scholarly journals Sprint training reduces urinary purine loss following intense exercise in humans

2006 ◽  
Vol 31 (6) ◽  
pp. 702-708 ◽  
Author(s):  
Christos G. Stathis ◽  
Michael F. Carey ◽  
Alan Hayes ◽  
Andrew P. Garnham ◽  
Rodney J. Snow

The influence of sprint training on endogenous urinary purine loss was examined in 7 active male subjects (age, 23.1 ± 1.8 y; body mass, 76.1 ± 3.1 kg; VO2 peak, 56.3 ± 4.0 mL·kg–1·min–1). Each subject performed a 30 s sprint performance test (PT), before and after 7 d of sprint training. Training consisted of 15 sprints, each lasting 10 s, on an air-braked cycle ergometer performed twice each day. A rest period of 50 s separated each sprint during training. Sprint training resulted in a 20% higher muscle ATP immediately after PT, a lower IMP (57% and 89%, immediately after and 10 min after PT, respectively), and inosine accumulation (53% and 56%, immediately after and 10 min after the PT, respectively). Sprint training also attenuated the exercise-induced increases in plasma inosine, hypoxanthine (Hx), and uric acid during the first 120 min of recovery and reduced the total urinary excretion of purines (inosine + Hx + uric acid) in the 24 h recovery period following intense exercise. These results show that intermittent sprint training reduces the total urinary purine excretion after a 30 s sprint bout.


1991 ◽  
Vol 71 (4) ◽  
pp. 1289-1295 ◽  
Author(s):  
I. B. Mekjavic ◽  
C. J. Sundberg ◽  
D. Linnarsson

An experimental protocol was designed to investigate whether human core temperature is regulated at a “set point” or whether there is a neutral zone between the core thresholds for shivering thermogenesis and sweating. Nine male subjects exercised on an underwater cycle ergometer at a work rate equivalent to 50% of their maximum work rate. Throughout an initial 2-min rest period, the 20-min exercise protocol, and the 100-min recovery period, subjects remained immersed to the chin in water maintained at 28 degrees C. On completion of the exercise, the rate of forehead sweating (Esw) decayed from a mean peak value of 7.7 +/- 4.2 (SD) to 0.6 +/- 0.3 g.m-2.min-1, which corresponds to the rate of passive transpiration, at core temperatures of 37.42 +/- 0.29 and 37.39 +/- 0.48 degrees C, as measured in the esophagus (Tes) and rectum (Tre), respectively. Oxygen uptake (VO2) decreased rapidly from an exercising level of 2.11 +/- 0.25 to 0.46 +/- 0.09 l/min within 4 min of the recovery period. Thereafter, VO2 remained stable for approximately 20 min, eventually increased with progressive cooling of the core region, and was elevated above the median resting values determined between 15 and 20 min at Tes = 36.84 +/- 0.38 degrees C and Tre = 36.80 +/- 0.39 degrees C. These results indicate that the core temperatures at which sweating ceases and shivering commences are significantly different (P less than 0.001) regardless of whether core temperature is measured within the esophagus or rectum.(ABSTRACT TRUNCATED AT 250 WORDS)



1993 ◽  
Vol 75 (1) ◽  
pp. 173-180 ◽  
Author(s):  
M. J. McKenna ◽  
T. A. Schmidt ◽  
M. Hargreaves ◽  
L. Cameron ◽  
S. L. Skinner ◽  
...  

This study investigated the effects of sprint training on muscle Na(+)-K(+)-adenosinetriphosphatase (ATPase) concentration, plasma [K+] regulation, muscle performance, and fatigue during severe intermittent exercise. Six untrained male subjects underwent intensive cycle-sprint training for 7 wk. Muscle biopsies were taken at rest from the vastus lateralis muscle before and after 7 wk of training and were assayed for Na(+)-K(+)-ATPase concentration using vanadate-facilitated [3H]ouabain binding to intact samples. Before and after the training period, subjects performed four maximal 30-s exercise bouts (EB) on a cycle ergometer, each separated by a 4-min recovery. Arterialized venous blood samples were drawn immediately before and after each sprint bout and were analyzed for plasma [K+]. The work output was significantly elevated (11%) across all four EBs after training. The muscle [3H]ouabain binding site concentration was significantly increased (16%) from 333 +/- 19 to 387 +/- 15 (SE) pmol/g wet wt after training but was unchanged in muscle obtained from three control subjects. Plasma [K+] rose by 1–2 mmol/l with each EB and declined rapidly by the end of each recovery period. The increases in plasma [K+] resulting from each EB were significantly lower (19%) after training. The ratios of rise in plasma [K+] relative to work output during each EB were also significantly lower (27%) after training. The increased muscle [3H]ouabain binding site concentration and the reduced ratio of rise in [K+] relative to work output with exercise are both consistent with improved plasma and skeletal muscle K+ regulation after sprint training.



1997 ◽  
Vol 82 (4) ◽  
pp. 1360-1369 ◽  
Author(s):  
Anne L. Friedlander ◽  
Gretchen A. Casazza ◽  
Michael A. Horning ◽  
Melvin J. Huie ◽  
George A. Brooks

Friedlander, Anne L., Gretchen A. Casazza, Michael A. Horning, Melvin J. Huie, and George A. Brooks. Training-induced alterations of glucose flux in men. J. Appl. Physiol. 82(4): 1360–1369, 1997.—We examined the hypothesis that glucose flux was directly related to relative exercise intensity both before and after a 10-wk cycle ergometer training program in 19 healthy male subjects. Two pretraining trials [45 and 65% of peak O2 consumption (V˙o 2 peak)] and two posttraining trials (same absolute and relative intensities as 65% pretraining) were performed for 90 min of rest and 1 h of cycling exercise. After training, subjects increasedV˙o 2 peak by 9.4 ± 1.4%. Pretraining, the intensity effect on glucose kinetics was evident with rates of appearance (Ra; 5.84 ± 0.23 vs. 4.73 ± 0.19 mg ⋅ kg−1 ⋅ min−1), disappearance (Rd; 5.78 ± 0.19 vs. 4.73 ± 0.19 mg ⋅ kg−1 ⋅ min−1), oxidation (Rox; 5.36 ± 0.15 vs. 3.41 ± 0.23 mg ⋅ kg−1 ⋅ min−1), and metabolic clearance (7.03 ± 0.56 vs. 5.20 ± 0.28 ml ⋅ kg−1 ⋅ min−1) of glucose being significantly greater ( P ≤ 0.05) in the 65% than the 45%V˙o 2 peak trial. When Rd was expressed as a percentage of total energy expended per minute (Rd E), there was no difference between the 45 and 65% intensities. Training did reduce Ra (4.63 ± 0.25), Rd (4.65 ± 0.24), Rox (3.77 ± 0.43), and Rd E (15.30 ± 0.40 to 12.85 ± 0.81) when subjects were tested at the same absolute workload ( P ≤ 0.05). However, when they were tested at the same relative workload, Ra, Rd, and Rd E were not different, although Rox was lower posttraining (5.36 ± 0.15 vs. 4.41 ± 0.42, P ≤ 0.05). These results show 1) glucose use is directly related to exercise intensity; 2) training decreases glucose flux for a given power output; 3) when expressed as relative exercise intensity, training does not affect the magnitude of blood glucose use during exercise; 4) training alters the pathways of glucose disposal.



2014 ◽  
Vol 116 (8) ◽  
pp. 1068-1077 ◽  
Author(s):  
Mariasole Da Boit ◽  
Stephen J. Bailey ◽  
Steven Callow ◽  
Fred J. DiMenna ◽  
Andrew M. Jones

The purpose of this study was to test the hypothesis that V̇o2 kinetics would be speeded to a greater extent following repeated sprint training (RST), compared with continuous endurance training (ET), in the transition from moderate- to severe-intensity exercise. Twenty-three recreationally active subjects were randomly assigned to complete six sessions of ET (60–110 min of moderate-intensity cycling) or RST (four to seven 30-s all-out Wingate tests) over a 2-wk period. Subjects completed three identical work-to-work cycling exercise tests before and after the intervention period, consisting of baseline cycling at 20 W followed by sequential step increments to moderate- and severe-intensity work rates. The severe-intensity bout was continued to exhaustion on one occasion and was followed by a 60-s all-out sprint on another occasion. Phase II pulmonary V̇o2 kinetics were speeded by a similar magnitude in both the lower (ET pre, 28 ± 4; ET post, 22 ± 4 s; RST pre, 25 ± 8; RST post, 20 ± 7 s) and upper (ET pre, 50 ± 10; ET post, 39 ± 11 s; RST pre, 54 ± 7; RST post, 40 ± 11 s) steps of the work-to-work test following ET and RST ( P < 0.05). The tolerable duration of exercise and the total amount of sprint work completed in the exercise performance test were also similarly enhanced by ET and RST ( P < 0.05). Therefore, ET and RST provoked comparable improvements in V̇o2 kinetics and exercise performance in the transition from an elevated baseline work rate, with RST being a more time-efficient approach to elicit these adaptations.



Author(s):  
Alina Gailiūnienė ◽  
Arvydas Stasiulis ◽  
Jolanta Michailovienė

There are numerous studies about exercise-induced sports hematuria, proteinuria, acute renal failure following a marathon (Steward, Posen, 1980; Poortmans et al., 2001; Ayca et al., 2006). But studies investigating the effects of exercise on blood indicators of renal function are quite few.The aim of this study was to investigate the effects of submaximal veloergometric exercise on very important bio-chemical indicators of renal function — level nitrogen compounds in the blood. We investigated concentration of creatinine, urea, total protein and uric acid in venous blood samples before and after submaximal veloergometric exercise. Those nitrogen compounds were studied in three groups of subjects.The study was performed with 10 trained (Group 1), 10 untrained subjects (Group 2) and 10 subjects with I o  hiper-tensive status (Group 3). The age range was 20.5—21.3 years, weight — 71.8—77.3 kg, height — 180—177 cm. All subjects voluntered to participate in the study after providing written informed consent. The study was approved in accordance with the Declaration of Helsinki. Blood samples were collected before and after the submaximal velo-ergometric test into vacumtrainer tubes. Concentrations of creatinine, urea, total protein and uric acid in the serum were determined using Technicon Auto Analyzer ADVIA 1650 system.All data were reported as mean ± standard deviation (SD) unless otherwise specifi ed, and statistical signifi cance was recognized when p ≤ 0.05.No statistically signifi cant difference was observed between pre- and post exercise blood creatinine, urea, total protein and uric acid mean levels of all group subjects. A marked exercise induced increase in blood creatinine and total protein concentrations was observed when the results of trained and untrained participants’ parameter differences were compared after the exercise.A signifi cant (p < 0.05) exercise-induced increase in blood urea and total protein concentration was observed when the mean values of Group 1 and Group 2 before the exercise and parameters after the exercise were compared.When blood creatinine, urea, total protein and uric acid levels were compared separately for the participants, it was observed that seven persons in Group 1 and three persons in Group 2 showed a marked exercise-induced increase in the blood nitrogen compounds level.Research results suggest that 1) the testing exercise-induced statistically insignifi cant (p > 0.05) increases in the blood parameters of nitrogen compounds (creatinine, urea, total protein and uric acid) could be due to the common phenomenon of the physical stress and catecholamine effects, 2) postexercise changes of blood nitrogen compounds were signifi cant (p < 0.05) when the results of Group 1 with Group 2 participants were compared. The signifi cant differences in metabolic responce in Group 1 and  Group 2 participants probably refl ect differences in work volume and intensity, and 3) further studies are needed to be performed on more subjects to evaluate exercise-specifi c effects on postexercise changes of blood nitrogen compounds in athletes and nonathletes.Keywords: blood, creatinine, urea, total protein, uric acid. 



2013 ◽  
Vol 110 (6) ◽  
pp. 1133-1142 ◽  
Author(s):  
Keyne Charlot ◽  
Didier Chapelot

There is general agreement that exercise-induced energy expenditure is not entirely compensated for at the next meal or over the following 24 h, but inter-individual variability is high. The role of ‘fatness and fitness’ in this variability has never been assessed. Therefore, eighteen non-obese male subjects aged 22·2 (sd2·0) years were selected and separated into a ‘high-fatness and low-fitness’ (Hfat/Lfit,n9) and a ‘low-fatness and high-fitness’ (Lfat/Hfit,n9) group, according to three criteria: maximal oxygen uptake; weekly hours of physical activity; fat mass index. At 1 h before lunch, they were subjected to 60 min of exercise on a cycle ergometer (70 % VO2max), or stayed at rest. Then, they self-reported food intake in diaries until the next breakfast. Intake at lunch was not different between conditions, but was higher after exercise than after rest over the 24 h, leading to a significant but partial mean level of compensation of 49·8 (sem16·5) and 37·8 (sem24·6) % for the Hfat/Lfit and Lfat/Hfit groups, respectively. Energy compensation at lunch and over the 24 h were strongly correlated (r0·76,P< 0·001). Both groups consumed more fat and protein after exercise than after rest over the 24 h, but the percentage of energy derived from fat increased only in the Hfat/Lfit group (2·1 (sem0·6) %,P= 0·026). Thus, the energy cost of an aerobic exercise session was partially compensated over the next 24 h independently of the ‘fatness and fitness’ status, but ‘high-fat and low-fit’ individuals compensated more specifically on fats.



1999 ◽  
Vol 276 (1) ◽  
pp. E106-E117 ◽  
Author(s):  
B. C. Bergman ◽  
G. E. Butterfield ◽  
E. E. Wolfel ◽  
G. A. Casazza ◽  
G. D. Lopaschuk ◽  
...  

To evaluate the hypothesis that endurance training increases intramuscular triglyceride (IMTG) oxidation, we studied leg net free fatty acid (FFA) and glycerol exchange during 1 h of cycle ergometry at two intensities before training [45 and 65% of peak rate of oxygen consumption (V˙o 2 peak)] and after training [65% pretrainingV˙o 2 peak, same absolute workload (ABT), and 65% posttrainingV˙o 2 peak, same relative intensity (RLT)]. Nine male subjects (178.1 ± 2.5 cm, 81.8 ± 3.3 kg, 27.4 ± 2.0 yr) were tested before and after 9 wk of cycle ergometer training, five times per week at 75%V˙o 2 peak. The power output that elicited 66.1 ± 1.1% ofV˙o 2 peak before training elicited 54.0 ± 1.7% after training due to a 14.6 ± 3.1% increase inV˙o 2 peak. Training significantly ( P < 0.05) decreased pulmonary respiratory exchange ratio (RER) values at ABT (0.96 ± 0.01 at 65% pre- vs. 0.93 ± 0.01 posttraining) but not RLT (0.95 ± 0.01). After training, leg respiratory quotient (RQ) was not significantly different at either ABT (0.98 ± 0.02 pre- vs. 0.98 ± 0.03 posttraining) or RLT (1.01 ± 0.02). Net FFA uptake was increased at RLT but not ABT after training. FFA fractional extraction was not significantly different after training or at any exercise intensity. Net glycerol release, and therefore IMTG lipolysis calculated from three times net glycerol release, did not change from rest to exercise or at ABT but decreased at the same RLT after training. Muscle biopsies revealed minor muscle triglyceride changes during exercise. Simultaneous measurements of leg RQ, net FFA uptake, and glycerol release by working legs indicated no change in leg FFA oxidation, FFA uptake, or IMTG lipolysis during leg cycling exercise that elicits 65% pre- and 54% posttrainingV˙o 2 peak. Training increases working muscle FFA uptake at 65%V˙o 2 peak, but high RER and RQ values at all work intensities indicate that FFA and IMTG are of secondary importance as fuels in moderate and greater-intensity exercise.



2007 ◽  
Vol 102 (6) ◽  
pp. 2158-2164 ◽  
Author(s):  
Kazushige Goto ◽  
Naokata Ishii ◽  
Ayuko Mizuno ◽  
Kaoru Takamatsu

This study compared the fat metabolism between “a single bout of prolonged exercise” and “repeated bouts of exercise” of equivalent exercise intensity and total exercise duration. Seven men performed three trials: 1) a single bout of 60-min exercise (Single); 2) two bouts of 30-min exercise, separated by a 20-min rest between exercise bouts (Repeated); and 3) rest. Each exercise was performed with a cycle ergometer at 60% of maximal oxygen uptake. In the Single and Repeated trials, serum glycerol, growth hormone, plasma epinephrine, and norepinephrine concentrations increased significantly ( P < 0.05) during the first 30-min exercise bout. In the Repeated trial, serum free fatty acids (FFA), acetoacetate, and 3-hydroxybutyrate concentrations showed rapid increases ( P < 0.05) during a subsequent 20-min rest period. During the second 30-min exercise bout, FFA and epinephrine responses were significantly greater in the Repeated trial than in the Single trial ( P < 0.05). Moreover, the Repeated trial showed significantly lower values of insulin and glucose than the Single trial. During the 60-min recovery period after the exercise, FFA, glycerol, and 3-hydroxybutyrate concentrations were significantly higher in the Repeated trial than in the Single trial ( P < 0.05). The relative contribution of fat oxidation to the energy expenditure showed significantly higher values ( P < 0.05) in the Repeated trial than in the Single trial during the recovery period. These results indicate that repeated bouts of exercise cause enhanced fat metabolism compared with a single bout of prolonged exercise of equivalent total exercise duration.



1991 ◽  
Vol 69 (8) ◽  
pp. 1222-1229 ◽  
Author(s):  
H. J. Green ◽  
S. Jones ◽  
M. Ball-Burnett ◽  
I. Fraser

This study was designed to investigate the effect of short-term, submaximal training on changes in blood substrates, metabolites, and hormonal concentrations during prolonged exercise at the same power output. Cycle training was performed daily by eight male subjects ([Formula: see text], [Formula: see text]) for 10–12 days with each exercise session lasting for 2 h at an average intensity of 59% of [Formula: see text]. This training protocol resulted in reductions (p < 0.05) in blood lactate concentration (mM) at 15 min (2.96 ± 0.46 vs. 1.73 ± 0.23), 30 min (2.92 ± 0.46 vs. 1.70 ± 0.22), 60 min (2.96 ± 0.53 vs. 1.72 ± 0.29), and 90 min (2.58 ± 1.3 vs. 1.62 ± 0.23) of exercise. The reduction in blood lactate was also accompanied by lower (p < 0.05) concentrations of both ammonia and uric acid. Similarly, following training lower concentrations (p < 0.05) were observed for blood β-hydroxybutyrate (60 and 90 min) and serum free fatty acids (90 min). Blood glucose (15 and 30 min) and blood glycerol (30 and 60 min) were higher (p < 0.05) following training, whereas blood alanine and pyruvate were unaffected. For the hormones insulin, glucagon, epinephrine, and norepinephrine, only epinephrine and norepinephrine were altered with training. For both of the catecholamines, the exercise-induced increase was blunted (p < 0.05) at both 60 and 90 min. As indicated by the changes in blood lactate, ammonia, and uric acid, a depression in glycolysis and IMP formation is suggested as an early adaptive response to prolonged submaximal exercise training.Key words: exercise, training, blood metabolites, substrates, hormones.



2021 ◽  
Vol 107 (4) ◽  
pp. 513-526
Author(s):  
R. Joro ◽  
A. Korkmaz ◽  
T.A. Lakka ◽  
A.L.T. Uusitalo ◽  
M. Atalay

AbstractIrisin is a novel exercise-induced myokine that may be involved in regulating energy metabolism. We determined whether overtraining syndrome (OTS) and its biochemical markers are associated with plasma irisin levels in athletes. Seven severely overtrained athletes (OA) and 10 healthy control athletes (CA) were recruited and examined at the time of diagnosis (baseline) and after 6- and 12-months follow-up. Training volume and intensity were initially restricted but progressively increased in OA as OTS symptoms alleviated; CA continued their normal training routine. A maximal cycle ergometer test was performed with irisin analyzed before and after the test. Before the exercise test, irisin levels tended to be lower in OA than in CA at baseline (154.5 ± 28.5 vs. 171.7 ± 58.7 ng/mL). In both groups, at rest irisin levels changed only marginally during follow-up and were not affected by maximal exercise, nor were they associated with physical performance or body fat percentage. Irisin concentration at rest correlated positively with an oxidative stress marker, malondialdehyde (MDA) and negatively with an antioxidant protection marker, oxygen radical absorbance capacity (ORAC) in response to the exercise test in OA at baseline. Our findings help to clarify the possible contribution of irisin and its association with oxidative stress in the pathophysiology of OTS.



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