scholarly journals Post-exercise urinary alpha-1 acid glycoprotein is not dependent on hypoxia

Author(s):  
Kelsey Elizabeth Joyce ◽  
George M. Balanos ◽  
Christopher Bradley ◽  
Amy Fountain ◽  
Arthur Randell Bradwell ◽  
...  

Introduction: Proteinuria is a transient physiologic phenomenon that occurs with a range of physical activities and during ascent to altitude. Exercise intensity appears to dictate the magnitude of post-exercise proteinuria; however, evidence also indicates possible contributions from exercise-induced hypoxemia or reoxygenation. Utilizing an environmental hypoxic chamber, this crossover designed study aimed to evaluate urinary alpha-1 acid glycoprotein (α1-AGP) excretion pre/post exercise performed in hypoxia and normoxia. Methods: Sixteen individuals underwent experimental sessions in normoxia (NOR, 20.9% O2) and hypoxia (HYP, 12.0% O2). Sessions began with a 2-hour priming period before completing a graded maximal exercise test (GXT) on a cycle ergometer, which was followed by continuation of exposure for an additional 2 hours. Physiologic responses (i.e., blood pressure, heart rate, and peripheral oxygenation), Lake Louise Scores, and urine specimens (analyzed for albumin and α1-AGP) were collected pre- and post-exercise (after 30, 60, and 120 minutes). Results: Peak power output was significantly reduced in HYP (193 ± 45 W) compared to NOR (249 ± 59 W, p < 0.01). Post-exercise urinary α1-AGP was greater in NOR (20.04 ± 14.84 μg•min-1) compared to HYP (15.08 ± 13.46 μg•min-1), albeit the difference was not significant (p > 0.05). Changes in urinary α1-AGP from pre- to post-30 minutes were not related to physiologic responses or performance outcomes observed during GXT in NOR or HYP. Conclusion: Despite profound systemic hypoxemia with maximal exercise in hypoxia, post-exercise α1-AGP excretion was not elevated above levels observed following normoxic exercise.

1994 ◽  
Vol 76 (3) ◽  
pp. 1346-1349 ◽  
Author(s):  
L. Kaijser ◽  
J. Pernow ◽  
B. Berglund ◽  
J. Grubbstrom ◽  
J. M. Lundberg

To evaluate the effect of hypoxemia on cardiac release of neuropeptide Y-like immunoreactivity (NPY-LI) and norepinephrine (NE), arterial and coronary sinus blood was sampled and coronary sinus blood flow was measured by thermodilution in nine healthy volunteers at rest and during supine cycle ergometer exercise while they breathed air and 12% O2, which reduced arterial O2 saturation to approximately 68%. Five subjects started to exercise for 30 min breathing air and continued for 30 min breathing 12% O2; four subjects breathed 12% O2 and air in the reverse order. The load was adjusted to give the same heart rate during O2 and air breathing. No significant cardiac net release of NPY-LI or NE was seen at rest. Exercise induced release of NPY-LI and NE. The net release of NPY-LI was 0.7 +/- 0.4 pmol/min during air breathing (average 12 and 30 min) and 2.8 +/- 0.6 pmol/min during 12% O2 breathing. The difference was not influenced by the order of the breathing periods. The NE coronary sinus-arterial difference was not significantly different between 12% O2 and air breathing, whereas the net release was significantly larger during 12% O2 breathing (0.6 +/- 0.1 vs. 0.4 +/- 0.1 nmol/min). Thus, NPY is released with NE from the heart during exercise. Arterial hypoxemia seems to be an additional stimulus of preferential NPY release.


2020 ◽  
Vol 6 (2) ◽  
pp. 00271-2019
Author(s):  
Anna R. Jackson ◽  
J.H. Hull ◽  
James G. Hopker ◽  
Hannah Fletcher ◽  
William Gowers ◽  
...  

Respiratory symptoms, including cough, are prevalent in individuals with asthma when exercising. This study investigates whether a heat and moisture exchanger (HME) face mask is effective in modulating exercise-induced bronchoconstriction (EIB) and post-exercise cough in a cold, dry environment in individuals with asthma.Twenty-six participants diagnosed with asthma (20 males, 6 females) completed three cycling exercise challenges at 8°C and 24% relative humidity in a randomised order. Participants wore either an HME mask (MASK), sham mask (SHAM), or no mask (CONT). Following a 3-min warm-up, participants completed 6-min cycling at 80% peak power output. Before and after exercise, maximal flow-volume loops were recorded. Post-exercise cough was monitored with a Leicester Cough Monitor (LCM) for 24 h. Results were analysed using repeated-measures ANOVA and Friedman's tests and data were presented as the mean±sd or median (interquartile range (IQR)).Eleven participants failed to demonstrate EIB (i.e. >10% fall in forced expiratory volume in 1 s after exercise) and were removed from analysis. The percentage fall in forced expiratory volume in 1 s following exercise in CONT was greater than MASK (MASK: −6% (7%), SHAM: −11% (11%), CONT: −13% (9%); p<0.01). No difference was found between exercise in cough count per hour over the 24-h monitoring period or the number of coughs in the first hour after exercise.HME masks can attenuate EIB when exercising in cold, dry environments. The SHAM mask may not have been entirely inert, demonstrating the challenges of running randomised control trials utilising control and sham conditions.


2014 ◽  
Vol 2014 ◽  
pp. 1-6 ◽  
Author(s):  
Aneta Otocka-Kmiecik ◽  
Marek Lewandowski ◽  
Urszula Szkudlarek ◽  
Dariusz Nowak ◽  
Monika Orlowska-Majdak

The aim of the study was to compare the effect of maximal exercise (ME) on paraoxonase (PON) and arylesterase (ARE) activity depending on lifestyle in respect to physical activity. The study was performed on 46 young men divided into two groups: sedentary (S) and physically active (PA). All participants performed ME on a treadmill. PON1 activities, FRAP, uric acid, bilirubin, TBARS, and lipid profile were determined in their blood before, at the bout of, and after ME. No significant differences in PON1 activities were found between S and PA subjects at baseline. Nearly all biochemicals increased at ME in both groups. Both PON and ARE activity increased at the bout of ME in PA subjects and only ARE activity in S subjects. ARE/HDL-C ratio increased at the bout of ME in PA and S subjects. The difference in PON1 activity response to ME between study groups may be a result of adaptation of PA subjects to regular physical activity. We suggest that PON1 activity may be a marker of antioxidant protection at ME and an indicator of adaptation to exercise.


2002 ◽  
Vol 93 (2) ◽  
pp. 724-731 ◽  
Author(s):  
Henning B. Nielsen ◽  
Per P. Bredmose ◽  
Morten Strømstad ◽  
Stefanos Volianitis ◽  
Bjørn Quistorff ◽  
...  

The contribution of pH to exercise-induced arterial O2 desaturation was evaluated by intravenous infusion of sodium bicarbonate (Bic, 1 M; 200–350 ml) or an equal volume of saline (Sal; 1 M) at a constant infusion rate during a “2,000-m” maximal ergometer row in five male oarsmen. Blood-gas variables were corrected to the increase in blood temperature from 36.5 ± 0.3 to 38.9 ± 0.1°C ( P < 0.05; means ± SE), which was established in a pilot study. During Sal exercise, pH decreased from 7.42 ± 0.01 at rest to 7.07 ± 0.02 but only to 7.34 ± 0.02 ( P < 0.05) during the Bic trial. Arterial Po 2 was reduced from 103.1 ± 0.7 to 88.2 ± 1.3 Torr during exercise with Sal, and this reduction was not significantly affected by Bic. Arterial O2 saturation was 97.5 ± 0.2% at rest and decreased to 89.0 ± 0.7% during Sal exercise but only to 94.1 ± 1% with Bic ( P < 0.05). Arterial Pco 2 was not significantly changed from resting values in the last minute of Sal exercise, but in the Bic trial it increased from 40.5 ± 0.5 to 45.9 ± 2.0 Torr ( P < 0.05). Pulmonary ventilation was lowered during exercise with Bic (155 ± 14 vs. 142 ± 13 l/min; P < 0.05), but the exercise-induced increase in the difference between the end-tidal O2 pressure and arterial Po 2 was similar in the two trials. Also, pulmonary O2 uptake and changes in muscle oxygenation as determined by near-infrared spectrophotometry during exercise were similar. The enlarged blood-buffering capacity after infusion of Bic attenuated acidosis and in turn arterial desaturation during maximal exercise.


1989 ◽  
Vol 66 (6) ◽  
pp. 2491-2495 ◽  
Author(s):  
S. K. Powers ◽  
J. Lawler ◽  
J. A. Dempsey ◽  
S. Dodd ◽  
G. Landry

Recent evidence suggests that heavy exercise may lower the percentage of O2 bound to hemoglobin (%SaO2) by greater than or equal to 5% below resting values in some highly trained endurance athletes. We tested the hypothesis that pulmonary gas exchange limitations may restrict VO2max in highly trained athletes who exhibit exercise-induced hypoxemia. Twenty healthy male volunteers were divided into two groups according to their physical fitness status and the demonstration of exercise-induced reductions in %SaO2 less than or equal to 92%: 1) trained (T), mean VO2max = 56.5 ml.kg-1.min-1 (n = 13) and 2) highly trained (HT) with maximal exercise %SaO2 less than or equal to 92%, mean VO2max = 70.1 ml.kg-1.min-1 (n = 7). Subjects performed two incremental cycle ergometer exercise tests to determine VO2max at sea level under normoxic (21% O2) and mild hyperoxic conditions (26% O2). Mean %SaO2 during maximal exercise was significantly higher (P less than 0.05) during hyperoxia compared with normoxia in both the T group (94.1 vs. 96.1%) and the HT group (90.6 vs. 95.9%). Mean VO2max was significantly elevated (P less than 0.05) during hyperoxia compared with normoxia in the HT group (74.7 vs. 70.1 ml.kg-1.min-1). In contrast, in the T group, no mean difference (P less than 0.05) existed between treatments in VO2max (56.5 vs. 57.1 ml.kg-1.min-1). These data suggest that pulmonary gas exchange may contribute significantly to the limitation of VO2max in highly trained athletes who exhibit exercise-induced reductions in %SaO2 at sea level.(ABSTRACT TRUNCATED AT 250 WORDS)


2013 ◽  
pp. 163-170 ◽  
Author(s):  
W. DUDZINSKA ◽  
A. LUBKOWSKA ◽  
K. JAKUBOWSKA ◽  
M. SUSKA ◽  
E. SKOTNICKA

Uridine is postulated to participate in the development of insulin resistance. Since exercise is an effective tool in the treatment of insulin resistance it appeared justified to assess the impact of maximal exercise on plasma uridine and insulin sensitivity indices (e.g. insulin and HOMA-IR) in healthy subjects. The study included forty-four healthy males (18.5±2.92 years, VO2max 50.2±6.26 ml kg-1 min-1). Subjects performed a single maximal exercise on a bicycle ergometer. Blood samples were taken three times: immediately before exercise, immediately after exercise and at the 30th min of rest. Uridine concentrations were determined in the whole blood using high-performance liquid chromatography. Serum insulin levels were measured by a specific ELISA method. Insulin sensitivity was assessed by homeostasis model assessment method (HOMA-IR). A maximal exercise-induced increase in the concentration of uridine correlated with post-exercise increases in insulin levels and HOMA-IR. Our results indicate a relationship between the concentration of uridine in the blood and indicators of insulin sensitivity in healthy subjects. We are the first to demonstrate that a maximal exercise-induced increase in the concentration of uridine is correlated with post-exercise increases in insulin levels and HOMA-IR in healthy subjects. It appears that uridine may be an indicator of insulin resistance.


1996 ◽  
Vol 75 (04) ◽  
pp. 612-616 ◽  
Author(s):  
Lothar Röcker ◽  
Martin Möckel ◽  
Klaus-Peter Westpfahl-W ◽  
Hanns-Christian Gunga

SummaryThe effects of moderate 30 min cycle ergometer exercise (aerobic metabolism; 0.85-3.71 mmol · 1−1 lactate) followed by short-term exercise at maximal capacity (anaerobic metabolism; 5.09 to 17.75 mmol · 1−1 lactate) on endothelin (ET) and hemostatic variables (tissue plasminogen activator [t-PA] antigen, prothrombin fragments [F1,2], thrombin-antithrombin III complex [TAT], prothrombin time and partial thromboplastin time) were investigated in 15 male healthy subjects of varying fitness levels. Endothelin was measured twice, before and immediately after maximal cycle exercise. The results show an increase in endothelin concentration [10.0 pg · m1−1 (baseline) + 6.1 pg · m1−1 (increase post exercise)]. ET did not increase under control conditions. Moderate 30 min exercise caused an increase in t-PA antigen concentration (3.66 + 3.15 ng · m1−1) and short-term maximal exercise produced a markedly higher elevation in this variable (+10.6 ng · m1−1). F1,2 increased (810 + 40 pmol · 1−1) under moderate and by 150 pmol · 1−1 under anaerobic exercise. TAT increased only at maximal exercise levels (1.01 + 0.32 ng · 1−1). No changes were found in any of these variables under control conditions. No correlation of endothelin and the hemostatic variables was found.It is concluded that endothelin and hemostatic markers increase independently during moderate and maximal exercise.


Thorax ◽  
2001 ◽  
Vol 56 (9) ◽  
pp. 675-679
Author(s):  
C Goubault ◽  
M-C Perault ◽  
E Leleu ◽  
S Bouquet ◽  
P Legros ◽  
...  

BACKGROUNDBeta-2 agonists such as salbutamol are used, not only by asthmatic athletes to prevent exercise induced asthma, but also by non-asthmatic athletes as a potentially ergogenic agent. We have investigated whether inhaled salbutamol enhances endurance performance in non-asthmatic athletes.METHODSA prospective double blind, randomised, three way crossover design was used to study the effects of 200 μg and 800 μg inhaled salbutamol versus a placebo in 12 trained triathletes. The treatments were compared in three identical cycle ergometer sessions at 85% of the predetermined maximal oxygen uptake. Lung function, endurance time, metabolic parameters (glucose, potassium, lactate, free fatty acid, and glycerol), and psychomotor performance were evaluated.RESULTSNeither endurance time nor post-exercise bronchodilation were significantly different between the treatments. Metabolic parameters were affected by exercise but not by treatment.CONCLUSIONSInhaled salbutamol, even in a high dose, did not have a significant effect on endurance performance in non-asthmatic athletes, although the bronchodilating effect of the drug at the beginning of exercise may have improved respiratory adaptation. Our results do not preclude an ergogenic effect of β2 agonists given by other routes or for a longer period.


2015 ◽  
pp. 467-477 ◽  
Author(s):  
W. DUDZINSKA ◽  
A. LUBKOWSKA ◽  
B. DOLEGOWSKA ◽  
M. SUSKA ◽  
M. JANIAK

Studies have shown that uridine concentration in plasma may be an indicator of uric acid production in patients with gout. It has been also postulated that uridine takes part in blood pressure regulation. Since physical exercise is an effective tool in treatment and prevention of cardio-vascular diseases that are often accompanied by hyperuricemia and hypertension, it seemed advisable to attempt to evaluate the relationship between oxypurine concentrations (Hyp, Xan and UA) and that of Urd and BP after physical exercise in healthy subjects. Sixty healthy men (17.2±1.71 years, BMI 23.2±2.31 kg m−2, VO2max 54.7±6.48 ml kg−1 min−1) took part in the study. The subjects performed a single maximal physical exercise on a bicycle ergometer. Blood for analyses was sampled three times: immediately before exercise, immediately after exercise, and in the 30th min of rest. Concentrations of uridine and hypoxanthine, xanthine and uric acid were determined in whole blood using high-performance liquid chromatography. We have shown in this study that the maximal exercise-induced increase of uridine concentration correlates with the post-exercise increase of uric acid concentration and systolic blood pressure. The results of our study show a relationship between uridine concentration in blood and uric acid concentration and blood pressure. We have been the first to demonstrate that a maximal exercise-induced increase in uridine concentration is correlated with the post-exercise and recovery-continued increase of uric acid concentration in healthy subjects. Thus, it appears that uridine may be an indicator of post-exercise hyperuricemia and blood pressure.


1997 ◽  
Vol 82 (1) ◽  
pp. 364-370 ◽  
Author(s):  
Carl De Crée ◽  
Peter Ball ◽  
Bärbel Seidlitz ◽  
Gerrit Van Kranenburg ◽  
Peter Geurten ◽  
...  

De Crée, Carl, Peter Ball, Bärbel Seidlitz, Gerrit Van Kranenburg, Peter Geurten, and Hans A. Keizer. Plasma 2-hydroxycatecholestrogen responses to acute submaximal and maximal exercise in untrained women. J. Appl. Physiol. 82(1): 364–370, 1997.—Exercise-induced menstrual problems are accompanied by an increase in catecholestrogen (CE) formation. It has been hypothesized that hypoestrogenemia may be secondary to an increased turnover from estrogens to CE, which then may disrupt luteinizing hormone release. In addition, the strong affinity of CE for the catecholamine-deactivating enzyme catechol- O-methyltransferase (COMT) has led to speculations about their possible role in safeguarding norepinephrine from premature decomposition during exercise. We investigated whether acute exercise on a cycle ergometer produces any changes in CE homeostasis. Nine untrained eumenorrheic women (body fat, 24.8 ± 3.1%) volunteered for this study. Baseline plasma CE averages for total 2-hydroxyestrogens (2-OHE) were 218 ± 29 (SE) pg/ml during the follicular phase (FPh) and 420 ± 58 pg/ml during the luteal phase (LPh). 2-Methoxyestrogens (2-MeOE) measured 257 ± 17 pg/ml in the FPh and 339 ± 39 pg/ml in the LPh. During incremental exercise, total estrogens (E) increased, but 2-OHE and 2-MeOE levels did not significantly change in either phase. The 2-OHE/E ratio (measure of CE turnover) decreased during exercise in both menstrual phases, whereas the 2-MeOE/2-OHE ratio (correlates with COMT activity) did not significantly change. These findings suggest that there is insufficient evidence to conclude that brief incremental exercise in untrained eumenorrheic females acutely produces increased CE formation.


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