Effect of exercise hemoconcentration and hyperosmolality on exercise responses

1988 ◽  
Vol 65 (2) ◽  
pp. 519-524 ◽  
Author(s):  
S. M. Fortney ◽  
N. B. Vroman ◽  
W. S. Beckett ◽  
S. Permutt ◽  
N. D. LaFrance

We investigated the effects of a decrease in plasma volume (PV) and an increase in plasma osmolality during exercise on circulatory and thermoregulatory responses. Six subjects cycled at approximately 65% of their maximum O2 uptake in a warm environment (30 degrees C, 40% relative humidity). After 30 min of control (C) exercise (no infusion), PV decreased 13.0%, or 419 +/- 106 (SD) ml, heart rate (HR) increased to 167 +/- 3 beats/min, and esophageal temperature (Tes) rose to 38.19 +/- 0.09 degrees C (SE). During infusion studies (INF), infusates were started after 10 min of exercise. The infusates contained 5% albumin suspended in 0.45, 0.9, or 3.0% saline. The volume of each infusate was adjusted so that during the last 10 min of exercise PV was maintained at the preexercise level and osmolality was allowed to differ. HR was significantly lower (10-16 beats/min) during INF than during C. Tes was reduced significantly during INF, with trends for increased skin blood flow and decreased sweating rates. No significant differences in HR, Tes, or sweating rate occurred between the three infusion conditions. We conclude that the decrease in PV, which normally accompanies moderate cycle exercise, compromises circulatory and thermal regulations. Increases in osmolality appear to have small if any effects during such short-term exercise.

1992 ◽  
Vol 73 (4) ◽  
pp. 1340-1350 ◽  
Author(s):  
S. J. Montain ◽  
E. F. Coyle

This investigation determined the effect of different rates of dehydration, induced by ingesting different volumes of fluid during prolonged exercise, on hyperthermia, heart rate (HR), and stroke volume (SV). On four different occasions, eight endurance-trained cyclists [age 23 +/- 3 (SD) yr, body wt 71.9 +/- 11.6 kg, maximal O2 consumption 4.72 +/- 0.33 l/min] cycled at a power output equal to 62-67% maximal O2 consumption for 2 h in a warm environment (33 degrees C dry bulb, 50% relative humidity, wind speed 2.5 m/s). During exercise, they randomly received no fluid (NF) or ingested a small (SF), moderate (MF), or large (LF) volume of fluid that replaced 20 +/- 1, 48 +/- 1, and 81 +/- 2%, respectively, of the fluid lost in sweat during exercise. The protocol resulted in graded magnitudes of dehydration as body weight declined 4.2 +/- 0.1, 3.4 +/- 0.1, 2.3 +/- 0.1, and 1.1 +/- 0.1%, respectively, during NF, SF, MF, and LF. After 2 h of exercise, esophageal temperature (Tes), HR, and SV were significantly different among the four trials (P < 0.05), with the exception of NF and SF. The magnitude of dehydration accrued after 2 h of exercise in the four trials was linearly related with the increase in Tes (r = 0.98, P < 0.02), the increase in HR (r = 0.99, P < 0.01), and the decline in SV (r = 0.99, P < 0.01). LF attenuated hyperthermia, apparently because of higher skin blood flow, inasmuch as forearm blood flow was 20–22% higher than during SF and NF at 105 min (P < 0.05). There were no differences in sweat rate among the four trials. In each subject, the increase in Tes from 20 to 120 min of exercise was highly correlated to the increase in serum osmolality (r = 0.81-0.98, P < 0.02-0.19) and the increase in serum sodium concentration (r = 0.87-0.99, P < 0.01-0.13) from 5 to 120 min of exercise. In summary, the magnitude of increase in core temperature and HR and the decline in SV are graded in proportion to the amount of dehydration accrued during exercise.


1989 ◽  
Vol 66 (1) ◽  
pp. 336-341 ◽  
Author(s):  
S. P. Sady ◽  
M. W. Carpenter ◽  
P. D. Thompson ◽  
M. A. Sady ◽  
B. Haydon ◽  
...  

Our purpose was to determine if pregnancy alters the cardiovascular response to exercise. Thirty-nine women [29 +/- 4 (SD) yr], performed submaximal and maximal exercise cycle ergometry during pregnancy (antepartum, AP, 26 +/- 3 wk of gestation) and postpartum (PP, 8 +/- 2 wk). Neither maximal O2 uptake (VO2max) nor maximal heart rate (HR) was different AP and PP (VO2 = 1.91 +/- 0.32 and 1.83 +/- 0.31 l/min; HR = 182 +/- 8 and 184 +/- 7 beats/min, P greater than 0.05 for both). Cardiac output (Q, acetylene rebreathing technique) averaged 2.2 to 2.8 l/min higher AP (P less than 0.01) at rest and at each exercise work load. Increases in both HR and stroke volume (SV) contributed to the elevated Q at the lower exercise work loads, whereas an increased SV was primarily responsible for the higher Q at higher levels. The slope of the Q vs. VO2 relationship was not different AP and PP (6.15 +/- 1.32 and 6.18 +/- 1.34 l/min Q/l/min VO2, P greater than 0.05). In contrast, the arteriovenous O2 difference (a-vO2 difference) was lower at each exercise work load AP, suggesting that the higher Q AP was distributed to nonexercising vascular beds. We conclude that Q is greater and a-vO2 difference is less at all levels of exercise in pregnant subjects than in the same women postpartum but that the coupling of the increase in Q to the increase in systemic O2 demand (VO2) is not different.(ABSTRACT TRUNCATED AT 250 WORDS)


1989 ◽  
Vol 256 (6) ◽  
pp. R1340-R1347 ◽  
Author(s):  
T. Kitanaka ◽  
R. D. Gilbert ◽  
L. D. Longo

To determine the maternal cardiovascular responses to long-term hypoxemia, we studied three groups of animals: 1) pregnant ewes (n = 20) at 110-115 days gestation subjected to hypoxia for up to 28 days; 2) pregnant ewes (n = 4) that served as normoxic controls; and 3) nonpregnant ewes (n = 6) subjected to hypoxemia for up to 28 days. We measured mean arterial pressure, heart rate, uterine blood flow, and uterine vascular resistance continuously for 1 h/day while the ewe was exposed to an inspired O2 fraction of 12-13% for at least 17 days. Arterial PO2, O2 saturation, hemoglobin, arteriovenous O2 difference, and uterine O2 uptake were measured daily while blood volume and erythropoietin concentration were measured weekly. In the pregnant hypoxic group arterial PO2 decreased from a control value of 101.5 +/- 5.1 to 59.2 +/- 5.1 Torr within a few minutes, where it remained throughout the study. The hemoglobin concentration increased from 8.9 +/- 0.5 to 10.0 +/- 0.5 g/dl within 24 h where it remained, whereas erythropoietin concentration increased from 16.6 +/- 2.1 to 39.1 +/- 7.8 mU/ml at 24 h but then returned to near-control levels. Arterial glucose concentration, mean arterial pressure, and cardiac output decreased slightly but insignificantly. In contrast, body weight, heart rate, blood volume, uterine blood flow, uterine O2 flow, uteroplacental O2 uptake, and the concentrations of catecholamines and cortisol remained relatively constant. Thus both pregnant and nonpregnant sheep experience relatively minor cardiovascular and hematologic responses in response to long-term hypoxemia of moderate severity.


2000 ◽  
Vol 278 (2) ◽  
pp. H321-H330 ◽  
Author(s):  
José González-Alonso ◽  
Ricardo Mora-Rodríguez ◽  
Edward F. Coyle

Euhydrated and dehydrated subjects exercised in a hot and a cold environment with our aim to identify factors that relate to reductions in stroke volume (SV). We hypothesized that reductions in SV with heat stress are related to the interaction of several factors rather than the effect of elevated skin blood flow. Eight male endurance-trained cyclists [maximal O2 consumption (V˙o 2 max) 4.5 ± 0.1 l/min; means ± SE] cycled for 30 min (72%V˙o 2 max) in the heat (H; 35°C) or the cold (C; 8°C) when euhydrated or dehydrated by 1.5, 3.0, or 4.2% of their body weight. When euhydrated, SV and esophageal temperature (Tes 38.2–38.3°C) were similar in H and C, whereas skin blood flow was much higher in H vs. C (365 ± 64% higher; P < 0.05). With each 1% body weight loss, SV declined 6.4 ± 1.3 ml (4.8%) in H and 3.4 ± 0.4 ml (2.5%) in C, whereas Tes increased 0.21 ± 0.02 and 0.10 ± 0.02°C in H and C, respectively ( P < 0.05). However, reductions in SV were not associated with increases in skin blood flow. The reduced SV was highly associated with increased heart rate and reduced blood volume in both H ( R = 0.96; P < 0.01) and C ( R = 0.85; P < 0.01). In conclusion, these results suggest that SV is maintained in trained subjects during exercise in euhydrated conditions despite large differences in skin blood flow. Furthermore, the lowering of SV with dehydration appears largely related to increases in heart rate and reductions in blood volume.


1992 ◽  
Vol 73 (4) ◽  
pp. 1232-1237 ◽  
Author(s):  
C. G. Tankersley ◽  
D. H. Zappe ◽  
T. G. Meister ◽  
W. L. Kenney

Elevated body core temperature stimulates cutaneous vasodilation, which can be modified by nonthermal factors. To test whether hypohydration affects forearm vascular conductance discretely from relative alterations in heart rate (HR), eight trained cyclists exercised progressively for 20 min each at 60, 120, and 180 W [approximately 22, 37, and 55% of maximal cycling O2 consumption (VO2peak), respectively] in a warm humid environment (dry bulb temperature 30 degrees C; wet bulb temperature 24 degrees C). Esophageal temperature and forearm blood flow were measured every 30 s, and mean arterial pressure and HR were measured at rest and during each exercise intensity (minutes 15, 35, and 55). In the hypovolemic (HP) compared with the euvolemic (EU) state, blood volume was contracted by 24-h fluid restriction an average of 510 ml, and this difference was sustained throughout exercise. The esophageal temperature and HR responses were similar between EU and HP states at 60 and 120 W but were significantly (P < 0.05) higher in HP by the end of 180 W. In contrast, the forearm blood flow response was significantly (P < 0.05) depressed during exercise at 120 and 180 W in HP, whereas mean arterial pressure remained similar between conditions. When body core temperature is elevated in a hypohydrated state, forearm vascular conductance is reduced at exercise intensities of approximately 37% VO2peak, which is independent of relative changes in HR. These findings are consistent with the notion that during exercise an attenuated cutaneous vasodilation is elicited by alterations in regionalized sympathetic outflow, which is unaccompanied by activation of cardiac pacemaker cells.


1984 ◽  
Vol 56 (5) ◽  
pp. 1411-1417 ◽  
Author(s):  
J. D. Shaffrath ◽  
W. C. Adams

Cardiovascular drift (CVD) can be defined as a progressive increase in heart rate (HR), decreases in stroke volume (SV) and mean arterial pressure (MAP), and a maintained cardiac output (Q) during prolonged exercise. To test the hypothesis that the magnitude of CVD would be related to changes in skin blood flow ( SkBF ), eight healthy, moderately trained males performed 70-min bouts of cycle ergometry in a 2 X 2 assortment of airflows (less than 0.2 and 4.3 m X s-1) and relative work loads (43.4% and 62.2% maximal O2 uptake). Ambient temperature and relative humidity were controlled to mean values of 24.2 +/- 0.8 degrees C and 39.5 +/- 2.4%, respectively. Q, HR, MAP, SkBF , skin and rectal temperatures, and pulmonary gas exchange were measured at 10-min intervals during exercise. Between the 10th and 70th min during exercise at the higher work load with negligible airflow, HR and SkBF increased by 21.6 beats X min-1 and 14.0 ml X 100 ml-1 X min-1, respectively, while SV and MAP decreased by 16.4 ml and 11.3 mmHg. The same work load in the presence of 4.3 m X s-1 airflow resulted in nonsignificant changes of 7.6 beats X min-1, 4.0 ml X (100 ml-1 X min)-1, -2.7 ml, and -1.7 mmHg for HR, SkBF , SV, and MAP. Since nonsignificant changes in HR, SkBF , SV, and MAP were observed at the lower work load in both airflow conditions, the results emphasize that CVD occurs only in conditions which combine high metabolic and thermal circulatory demands.(ABSTRACT TRUNCATED AT 250 WORDS)


1992 ◽  
Vol 73 (4) ◽  
pp. 1238-1245 ◽  
Author(s):  
C. G. Tankersley ◽  
W. C. Nicholas ◽  
D. R. Deaver ◽  
D. Mikita ◽  
W. L. Kenney

Thermoregulatory, cardiovascular, and body fluid responses during exercise in the heat were tested in five middle-aged (48 +/- 2 yr) women before and after 14–23 days of estrogen replacement therapy (ERT). The heat and exercise challenge consisted of a 40-min rest period followed by semirecumbent cycle exercise (approximately 40% maximal O2 uptake) for 60 min. At rest, the ambient temperature was elevated from a thermoneutral (dry bulb temperature 25 degrees C; wet bulb temperature 17.5 degrees C) to a warm humid (dry bulb temperature 36 degrees C; wet bulb temperature 27.5 degrees C) environment. Esophageal (Tes) and rectal (Tre) temperatures were measured to estimate body core temperature while arm blood flow and sweating rate were measured to assess the heat loss response. Mean arterial pressure and heart rate were measured to evaluate the cardiovascular response. Blood samples were analyzed for hematocrit (Hct), hemoglobin ([Hb]), plasma 17 beta-estradiol (E2), progesterone (P4), protein, and electrolyte concentrations. Plasma [E2] was significantly (P < 0.05) elevated by ERT without affecting the plasma [P4] levels. After ERT, Tes and Tre were significantly (P < 0.05) depressed by approximately 0.5 degrees C, and the Tes threshold for the onset of arm blood flow and sweating rate was significantly (P < 0.05) lower during exercise. After ERT, heart rate during exercise was significantly lower (P < 0.05) without notable variation in mean arterial pressure. Isotonic hemodilution occurred with ERT evident by significant (P < 0.05) reductions in Hct and [Hb], whereas plasma tonicity remained unchanged.(ABSTRACT TRUNCATED AT 250 WORDS)


1985 ◽  
Vol 59 (5) ◽  
pp. 1394-1401 ◽  
Author(s):  
M. N. Sawka ◽  
A. J. Young ◽  
R. P. Francesconi ◽  
S. R. Muza ◽  
K. B. Pandolf

We studied the effects of graded hypohydration levels on thermoregulatory and blood responses during exercise in the heat. Eight heat-acclimated male subjects attempted four heat-stress tests (HSTs). One HST was attempted during euhydration, and three HSTs were attempted while the subjects were hypohydrated by 3, 5, and 7% of their body weight. Hypohydration was achieved by an exercise-heat regimen on the day prior to each HST. After 30 min of rest in a 20 degrees C antechamber the HST consisted of a 140-min exposure (4 repeats of 10 min rest and 25 min treadmill walking) in a hot-dry (49 degrees C, 20% relative humidity) environment. The following observations were made: 1) a low-to-moderate hypohydration level primarily reduced plasma volume with little effect on plasma osmolality, whereas a more severe hypohydration level resulted in no further plasma volume reduction but a large increment in plasma osmolality; 2) core temperature and heart rate responses increased with severity of hypohydration; 3) sweating rate responses for a given rectal temperature were systematically decreased with severity of hypohydration; and 4) the reduction in sweating rate was more strongly associated with plasma hyperosmolality than hypovolemia. In conclusion, an individual's thermal strain increases linearly with the severity of hypohydration during exercise in the heat, and plasma hyperosmolality influences the reduction in sweating more profoundly than hypovolemia.


1986 ◽  
Vol 112 (2) ◽  
pp. 166-171 ◽  
Author(s):  
J. P. Bussien ◽  
R. C. Gaillard ◽  
J. Nussberger ◽  
B. Waeber ◽  
K. G. Hofbauer ◽  
...  

Abstract. The effect of vasopressin released during Finnish sauna on blood pressure, heart rate and skin blood flow was investigated in 12 healthy volunteers. Exposure to the hot air decrease body weight by 0.6 to 1.25 kg (mean = 0.8 kg, P < 0.001). One hour after the end of the sauna sessions, plasma vasopressin was higher (1.7 ± 0.2 pg/ml, P < 0.01 mean ± sem) than before the sauna (1.0 ± 0.1 pg/ml). No simultaneous change in plasma osmolality, plasma renin activity, plasma norepinephrine, epinephrine, cortisol, aldosterone, beta-endorphin and metenkephalin levels was observed. Despite the slight sauna-induced elevation in circulating vasopressin, intravenous injection of the specific vascular vasopressin antagonist d(CH2)5Tyr-(Me)AVP (5 μg/kg) 1 h after the sauna had no effect on blood pressure, heart rate or skin blood flow. These data suggest that vasopressin released into the circulation during a sauna session reaches concentrations which are not high enough to interfere directly with vascular tone.


1988 ◽  
Vol 65 (2) ◽  
pp. 657-661 ◽  
Author(s):  
S. P. Sady ◽  
M. W. Carpenter ◽  
M. A. Sady ◽  
B. Haydon ◽  
B. Hoegsberg ◽  
...  

We measured maximal O2 uptake (VO2max) during stationary cycling in 40 pregnant women [aged 29.2 +/- 3.9 (SD) yr, gestational age 25.9 +/- 3.3 wk]. Data from 30 of these women were used to develop an equation to predict the percent VO2max from submaximal heart rates. This equation and the submaximal VO2 were used to predict VO2max in the remaining 10 women. The accuracy of VO2max values estimated by this procedure was compared with values predicted by two popular methods: the Astrand nomogram and the VO2 vs. heart rate (VO2-HR) curve. VO2max values estimated by the derived equation method in the 10 validation subjects were only 3.7 +/- 12.2% higher than actual values (P greater than 0.05). The Astrand method overestimated VO2max by 9.0 +/- 19.4% (P greater than 0.05), whereas the VO2-HR curve method underestimated VO2max by only 1.6 +/- 10.3% in the same 10 subjects (P greater than 0.05). Both the Astrand and the VO2-HR curve methods correlated well with the actual values when all 40 subjects were considered (r = 0.77 and 0.85, respectively), but the VO2-HR curve method had a lower SE of prediction than the Astrand method (8.7 vs. 10.4%). In a comparison group of 10 nonpregnant sedentary women (29.9 +/- 4.5 yr), an equation relating %VO2max to HR nearly identical to that obtained in the pregnant women was found, suggesting that pregnancy does not alter this relationship. We conclude that extrapolating the VO2-HR curve to an estimated maximal HR is the most accurate method of predicting VO2max in pregnant women.


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