Effects of ACE inhibition on endurance exercise haemodynamics in trained subjects with mild hypertension

Palatini, Paolo; Bongiovi, Stefano; Mario, Luca; Mormino, Paolo; Raule, Gino; Pessina, Achille C.

doi:10.1007/bf00194331

Cited by 10 publications

(5 citation statements)

References 32 publications

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“…Systemic angiotensin II levels and blood pressure seem to be unaffected by the ACE ID genotyperelated variation in plasma ACE levels (17). In addition, treatment with ACE inhibitors causes a drastic decrease in ACE activity and angiotensin II levels but has no effect on endurance performance in healthy or mildly hypertensive subjects (2,27,28). It has been suggested that the greater ACE II genotype frequency in endurance athletes could reflect the selection of individuals with a ''healthier'' cardiovascular system and, thus a higher aerobic capacity (12,24,26).…”

Section: Discussionmentioning

confidence: 99%

No association between the angiotensin-converting enzyme ID polymorphism and elite endurance athlete status

Rankinen

Wolfarth

Simoneau

et al. 2000

Journal of Applied Physiology

184

132

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Several studies have reported that the insertion (I) allele of the angiotensin-converting enzyme ( ACE) I/deletion (D) polymorphism is associated with enhanced responsiveness to endurance training and is more common in endurance athletes than in sedentary controls. We tested the latter hypothesis in a cohort of 192 male endurance athletes with maximal oxygen uptake ≥75 ml ⋅ kg−1 ⋅ min−1and 189 sedentary male controls. The ACE ID polymorphism in intron 16 was typed with the three-primer polymerase chain reaction method. Both the genotype ( P = 0.214) and allele ( P = 0.095) frequencies were similar in the athletes and the controls. Further analyses in the athletes revealed no excess of the I allele among the athletes within the highest quartile (> 80 ml ⋅ kg−1 ⋅ min−1) or decile (>83 ml ⋅ kg−1 ⋅ min−1) of maximal oxygen uptake. These data from the GENATHLETE cohort do not support the hypothesis that the ACE ID polymorphism is associated with a higher cardiorespiratory endurance performance level.

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Section: Discussionmentioning

confidence: 99%

No association between the angiotensin-converting enzyme ID polymorphism and elite endurance athlete status

Rankinen

Wolfarth

Simoneau

et al. 2000

Journal of Applied Physiology

184

132

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“…Although the renin-angiotensin system does interact with the sympathetic nervous system, this control is primarily involved in the regulation of peripheral vascular smooth muscle tone (9) and not central CV chronotropic responses. In fact, angiotensin I infusions have, at best, only a minimal impact on HR (7,21). Furthermore, angiotensin converting enzyme (ACE) inhibitors are believed to be an optimal medication for hypertensives who want to exercise, because they have negligible effects on exercise HR responses and maximal exercise capacities (12,21).…”

Section: Discussionmentioning

confidence: 99%

“…In fact, angiotensin I infusions have, at best, only a minimal impact on HR (7,21). Furthermore, angiotensin converting enzyme (ACE) inhibitors are believed to be an optimal medication for hypertensives who want to exercise, because they have negligible effects on exercise HR responses and maximal exercise capacities (12,21). Thus it is entirely possible that the AGT M235T locus is simply a marker for another adjacent genetic variant that may be within the sympathetic nervous system and which would be better linked, in mechanistic terms, to our findings of altered exercise HR responses associated with AGT M235T genotypes.…”

Section: Discussionmentioning

confidence: 99%

Angiotensinogen M235T polymorphism associates with exercise hemodynamics in postmenopausal women

McCole

Brown

Moore

et al. 2002

Physiological Genomics

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.-We sought to determine whether the M235T angiotensinogen (AGT) polymorphism, either interacting with habitual physical activity (PA) levels or independently, was associated with cardiovascular (CV) hemodynamics during maximal and submaximal exercise. Sixty-one healthy postmenopausal women (16 sedentary, 21 physically active, and 24 endurance athletes) had heart rate (HR), blood pressure (BP), cardiac output, stroke volume (SV), total peripheral resistance (TPR), and arteriovenous O 2 difference (a-vDO2) assessed during 40, 60, 80, and ϳ100% of VO 2 max treadmill exercise. VO 2 max did not differ among AGT genotype groups; however, maximal HR was 14 beats/min higher in AGT TT than MM genotype women (P Ͻ 0.05). AGT TT genotype women also had 19 beats/min higher HR during ϳ100% VO 2 max exercise than AGT MM genotype women (P ϭ 0.008). AGT genotype also interacted with habitual PA levels to associate with systolic BP and a-vDO 2 during ϳ100% VO2 max exercise (both P Ͻ 0.01). AGT TT genotype women had 11 beats/min higher HR during submaximal exercise than MM genotype women (P Ͻ 0.05). AGT genotype interacted with habitual PA levels to associate with systolic BP during submaximal exercise (P ϭ 0.009). AGT genotype, independently or interacting with habitual PA levels, did not associate significantly with diastolic BP, cardiac output, SV, or TPR during maximal or submaximal exercise. Thus this common genetic variant in the renin-angiotensin system appears to associate, both interactively with habitual PA levels and independently, with HR, systolic BP, and a-vDO 2 responses to maximal and submaximal exercise in postmenopausal women. heart rate; blood pressure; cardiac output; stroke volume; genetics THE RENIN-ANGIOTENSIN-ALDOSTERONE system is intimately involved in the regulation of blood pressure (BP) and cardiovascular (CV) hemodynamics through its effects on angiotensin II, a potent vasoconstrictor, and fluid and electrolyte balance. A common genetic polymorphism within the renin-angiotensin-aldosterone system, a T-for-C substitution at nucleotide 704 of the angiotensinogen (AGT) gene leading to a methionine-to-threonine substitution at codon 235 in some but not all studies, has been associated with hypertension and BP (2, 5, 10, 13, 23). This variant is especially appealing as a candidate locus that might affect CV hemodynamics because it is relatively common (15). Furthermore, it has been shown to affect plasma angiotensinogen levels (11), which are normally close to the K m for the conversion of angiotensinogen to angiotensin I by renin (6). Therefore, changes in angiotensinogen levels could potentially alter angiotensin I and II levels. Thus the AGT locus would appear to be a putative candidate locus that might affect CV hemodynamics.Previously Krizanova and coworkers (14) assessed the association of BP and heart rate (HR) during rest and submaximal exercise with AGT M235T polymorphisms. The primary aim of a second study, by Rankinen et al. (22), was to examine the association between this common genetic polymo...

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“…Thus ACE inhibition did not alter oxidative capacity, in line with the maintained endurance capacity of the animals. Similarly, in trained human subjects with or without mild hypertension, ACE inhibition does not affect endurance exercise hemodynamics and V O 2 max or parameters of energy metabolism (26,28).…”

Section: Discussionmentioning

confidence: 99%

Does ACE inhibition enhance endurance performance and muscle energy metabolism in rats?

Bahi

Koulmann²,

Sanchez³

et al. 2004

Journal of Applied Physiology

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The renin-angiotensin-aldosterone system plays an important role in the hydroelectrolytic balance, blood pressure regulation, and cell growth. In some studies, the insertion (I) allele of the angiotensin-converting enzyme (ACE) gene, associated with a lower ACE activity, has been found in excess frequency in elite endurance athletes, suggesting that decreased ACE activity could be involved in endurance performance (Myerson S, Hemingway H, Budget R, Martin J, Humphries S, and Montgomery H. J Appl Physiol 87: 1313-1316, 1999). To test this hypothesis, we evaluated whether ACE inhibition could be associated with improved endurance performance and muscle oxidative capacity in rats. Eight male Wistar rats were treated for 10-12 wk with an ACE inhibitor, perindopril (2 mg.kg-1.day-1), and compared with eight control rats. Endurance time was measured on a treadmill, and oxidative capacity and regulation of mitochondrial respiration by substrates were evaluated in saponin-permeabilized fibers of slow soleus and fast gastrocnemius muscles. Endurance time did not differ between groups (57 +/- 5 min for perindopril vs. 55 +/- 6 min for control). Absolute and relative (to body weight) left ventricular weight was 20% (P < 0.01) and 12% (P < 0.01) lower, respectively, in the treated group. No difference in oxidative capacity, mitochondrial enzyme activities, or mitochondrial regulation by ADP was observed in soleus or gastrocnemius. Mitochondrial respiration with glycerol 3-phosphate was 17% higher in gastrocnemius (P < 0.03) and with octanoylcarnitine 14% greater in soleus (P < 0.01) of treated rats. These results demonstrate that ACE inhibition was not associated with improved endurance time and maximal oxidative capacity of skeletal muscles. This suggests that ACE activity has no implication in endurance capacity and only minor effects on mitochondrial function in sedentary animals.

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Effects of ACE inhibition on endurance exercise haemodynamics in trained subjects with mild hypertension

Cited by 10 publications

References 32 publications

No association between the angiotensin-converting enzyme ID polymorphism and elite endurance athlete status

No association between the angiotensin-converting enzyme ID polymorphism and elite endurance athlete status

Angiotensinogen M235T polymorphism associates with exercise hemodynamics in postmenopausal women

Does ACE inhibition enhance endurance performance and muscle energy metabolism in rats?

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