A genetic study of sex hormone—Binding globulin measured before and after a 20-week endurance exercise training program: The HERITAGE Family Study

Metabolism ◽  
2000 ◽  
Vol 49 (8) ◽  
pp. 1014-1020 ◽  
Author(s):  
Ping An ◽  
Treva Rice ◽  
Jacques Gagnon ◽  
Yuling Hong ◽  
Arthur S. Leon ◽  
...  
1990 ◽  
Vol 258 (3) ◽  
pp. H842-H847 ◽  
Author(s):  
S. E. DiCarlo ◽  
V. S. Bishop

This study was designed to determine whether cardiac vagal afferents exert an inhibitory influence on increases in regional vascular resistance during exercise and to determine whether endurance exercise training enhances the inhibitory influence of cardiac vagal afferents. We measured changes in regional vascular resistance in 12 rabbits at rest and during running at 12.6 m/min, 20% grade, before and after reversible denervation of cardiac afferents (intrapericardial procainamide HCl, 2%). In addition, these procedures were repeated in five of these rabbits following an 8-wk endurance exercise training program. Because intrapericardial injections of procainamide anesthetize both the efferent as well as the afferent innervation to the heart, it was necessary to determine the effects of blocking the efferent innervation on the regulation of regional vascular resistance during exercise. Rabbits were instrumented with Doppler ultrasonic flow probes around the renal (R), mesenteric (M), ascending, and terminal aortic (TA) arteries. Catheters were positioned in the central ear artery and vein and pericardial sac. Mean arterial pressure, heart rate, cardiac output, R, M, TA, and systemic (S) resistances were determined. Exercise changed R (+37 +/- 4%), M (+88 +/- 9%), TA (-62 +/- 6%), and S (-34 +/- 3) resistances. Subsequent cardiac efferent blockade alone had no significant effect on regional vascular resistance during exercise. Combined efferent and afferent blockade resulted in significant increases in R (+62 +/- 6%) and M resistance (+134 +/- 13%) but did not alter TA (-51 +/- 4%) or S (-27 +/- 2%) resistance during exercise. Exercise training significantly enhanced the inhibitory influence of cardiac afferents on R and M regional vascular resistance.(ABSTRACT TRUNCATED AT 250 WORDS)


1978 ◽  
Vol 44 (6) ◽  
pp. 877-881 ◽  
Author(s):  
R. C. Hickson ◽  
H. A. Bomze ◽  
J. O. Hollozy

The purpose of this study was to determine the effect of endurance exercise training on the time course of the increase in VO2 toward steady state in response to submaximal constant load work. Seven men participated in a strenuous program of endurance exercise for 40 min/day, 6 days/wk for 10 wk. Their average VO2max increased from 3.29 liters before training to 4.53 liters at the end of the training program. VO2 was measured continuously on a breath-by-breath basis at work rates requiring 40%, 50%, 60%, or 70% of VO2max before training. After training the subjects were retested both at the same absolute and the same relative work rates. The increases in VO2 toward steady state occurred more rapidly in the trained than in the untrained state both at the same absolute and at the same relative work rates. The finding that O2 uptake rises to meet O2 demand more rapidly in the trained than in the untrained state provides evidence that the working muscles become less hypoxic at the onset of exercise of the same intensity after training.


2000 ◽  
Vol 278 (4) ◽  
pp. E580-E587 ◽  
Author(s):  
Scott McKenzie ◽  
Stuart M. Phillips ◽  
Sherry L. Carter ◽  
Stuart Lowther ◽  
Martin J. Gibala ◽  
...  

We studied the effects of a 38-day endurance exercise training program on leucine turnover and substrate metabolism during a 90-min exercise bout at 60% peak O2 consumption (V˙o 2 peak) in 6 males and 6 females. Subjects were studied at both the same absolute (ABS) and relative (REL) exercise intensities posttraining. Training resulted in a significant increase in whole bodyV˙o 2 peak and skeletal muscle citrate synthase (CS; P < 0.001), complex I-III ( P < 0.05), and total branched-chain 2-oxoacid dehydrogenase (BCOAD; P < 0.001) activities. Leucine oxidation increased during exercise for the pretraining trial (PRE, P < 0.001); however, there was no increase for either the ABS or REL posttraining trial. Leucine oxidation was significantly lower for females at all time points during rest and exercise ( P < 0.01). The percentage of BCOAD in the activated state was significantly increased after exercise for both the PRE and REL exercise trials, with the increase in PRE being greater ( P < 0.001) compared with REL ( P < 0.05). Females oxidized proportionately more lipid and less carbohydrate during exercise compared with males. In conclusion, we found that 38 days of endurance exercise training significantly attenuated both leucine oxidation and BCOAD activation during 90 min of endurance exercise at 60%V˙o 2 peak for both ABS and REL exercise intensities. Furthermore, females oxidize proportionately more lipid and less carbohydrate compared with males during endurance exercise.


2002 ◽  
Vol 92 (6) ◽  
pp. 2368-2374 ◽  
Author(s):  
Annette N. Senitko ◽  
Nisha Charkoudian ◽  
John R. Halliwill

In sedentary individuals, postexercise hypotension after a single bout of aerobic exercise is due to a peripheral vasodilation. Endurance exercise training has the potential to modify this response and perhaps reduce the degree of postexercise hypotension. We tested the hypothesis that endurance exercise-trained men and women would have blunted postexercise hypotension compared with sedentary subjects but that the mechanism of hypotension would be similar (i.e., vasodilation). We studied 16 endurance-trained and 16 sedentary men and women. Arterial pressure, cardiac output, and total peripheral resistance were determined before and after a single 60-min bout of exercise at 60% peak oxygen consumption. All groups exhibited a similar degree of postexercise hypotension (∼4–5 mmHg; P < 0.05 vs. preexercise). In sedentary men and women, hypotension was the result of vasodilation (Δresistance: −8.9 ± 2.2%). In endurance-trained women, hypotension was also the result of vasodilation (−8.1 ± 4.1%). However, in endurance-trained men, hypotension was the result of a reduced cardiac output (−5.2 ± 2.4%; P < 0.05 vs. all others) and vasodilation was absent (−0.7 ± 3.3%; P < 0.05 vs. all others). Thus we conclude the magnitude of postexercise hypotension is similar in sedentary and endurance-trained men and women but that endurance-trained men and women achieve this fall in pressure via different mechanisms.


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