Post-exercise Proteinuria Research Articles

Hypoxia is not the primary mechanism contributing to exercise-induced proteinuria

IntroductionProteinuria increases at altitude and with exercise, potentially as a result of hypoxia. Using urinary alpha-1 acid glycoprotein (α1-AGP) levels as a sensitive marker of proteinuria, we examined the impact...

Factors influencing post-exercise proteinuria after marathon and ultramarathon races.

Post-exercise proteinuria is one of the most common findings observed after short and intensive physical activity, but is observed also after long runs with low intensity. The aim of this study was to analyze factors influencing proteinuria after marathon runs. Two groups of male amateur runners were studied. The results of 20 marathon finishers (42.195 m), with a mean age of 49.3 ± 6.85 years; and 17 finishers of a 100-km ultramarathon with a mean age of 40.18±4.57 years were studied. Urine albumin to creatinine ratio (ACR) was calculated before and after both races. The relationship between ACR and run pace, metabolites (lactate, beta hydroxybutyrate), markers of inflammation (CRP, IL-6) and insulin was studied. The significant increase in ACR was observed after both marathon races. ACR increased from 6.41 to 21.96 mg/g after the marathon and from 5.37 to 49.64 mg/g after the ultramarathon (p<0.05). The increase in ACR was higher after the ultramarathon that after the marathon. There was no correlation between run pace and proteinuria. There was no correlation between ACR and glucose, free fatty acids, lactate, beta-hydroxybutyrate and insulin levels. There was significant negative correlation between ACR and interleukin 6 (IL-6) (r =-0.59, p< 0.05) after ultramarathon. Proteinuria is a common finding after physical exercise. After very long exercises it is related to duration but not to intensity. There is no association between metabolic and hormonal changes and ACR after marathon runs. The role on inflammatory cytokines in albuminuria is unclear.

Nitric oxide involvement in post-exercise proteinuria of sedentary young men

Summary Objectives Post-exercise proteinuria is generally characterised based on the alterations in renal hemodynamics. The present study was focused on the role of nitric oxide in post-exercise proteinuria; nitric oxide is a biomolecule involved in mechanisms that affect renal hemodynamics and is a mediator that rises during exercise bouts. Methods Healthy human subjects performed three high-intensity exercise sessions with a one-week interval; control, NO donor (isosorbide mononitrate) and vasodilator that unrelated nitric oxide (diltiazem). Urine samples obtained immediately before and 30 and 120 minutes after the exercise session were examined for proteinuria. The alterations in systemic blood pressure induced by the drugs were evaluated by performing blood pressure measurements. Results Both the agents that were administered caused a significant decrease in the systolic or diastolic blood pressure; however, the extent of reduction was not different between the two agents. Exercise session induced apparent proteinuria at 30 minutes post-exercise during all the protocols. Exercise-induced rise in urinary protein excretion was significantly reduced by isosorbide mononitrate, while a similar effect was not observed for diltiazem. Conclusion Our results revealed that exogenous nitric oxide could alter the hemodynamic changes during exercise and thus reduce post-exercise proteinuria. Further, endogenous nitric oxide may prevent excessive elevation in the post-exercise proteinuria during normal physiological conditions.

Biochemical Markers of Renal Hypoperfusion, Hemoconcentration, and Proteinuria after Extreme Physical Exercise.

Background and Objectives: Physical exercise increases the blood perfusion of muscles, but decreases the renal blood flow. There are several markers of renal hypoperfusion which are used in the differential diagnosis of acute kidney failure. Albuminuria is observed after almost any exercise. The aim of this study was to assess changes in renal hypoperfusion and albuminuria after a 100-km race. Materials and Methods: A total of 27 males who finished a 100-km run were studied. The mean age of the runners was 38.04 ± 5.64 years. The exclusion criteria were a history of kidney disease, glomerular filtration rate (GFR) <60 ml/min, and proteinuria. Blood and urine were collected before and after the race. The urinary albumin/creatinine ratio (ACR), fractional excretion of urea (FeUrea) and sodium (FeNa), plasma urea/creatinine ratio (sUrea/Cr), urine/plasma creatinine ratio (u/pCr), urinary sodium to potassium ratio (uNa/K), and urinary potassium to urinary potassium plus sodium ratio (uK/(K+Na)) were calculated. Results: After the race, significant changes in albuminuria and markers of renal hypoperfusion (FeNa, FeUrea, sUrea/Cr, u/sCr, urinary Na, uNa/K, uK/(K+Na)) were found. Fifteen runners (55.56%) had severe renal hypoperfusion (FeUrea <35, uNa/K <1, and uK/(Na+K) >0.5) after the race. The mean ACR increased from 6.28 ± 3.84 mg/g to 48.43 ± 51.64 mg/g (p < 0.001). The ACR was higher in the group with severe renal hypoperfusion (59.42 ± 59.86 vs. 34.68 ± 37.04 mg/g), but without statistical significance. Conclusions: More than 50% of the runners had severe renal hypoperfusion after extreme exercise. Changes in renal hemodynamics are probably an important, but not the only, factor of post-exercise proteinuria.

The Renin–Angiotensin System, Not the Kinin–Kallikrein System, Affects Post-Exercise Proteinuria

Background/Aims: Temporary proteinuria post-exercise is common and is caused predominantly by renal haemodynamic alterations. One reason is up-regulation of angiotensin II (Ang II) due to the reducing effect of angiotensin-converting enzyme (ACE) inhibitors. However, another, ignored, reason could be the kininase effect of ACE inhibition. This study investigated how ACE inhibition reduces post-exercise proteinuria: by either Ang II up-regulation inhibition or bradykinin elevation due to kininase activity inhibition. Methods: Our study included 10 volunteers, who completed 3 high-intensity exercise protocols involving cycling at 1-week intervals. The first protocol was a control arm, the second evaluated the effect of ACE inhibition and the third examined the effect of angiotensin type 1 receptor blockade. Upon application, both agents reduced systolic and diastolic blood pressure; however, there were no statistically significant ­differences. In addition, total protein, microalbumin and ­β₂-microglobulin excretion levels in urine specimens were analysed before, 30 min after and 120 min after the exercise protocols. Results: Total protein levels in urine samples were elevated in all 3 protocols after 30 min of high-intensity exercise, compared to baseline levels. However, both ACE inhibition and angiotensin type 1 receptor blockade suppressed total protein in the 30th min. In each protocol, total protein levels returned to the baseline after 120 min. Urinary microalbumin and β₂-microglobulin levels during the control protocol were significantly higher 30 min post-exercise; however, only angiotensin type 1 receptor blockade suppressed microalbumin levels. Conclusion: The results indicated Ang II up-regulation, not bradykinin elevation, plays a role in post-exercise proteinuria.

Impact of Moderate Intensity Endurance Exercise on Kidney Injury

PURPOSE: Exercise-induced redistribution of blood results in a decreased renal perfusion and changes in glomerular permeability and filtration ratio. These alterations may lead to a deterioration of renal function or even acute, but transient, renal failure. Kidney Injury Molecule-1 (KIM1) and Neutrophil gelatinase-associated lipocalin (NGAL) are new urinary biomarkers to detect kidney injury in an early stage. Therefore, the purpose of this study was to examine the effects of an acute bout of endurance exercise on urinary KIM1 and NGAL levels. METHODS: A total of 60 subjects (56±10 years) participated in an annual walking event and walked 30-50 km at a self-selected pace. Heart rate was recorded every 5 km. Baseline and post-exercise blood and urine samples were taken to assess fluid balance and kidney injury and body mass was measured to determine the relative body mass loss. Urinary KIM1 and NGAL levels were corrected for variations in urine volume and for urinary concentration changes using urinary cystatin C. RESULTS: Subjects completed the exercise bout at 71±9% of their predicted maximal heart rate. At baseline, kidney function, measured as estimated glomerular filtration rate (eGFR) was 89.3±11.6 mL/min, whereas 49% of the subjects had a slightly decreased kidney function (eGFR<90 mL/min). Post-exercise body mass loss was 0.9±1.2% and 20% of the subjects were dehydrated after exercise (relative body mass loss >2%). We observed a significant increase in post-exercise cystatin C-corrected urinary NGAL levels (3.0±1.5 ng/10μg cystatin C) compared to baseline (2.3±1.3 ng/10μg cystatin C, p=0.025). Moreover, 65% of subjects demonstrated elevated NGAL levels after exercise. In contrary, corrected urinary KIM1 levels did not change after exercise (0.70±0.45 versus 0.74±0.49 ng/10μg cystatin C, p=0.63). At baseline, 2 subjects were detected with proteinuria, whereas 8 subjects had post-exercise proteinuria (p=0.048). CONCLUSION: The increased levels of cystatin C corrected NGAL and proteinuria after an acute bout of endurance exercise suggest that an acute bout of endurance exercise may cause transient kidney injury.

What Does Post-Exercise Proteinuria Tell Us About Kidneys?

What Does Post-Exercise Proteinuria Tell Us About Kidneys?

Post-exercise proteinuria in the cadets trained on Special Aerial Gymnastics Instruments.

Assessment of the effect of training on Special Aerial Gymnastics Instruments (SAGI) on the urine β-2- microglobulin (β-2M), albumin (ALB), total protein (TP), N-acetyl-β-D-glucosaminidase EC.3.2.1.30 (NAG), expressed as creatinine (Cr) and on the physical fitness of the examined cadets in comparison with the control group. The study involved 55 cadets aged 20, divided into group A (N = 41) trained on SAGI, and group B (N = 14) - a control group. The urine was collected twice: before the training (BT) and after the training (AT) at the start (training I), during (training II), and after completion of the training program (training III). Urine proteins were assayed with commercially available kits. In group A, results obtained in trainings I, II and III showed a statistically significant increase in β-2M/Cr, NAG/Cr, TP/Cr, ALB/Cr indices in AT compared with the baseline BT values. Similarly in group B, a statistically significant increase in β-2M/Cr, NAG/Cr (trainings I, II), TP/Cr, AT compared with the baseline BT values in trainings I, II, and III was noted. Comparison of both groups showed a higher value of the post-exercise proteinuria in group B than in group A. In group A, a significant correlation between TP/Cr vs. ALB/Cr, NAG/Cr vs. TP/Cr, β-2M/Cr vs. TP/Cr, i.e., r = 0.62 at p < 0.001; r = 0.33 at p = 0.03; r = 0.60 at p < 0.001, and r = 0.52 at p < 0.001, respectively, was observed in group A, training III, AT. Assayed urine proteins depend on the intensity of physical exercise, the type of exercise, and the level of physical fitness.

The effect of competition on gamma-glutamyl transferase, creatinine and protein levels of taekwondo players

Post-exercise proteinuria and increased urinary gamma-glutamyl transferase (GGT) levels can be predictive of exercise induced renal damage. In the literature, numerous studies exist on exercise induced proteinuria, but studies investigating the effects of exercise on urinary GGT levels are quite few in martial arts. The purpose of this study was to determine that changes in serum and urinary GGT activity and creatinine levels, and also urinary protein levels in order to assess any potential exercise induced tubular damage on taekwondo players. The study was performed on 18 female and 17 male taekwondo players who were participants in A°stanbul Taekwondo Championships. Blood and urine samples collected pre- and 1 h post competition were analyzed for serum GGT and creatinine, urinary GGT, creatinine and protein levels. The post competition serum creatinine level (p = 0.002), urinary GGT (p = 0.010) and protein levels (p = 0.000) were higher than the pre- competition levels in female players. The post competition serum creatinine level (p = 0.006), urinary GGT (p = 0.005) and protein levels (p = 0.000) were higher than the pre-competition levels in male players. We suggest that high-intensity short duration exercise does not lead to increase in serum GGT levels, but lead to increase in serum creatinine levels, as well as induced excretion urinary GGT and protein levels. Key words: Exercise, gamma-glutamyltransferase, serum, urine, enzyme, protein, creatinine, taekwondo.

Does Proteinuria-Inducing Physical Activity Increase Biomarkers of Acute Kidney Injury?

Aim: We sought to determine if an acute kidney injury biomarker, neutrophil gelatinaseassociated lipocalin (NGAL), would be up-regulated by high-intensity proteinuria-inducing exercise. Methods: A prospective cohort design was utilised. 100 healthy, active adults (mean age 24 ± 4 (SD) years) were screened for post-exercise proteinuria (PeP); 10 PeP positive and 10 PeP negative participants then completed a high-intensity exercise protocol involving an 800 meter sprint. Plasma and urinary NGAL, urinary creatinine, urinary albumin and urine volume were obtained at the following time points: pre-run, immediately post-, 25 minutes, one hour and two hours post-run. Results: Following high-intensity exercise, 64% of participants had urinary NGAL concentrations above the normal range, particularly at 25 minutes post (P = 0.002). However, there was no difference in NGAL response between PeP positive and negative groups and plasma NGAL was decreased, not elevated, following exercise (P = 0.002). In some individuals normalizing urinary NGAL for urinary creatinine attenuated elevations. Urinary NGAL was also negatively correlated with urine volume (r = -0.701, P = 0.005). Conclusion: Proteinuria susceptibility did not influence an acute injury biomarker response to exercise. Nevertheless, urinary NGAL was elevated by exercise, possibly due to increased production by the proximal tubule, increased plasma clearance (given the decrease in plasma NGAL) and/or a concentrating effect of exercise-induced oliguria. Until correct normalisation of urinary biomarkers is determined, NGAL should be interpreted cautiously in exercise and acute kidney injury-induced oliguria. The inter-individual NGAL response to exercise also warrants further investigation.

The pattern of proteinuria following karate (Kumite) competitions.

Sir, Despite the large amount of proteins in the plasma, the urine is virtually protein free due to the selectivity of the glomerular barrier [1]. The major component of urinary protein is a tubular protein (Tamm-Horsfall) while albumin constitutes 30–40% of the total urinary protein. Various physiologic settings, including exercise, can induce a transient increase in the urinary protein excretion that is usually benign and reversible. The type of post-exercise proteinuria depends on the intensity of exercise rather than its duration, so that moderate exercise induces glomerular and heavy exercise glomerular-tubular mixed-type protein loss [2]. Post-exercise proteinuria may be due to the loss of the charge selectivity from the glomerular capillary wall, a relative preservation of the glomerular filtration rate, proteinuria out of proportion of maximal tubular reabsorption capacity following heavy exercise [2,3] and oxidative stress produced by free radicals due to enhanced oxygen consumption in muscles [4]. The purpose of our study was to compare the amount and pattern of proteinuria before and after karate (Kumite) competition in 18 male practitioners, aged 18–21 years, with similar physical characteristics. All practitioners competed in three rounds, each lasted 3 min, with a 10 min resting interval between them. Urine samples were collected just before the competition and during 24 h thereafter. Total urinary protein, urinary beta2-microglobulin B2M as tubular and albumin as glomerular protein were assayed. Before competition, the mean value of total urinary protein, albumin and B2M as basal levels were 70.68 ± 12.5, 4.84 ± 3.17 and 0.0217 ± 0.0133 mg/day, respectively. After competition, the mean values of 24-h total urine protein (196.05 ± 70.88 mg/day), albumin (34.07 ± 32.88 mg/day) and B2M (0.0933 ± 0.0372 mg/day) levels were significantly increased (P = 0.023, P = 0.001 and P < 0.001). This study revealed significantly increased proteinuria of a mixed type (albumin and B2M) in all practitioners following exhaustive short-term competition. Despite the mixed type of proteinuria, we observed a six-fold increase compared to the basal level in urine albumin (versus four-fold increase for urinary B2M) suggesting a more prominent role of glomerular proteinuria probably due to glomerular membrane permeability changing factors, such as sympathetic overactivity and competitive stress. Conflict of interest statement. None.

Potential sources of oxidative stress that induce postexercise proteinuria in rats

Exercise-induced proteinuria is a common consequence of physical activity and is caused predominantly by alterations in renal hemodynamics. Although it has been shown that exercise-induced oxidative stress can also contribute to the occurrence of postexercise proteinuria, the sources of reactive oxygen species that promote it are unknown. We investigated the enzymes nicotinamide adenine dinucleotide phosphate (NADPH) oxidase and xanthine oxidase (XO) as possible sources of oxidative stress in postexercise proteinuria. First, we evaluated the effect of blocking the NADPH oxidase enzyme on postexercise proteinuria. We found a significant increase in urinary protein level, kidney thiobarbituric acid-reactive substances (TBARS), and protein carbonyl content after exhaustive exercise, and NADPH oxidase activity was induced by exercise. Rats that were treated with an NADPH oxidase inhibitor for 4 days before exhaustive exercise showed no increase in kidney TBARS or protein carbonyl derivative level and no proteinuria or NADPH oxidase activation. In the next set of experiments, we investigated the effect of XO blockage on postexercise proteinuria. Oxypurinol, an XO inhibitor was administered to rats for 3 days before exercise. Although XO inhibition significantly decreased kidney TBARS levels and protein carbonyl content in exercised rats, the inhibition did not prevent exercise-induced proteinuria. However, plasma and kidney XO activity was not induced by exercise, but rather it was suppressed under oxypurinol treatment. These results suggest that increased NADPH oxidase activity induced by exhaustive exercise is an important source of elevated oxidative, stress during exercise, which contributes to the occurrence of postexercise proteinuria.

Biphasic Pattern of Exercise-Induced Proteinuria in Sedentary and Trained Men

Background/Aims: Exercise-induced proteinuria is a common consequence of physical activity, although its mechanism is not clear. Oxidant stress has been proposed as one of different factors involved in postexercise proteinuria in rats. In this study we investigated whether reactive oxygen radicals generated during exercise play a role in exercise-induced proteinuria in sedentary and trained men. Methods: The validity of oxidant stress following stepwise maximal exercise on proteinuria was investigated in sedentary and trained subjects before and after antioxidant vitamin treatment (A, C, and E) for 2 months. While protein carbonyl content in serum and thiobarbituric acid reactive substances (TBARS) in erythrocytes and urine were used as oxidant stress markers, total protein, albumin, β₂-microglobulin in urine were assayed for proteinuria in five consecutive specimens after exercise. Urines were collected before exercise, then 30 min, 2, 8 and 24 h postexercise. Results: Increased urinary protein levels and mixed type proteinuria were determined after 30 min of exercise in sedentary and trained subjects. Proteinuria was normalized at 2 and 8 h specimens. However, glomerular type proteinuria was identified at 24 h specimen in both groups. Oxidant stress markers were significantly elevated in sedentary and trained subjects. Antioxidant treatment prevented the increase in oxidant stress markers, urinary protein levels and the occurrence of glomerular type proteinuria after exhaustive exercise at 24 h in both groups. Conclusions: These findings suggest that the exercise-induced oxidant stress may contribute to exercise-induced proteinuria in sedentary and trained men.

Angiotensin II Inhibition Attenuates Postexercise Proteinuria in Rats

An important explanatory theory for the mechanism of postexercise proteinuria is that angiotensin II could be inhibited by angiotensin converting enzyme inhibitors. Because of the kininase effect of the angiotensin converting enzyme, it is unclear whether the kallikrein-kinin system contributes to the effect of angiotensin converting enzyme inhibitors on postexercise proteinuria. The aim of this study was to evaluate any possible involvement of the kallikrein-kinin system in the therapeutic effect of angiotensin converting enzyme inhibitors on postexercise proteinuria. We evaluated urinary protein levels in exhausted rats receiving an angiotensin converting enzyme inhibitor (enalapril) or an angiotensin II type I receptor antagonist (losartan). Enalapril (30 mg/kg/day, two days) or losartan (20 mg/kg/day, two days) were given to animals using an intragastric catheter. Urinary protein levels increased (41 %) in rats which were exhausted via treadmill running (p < 0.05). In animals that received drug treatment (enalapril or losartan), but did not exercise to exhaustion, urinary protein levels were not different from the control group. Urinary protein levels were found to be significantly lower (p < 0.05) in animals which performed acute exhaustive exercise after enalapril or losartan administration, compared to rats which were exhausted without drug administration. Inhibition of postexercise proteinuria by either enalapril or losartan suggested that angiotensin II plays an important role in postexercise proteinuria, however, it appears the kallikrein-kinin system is not involved in angiotensin converting enzyme inhibitors effect.

Urinary insulin-like growth factor-I measurement in an actual sport competition, an additional approach in laboratory antidoping tests

Background The insulin-like growth factor hormone (IGF-I) is an important protein hormone under investigation with physical exercise and for doping detection. Urinary IGF-I level in fact represents a relevant measurement when the postexercise proteinuria is under analysis. To verify the IGF-I level variation in the circulation and in urinary excretion in the occasion of a competition, the plasma and urine IGF-I in athletes before and after an actual competitive event were measured. Methods Twenty well-trained cyclists took part in a competition (102 km) and concluded the intense physical exercise in approximately 2 1/2 h. Urine and blood samples were collected from each athlete 10–20 min before and at the end of the competition. Plasma and urine total IGF-I (pIGF, uIGF), total urinary proteins (uPr), and creatinine (uCr) concentrations were measured. Results The uIGF [from 76.2±15.8 to 256.9±29.1 ng/l ( p<0.001)], uPr [from 29.4±6.7 to 325.9±95.1 mg/l ( p<0.005)], and uCr [from 6.3±1.0 to 10.0±0.8 mmol/l ( p<0.005)] significantly increased. The pIGF was 262.6±14.3 and 247.3±11.8 μg/l before and end-exercise, respectively. A statistical correlation between uIGF and uPr was demonstrated ( p<0.001). The pIGF/uIGF ratio was significantly ( p<0.05) decreased comparing the end with before the competition. Conclusions The pIGF/uIGF significantly decreased at the end, compared with before the competition, suggesting a changed uIGF excretion. This increment appeared to be increased, although not significantly, considering the ratio with uCr.

The effect of reactive oxidant generation in acute exercise-induced proteinuria in trained and untrained rats.

Exercise-induced proteinuria is a common consequence of physical activity, although its mechanism is not clear. We investigated whether free radicals generated during exercise play a role in post-exercise proteinuria in sedentary and treadmill-running trained rats, separately. Sedentary and trained rats were randomly divided into four sub-groups: control, antioxidant treatment, exhaustive exercise and an exhaustive exercise plus antioxidant treatment group. Antioxidant therapy was applied by intragastric catheter for 4 weeks with vitamin C (ascorbic acid, 50 mg x kg(-1) x day(-1)) and vitamin E (alpha-tocopherol, 20 mg x kg(-1).day(-1)). Twenty-four-hour urine samples were used for measuring protein levels and protein electrophoresis. Thiobarbituric acid (TBARS) and glutathione (GSH) levels, superoxide dismutase (SOD) and catalase (CAT) activities were assayed in blood and tissues. Increased urinary protein levels and mixed type proteinuria in electrophoresis were identified after exhaustive exercise in sedentary rats. Erythrocyte, kidney and muscle TBARS levels were significantly elevated in this group. Antioxidant treatment prevented the increase in urinary protein levels, TBARS levels and the occurrence of mixed type proteinuria after exhaustive exercise in sedentary rats. Exhaustive exercise in trained rats resulted in elevation of urine protein levels and mixed type proteinuria although kidney TBARS levels were not changed compared to those of the trained controls. Antioxidant therapy in trained and exhausted-trained animals resulted in decreased TBARS levels in the kidney but it did not affect urinary-increased protein levels or electrophoresis in exhausted animals. This findings suggest that the exercise-induced oxidant stress may contribute to post-exercise proteinuria in sedentary rats. However, this mechanism may not be responsible for proteinuria in trained rats.

Effect of nitric oxide on exercise-induced proteinuria in rats.

Temporary proteinuria occurring after exercise is a common finding, and it is explained predominantly by alterations in renal hemodynamics. In this study, we investigated whether nitric oxide (NO), which is known to have an effect on renal hemodynamics and to increase during exercise, has a role in postexercise proteinuria. In the first step of this study, the effect of acute NO synthase blockage on exercise proteinuria was evaluated. The urinary protein levels in animals that performed acute exhaustive treadmill running exercise were considerably elevated compared with the control animals. Significantly elevated urinary protein levels were also detected in animals that received Nomega-nitro-L-arginine methyl ester before exhaustion, compared with both control and exhausted groups, and mixed-type proteinuria was detected in electrophoresis, as in all exhausted animals. In the second step of the study, a NO donor (isosorbide mononitrate) was given to rats 1 h before exhaustive exercise. Mixed-type proteinuria and the elevation in urinary protein levels that occur as a consequence of exhaustive exercise were prevented by NO donor treatment. Finally, in the third step of our study, a calcium channel blocker (diltiazem), another vasodilator, was applied to the rats 1 h before exhaustive exercise. Urinary protein levels were not different in exhausted rats with or without calcium channel blocker treatment. On the other hand, in both groups, urinary protein levels were higher than in the control group. The tail-cuff blood pressure alterations caused by vasodilator drug applications before exercise were not different for NO donor and calcium channel blocker groups. These results suggest that endogenous NO might prevent the postexercise proteinuria from becoming more severe by affecting hemodynamic changes that occur during exercise.

Effects of acute, heavy-resistance exercise on urinary peptide hormone excretion in humans.

To examine physical exercise-related changes in urinary excretion of protein/peptide hormones and to correlate modifications with the general increase in post-exercise proteinuria, urine C-peptide, insulin and insulin-like growth factor-I (IGF-I) and their plasma concentrations were measured. Plasma and urinary C-peptide, insulin and IGF-I before (Bex) and at the end (Eex) of physical exercise (a 2.5-hour competition, 102 km) were analysed in 20 young cyclists. At Eex compared with Bex, concentration of urinary C-peptide decreased slightly but significantly (21.3 +/- 2.7 vs. 13.5 +/- 1.7 nmol/l), but urinary insulin and urinary IGF-I concentrations significantly increased at Eex (92.5 +/- 4.2 vs. 131.4 +/- 15.7 pmol/l and 10.0 +/- 2.1 vs. 33.6 +/- 3.8 pmol/l, respectively). Plasma insulin and plasma C-peptide significantly decreased, whereas plasma IGF-I was unchanged. Urinary concentrations of total proteins and creatinine significantly increased. Both Eex urinary C-peptide/urinary protein and urinary C-peptide/urinary creatinine ratios were significantly reduced. The correlation between C-peptide and insulin in plasma was confirmed at Bex as well as Eex, but in urine only at Bex. An increased renal tubular reabsorption of C-peptide at the end of exercise might be suggested, but the expected values considering creatinine excretion were almost three times less. The Eex urinary insulin concentration was higher than expected, considering the circulation levels, but lower when compared with the expected concentration considering creatinine excretion. Physical exercise proteinuria, related to an increased protein filtration and a saturation of the mechanisms responsible for the reabsorption, does not appear similar for all peptide hormones.

Continuous versus intermittent exercise effects on urinary excretion of albumin and total protein

Several studies have reported post-exercise increases of urinary concentrations of plasma proteins. However, under normal conditions, through mechanisms of size and electrical charge selection, the kidney restricts the clearance of molecules as large as albumin. Post-exercise increases in albuminuria occur following the physiological stress of intense exercise, most likely as a result of the exercise induced blood acidity changes which lead to a change in the arrangement of the albumin molecule, and subsequently the filtration characteristics of the glomerular capillary wall. The purpose of the present study was therefore to determine the extent to which different types of exercise could induce a transient condition of post-exercise increases in the urinary output of total protein and albumin. All 14 males, who agreed to participate in the study, performed a continuous and an intermittent cycling protocol on a stationary bicycle ergometer. The results showed that: a) intermittent exercise had a greater influence than continuous exercise on the total output of urine albumin, and of urine total protein; b) concentrations of blood pH and blood lactate, were associated with changes in the clearance of urine albumin and urine total protein. Post-exercise proteinuria response seems to be transient and therefore renal trauma is not suspected at the early stages of observation. Furthermore, these results indicate that the kidney undergoes distinct physiological adjustments during exercise, and that these adjustments are relative to the intensity of the exercise stress.

Urinary insulin-like growth factor I in athletes, before and after physical exercise, and in sedentary subjects

Background: Insulin-like growth factor I (IGF-I), like growth hormone (GH), is excreted in urine in a smaller fraction than the concentration found in blood. Exercising subjects undergo post-exercise proteinuria. The present work aims to propose a method for urinary IGF-I analysis (uIGF-I) by defining urinary concentration in sedentary individuals and athletes before and after strenuous exercise. Methods: Urine samples were collected from 30 sedentary healthy male individuals during the morning and from 30 well-trained cyclists, before and after a competition of about 3 h (150 km). uIGF-I was measured in undiluted acidified urine by radioimmunoassay (RIA) method using a purified polyclonal rabbit antibody, human 125I-IGF-I and a second anti-rabbit antiserum. The acidification of the urine samples and the excess of IGF-II addition in the incubation medium of the assay were used to dissociate the binding and to block the interference from IGF binding proteins (IGFBPs). Urinary growth hormone (uGH), total protein (utPr) and creatinine (ucr) concentrations were also measured by immunoradiometric assay (IRMA), colorimetric and capillary electrophoresis methods, respectively. Results: The analysis range was 0–2500 ng/l (0–327 pmol/l), the intra- and inter-assay coefficients of variations (CVs) ranged from 2.3% to 7.8%, respectively. The detection limit was 0.6 pg/tube. The uIGF-I/creatinine (cr) ratio in healthy subjects was 70±8 pg/mg cr. The uIGF-I/creatinine ratio (pg/mg cr) was different ( p<0.001) in athletes before vs. after competition 93±27 vs. 136±13. Athletes' [uIGF-I/total proteins] ratio (ng/mg tPr) before and post-exercise was 2.3±0.5 and 2.5±0.3, respectively. Conclusions: uIGF-I assay appears to be an effective way of monitoring IGF-I excretion. In the cyclists, in the pre-exercise state, uIGF-I was comparable with that measured in sedentary healthy individuals. In the cyclists, after strenuous exercise, the increased uIGF-I/cr and uGH/cr ratios suggested a relation with the post-exercise proteinuria. In conclusion, proteinuria physiologically obtained, such as post-exercise proteinuria, might be a new approach in IGF-I system investigation.