Related Experiment Video
Updated: Sep 9, 2025
10:18
Ascending Aortic Constriction in Rats for Creation of Pressure Overload Cardiac Hypertrophy Model
Published on: June 29, 2014
17.2K
Angiotensin-converting enzyme and exercise adaptations: Genetic variability, pharmacological modulation and future
Tórur Sjúrðarson1, Nikolai B Nordsborg2
1Centre of Health Science, Faculty of Health, University of the Faroe Islands, Tórshavn, Faroe Islands.
The Journal of Physiology
|September 2, 2025
Summary
Individual responses to exercise training vary. Angiotensin-converting enzyme (ACE) activity influences muscle growth and endurance, but ACE inhibitors don't affect exercise performance. Precision exercise medicine needs direct ACE activity measurement.
Area of Science:
- Exercise physiology
- Pharmacology
- Genetics
Background:
- Individual variability in exercise response impacts athletic performance and health.
- Angiotensin-converting enzyme (ACE) activity, influenced by genetics and drugs, plays a role in exercise adaptations.
Purpose of the Study:
- To review how ACE activity affects skeletal muscle, cardiac, and blood adaptations to exercise.
- To explore the impact of ACE inhibition on exercise outcomes.
- To discuss future research directions for understanding training variability.
Main Methods:
- Literature review synthesizing evidence on ACE activity and exercise adaptations.
- Analysis of studies involving genetic variation, epigenetic regulation, and pharmacological ACE inhibition.
- Examination of exercise-induced modulation of the renin-angiotensin system.
Main Results:
- Pharmacological ACE inhibition selectively reduces cardiac and hematological adaptations (e.g., hemoglobin mass) but not peripheral muscle adaptations or aerobic performance.
- Exercise modulates ACE expression and renin-angiotensin system signaling in a context-dependent manner.
- Genotype alone is a poor predictor of ACE levels or downstream signaling.
Conclusions:
- ACE plays a complex role in exercise adaptations, with pharmacological inhibition having specific effects.
- Future research should focus on direct phenotyping of ACE activity and the renin-angiotensin system axis.
- ACE inhibition serves as a model for advancing precision exercise medicine by studying individual training response variability.
Related Concept Videos
01:26Heart Failure Drugs: Inhibitors of Renin-Angiotensin System
505
The activation of the sympathetic nervous system and the renin-angiotensin-aldosterone system (RAAS) contributes to cardiac remodeling, and inhibiting the RAAS is a pharmacological target in heart failure management. As a result, neurohumoral modulation is a crucial treatment principle for managing heart failure. This approach involves using medications like ACE inhibitors (ACEIs), angiotensin receptor blockers (ARBs), β-blockers, mineralocorticoid receptor antagonists (MRAs), and neutral...
505
01:30Antihypertensive Drugs: Angiotensin-Converting Enzyme Inhibitors
871
Angiotensin-converting enzyme (ACE), a vital component of the renin-angiotensin-aldosterone system, is abundant in lung endothelial cells. ACE converts the inactive decapeptide, angiotensin I, into the active octapeptide, angiotensin II. This potent vasoconstrictor narrows blood vessels, increasing resistance to blood flow and elevating blood pressure. Angiotensin II also stimulates aldosterone production, encouraging kidney cells to reabsorb more sodium and water from urine, thereby increasing...
871
01:29Heart Failure II: Pathophysiology
37
Systolic Heart Failure and Compensatory MechanismsSystolic heart failure (also termed HFrEF, Heart Failure with Reduced Ejection Fraction) is the most prevalent type of heart filure. It results in a decreased volume of blood being pumped from the ventricle. The aortic arch and carotid sinuses have baroreceptors that detect reduced blood pressure, triggering the sympathetic nervous system (SNS) to release epinephrine and norepinephrine. Initially, this response aims to boost heart rate and...
37
01:30Heart Failure V: Medical Management
23
Medical Management of Acute Decompensated Heart Failure (ADHF)The primary goals of therapy for patients hospitalized with acute decompensated heart failure (ADHF) include:Relieving symptomsOptimizing volume statusSupporting oxygenation and ventilationMaintaining cardiac output (CO) and end-organ perfusionIdentifying and addressing the cause of ADHFPreventing complicationsProviding patient education on factors precipitating HF exacerbationPlanning for dischargeOngoing monitoring and assessment...
23
01:29Hypertension II: Pathophysiology
77
Hypertension is a chronic condition in which the blood's force against artery walls is excessively high, posing risks such as heart disease. The condition's underlying mechanisms involve complex interactions among the cardiovascular, kidney, and autonomic nervous systems.Renin-Angiotensin-Aldosterone System (RAAS): This system significantly influences blood pressure regulation. When blood pressure decreases, the kidneys secrete renin. This enzyme transforms angiotensinogen, a plasma protein,...
77
01:30Antihypertensive Drugs: Angiotensin II Receptor Blockers
911
In the renin-angiotensin-aldosterone system, a hormone called angiotensin II plays a crucial role. It binds to the AT1 receptors in vascular smooth muscles coupled with Gq proteins. The activation of these receptors activates an enzyme called phospholipase C, which releases two molecules: inositol trisphosphate and diacylglycerol. These molecules cause a chain reaction that leads to the phosphorylation of myosin light chains and promotes interaction between actin and myosin, leading to smooth...
911