Dynamic exercise in senescent beagles: oxygen consumption and hemodynamic responses

1989 ◽  
Vol 257 (5) ◽  
pp. H1428-H1437 ◽  
Author(s):  
G. C. Haidet

Seven senescent beagles and seven younger mature beagles were studied at rest, as well as during maximal and submaximal exercise on a motor-driven treadmill. Maximal exercise capacity was significantly (P less than 0.05) reduced, and maximal total body O2 consumption (VO2 max) was 31% lower in senescent beagles. VO2 was also significantly reduced in old dogs, when directly compared at the same relative workloads in old and younger mature dogs. However, VO2 was very similar in both groups during each of the absolute levels of directly comparable exercise. The observed age-related reduction in VO2 max was associated with a significant 25% reduction in maximal cardiac output (CO) in senescent beagles, and with an 11% reduction in maximal arteriovenous O2 difference. CO was also significantly reduced in old dogs at the same relative levels of submaximal exercise evaluated. Combined effects of reductions in stroke volume and in heart rate both contributed to the observed reductions in CO observed in senescent dogs during maximal exercise, as well as during relative levels of submaximal exercise. However, CO responses at each absolute level of submaximal exercise were similar in senescent and younger mature beagles, and the relationship between CO and VO2 was also similar in both groups. Increases in stroke volume significantly contributed to observed increases in CO beginning at the same relative level of exercise in both old and young dogs. Results of this study demonstrate that significant age-related changes in VO2max and in other associated hemodynamic parameters occur during maximal exercise. Many of these changes are also apparent when relative levels of submaximal exercise are directly compared in senescent and in younger mature beagles. However, most hemodynamic responses during absolute levels of exercise are similar in both groups, unless these parameters reflect the relative workload performed, indicating that these responses are appropriate for each absolute level of work that can be performed in the senescent dogs.

1985 ◽  
Vol 59 (1) ◽  
pp. 183-189 ◽  
Author(s):  
T. I. Musch ◽  
G. C. Haidet ◽  
G. A. Ordway ◽  
J. C. Longhurst ◽  
J. H. Mitchell

Ten foxhounds were studied during maximal and submaximal exercise on a motor-driven treadmill before and after 8–12 wk of training. Training consisted of working at 80% of maximal heart rate 1 h/day, 5 days/wk. Maximal O2 consumption (VO2max) increased 28% from 113.7 +/- 5.5 to 146.1 +/- 5.4 ml O2 X min-1 X kg-1, pre- to posttraining. This increase in VO2max was due primarily to a 27% increase in maximal cardiac output, since maximal arteriovenous O2 difference increased only 4% above pretraining values. Mean arterial pressure during maximal exercise did not change from pre- to posttraining, with the result that calculated systemic vascular resistance (SVR) decreased 20%. There were no training-induced changes in O2 consumption, cardiac output, arteriovenous O2 difference, mean arterial pressure, or SVR at any level of submaximal exercise. However, if post- and pretraining values are compared, heart rate was lower and stroke volume was greater at any level of submaximal exercise. Venous lactate concentrations during a given level of submaximal exercise were significantly lower during posttraining compared with pretraining, but venous lactate concentrations during maximal exercise did not change as a result of exercise training. These results indicate that a program of endurance training will produce a significant increase in VO2max in the foxhound. This increase in VO2max is similar to that reported previously for humans and rats but is derived primarily from central (stroke volume) changes rather than a combination of central and peripheral (O2 extraction) changes.


1990 ◽  
Vol 68 (2) ◽  
pp. 586-593 ◽  
Author(s):  
E. E. Wolfel ◽  
W. R. Hiatt ◽  
H. L. Brammell ◽  
V. Travis ◽  
L. D. Horwitz

Exercise training has been shown to decrease plasma norepinephrine (NE) and epinephrine (EPI) levels during absolute levels of submaximal exercise, which may reflect alterations in sympathetic tone as a result of training. To determine if beta-adrenergic blockade altered these changes in the plasma concentration of catecholamines with exercise conditioning, we studied the effects of beta-adrenergic blockade on NE and EPI at rest and during exercise in 24 healthy, male subjects after a 6-wk exercise training program. The subjects were randomized to placebo (P), atenolol 50 mg twice daily (A), and nadolol 40 mg twice daily (N). There were no changes in resting NE and EPI compared with pretraining values in any subject group. During the same absolute level of submaximal exercise NE decreased in P and A but was unchanged in N, whereas EPI decreased only in P. At maximal exercise all three groups developed significant increases in NE after training that paralleled increases in systolic blood pressure. EPI at maximal exercise increased after training with N but was unchanged with P or A. These training-induced changes in plasma catecholamine levels were masked or blunted when the A and N groups were studied while still on medication after training. Thus beta-adrenergic blockade has important effects on adaptations of the sympathetic nervous system to training, especially during submaximal exercise.


2006 ◽  
Vol 101 (3) ◽  
pp. 938-944 ◽  
Author(s):  
Edward P. Weiss ◽  
Robert J. Spina ◽  
John O. Holloszy ◽  
Ali A. Ehsani

We investigated the hemodynamic determinants of the age-associated decline in maximal oxygen uptake (V̇o2 max) and the influence of gender on the decline in V̇o2 max and its determinants in old and very old men and women. Sedentary, 60- to 92-yr-old women ( n = 71) and men ( n = 29), with no evidence of cardiovascular disease, underwent maximal treadmill exercise tests during which V̇o2 max and maximal cardiac output (Q̇max) were determined. V̇o2 max and age were inversely related in both women (−23 ± 2 ml·min−1·yr−1; P < 0.0001) and men (−57 ± 5 ml·min−1·yr−1; P < 0.0001). The absolute slope of the V̇o2 max vs. age relationship was twofold steeper in men than in women ( P < 0.0001). Q̇max was also inversely related to age in a gender-specific manner (women = −87 ± 25 ml·min−1·yr−1, P = 0.0009; men = −215 ± 50 ml·min−1·yr−1, P = 0.0002; P = 0.01 women vs. men). Age-related changes in maximal exercise arteriovenous oxygen content difference (a-vDo2) were marginally different ( P = 0.08) between women (−0.12 ± 0.03 ml·dl−1·yr−1, P = 0.0003) and men (−0.22 ± 0.04 ml·dl−1·yr−1, P < 0.0001). Age-associated decreases in Q̇max and a-vDo2 contributed equally to the declines in V̇o2 max in both men and women. In the later stages of life, V̇o2 max, Q̇max, and a-vDo2 decrease with age more rapidly in older men than they do in older women. As a result, the gender differences dissipate in the later decades of life. Declines in Q̇max and a-vDo2 contribute equally to the age-related decrease in V̇o2 max in men and women.


1989 ◽  
Vol 66 (3) ◽  
pp. 1506-1508 ◽  
Author(s):  
R. S. Mazzeo ◽  
P. A. Grantham

It was the purpose of this investigation to examine any age-related changes in norepinephrine turnover (NEt) in four tissues at rest and during exercise. Fischer 344 rats 6 (n = 20) and 25 mo of age (n = 20) were received from the National Institute on Aging. NEt was determined at rest, during 30 min of submaximal exercise, and at maximal exercise by administration of alpha-methyl-p-tyrosine, a competitive inhibitor of tyrosine hydroxylase. Resting NE declined with age in both heart (38.2 vs. 30.5 ng.g-1.h-1) and liver (11.2 vs. 6.4 ng.g-1.h-1). NEt was greater in the older animals compared with the young animals in heart (120.9 vs. 169.5 ng.g-1.h-1), liver (23.1 vs. 38.9 ng.g-1.h-1), and adrenals (74.0 vs. 98.4 ng.mg-1.h-1) during submaximal exercise. In response to maximal exercise, NEt varied depending on age and tissue. It was concluded that, in response to exercise stress, the older animals generally demonstrated a higher NEt (reflecting elevated sympathetic activity) perhaps because of a decreased adrenergic receptor sensitivity and/or responsiveness.


1994 ◽  
Vol 77 (3) ◽  
pp. 1341-1348 ◽  
Author(s):  
N. C. Gonzalez ◽  
L. P. Erwig ◽  
C. F. Painter ◽  
R. L. Clancy ◽  
P. D. Wagner

The effect of hematocrit (Hct) on O2 transport in hypoxic [inspired PO2 (PIO2) approximately 70 Torr] and normoxic (PIO2 approximately 145 Torr) exercise was studied in rats acclimatized to 3 wk of PIO2 at approximately 70 Torr (A rats) and in nonacclimatized littermates (NA rats). Isovolumic exchange transfusion of plasma or red blood cells was used to lower Hct in A rats from approximately 60 to 45% and to raise Hct of NA rats from 45 to 60%: Controls were A and NA rats exchange transfused with whole blood at constant Hct. Lowering Hct of A rats lowered the arterial O2 concentration (CaO2) and the arterial-mixed venous O2 difference and increased the maximal cardiac output (Qmax) without changes in maximal O2 uptake (VO2 max) or in the product of Qmax x CaO2, circulatory O2 convection at maximal exercise (TO2 max). Raising Hct in NA rats produced the opposite changes in CaO2, arterial-mixed venous O2 difference, and Qmax, but VO2 max and TO2 max increased significantly, both in hypoxia and normoxia, because of relatively small changes in Qmax. In NA rats, a steeper slope of the line relating VO2 max to calculated mean capillary PO2 at high Hct suggested a higher tissue O2 diffusing capacity with high Hct. For a given Hct and Qmax, systemic arterial pressure was higher in A rats. The data suggest that 1) the effect of Hct on systemic hemodynamics is different in A and NA rats, resulting in different effects on VO2 max; 2) factors in addition to Hct contribute to the high systemic vascular resistance of A rats; and 3) increased diffusive conductance for O2, as well as increased TO2 max, could be responsible for the effect of Hct on VO2 max of NA rats.


1988 ◽  
Vol 64 (1) ◽  
pp. 404-408 ◽  
Author(s):  
M. K. Hopper ◽  
A. R. Coggan ◽  
E. F. Coyle

The effects of plasma-volume (PV) expansion on stroke volume (SV) (CO2 rebreathing) during submaximal exercise were determined. Intravenous infusion of 403 +/- 21 ml of a 6% dextran solution before exercise in the upright position increased SV 11% (i.e., 130 +/- 6 to 144 +/- 5 ml; P less than 0.05) in untrained males (n = 7). Further PV expansion (i.e., 706 +/- 43 ml) did not result in a further increase in SV (i.e., 145 +/- 4 ml). SV was somewhat higher during supine compared with upright exercise when blood volume (BV) was normal (i.e., 138 +/- 8 vs. 130 +/- 6 ml; P = 0.08). PV expansion also increased SV during exercise in the supine position (i.e., 138 +/- 8 to 150 +/- 8 ml; P less than 0.05). In contrast to these observations in untrained men, PV expansion of endurance-trained men (n = 10), who were naturally PV expanded, did not increase SV during exercise in the upright or supine positions. When BV in the untrained men was increased to match that of the endurance-trained subjects, SV was observed to be 15% higher (165 +/- 7 vs. 144 +/- 5 ml; P less than 0.05), whereas mean blood pressure and total peripheral resistance were significantly lower (P less than 0.05) in the trained compared with untrained subjects during upright exercise at a similar heart rate. The present findings indicate that exercise SV in untrained men is preload dependent and that increases in exercise SV occur in response to the first 400 ml of PV expansion. It appears that approximately one-half of the difference in SV normally observed between untrained and highly endurance-trained men during upright exercise is due to a suboptimal BV in the untrained men.


1988 ◽  
Vol 65 (2) ◽  
pp. 964-970 ◽  
Author(s):  
T. I. Musch ◽  
A. Bruno ◽  
G. E. Bradford ◽  
A. Vayonis ◽  
R. L. Moore

Two different open-circuit techniques of measuring metabolic rate were examined in rats at rest and during exercise. With one technique ambient air was drawn through a tightly fitting mask that was secured to the rat's head, whereas with the other technique the rat was placed into and ambient air was drawn through a Plexiglas box. Two series of experiments were performed. In series I, two groups were studied that consisted of rats that had received myocardial infarctions produced by coronary arterial ligations and rats that had received sham operations. In this series of experiments O2 uptake (VO2) and CO2 production (VCO2) were measured at rest, during four levels of submaximal exercise, and during maximal treadmill exercise in the same group of rats by use of both techniques in random order. VO2, VCO2, and the calculated respiratory exchange ratio (R) were similar at rest, during the highest level of submaximal exercise (20% grade, 37 m/min), and during maximal exercise; however, VO2 and VCO2 were significantly lower with the metabolic box technique compared with the mask technique during the three lowest work loads (5% grade, 19 m/min; 10% grade, 24 m/min; and 15% grade, 31 m/min). These differences appeared to be associated with a change in gait produced when the mask was worn. In series II, the arterial blood gas and acid-base responses to both submaximal and maximal exercise were measured using both techniques in a group of instrumented rats that had a catheter placed into the right carotid artery.(ABSTRACT TRUNCATED AT 250 WORDS)


1992 ◽  
Vol 72 (4) ◽  
pp. 1437-1443 ◽  
Author(s):  
T. I. Musch

The hemodynamic response to maximal exercise was determined in rats with a chronic myocardial infarction (MI) that were subjected to 6–8 wk of high-intensity sprint training (HIST) or limited exercise activity (sedentary control). Training was performed 6 days/wk and consisted of five 1-min bouts of treadmill running at work loads (15% grade, 97 m/min) in excess of the animal's maximal O2 uptake (VO2max). The left ventricular infarct size for the HIST and sedentary control rats was 35 +/- 4 and 34 +/- 3% of the total endocardial circumference, respectively. VO2max was significantly greater for MI rats subjected to the HIST paradigm than for sedentary control rats. This increase in VO2max was due to an increase in the maximal stroke volume that could be generated by the HIST rat during exercise, inasmuch as the maximal heart rate response and the ability to extract O2 from the blood were similar between the two groups of rats. Citrate synthase activities measured in the plantaris muscle of the HIST and sedentary control rats were similar. These results suggest that the increase in VO2max produced with HIST in MI rats may be linked to changes in central cardiac function, as indicated by the increase in maximal stroke volume that could be generated by the MI rat during maximal exercise conditions.


1989 ◽  
Vol 66 (2) ◽  
pp. 949-954 ◽  
Author(s):  
A. M. Rivera ◽  
A. E. Pels ◽  
S. P. Sady ◽  
M. A. Sady ◽  
E. M. Cullinane ◽  
...  

We examined the hemodynamic factors associated with the lower maximal O2 consumption (VO2max) in older formerly elite distance runners. Heart rate and VO2 were measured during submaximal and maximal treadmill exercise in 11 master [66 +/- 8 (SD) yr] and 11 young (32 +/- 5 yr) male runners. Cardiac output was determined using acetylene rebreathing at 30, 50, 70, and 85% VO2max. Maximal cardiac output was estimated using submaximal stroke volume and maximal heart rate. VO2max was 36% lower in master runners (45.0 +/- 6.9 vs. 70.4 +/- 8.0 ml.kg-1.min-1, P less than or equal to 0.05), because of both a lower maximal cardiac output (18.2 +/- 3.5 vs. 25.4 +/- 1.7 l.min-1) and arteriovenous O2 difference (16.6 +/- 1.6 vs. 18.7 +/- 1.4 ml O2.100 ml blood-1, P less than or equal to 0.05). Reduced maximal heart rate (154.4 +/- 17.4 vs. 185 +/- 5.8 beats.min-1) and stroke volume (117.1 +/- 16.1 vs. 137.2 +/- 8.7 ml.beat-1) contributed to the lower cardiac output in the older athletes (P less than or equal 0.05). These data indicate that VO2max is lower in master runners because of a diminished capacity to deliver and extract O2 during exercise.


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