To examine the effects of elk velvet antler supplementation (EVA) combined with training on resting and exercise-stimulated hormonal response, male (n = 25) and female (n = 21) rowers ingested either E VA (560 mg/d) or placebo (PL) during 10 wk of training. VO2max, 2000 m rowing time, leg and bench press strength were determined before and after 5 and 10 wk of training. Serum hormone levels were measured prior to and 5 and 60 min after a simulated 2000 m rowing race. VO2max and strength increased and 2000 m times decreased similarly (P < 0.05) with training. There was no significant difference between the EVA and PL group for any hormonal response. Testosterone (males only) and growth hormone (both genders) were higher 5 min after the simulated race (P < 0.05) but returned to baseline at 60 min. Cortisol was higher 5 and 60 min compared to rest (both genders) (P < 0.05) and was higher 60 min post-exercise following 5 and 10 wk of training. It appears that 10 wk of EVA supplementation does not significantly improve rowing performance nor alter hormonal responses at rest or after acute exercise than training alone.
Daniel G. Syrotuik, Kirsten L. MacFadyen, Vicki J. Harber and Gordon J. Bell
Alex J. Wadley, Ida S. Svendsen and Michael Gleeson
Altitude exposure can exaggerate the transient increase in markers of oxidative stress observed following acute exercise. However, these responses have not been monitored in endurance-trained cyclists at altitudes typically experienced while training. Endurance trained males (n = 12; mean (± SD) age: 28 ± 4 years, V̇O2max 63.7 ± 5.3 ml/kg/min) undertook two 75-min exercise trials at 70% relative V̇O2max; once in normoxia and once in hypobaric hypoxia, equivalent to 2000m above sea level (hypoxia). Blood samples were collected before, immediately after and 2 h postexercise to assess plasma parameters of oxidative stress (protein carbonylation (PC), thiobarbituric acid reactive substances (TBARS), total antioxidant capacity (TAC) and catalase activity (CAT)). Participants cycled at 10.5% lower power output in hypoxia vs. normoxia, with no differences in heart rate, blood lactate or rating of perceived exertion observed. PC increased and decreased immediately after exercise in hypoxia and normoxia respectively (nmol/mg/protein: Normoxia—0.3 ± 0.1, Hypoxia + 0.4 ± 0.1; both p < .05). CAT increased immediately postexercise in both trials, with the magnitude of change greater in hypoxia (nmol/min/ml: Normoxia + 12.0 ± 5.0, Hypoxia + 27.7 ± 4.8; both p < .05). CAT was elevated above baseline values at 2 h postexercise in Hypoxia only (Normoxia + 0.2 ± 2.4, Hypoxia + 18.4 ± 5.2; p < .05). No differences were observed in the changes in TBARS and TAC between hypoxia and normoxia. Trained male cyclists demonstrated a differential pattern/ timecourse of changes in markers of oxidative stress following submaximal exercise under hypoxic vs. normoxic conditions.
Romain Meeusen and Phil Watson
It is clear that the cause of fatigue is complex, infuenced by both events occurring in the periphery and the central nervous system (CNS). It has been suggested that exercise-induced changes in serotonin (5-HT), dopamine (DA), and noradrenaline (NA) concentrations contribute to the onset of fatigue during prolonged exercise. Serotonin has been linked to fatigue because of its documented role in sleep, feelings of lethargy and drowsiness, and loss of motivation, whereas increased DA and NA neurotransmission favors feelings of motivation, arousal, and reward. 5-HT has been shown to increase during acute exercise in running rats and to remain high at the point of fatigue. DA release is also elevated during exercise but appears to fall at exhaustion, a response that may be important in the fatigue process. The rates of 5-HT and DA/NA synthesis largely depend on the peripheral availability of the amino acids tryptophan (TRP) and tyrosine (TYR), with increased brain delivery increasing serotonergic and DA/NA activity, respectively. TRP, TYR, and the branched-chained amino acids (BCAAs) use the same transporter to pass through the blood-brain barrier, meaning that the plasma concentration ratio of these amino acids is thought to be a very important marker of neurotransmitter synthesis. Pharmacological manipulation of these neurotransmitter systems has provided support for an important role of the CNS in the development of fatigue. Work conducted over the last 20 y has focused on the possibility that manipulation of neurotransmitter precursors may delay the onset of fatigue. Although there is evidence that BCAA (to limit 5-HT synthesis) and TYR (to elevate brain DA/NA) ingestion can influence perceived exertion and some measures of mental performance, the results of several apparently well-controlled laboratory studies have yet to demonstrate a clear positive effect on exercise capacity or performance. There is good evidence that brain neurotransmitters can play a role in the development of fatigue during prolonged exercise, but nutritional manipulation of these systems through the provision of amino acids has proven largely unsuccessful.
Dariush Sheikholeslami-Vatani, Slahadin Ahmadi and Hassan Faraji
sensitive tools for evaluating these physiological processes ( Kangas et al., 2017 ). Various types of cellular stress stimuli have been shown to trigger apoptosis. Strenuous acute exercise directly or indirectly can induce a stress response and apoptosis in working skeletal muscles ( Podhorska-Okołów et
Blai Ferrer-Uris, Albert Busquets and Rosa Angulo-Barroso
associated with repeated bouts of acute exercise ( Griffin et al., 2011 ; Hopkins, Davis, Vantieghem, Whalen, & Bucci, 2012 ). In adults, acute exercise seems to transiently affect brain function through an increase in the concentration of certain neurochemicals, such as neurotransmitters (e
Thomas Finkenzeller, Sabine Würth, Michael Doppelmayr and Günter Amesberger
, perceptual tasks, visual search tasks, memory tasks), exercise duration, exercise intensity, and fitness level. Furthermore, Lambourne and Tomporowski ( 2010 ) obtained different effect sizes depending on when the cognitive assessment was taken during acute exercise, indicating a decline in the initial 20
Keishi Soga, Keita Kamijo and Hiroaki Masaki
studies have explored the effects of a single bout of acute exercise on memory functions. These studies have consistently indicated that retrieval performance improved when learning or when the encoding phase was performed after acute aerobic exercise ( Etnier, Labban, Piepmeier, Davis, & Henning, 2014
Carolina Menezes Fiorelli, Emmanuel Gomes Ciolac, Lucas Simieli, Fabiana Araújo Silva, Bianca Fernandes, Gustavo Christofoletti and Fabio Augusto Barbieri
regulation of exercise-induced cognitive responses. However, the previous studies have analyzed the effects of acute exercise in neurologically healthy individuals. Therefore, an important lack in literature is about the effects of acute aerobic exercise in cognition impairments in PD. Therefore, 2 questions
Austin T. Robinson, Adriana Mazzuco, Ahmad S. Sabbahi, Audrey Borghi-Silva and Shane A. Phillips
.4 Note . Data presented as mean ± SD . There was no significant main effect for supplementation or acute exercise or an interaction effect for these measures. SBP = systolic blood pressure; DBP = diastolic blood pressure; MAP = mean arterial pressure; AUX = augmentation index; AUX75 = a normalization
Ilkka Heinonen, Jukka Kemppainen, Toshihiko Fujimoto, Juhani Knuuti and Kari K. Kalliokoski
-Czernik, 2012 ). Human bone marrow circulation responds to acute exercise ( Heinonen et al., 2013a , 2013b ) and local heat stress ( Heinonen et al., 2011a ), although to a lesser degree than in contracting skeletal muscles ( Heinonen et al., 2007 , 2010a , 2011b , 2015 ). In addition to its perfusion, the