta-alanine supplementation was 44% likely to increase average power output during the 4-minute cycling time trial when compared with the placebo, although this was not statistically significant (p = .25). Isokinetic average power/repetition was significantly increased post beta-alanine supplementation compared with placebo (beta-alanine: 6.8 ± 9.9W, placebo: –4.3 ± 9.5 W, p = .04, 85% likely benefit), while fatigue index was significantly reduced (p = .03, 95% likely benefit). TWD was 89% likely to be improved following beta-alanine supplementation; however, this was not statistically significant (p = .09). There were no significant differences in blood pH, lactate, and HCO3 − between groups (p > .05). Four weeks of beta-alanine supplementation resulted in worthwhile changes in time-trial performance and short-duration muscular force production in highly trained cyclists.
Hee-Tae Roh, Su-Youn Cho, Hyung-Gi Yoon and Wi-Young So
We investigated the effects of aerobic exercise intensity on oxidative–nitrosative stress, neurotrophic factor expression, and blood–brain barrier (BBB) permeability. Fifteen healthy men performed treadmill running under low-intensity (LI), moderate-intensity (MI), and high-intensity (HI) conditions. Blood samples were collected immediately before exercise (IBE), immediately after exercise (IAE), and 60 min after exercise (60MAE) to examine oxidative–nitrosative stress (reactive oxygen species [ROS]; nitric oxide [NO]), neurotrophic factors (brain-derived neurotrophic factor [BDNF]; nerve growth factor [NGF]), and blood-brain barrier (BBB) permeability (S-100β; neuron-specific enolase). ROS concentration significantly increased IAE and following HI (4.9 ± 1.7 mM) compared with that after LI (2.8 ± 1.4 mM) exercise (p < .05). At 60MAE, ROS concentration was higher following HI (2.5 ± 1.2 mM) than after LI (1.5 ± 0.5 mM) and MI (1.4 ± 0.3 mM) conditions (p < .05). Plasma NO IAE increased significantly after MI and HI exercise (p < .05). Serum BDNF, NGF, and S-100b levels were significantly higher IAE following MI and HI exercise (p < .05). BDNF and S-100b were higher IAE following MI (29.6 ± 3.4 ng/mL and 87.1 ± 22.8 ng/L, respectively) and HI (31.4 ± 3.8 ng/mL and 100.6 ± 21.2 ng/L, respectively) than following LI (26.5 ± 3.0 ng/mL and 64.8 ± 19.2 ng/L, respectively) exercise (p < .05). 60MAE, S-100b was higher following HI (71.1 ± 14.5 ng/L) than LI (56.2 ± 14.7 ng/L) exercise (p < .05). NSE levels were not significantly different among all intensity conditions and time points (p > .05). Moderate- and/or high-intensity exercise may induce higher oxidative-nitrosative stress than may low-intensity exercise, which can increase peripheral neurotrophic factor levels by increasing BBB permeability.
Simon P. Roberts, Keith A. Stokes, Lee Weston and Grant Trewartha
This study presents an exercise protocol utilizing movement patterns specific to rugby union forward and assesses the reproducibility of scores from this test.
After habituation, eight participants (mean ± SD: age = 21 ± 3 y, height = 180 ± 4 cm, body mass = 83.9 ± 3.9 kg) performed the Bath University Rugby Shuttle Test (BURST) on two occasions, 1 wk apart. The protocol comprised 16 × 315-s cycles (4 × 21-min blocks) of 20-m shuttles of walking and cruising with 10-m jogs, with simulated scrummaging, rucking, or mauling exercises and standing rests. In the last minute of every 315-s cycle, a timed Performance Test was carried out, involving carrying a tackle bag and an agility sprint with a ball, followed by a 25-s recovery and a 15-m sprint.
Participants traveled 7078 m, spending 79.8 and 20.2% of time in low- and high-intensity activity, respectively. The coefficients of variation (CV) between trials 1 and 2 for mean time on the Performance Test (17.78 ± 0.71 vs 17.58 ± 0.79 s) and 15-m sprint (2.69 ± 0.15 vs 2.69 ± 0.15 s) were 1.3 and 0.9%, respectively. There was a CV of 2.2% between trials 1 and 2 for mean heart rate (160 ± 5 vs 158 ± 5 beats⋅min−1) and 14.4% for blood lactate (4.41 ± 1.22 vs 4.68 ± 1.68 mmol⋅L−1).
Results suggest that measures of rugby union-specifc high-intensity exercise performed during the BURST were reproducible over two trials in habituated participants.