Exercise-induced changes in blood zinc and related proteins in humans

1985 ◽  
Vol 58 (5) ◽  
pp. 1453-1458 ◽  
Author(s):  
H. Ohno ◽  
K. Yamashita ◽  
R. Doi ◽  
K. Yamamura ◽  
T. Kondo ◽  
...  

Effects of cycle ergometer exercise (approximately 75% maximum ventilatory O2 consumption for 30 min) on the concentrations of zinc and related proteins in erythrocytes and/or plasma were studied on 11 sedentary male students. Lower concentrations of total zinc and of zinc derived from carbonic anhydrase I type (CA-I) in erythrocytes were observed immediately after exercise, but they disappeared after 30 min of rest. The change in total zinc concentration in erythrocytes correlated well with that in CA-I concentration immediately after exercise, as well as after rest. The concentration of carbonic anhydrase II type (CA-II)-derived zinc did not vary substantially at any time. On the other hand, there were significant increases in the plasma concentrations of total zinc and of alpha 2-macroglobulin (alpha 2-MG)-bound zinc immediately after exercise, whereas no such effect was noted in albumin-bound zinc. A positive correlation was found between total zinc and alpha 2-MG concentrations in plasma immediately after exercise. In addition, the change in the activity of alkaline phosphatase, a zinc metalloenzyme, correlated well with that in the total zinc concentration in plasma. These results suggest that a brief physical exercise induces the movement of zinc into plasma.

1997 ◽  
Vol 82 (4) ◽  
pp. 1107-1111 ◽  
Author(s):  
Seiji Maeda ◽  
Takashi Miyauchi ◽  
Michiko Sakane ◽  
Makoto Saito ◽  
Shinichi Maki ◽  
...  

Maeda, Seiji, Takashi Miyauchi, Michiko Sakane, Makoto Saito, Shinichi Maki, Katsutoshi Goto, and Mitsuo Matsuda. Does endothelin-1 participate in the exercise-induced changes of blood flow distribution of muscles in humans? J. Appl. Physiol. 82(4): 1107–1111, 1997.—Endothelin-1 (ET-1) is an endothelium-derived potent vasoconstrictor peptide that potentiates contractions to norepinephrine in human vessels. We previously reported that the circulating plasma concentration of ET-1 is significantly increased after exercise (S. Maeda, T. Miyauchi, K. Goto, and M. Matsuda. J. Appl. Physiol. 77: 1399–1402, 1994). To study the roles of ET-1 during and after exercise, we investigated whether endurance exercise affects the production of ET-1 in the circulation of working muscles and nonworking muscles. Male athletes performed one-leg cycle ergometer exercise of 30-min duration at intensity of 110% of their individual ventilatory threshold. Plasma concentrations of ET-1 in both sides of femoral veins (veins in the working leg and nonworking leg) and in the femoral artery (artery in the nonworking leg) were measured before and after exercise. The plasma ET-1 concentration in the femoral vein in the nonworking leg was significantly increased after exercise, whereas that in femoral vein in the working leg was not changed. The arteriovenous difference in ET-1 concentration was significantly increased after exercise in the circulation of the nonworking leg but not of the working leg, which suggests that the production of ET-1 was increased in the circulation of the nonworking leg by exercise. The present study also demonstrated that the plasma norepinephrine concentrations were elevated by exercise in the femoral veins of both the working and nonworking legs, suggesting that the sympathetic nerve activity was augmented in both legs during exercise. Therefore, the present study demonstrates the possibility that the increase in production of ET-1 in nonworking muscles may cause vasoconstriction and hence decrease blood flow in nonworking muscles through its direct vasoconstrictive action or through an indirect effect of ET-1 to enhance vasoconstrictions to norepinephrine and that these responses may be helpful in increasing blood flow in working muscles. We propose that endogenous ET-1 contributes to the exercise-induced redistribution of blood flow in muscles.


1994 ◽  
Vol 266 (1) ◽  
pp. E136-E143 ◽  
Author(s):  
L. A. Mendenhall ◽  
S. C. Swanson ◽  
D. L. Habash ◽  
A. R. Coggan

We have previously shown that 12 wk of endurance training reduces the rate of glucose appearance (Ra) during submaximal exercise (Coggan, A. R., W. M. Kohrt, R. J. Spina, D. M. Bier, and J. O. Holloszy. J. Appl. Physiol. 68: 990-996, 1990). The purpose of the present study was to examine the time course of and relationship between training-induced alterations in glucose kinetics and endocrine responses during prolonged exercise. Accordingly, seven men were studied during 2 h of cycle ergometer exercise at approximately 60% of pretraining peak oxygen uptake on three occasions: before, after 10 days, and after 12 wk of endurance training. Ra was determined using a primed, continuous infusion of [6,6-2H]glucose. Ten days of training reduced mean Ra during exercise from 36.9 +/- 3.3 (SE) to 28.5 +/- 3.4 mumol.min-1.kg-1 (P < 0.001). Exercise-induced changes in insulin, C-peptide, glucagon, norepinephrine, and epinephrine were also significantly blunted. After 12 wk of training, Ra during exercise was further reduced to 21.5 +/- 3.1 mumol.min-1.kg-1 (P < 0.001 vs. 10 days), but hormone concentrations were not significantly different from 10-day values. The lower glucose Ra during exercise after short-term (10 days) training is accompanied by, and may be due to, altered plasma concentrations of the major glucoregulatory hormones. However, other adaptations must be responsible for the further reduction in Ra with more prolonged training.


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 41 (Supplement_2) ◽  
Author(s):  
C Nakata ◽  
A Goda ◽  
K Takeuchi ◽  
H Kikuchi ◽  
T Inami ◽  
...  

Abstract Background Exercise-induced elevation of pulmonary arterial wedge pressure (PAWP) may show preclinical or exercise-induced left ventricular diastolic dysfunction. Invasive hemodynamic assessment during provocative maneuvers, like exercise and volume challenge, in these patients allows greater sensitivity to diagnose or exclude HFpEF. The aim of this study was to examine how the leg raise, which is a simple way to increase preload, can detect exercise-induced PAWP elevation. Methods Four hundred seventy-nine patients (60±14y.o, mean pulmonary arterial pressure (PAP) 19mmHg, PAWP 8mmHg, CTEPH /IPAH/CTD-PH/SOB unknown reason: 357/56/38/28pts) with near-normal PAP and normal PAWP at rest underwent symptom-limited exercise test using supine cycle ergometer with right heart catheter. Exercise-induced elevation in PAWP of over 20mmHg was defined as exercise-induced elevation group. Results ΔPAWP (after leg raise - rest) in the exercise-induced elevation group was significantly higher (6.0±4.1 vs. 2.7±3.9mmHg, p&lt;0.001, in the older (age≥60y.o) group (n=276); 3.4±3.5 vs. 1.9±3.4mmHg, p&lt;0.001, in the younger (age&lt;60y.o) group (n=203)) than that in the non-elevation group after legs raise for cycle ergometer exercise. The area under the ROC curve for ΔPAWP was 0.72 (95% CI: 0.65–0.78) in the older and 0.64 (95% CI: 0.53–0.75) in the younger. In the older, the cut-off value for detect exercise-induced PAWP elevation of ΔPAWP was 4mmHg, with 72% sensitivity and 58% specificity. On the other hand, in the younger, the cut-off value was 3mmHg, with 69% sensitivity and 59% specificity. Conclusion Leg raise can easily detect occult left ventricular diastolic dysfunction. Funding Acknowledgement Type of funding source: None


1997 ◽  
Vol 83 (2) ◽  
pp. 407-413 ◽  
Author(s):  
Andrew Haskell ◽  
Ethan R. Nadel ◽  
Nina S. Stachenfeld ◽  
Kei Nagashima ◽  
Gary W. Mack

Haskell, Andrew, Ethan R. Nadel, Nina S. Stachenfeld, Kei Nagashima, and Gary W. Mack. Transcapillary escape rate of albumin in humans during exercise-induced hypervolemia. J. Appl. Physiol. 83(2): 407–413, 1997.—To test the hypotheses that plasma volume (PV) expansion 24 h after intense exercise is associated with reduced transcapillary escape rate of albumin (TERalb) and that local changes in transcapillary forces in the previously active tissues favor retention of protein in the vascular space, we measured PV, TERalb, plasma colloid osmotic pressure (COPp), interstitial fluid hydrostatic pressure (Pi), and colloid osmotic pressure in leg muscle and skin and capillary filtration coefficient (CFC) in the arm and leg in seven men and women before and 24 h after intense upright cycle ergometer exercise. Exercise expanded PV by 6.4% at 24 h (43.9 ± 0.8 to 46.8 ± 1.2 ml/kg, P< 0.05) and decreased total protein concentration (6.5 ± 0.1 to 6.3 ± 0.1 g/dl, P < 0.05) and COPp (26.1 ± 0.8 to 24.3 ± 0.9 mmHg, P < 0.05), although plasma albumin concentration was unchanged. TERalb tended to decline (8.4 ± 0.5 to 6.5 ± 0.7%/h, P = 0.11) and was correlated with the increase in PV ( r = −0.69, P < 0.05). CFC increased in the leg (3.2 ± 0.2 to 4.3 ± 0.5 μl ⋅ 100 g−1 ⋅ min−1 ⋅ mmHg−1, P < 0.05), and Pi showed a trend to increase in the leg muscle (2.8 ± 0.7 to 3.8 ± 0.3 mmHg, P = 0.08). These data demonstrate that TERalb is associated with PV regulation and that local transcapillary forces in the leg muscle may favor retention of albumin in the vascular space after exercise.


1980 ◽  
Vol 239 (3) ◽  
pp. G136-G140 ◽  
Author(s):  
J. Hilsted ◽  
H. Galbo ◽  
B. Sonne ◽  
T. Schwartz ◽  
J. Fahrenkrug ◽  
...  

Peripheral plasma concentrations of gastroenteropancreatic peptides were measured during a 3-h period of bicycle exercise at 40% of maximal oxygen uptake in six normal men. Marked increases (P < 0.02) were found in vasoactive intestinal polypeptide (VIP) [1.8 +/- 0.7 (rest) vs. 22.3 +/- 5.4 pmol x l-1 (mean +/- SE) (3 h)], secretin (0.5 +/- 0.5 vs. 11.1 +/- 2.7 pmol x l-1), pancreatic polypeptide (PP) (4.0 +/- 1.5 vs. 46.3 +/- 11.5 pmol x l-1), somatostatin (SRIF) (12.8 +/- 1.2 vs. 17.7 +/- 0.6 pmol x l-1), whereas no changes occurred in gastric inhibitory polypeptide (37.3 +/- 5.9 vs. 39.2 +/- 9.8 pmol x l-1). Immunoreactive insulin and C-peptide decreased from 0.08 +/- 0.004 and 0.39 +/- 0.03 pmol x l-1, respectively, to 0.04 +/- 0.003 (P < 0.005) and 0.13 +/- 0.02 (P < 0.001). The significant decrease in C-peptide and in the C-peptide-to-insulin molar ratio indicate decreased insulin secretion and clearance, respectively, during exercise. Plasma glucose decreased [5.0 +/- 0.1 (rest) vs. 4.2 +/- 0.3 mmol.l-1 (3 h)] (P < 0.01). During 3 h of rest, none of the measured parameters had changed. The marked exercise-induced changes in plasma concentrations of PP, secretin, VIP, and SRIF are provocative. We know in detail neither the stimuli for the release of these peptides nor their physiological role during exercise.


Author(s):  
Giovanni Messina ◽  
Giovanni Di Bernardo ◽  
Andrea Viggiano ◽  
Vincenzo De Luca ◽  
Vincenzo Monda ◽  
...  

AbstractBackground:The purpose of this research was to study the effects of exercise on the concentration of plasma orexin A, a peptide regulating several physiological functions.Methods:Blood samples were collected from participants (men, n=10; age: 24.4±2.93 years) 15, 0 min before the start of exercise, and 30, 45, 60 min after a cycle ergometer exercise at 75 W for 15 min. Also heart rate (HR), galvanic skin response (GSR), and rectal temperature were monitored.Results:The exercise induced a significant increase (p<0.01) in plasmatic orexin A with a peak at 30 min after the exercise bout, in association with an increase of the other three monitored variables: HR (p<0.01), GSR (p<0.05), and rectal temperature (p<0.01).Conclusions:Our findings indicate that plasmatic orexin A is involved in the reaction to physical activity.


2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
S.J Hwang ◽  
M.G Kang ◽  
K.H Kim ◽  
H.W Park ◽  
J.S Koh ◽  
...  

Abstract Background Invasive diastolic stress test using cycle ergometer is gold standard for diagnosis of heart failure with preserved ejection fraction (HFpEF) by demonstrating elevation of left ventricular end diastolic pressure (LVEDP) during exercise. It is well known that passive leg raising increases preload and augments LVEDP in HFpEF patients. However correlation between passive leg raising induced increase of LVEDP and cycle ergometer exercise induced increase of LVEDP is not well established. Therefore we investigated whether passive leg raising test could substitute cycle exercise test for diagnosis of HFpEF. Method Forty-five patients with unexplained dyspnea and ejection fraction &gt;50% underwent invasive exercise test. After measuring baseline LVEDP in supine position using pigtail catheter through radial artery approach, LVEDP during passive leg raising was evaluated. Then exercise LVEDP was measured after 3 minutes of 20 watt supine cycle ergometer exercise. Patients with normal resting LVEDP &lt;16mmHg were enrolled. Patients with cycle ergometer exercise LVEDP &gt;26mmHg were classified as HFpEF and exercise LVEDP &lt;26mmHg were defined as noncardiac dyspnea. Results Among 45 patients with unexplained dyspnea with preserved EF, 30 patients with ergometer exercise LVEDP &gt;26mmHg were grouped as HFpEF and 15 patients with exercise LVEDP &lt;26mmHg grouped as noncardiac dyspnea (NCD). Resting LVEDP was higher in HFpEF than NCD (14±2mmHg vs 11±3mmHg, P=0.01) but there was substantial overlap (figure 1) showing poor differentiation power of resting LVEDP. Passive leg raising increased LVEDP in both HFpEF and NCD but this was more marked in HFpEF group than in NCD group with minimal overlap (24±4mmHg vs 17±2mmHg, P&lt;0.001) (figure 2). Passive leg raising LVEDP was well correlated with cycle ergometer exercise LVEDP (R2=0.60, P&lt;0.01). The best cutoff value for passive leg raising LVEDP to detect HFpEF was 20mmHg (sensitivity, 0.87; specificity, 1.00), giving an area under the curve of 0.93 (95% confidence interval, 0.80 to 0.99). Positive predictive value of passive leg raising LVEDP &gt;20mmHg for diagnosis of HFpEF was 96% and negative predictive value was 77%. Conclusion Passive leg raising induced augmentation of left ventricular end diastolic pressure (LVEDP) was well correlated with cycle exercise induced elevation of LVEDP in HFpEF patients. Passive leg raising test may be used for detecting HFpEF with good accuracy in substitution for cycle ergometer exercise test. Funding Acknowledgement Type of funding source: None


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)


1994 ◽  
Vol 77 (3) ◽  
pp. 1399-1402 ◽  
Author(s):  
S. Maeda ◽  
T. Miyauchi ◽  
K. Goto ◽  
M. Matsuda

The purpose of this study was to investigate whether the release of endothelin-1 (ET-1), a potent vasoconstrictor peptide produced by vascular endothelial cells, is induced by exercise. Venous plasma concentrations of ET-1 were measured by sandwich-enzyme immunoassay before and after endurance exercise with a cycle ergometer at different intensities. Male intercollegiate athletes participated in the study and performed cycle ergometer exercise of 30 min duration at intensities of 90 or 130% of their individual ventilatory threshold (VT). The plasma concentration of ET-1 was slightly but significantly increased after exercise at 90% and markedly increased after exercise at 130% of individual VT. The increase in ET-1 was greatest 30 min after exercise at both intensities. It was first demonstrated that the plasma concentration of ET-1 was significantly increased after exercise: the greater the intensity, the greater the extent of the increase in plasma ET-1 concentration. However, the precise physiological roles of ET-1 during exercise remain to be elucidated.


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