TGF-β1 gene-race interactions for resting and exercise blood pressure in the HERITAGE Family Study

2001 ◽  
Vol 91 (4) ◽  
pp. 1808-1813 ◽  
Author(s):  
Miguel A. Rivera ◽  
Marcos Echegaray ◽  
Tuomo Rankinen ◽  
Louis Pérusse ◽  
Treva Rice ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Acute Exercise ◽  
Transforming Growth Factor ◽  
Family Study ◽  
Maximal Oxygen Consumption ◽  
Acute Response ◽  
Exercise Blood Pressure ◽  
Before And After ◽  
Normotensive Subjects ◽  
Response To Exercise

We examined the possible association between a transforming growth factor (TGF)-β1 gene polymorphism in codon 10 and blood pressure (BP) at rest, in acute response to exercise in the pretrained (sedentary) and trained states, as well as in its training response (Δ) to 20 wk of endurance exercise. Subjects were 257 black and 480 white, healthy sedentary normotensive subjects from the HERITAGE Family Study. The polymorphism was detected by polymerase chain reaction and digestion with the Msp A1 I endonuclease yielding a wild (leucine-10) and a mutant (proline-10) allele. Resting and exercise [50 W plus 60, 80, and 100% maximal oxygen consumption (V˙o 2 max)] BP were determined before and after training. Significant ( P < 0.05) race-genotype interactions were found for systolic (S) BP in both the sedentary and trained states. Among whites but not in blacks, the TGF-β1 genotypes were significantly ( P < 0.05) associated with sedentary-state SBP at rest, at 50 W, and at 60 and 100% V˙o 2 max as well as with trained-state SBP at rest and at 80 and 100%V˙o 2 max. The leucine-10 homozygotes had significantly ( P < 0.05) lower SBP than proline-10 homozygotes. ΔBP was not significantly associated with genotype. These results support the hypothesis of an association between the TGF-β1 marker in codon 10 and SBP at rest and in response to acute exercise in whites but not in blacks.

scholarly journals AGT M235T and ACE ID polymorphisms and exercise blood pressure in the HERITAGE Family Study

2000 ◽  
Vol 279 (1) ◽  
pp. H368-H374 ◽  
Author(s):  
Tuomo Rankinen ◽  
Jacques Gagnon ◽  
Louis Pérusse ◽  
Yvon C. Chagnon ◽  
Treva Rice ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Endurance Training ◽  
Gene Polymorphisms ◽  
Maximal Exercise ◽  
Family Study ◽  
Submaximal Exercise ◽  
Exercise Tests ◽  
Exercise Blood Pressure ◽  
Before And After ◽  
The Difference

We investigated the association between angiotensinogen (AGT) and angiotensin-converting enzyme (ACE) gene polymorphisms and exercise training responses of resting and exercise blood pressure (BP). BP at rest and during submaximal (50 watts) and maximal exercise tests was measured before and after 20 wk of endurance training in 476 sedentary normotensive Caucasian subjects from 99 families. AGT M235T and ACE insertion/deletion polymorphisms were typed with PCR-based methods. Men carrying the AGT MM and MT genotypes showed 3.7 ± 0.6 and 3.2 ± 0.5 (SE) mmHg reductions, respectively, in diastolic BP at 50 watts (DBP50), whereas, in the TT homozygotes, the decrease was 0.4 ± 1.0 mmHg ( P = 0.016 for trend, adjusted for age, body mass index, and baseline DBP50). Men with the ACE DD genotype showed a slightly greater decrease in DBP50 (4.4 ± 0.6 mmHg) than the II and ID genotypes (2.8 ± 0.7 and 2.4 ± 0.5 mmHg, respectively, P = 0.050). Furthermore, a significant ( P = 0.022) interaction effect between the AGT and ACE genes was noted for DBP50; the AGT TT homozygotes carrying the ACE D allele showed no response to training. Men with the AGT TT genotype had greater ( P = 0.007) diastolic BP (DBP) response to acute maximal exercise at baseline. However, the difference disappeared after the training period. No associations were found in women. These data suggest that, in men, the genetic variation in the AGT locus modifies the responsiveness of submaximal exercise DBP to endurance training, and interactions between the AGT and ACE loci can alter this response.

Angiogenin gene-race interaction for resting and exercise BP phenotypes: the HERITAGE Family Study

2001 ◽  
Vol 90 (4) ◽  
pp. 1232-1238 ◽  
Author(s):  
Miguel A. Rivera ◽  
Marcos Echegaray ◽  
Tuomo Rankinen ◽  
Louis Pérusse ◽  
Treva Rice ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Gene Polymorphism ◽  
Training Program ◽  
High Intensity ◽  
Acute Exercise ◽  
Family Study ◽  
Rare Allele ◽  
Genotypic Effect ◽  
Before And After ◽  
Rest And Exercise

We examined the association between an angiogenin gene polymorphism and blood pressure (BP) at rest and in response to acute exercise before and after a 20-wk endurance-training program. Subjects were 737 normotensive and borderline hypertensive subjects (257 black and 480 white). The polymorphism was detected by PCR and digestion with AvaII, yielding an allele of 253 bp or a rare allele of 194 + 59 bp. Resting and exercise [50 W; 60, 80, and 100% of maximal O2 consumption (V˙o 2 max)] systolic (SBP) and diastolic BP were determined before and after training. Among blacks, adjusted SBP in the sedentary state was significantly lower in carriers of the rare allele at rest and exercise intensities of 60, 80, and 100% ofV˙o 2 max. In the trained state, carriers of the rare allele had a significantly ( P < 0.05) lower SBP than did noncarriers at rest and at 80 and 100% ofV˙o 2 max. The genotypic effect observed among blacks was not evident among whites. Furthermore, change in BP (after − before) was not significantly associated with the genotype. In conclusion, the angiogenin gene AvaII polymorphism is associated with a lower SBP at rest and in response to acute high-intensity exercise in blacks but not in whites.

Effects of combined histamine H1 and H2 receptor blockade on hemodynamic responses to dynamic exercise in males with high-normal blood pressure

2020 ◽  
Vol 45 (7) ◽  
pp. 769-776
Author(s):  
Ashley Naylor ◽  
Brian Shariffi ◽  
Trevor L. Gillum ◽  
Boyer William ◽  
Sean Sullivan ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Dynamic Exercise ◽  
Histamine Receptors ◽  
Normal Group ◽  
Receptor Blockade ◽  
Peripheral Vasoconstriction ◽  
Before And After ◽  
Group A ◽  
Postexercise Hypotension ◽  
Response To Exercise

While postexercise hypotension is associated with histamine H1 and H2 receptor-mediated postexercise vasodilation, effects of histaminergic vasodilation on blood pressure (BP) in response to dynamic exercise are not known. Thus, in 20 recreationally active male participants (10 normotensive and 10 with high-normal BP) we examined the effects of histamine H1 and H2 receptor blockade on cardiac output (CO), mean atrial pressure (MAP), aortic stiffness (AoStiff), and total vascular conductance (TVC) at rest and during progressive cycling exercise. Compared with the normotensive group, MAP, CO, and AoStiff were higher in the high-normal group before and after the blockade at rest, while TVC was similar. At the 40% workload, the blockade significantly increased MAP in both groups, while no difference was found in the TVC. CO was higher in the high-normal group than the normotensive group in both conditions. At the 60% workload, the blockade substantially increased MAP and decreased TVC in the normotensive group, while there were no changes in the high-normal group. A similar CO response pattern was observed at the 60% workload. These findings suggest that the mechanism eliciting an exaggerated BP response to exercise in the high-normal group may be partially due to the inability of histamine receptors. Novelty Males with high-normal BP had an exaggerated BP response to exercise. The overactive BP response is known due to an increase in peripheral vasoconstriction. Increase in peripheral vasoconstriction is partially due to inability of histamine receptors.

Sex-based effects on the distribution of NK cell subsets in response to exercise and carbohydrate intake in adolescents

2006 ◽  
Vol 100 (5) ◽  
pp. 1513-1519 ◽  
Author(s):  
Brian W. Timmons ◽  
Mark A. Tarnopolsky ◽  
Oded Bar-Or
Keyword(s):  
Oxygen Consumption ◽  
Acute Exercise ◽  
Nk Cell ◽  
Maximal Oxygen Consumption ◽  
Exercise Immunology ◽  
Cell Counts ◽  
Flavored Water ◽  
Response To Exercise ◽  
Activation Marker Cd69 ◽  
Activation Status

Carbohydrate (CHO) supplementation and female sex independently influence the natural killer (NK) cell response to acute exercise. Consequently, this study sought to elucidate sex-based differences in the distribution of NK cell subsets (i.e., CD56dimand CD56bright) in response to exercise and CHO intake. Twenty-two healthy 14-yr-old girls ( n = 11) and boys ( n = 11) cycled for 60 min at 70% maximal oxygen consumption while drinking 6% CHO (CT) or flavored water (WT). Blood was collected at rest, during exercise (30 and 60 min), and during recovery (30 and 60 min) to identify CD3−CD56dimand CD3−CD56brightNK cells. The activation marker CD69 was also determined on CD3−CD56+cells. CD56dimresponses, expressed as proportions or cell counts, were greater ( P ≤ 0.01) in girls by 67 and 105%, respectively. CD56brightcell counts ( P = 0.006), but not CD56brightproportions ( P = 0.89), were greater in girls by 82%. Both CD56dimand CD56brightsubset responses, expressed as proportions or cell counts, were lower ( P ≤ 0.01) in CT vs. WT by 33–36%. The CD56bright-to-CD56dimratio decreased at 30 min of exercise but increased during recovery ( P < 0.001), with no effect of sex or CHO. Regardless of trial, CD3−CD56+cells expressed ∼18% higher levels of CD69 during recovery in girls but not boys ( P = 0.03), despite similar proportions and counts of CD69+cells. These results demonstrate sex-based differences in the distribution of NK cell subsets and activation status in response to exercise, but not CHO intake, and further support the need to control for sex in exercise immunology studies.

scholarly journals Blood Pressure Control at Rest and during Exercise in Obese Children and Adults

2012 ◽  
Vol 2012 ◽  
pp. 1-10 ◽  
Author(s):  
Konstantina Dipla ◽  
George P. Nassis ◽  
Ioannis S. Vrabas
Keyword(s):  
Blood Pressure ◽  
Nervous System ◽  
Acute Exercise ◽  
Blood Pressure Response ◽  
Physical Exertion ◽  
Exercise Bout ◽  
Pressure Response ◽  
Obese Children ◽  
Hemodynamic Responses ◽  
Response To Exercise

The hemodynamic responses to exercise have been studied to a great extent over the past decades, and an exaggerated blood pressure response during an acute exercise bout has been considered as an indicator of cardiovascular risk. Obesity is a major factor influencing the blood pressure response to exercise since evidence indicates that the arterial pressure response to exercise is exacerbated in obese compared with lean adults. Signs of augmented responses (such as an exaggerated blood pressure response) to physical exertion appear early in life (from the prepubertal years) in obese individuals. Understanding the mechanisms that drive the altered hemodynamic responses during exercise in obese individuals and prevent the progression to hypertension is vitally important. This paper focuses on the evidence linking obesity with alterations of the autonomic nervous system and discusses the potential mechanisms and consequences of the altered sympathetic nervous system behavior in obese individuals at rest and during exercise. Furthermore, this paper presents the alterations in the reflex regulatory mechanisms (“exercise pressor reflex” and baroreflex) in obese children and adults and addresses the effects of training on obesity-related disturbances.

Nitric oxide synthase inhibition attenuates the skeletal muscle VEGF mRNA response to exercise

2000 ◽  
Vol 88 (4) ◽  
pp. 1192-1198 ◽  
Author(s):  
Timothy P. Gavin ◽  
David A. Spector ◽  
Harrieth Wagner ◽  
Ellen C. Breen ◽  
Peter D. Wagner
Keyword(s):  
Nitric Oxide ◽  
Skeletal Muscle ◽  
Growth Factor ◽  
Methyl Ester ◽  
Acute Exercise ◽  
Transforming Growth Factor ◽  
No Production ◽  
Vegf Mrna ◽  
Exercise Induced ◽  
Response To Exercise

Vascular endothelial growth factor (VEGF), basic fibroblast growth factor (bFGF), and transforming growth factor-β1 (TGF-β1) mRNA increase in rat skeletal muscle in response to a single acute exercise bout. Nitric oxide (NO) is released locally by muscle vascular endothelium and muscle fibers during exercise, contributes to the blood flow response to exercise, and regulates mitochondrial respiration. We hypothesized that a reduction in NO production, via NO synthase inhibition, would demonstrate a link between NO and the VEGF, bFGF, and TGF-β1 gene responses to exercise. To investigate this hypothesis, 9-wk-old female Wistar rats were divided into eight treatment groups ( n = 6 each): 1) saline + rest, 2) saline + exercise, 3) 30 mg/kg N ω-nitro-l-arginine methyl ester (l-NAME, a known NOS inhibitor) + rest, 4) 30 mg/kgl-NAME + exercise, 5) 300 mg/kg l-NAME + rest, 6) 300 mg/kg l-NAME + exercise, 7) 300 mg/kg N ω-nitro-d-arginine methyl ester (d-NAME, inactive enantiomer of l-NAME) + rest, and 8) 300 mg/kg d-NAME + exercise. Exercise consisted of 1 h of running at 20 m/min on a 10° incline. VEGF, TGF-β1, and bFGF mRNA from left gastrocnemius were analyzed by quantitative Northern blot. Submaximal exercise for 1 h increased VEGF mRNA 4.2-fold and TGF-β1 mRNA 1.5-fold in untreated rats but did not increase bFGF mRNA. The exercise-induced increase in VEGF mRNA was attenuated ∼50% by 30 and 300 mg/kgl-NAME; the TGF-β1 mRNA increase was unaffected by 300 mg/kg l-NAME. In addition, 300 mg/kgd-NAME had no effect on the exercise-induced increase in VEGF mRNA. Administration of 300 mg/kg l-NAME had no effect on bFGF mRNA. These findings suggest that NO is important in the regulation of the VEGF gene response to exercise through increases in VEGF transcription or by increases in the VEGF mRNA half-life.

Physical fitness attenuates leukocyte-endothelial adhesion in response to acute exercise

2006 ◽  
Vol 101 (3) ◽  
pp. 785-788 ◽  
Author(s):  
Paul J. Mills ◽  
Suzi Hong ◽  
Laura Redwine ◽  
Steven M. Carter ◽  
Albert Chiu ◽  
...  
Keyword(s):  
Physical Fitness ◽  
Cardiovascular Health ◽  
Acute Exercise ◽  
Inflammatory Responses ◽  
Peak Oxygen Consumption ◽  
Peripheral Blood Mononuclear ◽  
Endothelial Adhesion Molecule ◽  
Exercise Challenge ◽  
Before And After ◽  
Response To Exercise

Studies suggest that physical fitness promotes cardiovascular health, including improved endothelial function and possibly reduced inflammatory responses to stressors. This study examined the effects of fitness on leukocyte-endothelial adhesion in response to an acute exercise challenge. Peripheral blood mononuclear cell (PBMC) adhesion to human umbilical venous endothelial cells (HUVEC) was examined in 18 more-fit and 19 less-fit individuals [mean age 39 yr (SD 11)] before and after a 20-min treadmill exercise at 65–70% peak oxygen consumption. PBMC were isolated from whole blood (Ficoll-Paque) at rest and immediately after exercise. HUVEC were incubated for 4 h in the presence of cytokines IL-1 and IL-8 to activate endothelial adhesion molecule expression. Fit subjects showed a significant reduction in PBMC-HUVEC adhesion after exercise ( P < 0.01) compared with less-fit subjects, who showed no significant change. Regardless of fitness levels, both at rest and in response to exercise, soluble ICAM-1 in the incubation media attenuated PBMC-HUVEC adhesion by ∼81% ( P < 0.001). The findings indicate that immune cells that demarginate in response to exercise have reduced ability to adhere in individuals who are physically fit, an effect apparently independent of ICAM-1 binding. The findings provide evidence of how physical fitness might protect individuals from inflammatory responses to exercise.

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