Exhaustive Endurance Exercise Research Articles

Exercise-induced cardiac troponin release in athletes with versus without coronary atherosclerosis.

The magnitude of exercise-induced cardiac troponin (cTn) elevations is dependent on cardiovascular health status, and previous studies have shown that occult coronary atherosclerosis is highly prevalent among amateur athletes. We tested the hypothesis that middle-aged and older athletes with coronary atherosclerosis demonstrate greater cTn elevations following a controlled endurance exercise test compared with healthy peers. We included 59 male athletes from the Measuring Athletes' Risk of Cardiovascular events 2 (MARC-2) study and stratified them as controls [coronary artery calcium score (CACS) = 0, n = 20], high CACS [≥300 Agatston units or ≥75th Multi-Ethnic Study of Atherosclerosis (MESA) percentile, n = 20] or significant stenosis (≥50% in any coronary artery, n = 19). Participants performed a cycling test with incremental workload until volitional exhaustion. Serial high-sensitivity cTn (hs-cTn) T and I concentrations were measured (baseline, after 30-min warm-up, and 0, 30, 60, 120, and 180 min postexercise). There were 58 participants (61 [58-69] yr) who completed the exercise test (76 ± 14 min) with a peak heart rate of 97.7 [94.8-101.8]% of their estimated maximum. Exercise duration and workload did not differ across groups. High-sensitivity cardiac troponin T (Hs-cTnT) and high-sensitivity cardiac troponin I (hs-cTnI) concentrations significantly increased (1.55 [1.33-2.14]-fold and 2.76 [1.89-3.86]-fold, respectively) over time, but patterns of cTn changes and the incidence of concentrations >99th percentile did not differ across groups. Serial sampling of hs-cTnT and hs-cTnI concentrations during and following an exhaustive endurance exercise test did not reveal differences in exercise-induced cTn release between athletes with versus without coronary atherosclerosis. These findings suggest that a high CACS or a >50% stenosis in any coronary artery does not aggravate exercise-induced cTn release in middle-aged and older athletes.NEW & NOTEWORTHY Exercise-induced cardiac troponin (cTn) release is considered to be dependent on cardiovascular health status. We tested whether athletes with coronary atherosclerosis demonstrate greater exercise-induced cTn release compared with healthy peers. Athletes with coronary atherosclerosis did not differ in cTn release following exercise compared with healthy peers. Our findings suggest that a high CACS or a >50% stenosis in any coronary artery does not aggravate exercise-induced cTn release in middle-aged and older athletes.

The Effect of Submaximal Exercise on Cutaneous Blood Flow, Thermoregulation and Recovery Hemodynamics Following Endurance Exercise

Aim. There are numerous reports of attenuation of cutaneous blood flow (CBF) during the recovery period after a single bout of exercise, but no one has investigated the CBF response to consecutive short-lasting aerobic exercise (SLAE) sessions following exhaustive endurance exercise (EEE) on daily basis, although this is a commonly used training regime in recreational athletes and could cause a cumulative increase in CBF that may be important for wound healing. This study examined the effects of EEE on forearm skin blood flow (LDF), cutaneous vascular conductance (CVC), and mean arterial pressure (MAP) in response to SLAE sessions performed for 7 days after EEE, as well as the correlation between cutaneous blood flow and indices associated with heart rate (HR) to examine the role of thermoregulation in post-exercise HR regulation. Methods. In 19 recreational runners, LDF, MAP, HR, heart rate recovery (HRR), and HR variability indices (lnRMSSD, lnHF, and lnLF/ HF) were measured after SLAE in the form of submaximal graded cycling performed on consecutive days after EEE in the form of a half marathon and compared with baseline values before EEE. A significant time effect was observed for all measured parameters throughout the study period. Results. Postexercise LDF increased 24 hours after EEE compared with baseline (77.814 AU compared with 54.712 AU). Postexercise hypotension was significantly more pronounced immediately after EEE compared with baseline (88.95.3 mmHg compared with 99.33.2 mmHg). However, postexercise CVC showed a progressive increase compared with baseline both immediately and 24 hours after EEE (0.53 0.07 AU/mmHg, 0.66 0.09 AU/mmHg compared with 0.4 0.09 AU/mmHg). A small negative correlation between LDF and HRR was observed throughout the experimental protocol. Conclusion. These results suggest that EEE strongly influences cutaneous and systemic hemodynamics and cardiac autonomic response during recovery after SLAE. Our most important finding was that EEE improved cutaneous perfusion 24 hours after completion of EEE, which may be important for wound healing. The results of our study are potentially applicable for patients with chronic wounds who should be encouraged to exercise moderately on daily basis and to include endurance exercises occasionally, as this strategy potentiates postexercise cutaneous perfusion.

Effects of Two-Week Betaine Supplementation on Apoptosis, Oxidative Stress, and Aerobic Capacity after Exhaustive Endurance Exercise.

This study evaluated the effects of 2 weeks of betaine supplementation on apoptosis, oxidative stress, and aerobic capacity after exhaustive endurance exercise (EEE). A double-blind, crossover, and counterbalanced design was adopted, with 10 healthy male participants asked to consume betaine (1.25 g of betaine mixed with 300 mL of sports beverage, twice per day for 2 weeks) or placebo (300 mL of sports beverage). All participants performed a graded exercise test on a treadmill to determine the maximal oxygen consumption (VO2max) before supplementation and then performed the EEE test at an intensity of 80% VO2max after 2 weeks of supplementation. The time to exhaustion, peak oxygen consumption, maximal heart rate, and average heart rate were recorded during the EEE test. Venous blood samples were drawn before, immediately after, and 3 h after the EEE test to assess apoptosis and the mitochondrial transmembrane potential (MTP) decline of lymphocytes as well as the concentrations of thiobarbituric acid reactive substance and protein carbonyl. The results indicated that lymphocyte apoptosis was significantly higher immediately after and 3 h after EEE than before exercise in participants in the placebo trial. However, lymphocyte apoptosis exhibited no significant differences among the three time points in participants in the betaine trial. Moreover, apoptosis in the betaine trial was significantly lower immediately after and 3 h after exercise compared with the placebo trial. No differences were noted for other variables. Thus, 2 weeks of betaine supplementation can effectively attenuate lymphocyte apoptosis, which is elevated by EEE. However, betaine supplementation exhibited no effects on MTP decline, oxidative stress, or aerobic capacity.

Testosterone Responses to Intensive, Prolonged Endurance Exercise in Women.

Objective:To examine the response of testosterone in women to an intensive, prolonged endurance exercise bout that mimicked a competitive event.Methods:Ten healthy eumenorrheic women ran to exhaustion at ~100% of their ventilatory threshold in their follicular menstrual cycle phase. Testosterone measures were assessed pre-exercise, immediately, 30 min, 60 min, 90 min, and 24 h post-exercise.Results:At exhaustion (75.1 ± 7.0 min), total (56%), free (36%), and bioavailable testosterone (50%) were increased from pre-exercise values (p< 0.05). At 24 h post-exercise, these measures were decreased from pre-exercise values (−21%, −31%, −18%, respectively; p < 0.05). Effect sizes for these changes ranged from medium to large in magnitude.Conclusion:Testosterone was elevated in the early recovery period following exhaustive endurance exercise but was reduced by 24 h afterward. These outcomes are comparable to responses seen in men when sex-based concentration differences are considered.

Effects Of Carbohydrate-Electrolyte Solution Supplementation On Fluid Retention And Aerobic Capacity After Exhaustive Exercise

Rehydration, or restoration of fluid spaces, is important when exhaustive endurance exercise (EEE) has compromised hydration status. Previous studies only investigated the effects of carbohydrate-electrolyte solution (CE) supplementation to facilitate replacement after exercise induced dehydration. CE supplementation for 1 hour before and 1 hour after EEE may play an important role in fluid retention and enhancing aerobic capacity. PURPOSE: To examine the effects of CE supplementation on fluid retention and aerobic capacity after EEE. METHODS: In a double-blind, crossover and counterbalanced designed study, nineteen health male participants were asked to intake ORS-SH@, an oral rehydration solution, (150 mL four times within an hour) or placebo (water) for 1 hour before and 1 hour after EEE. All participants completed graded exercise test to exhaustion on treadmill for determination of maximal oxygen consumption (VO2max) before supplementation, and then completed the exhaustive endurance exercise test at the intensity of 70% VO2max for 60 min. Then, the exercise intensity increased at 90% VO2max until exhaustion after supplementation. The average heart rate, maximal heart rate, running time to exhaustion and peak oxygen uptake were recorded during the exercise period. The body weight was recorded 15-min, 30-min, 45-min and 60-min of after EEE to calculate the dehydration rate and beverage hydration index (BHI). RESULTS: The dehydration rates in participants with ORS-SH@ treatment at 15-min, 30-min and 45-min of after EEE were significantly lower than with placebo treatment (-1.77±0.50% vs. -2.06±0.66%; -1.69±0.54% vs. -1.95±0.66%; -1.48±0.51% vs. -1.76±0.65%, respectively, p < .05). In addition, the BHI in participants with ORS-SH@ treatment at 15-min, 30-min and 45-min of after EEE (1.19±0.36, 1.22±0.43 and 1.27±0.54) were significantly higher than with placebo treatment (p < .05). However, there were no significant differences in other variables between treatments. CONCLUSIONS: ORS-SH@ supplementation can effectively enhance fluid retention after EEE. However, ORS-SH@ supplementation had no benefits on aerobic capacity. Supported by Panion & BF Biotech Inc. (Grant No: A-107-077)

Low-Osmolality Carbohydrate-Electrolyte Solution Ingestion Avoid Fluid Loss and Oxidative Stress After Exhaustive Endurance Exercise.

Low-osmolality carbohydrate–electrolyte solution (LCS) ingestion can replace losses from exercise-induced dehydration, but the benefits of LCS ingestion strategy after exhaustive endurance exercise (EEE) remain unknown. The present study evaluated the effects of LCS ingestion on dehydration, oxidative stress, renal function, and aerobic capacity after EEE. In our study with its double-blind, crossover, counterbalanced design, 12 healthy male participants were asked to consume LCS (150 mL four times per hour) or placebo (water) 1 h before and 1 h after EEE. All participants completed a graded exercise test to exhaustion on a treadmill for the determination of maximal oxygen consumption (), applied to further intensity calibration, and then completed the EEE test. The average heart rate, maximal heart rate, running time to exhaustion, and peak oxygen uptake (VO2peak) were recorded during the exercise period. The participants’ body weight was recorded at different time points before and after the EEE to calculate the dehydration rate. Blood samples were drawn at baseline and before, immediately after, 1 h after, and 2 h after EEE to determine indicators of oxidative stress and renal function. The results indicated that the dehydration rates in participants with LCS ingestion at 15 min, 30 min, and 45 min after EEE were significantly lower than in participants with placebo ingestion (−1.86 ± 0.47% vs. −2.24 ± 0.72%; −1.78 ± 0.50% vs. −2.13 ± 0.74%; −1.54 ± 0.51% vs. −1.94 ± 0.72%, respectively; p < 0.05). In addition, the concentration of catalase in participants with LCS ingestion immediately after EEE was significantly higher than in participants with placebo ingestion (2046.21 ± 381.98 nmol/min/mL vs. 1820.37 ± 417.35 nmol/min/mL; p < 0.05). Moreover, the concentration of protein carbonyl in participants with LCS ingestion immediately after EEE was slightly lower than in participants with placebo ingestion (2.72 ± 0.31 nmol carbonyl/mg protein vs. 2.89 ± 0.43 nmol carbonyl/mg protein; p = 0.06). No differences were noted for other variables. Our findings conclude that LCS ingestion can effectively avoid fluid loss and oxidative stress after EEE. However, LCS ingestion had no benefits for renal function or aerobic capacity.

Protein intake in the early recovery period after exhaustive exercise improves performance the following day.

The aim of the present study was to investigate the effect of protein and carbohydrate ingestion during early recovery from exhaustive exercise on performance after 18-h recovery. Eight elite cyclists (V̇o2max: 74.0 ± 1.6 ml·kg-1·min-1) completed two exercise and diet interventions in a double-blinded, randomized, crossover design. Participants cycled first at 73% of V̇o2max (W73%) followed by 1-min intervals at 90% of V̇o2max until exhaustion. During the first 2 h of recovery, participants ingested either 1.2 g carbohydrate·kg-1·h-1 (CHO) or 0.8 g carbohydrate + 0.4 g protein·kg-1·h-1 (CHO + PROT). The diet during the remaining recovery period was similar for both interventions and adjusted to body weight. After an 18-h recovery, cycling performance was assessed with a 10-s sprint test, 30 min of cycling at W73%, and a cycling time trial (TT). The TT was 8.5% faster (41:53 ± 1:51 vs. 45:26 ± 1:32 min; P < 0.03) after CHO + PROT compared with CHO. Mean power output during the sprints was 3.7% higher in CHO + PROT compared with CHO (1,063 ± 54 vs. 1,026 ± 53 W; P = 0.01). Nitrogen balance in the recovery period was negative in CHO and neutral in CHO + PROT (-82.4 ± 11.5 vs. 7.0 ± 15.4 mg/kg; P < 0.01). In conclusion, TT and sprint performances were improved 18 h after exhaustive cycling by CHO + PROT supplementation during the first 2 h of recovery compared with isoenergetic CHO supplementation. Our results indicate that intake of carbohydrate plus protein after exhaustive endurance exercise more rapidly converts the body from a catabolic to an anabolic state than carbohydrate alone, thus speeding recovery and improving subsequent cycling performance.NEW & NOTEWORTHY Prolonged high intensity endurance exercise depends on glycogen utilization and high oxidative capacity. Still, exhaustion develops and effective recovery strategies are required to compete in multiday stage races. We show that coingestion of protein and carbohydrate during the first 2 h of recovery is superior to isoenergetic intake of carbohydrate to stimulate recovery, and improves both endurance time-trial and 10-s sprint performance the following day in elite cyclists.

Circulating Small Non-coding RNAs as Biomarkers for Recovery After Exhaustive or Repetitive Exercise

Circulating microRNAs have proven to be reliable biomarkers, due to their high stability, both in vivo in the circulation, and ex vivo during sample preparation and storage. Small nucleolar RNAs (snoRNAs) are a different type of small non-coding RNAs that can also be reliably measured in plasma, but have only been studied sporadically. In this study, we aimed to identify RNA-biomarkers that can distinguish between different exercise regimes and that entail clues about muscle repair and recovery after prolonged exhaustive endurance exercise. We compared plasma microRNA profiles between two cohorts of elite cyclists, subjected to two different types of exercise regimes, as well as a cohort of patients with peripheral artery disease (PAD) that were scheduled to undergo lower limb amputation, due to critical limb ischemia. In elite athletes, muscle tissue recovers quickly even after exhaustive exercise, whereas in PAD patients, recovery is completely impaired. Furthermore, we measured levels of a specific group of snoRNAs in the plasma of both elite cyclists and PAD patients. Using a multiplex qPCR screening, we detected a total of 179 microRNAs overall, of which, on average, 161 microRNAs were detected per sample. However, only 30 microRNAs were consistently expressed in all samples. Of these, two microRNAs, miR-29a-3p and miR193a-5p, that responded differently two different types of exercise, namely exhaustive exercise and non-exhaustive endurance exercise. Using individual rt/qPCR, we also identified a snoRNA, SNORD114.1, which was significantly upregulated in plasma in response to endurance exercise. Furthermore, two microRNAs, miR-29a-3p and miR-495-3p, were significantly differentially expressed in athletes compared to PAD patients, but only following exercise. We suggest that these two microRNAs could function as markers of impaired muscle repair and recovery. In conclusion, microRNAs miR-29a-3p and miR-193a-5p may help us distinguish between repeated exhaustive and non-exhaustive endurance exercise. MicroRNA miR-29a-3p, as well as miR-495-3p, may further mark impaired muscle recovery in patients with severe critical limb ischemia. Furthermore, we showed for the first time that a circulating snoRNA, SNORD114.1, is regulated in response to exercise and may be used as biomarker.

Post‐exercise recovery of contractile function and endurance in humans and mice is accelerated by heating and slowed by cooling skeletal muscle

We investigated whether intramuscular temperature affects the acute recovery of exercise performance following fatigue-induced by endurance exercise. Mean power output was better preserved during an all-out arm-cycling exercise following a 2h recovery period in which the upper arms were warmed to an intramuscular temperature of ̴ 38°C than when they were cooled to as low as 15°C, which suggested that recovery of exercise performance in humans is dependent on muscle temperature. Mechanisms underlying the temperature-dependent effect on recovery were studied in intact single mouse muscle fibres where we found that recovery of submaximal force and restoration of fatigue resistance was worsened by cooling (16-26°C) and improved by heating (36°C). Isolated whole mouse muscle experiments confirmed that cooling impaired muscle glycogen resynthesis. We conclude that skeletal muscle recovery from fatigue-induced by endurance exercise is impaired by cooling and improved by heating, due to changes in glycogen resynthesis rate. Manipulation of muscle temperature is believed to improve post-exercise recovery, with cooling being especially popular among athletes. However, it is unclear whether such temperature manipulations actually have positive effects. Accordingly, we studied the effect of muscle temperature on the acute recovery of force and fatigue resistance after endurance exercise. One hour of moderate-intensity arm cycling exercise in humans was followed by 2h recovery in which the upper arms were either heated to 38°C, not treated (33°C), or cooled to ∼15°C. Fatigue resistance after the recovery period was assessed by performing 3×5min sessions of all-out arm cycling at physiological temperature for all conditions (i.e. not heated or cooled). Power output during the all-out exercise was better maintained when muscles were heated during recovery, whereas cooling had the opposite effect. Mechanisms underlying the temperature-dependent effect on recovery were tested in mouse intact single muscle fibres, which were exposed to ∼12min of glycogen-depleting fatiguing stimulation (350ms tetani given at 10s interval until force decreased to 30% of the starting force). Fibres were subsequently exposed to the same fatiguing stimulation protocol after 1-2h of recovery at 16-36°C. Recovery of submaximal force (30Hz), the tetanic myoplasmic free [Ca2+ ] (measured with the fluorescent indicator indo-1), and fatigue resistance were all impaired by cooling (16-26°C) and improved by heating (36°C). In addition, glycogen resynthesis was faster at 36°C than 26°C in whole flexor digitorum brevis muscles. We conclude that recovery from exhaustive endurance exercise is accelerated by raising and slowed by lowering muscle temperature.

Acute exhaustive aerobic exercise training impair cardiomyocyte function and calcium handling in Sprague-Dawley rats.

IntroductionRecent data from long-distance endurance participants suggest that cardiac function is impaired after completion. Existing data further indicate that right ventricular function is more affected than left ventricular function. The cellular mechanisms underpinning cardiac deterioration are limited and therefore the aim of this study was to examine cardiomyocyte and molecular responses of the right and left ventricle to an acute bout of exhaustive endurance exercise.Materials and methodsMale Sprague-Dawley rats were assigned to sedentary controls or acute exhaustive endurance exercise consisting of a 120 minutes long forced treadmill run. The contractile function and Ca2+ handling properties in isolated cardiomyocytes, protein expression levels of sarcoplasmic reticulum Ca2+-ATPase and phospholamban including two of its phosphorylated states (serine 16 and threonine 17), and the mitochondrial respiration in permeabilized cardiac muscle fibers were analyzed.ResultsThe exercise group showed a significant reduction in cardiomyocyte fractional shortening (right ventricle 1 Hz and 3 Hz p<0.001; left ventricle 1 Hz p<0.05), intracellular Ca2+ amplitude (right ventricle 1 and 3 Hz p<0.001; left ventricle 1 Hz p<0.01 and 3 Hz p<0.05) and rate of diastolic Ca2+ decay (right ventricle 1 Hz p<0.001 and 3 Hz p<0.01; left ventricle 1 and 3 Hz p<0.01). Cardiomyocyte relaxation during diastole was only significantly prolonged at 3 Hz in the right ventricle (p<0.05) compared to sedentary controls. We found an increase in phosphorylation of phospholamban at serine 16 and threonine 17 in the left (p<0.05), but not the right, ventricle from exhaustively exercised animals. The protein expression levels of sarcoplasmic reticulum Ca2+-ATPase and phospholamban was not changed. Furthermore, we found a reduction in maximal oxidative phosphorylation and electron transport system capacities of mitochondrial respiration in the right (p<0.01 and p<0.05, respectively), but not the left ventricle from rats subjected to acute exhaustive treadmill exercise.ConclusionAcute exhaustive treadmill exercise is associated with impairment of cardiomyocyte Ca2+ handling and mitochondrial respiration that causes depression in both contraction and diastolic relaxation of cardiomyocytes.

Increases in Brain 1H-MR Glutamine and Glutamate Signals Following Acute Exhaustive Endurance Exercise in the Rat.

Objective: Proton magnetic resonance spectroscopy (1H-MRS) in ultra-high magnetic field can be used for non-invasive quantitative assessment of brain glutamate (Glu) and glutamine (Gln) in vivo. Glu, the main excitatory neurotransmitter in the central nervous system, is efficiently recycled between synapses and presynaptic terminals through Glu-Gln cycle which involves glutamine synthase confined to astrocytes, and uses 60–80% of energy in the resting human and rat brain. During voluntary or involuntary exercise many brain areas are significantly activated, which certainly intensifies Glu-Gln cycle. However, studies on the effects of exercise on 1H-MRS Glu and/or Gln signals from the brain provided divergent results. The present study on rats was performed to determine changes in 1H-MRS signals from three brain regions engaged in motor activity consequential to forced acute exercise to exhaustion.Method: After habituation to treadmill running, rats were subjected to acute treadmill exercise continued to exhaustion. Each animal participating in the study was subject to two identical imaging sessions performed under light isoflurane anesthesia, prior to, and following the exercise bout. In control experiments, two imaging sessions separated by the period of rest instead of exercise were performed. 1H-NMR spectra were recorded from the cerebellum, striatum, and hippocampus using a 7T small animal MR scanner.Results: Following exhaustive exercise statistically significant increases in the Gln and Glx signals were found in all three locations, whereas increases in the Glu signal were found in the cerebellum and hippocampus. In control experiments, no changes in 1H-MRS signals were found.Conclusion: Increase in glutamine signals from the brain areas engaged in motor activity may reflect a disequilibrium caused by increased turnover in the glutamate-glutamine cycle and a delay in the return of glutamine from astrocytes to neurons. Increased turnover of Glu-Gln cycle may be a result of functional activation caused by forced endurance exercise; the increased rate of ammonia detoxification may also contribute. Increases in glutamate in the cerebellum and hippocampus are suggestive of an anaplerotic increase in glutamate synthesis due to exercise-related stimulation of brain glucose uptake. The disequilibrium in the glutamate-glutamine cycle in brain areas activated during exercise may be a significant contributor to the central fatigue phenomenon.

Cortisol and testosterone dynamics following exhaustive endurance exercise.

Cortisol (C) and testosterone (T) are impacted significantly by prolonged endurance exercise with inverse responses. Increases in C are witnessed concurrently with decrements in T, possibly impacting recovery. This study was conducted to assess the dynamics of C and free T (fT) concentration and recovery time following an exhaustive endurance exercise session (EES). 12 endurance-trained males (X±SD: VO2max 66.3±4.8ml/kg/min, age 22.8±3.1years, body fat 11.0±1.4%, training 7.1±3.2years) completed a treadmill EES at ventilatory threshold (74.7±4.6% of VO2max; 96.9±10.8min). Basal blood C and fT were collected at baseline: -48, -24h, and immediately before (0h) the EES as well as immediately (+0h), +24h, +48h, and +72h after the EES. Blood glucose (G) was measured to confirm no undue influence on C. Statistically data were analyzed with repeated measures ANOVA (LSD post hoc). C (nmol/L) increased significantly from -48h (321±59) to +0h (701±178) (p<0.001), and displayed a baseline overshoot with +24h (209±67) being significantly lower than -48 and +0h (p<0.03). fT (pmol/L) decreased significantly from -48h (161±40) to +0h (106±38) (p<0.01) and remained lower at +24h (110±33) and +48h (129±30) (p<0.001). G remained stable throughout. A moderately negative correlation (r=-0.636, p<0.026) was found between C and fT at +0h. EES recovery may require 48h for C and 72h for fT to return to baseline values. Furthermore, C and fT were only correlated immediately post-exercise. Future research should perform more frequent measurements throughout time course.

Cortisol and testosterone dynamics following exhaustive endurance exercise

Cortisol and testosterone dynamics following exhaustive endurance exercise

Pain thresholds following maximal endurance exercise.

Physical exercise causes alterations in pain sensitivity. Many studies verified so-called exercise-induced analgesia caused by submaximal aerobic intensity. This study aimed to determine the effect of an endurance exercise to exhaustion on pain sensitivity of healthy young men. Pressure pain thresholds (PPTs) [in Newton, (N)] of 50 healthy males (mean age 26 ± 4 years) were applied to knee, ankle and elbow joints as well as to the sternum and forehead. This was followed by a bout of cycling ergometer exercise to exhaustion. The whole process was repeated after 20 and 60 min respectively. Endurance exercise to exhaustion decreased PPTs at sternum and forehead significantly, while thresholds at the joints were not affected. Pain thresholds at forehead and sternum declined 20 min after exercise with the forehead's threshold being more reduced. PPTs remain decreased until 60 min after exercise (forehead: from 43.6 ± 15.2 N to 36.6 ± 19.8 N to 37.2 ± 13.4 N; sternum: from 46.8 ± 21.0 N to 42.5 ± 17.1 N to 44.8 ± 18.2 N). Modulation of pain sensitivity showed large effect sizes over time for both landmarks (forehead w = 0.65; sternum w = 0.50). Exhaustive endurance exercise is followed by a hyperalgetic condition at forehead and sternum. This may be due to either a reduction in pain inhibiting or an activation in pain stimulating pathways.

Relationship Between Cortisol and Free Testosterone in Response to Exhaustive Endurance Exercise

Research has shown intensive exercise to induce significant changes in cortisol (C) and testosterone (T). Typically, increases in C are witnessed concurrently to decreases in T. To determine whether there was the existence of a relationship between the changes observed in these two hormones, we measured the change scores (Δ) for 12 healthy, endurance trained males (X±SD: age 22.8±3.1y; VO2max 66.3±4.8 mL/kg/min) in response to an exhaustive exercise session (EES) (96.9±10.8 min at 74.7±4.6% of VO2max). The change scores were determined for basal levels of C and free T from pre to post EES (Δ0), post to +24h (Δ24), +48h (Δ48) and +72h (Δ72) into recovery. All basal hormonal levels were within acceptable clinical ranges for these subjects. The EES induced highly significant C increases (pre: 326.5±29.3nmol/L, post: 700.8±177.7nmol/L; p&lt;0.001) and free T decreases (pre: 162.3±23.6pmol/L, post: 106.1±38.6 pmol/L; p&lt;0.001) at Δ0. A significant negative correlation existed between C (Δ 374.3 nmol/L) and free T (Δ ‐56.2 pmol/L) at Δ0 (p=0.028, rs = ‐0.629; Spearman rho). No additional significant changes were detected into recovery. Cumming et al (J Clin Endocrinol Metab. 57:671, 1983) illustrated the phenomenon of C induced T reduction via pharmaceutical intervention. This study indicates a single bout of EES will induce similar effects endogenously, i.e., with elevated levels of C being associated with suppressed free T, perhaps through mechanisms directly associated with T production inhibition.

Current limitations and future perspectives of the Athlete Blood Passport

We read with interest the recent article of Ashenden et al. (2011) and, frankly, we are not really surprised about their findings, i.e., that the Athlete Blood Passport (ABP) software did not ‘‘flag’’ subjects who were receiving microdoses of recombinant human erythropoietin (rHuEPO). Despite its well-known analytical shortcomings, there is broad agreement that the ABP is currently a useful approach for safeguarding an athlete’s health in the presence of abnormal laboratory data (Zorzoli 2011). Nevertheless, for those who are familiar with sports and laboratory hematology, it would seem that the ABP has been mainly developed to detect substantial and acute variations in hematological parameters consistent with blood ‘‘boosting’’, and is therefore perhaps less effective at identifying mild or less pronounced abnormalities (Lippi and Plebani 2011). Several limitations have been noted with the ABP, which should be taken into consideration when interpreting test results. These include biological, pre-analytical (Lippi et al. 2010) and analytical variability (Banfi et al. 2011), as well as categorization according to different metabolic energy demands, hypoxia treatments during exercise, use of masking agents (Banfi 2011; Sanchis-Gomar et al. 2011), and now microdoses of rHuEpo. It is also conceivable that repeated ‘‘microtransfusions’’, as well as the combined use of minimal doses of rHuEpo in combination with ischemia modulators such as cobalt chloride, could produce substantial hematological improvements and performance benefits (Lippi et al. 2006), while remaining undetectable by current antidoping algorithms. Additional caveats include the lack of standardization and diagnostic thresholds for detecting doping which should be more clearly assessed to limit ambiguity (Banfi 2011; Sanchis-Gomar et al. 2011). The influence of factors such as exhaustive endurance exercise on vascular volumes should be considered to avoid misinterpretation of ABP software results (Sanchis-Gomar et al. 2011), especially because diurnal and exercise-related variations of hemoglobin levels have been reported due to plasma volume expansion following regular endurance exercise (Schumacher et al. 2010). Interestingly, Schumacher and Pottgiesser (2011) have recently shown that fluid loss associated with gastroenteritis, a condition not uncommon in athletes, is unlikely to cause blood data to reach levels of abnormality that would be consistent with blood doping. The results of this study are valuable, but additional investigations should be undertaken to clarify, for example, whether some common forms of bleeding (e.g., Communicated by Susan A. Ward.

Effects of Polyphenol-rich Diet on the Antioxidative and Physical Capacity After Exhaustive Endurance Exercise

Effects of Polyphenol-rich Diet on the Antioxidative and Physical Capacity After Exhaustive Endurance Exercise

Examination of the efficacy of acute L-alanyl-L-glutamine ingestion during hydration stress in endurance exercise

BackgroundThe effect of acute L-alanyl-L-glutamine (AG; Sustamine™) ingestion on performance changes and markers of fluid regulation, immune, inflammatory, oxidative stress, and recovery was examined in response to exhaustive endurance exercise, during and in the absence of dehydration.MethodsTen physically active males (20.8 ± 0.6 y; 176.8 ± 7.2 cm; 77.4 ± 10.5 kg; 12.3 ± 4.6% body fat) volunteered to participate in this study. During the first visit (T1) subjects reported to the laboratory in a euhydrated state to provide a baseline (BL) blood draw and perform a maximal exercise test. In the four subsequent randomly ordered trials, subjects dehydrated to -2.5% of their baseline body mass. For T2, subjects achieved their goal weight and were not rehydrated. During T3 - T5, subjects reached their goal weight and then rehydrated to 1.5% of their baseline body mass by drinking either water (T3) or two different doses (T4 and T5) of the AG supplement (0.05 g·kg-1 and 0.2 g·kg-1, respectively). Subjects then exercised at a workload that elicited 75% of their VO2 max on a cycle ergometer. During T2 - T5 blood draws occurred once goal body mass was achieved (DHY), immediately prior to the exercise stress (RHY), and immediately following the exercise protocol (IP). Resting 24 hour (24P) blood samples were also obtained. Blood samples were analyzed for glutamine, potassium, sodium, aldosterone, arginine vasopressin (AVP), C-reactive protein (CRP), interleukin-6 (IL-6), malondialdehyde (MDA), testosterone, cortisol, ACTH, growth hormone and creatine kinase. Statistical evaluation of performance, hormonal and biochemical changes was accomplished using a repeated measures analysis of variance.ResultsGlutamine concentrations for T5 were significantly higher at RHY and IP than T2 - T4. When examining performance changes (difference between T2 - T5 and T1), significantly greater times to exhaustion occurred during T4 (130.2 ± 340.2 sec) and T5 (157.4 ± 263.1 sec) compared to T2 (455.6 ± 245.0 sec). Plasma sodium concentrations were greater (p < 0.05) at RHY and IP for T2 than all other trials. Aldosterone concentrations at RHY and IP were significantly lower than that at BL and DHY. AVP was significantly elevated at DHY, RHY and IP compared to BL measures. No significant differences were observed between trials in CRP, IL-6, MDA, or in any of the other hormonal or biochemical measures.ConclusionResults demonstrate that AG supplementation provided a significant ergogenic benefit by increasing time to exhaustion during a mild hydration stress. This ergogenic effect was likely mediated by an enhanced fluid and electrolyte uptake.

β-Alanine Improves Sprint Performance in Endurance Cycling

Recent research has shown that chronic dietary beta-alanine (betaALA) supplementation increases muscle carnosine content, which is associated with better performance in short (1-2 min) maximal exercise. Success in endurance competitions often depends on a final sprint. However, whether betaALA can be ergogenic in sprint performance at the end of an endurance competition is at present unknown. Therefore, we investigated the effect of 8-wk betaALA administration in moderately to well-trained cyclists on sprint performance at the end of a simulated endurance cycling race. A double-blind study was performed, which consisted of two experimental test sessions interspersed by an 8-wk betaALA (2-4 g.d; n = 9) or matched placebo (PL; n = 8) supplementation period. In the pretesting and the posttesting, subjects performed a 10-min time trial and a 30-s isokinetic sprint (100 rpm) after a 110-min simulated cycling race. Capillary blood samples were collected for determination of blood lactate concentration and pH. Mean power output during the time trial was approximately 300 W and was similar between PL and betaALA during either the pretesting or the posttesting. However, compared with PL, during the final sprint after the time trial, betaALA on average increased peak power output by 11.4% (95% confidence interval = +7.8 to +14.9%, P = 0.0001), whereas mean power output increased by 5.0% (95% confidence interval = +2.0 to +8.1%, P = 0.005). Blood lactate and pH values were similar between groups at any time. Oral betaALA supplementation can significantly enhance sprint performance at the end of an exhaustive endurance exercise bout.

EFFECT OF ENDURANCE TRAINING ON HYPOTHALAMIC SEROTONIN CONCENTRATION AND PERFORMANCE

1. Serotonin is a neurotransmitter that modulates several functions, such as food intake, energy expenditure, motor activity, mood and sleep. Acute exhaustive endurance exercise increases the synthesis, concentration and metabolism of serotonin in the brain. This phenomenon could be responsible for central fatigue after prolonged and exhaustive exercise. However, the effect of chronic exhaustive training on serotonin is not known. The present study was conducted to examine the effect of exhaustive endurance training on performance and serotonin concentrations in the hypothalamus of trained rats. 2. Rats were divided into three groups: sedentary rats (SED), moderately trained rats (MOD) and exhaustively trained rats (EXT), with an increase of 200% in the load carried during the final week of training. 3. Hypothalamic serotonin concentrations were similar between the SED and MOD groups, but were higher in the EXT group (P < 0.05). Performance was lower in the EXT group compared with the MOD group (P < 0.05). 4. Thus, the present study demonstrates that exhaustive training increases serotonin concentrations in the hypothalamus, together with decreased endurance performance after inadequate recovery time. However, the mechanism underlying these changes remains unknown.