The effects of angiotensin receptor blockers vs. calcium channel blockers on the acute exercise-induced inflammatory and thrombotic response

Abstract

Arterial hypertension is an established risk factor for acute coronary syndromes, and physical exertion may trigger the onset of such an event. The mechanisms involved include the rupture of a small, inflamed, coronary plaque and the activation of thrombogenic factors. Blood pressure (BP)-lowering treatment has been associated with beneficial effects on subclinical inflammation and thrombosis at rest and during exercise. This prospective study sought to compare the effect of different antihypertensive drugs on the inflammatory and thrombotic response during exercise. A total of 60 never-treated hypertensive patients were randomized to an angiotensin receptor blocker (ARB)-or non-dihydropyridine calcium channel blocker (CCB)-based regimen. Patients with inflammatory or coronary artery disease were excluded. Six months after pharmaceutical BP normalization, the patients underwent a maximal treadmill exercise testing. High-sensitivity C-reactive protein (hsCRP), serum amyloid A (SAA), white blood cells (WBC), tumor necrosis factor-a (TNF-a), interleukin-6 (IL-6), total fibrinogen (TF) and von Willebrand factor (vWF) levels, as well as plasminogen activator inhibitor-1 (PAI-1) activity were measured in blood samples taken while the patients were at rest and during peak exercise. All of these biomarkers increased with exercise, except PAI-1, which decreased (Po0.05 for the difference between resting and peak exercise for all biomarkers). The ARB group had less marked (Po0.05) exercise-induced changes than the CCB group in hsCRP (5.8% vs. 7.7%), SAA (4.2% vs. 7.2%), WBC (46.8% vs. 52.6%), TNF-a (16.3% vs. 24.3%), TF (9.5% vs. 16.9%) and PAI-1 ( À9.5% vs. À12.3%) but a similar (P ¼ NS) change in IL-6 (39.4% vs. 38.6%) and vWF (29.2% vs. 28.6%). In conclusion, ARBs are most likely more effective than CCBs at suppressing the exercise-induced acute phase response. Potential protection against exercise-related coronary events remains to be elucidated.

Effects of Hyperbaric Oxygen Therapy on Inflammation, Oxidative/Antioxidant Balance, and Muscle Damage after Acute Exercise in Normobaric, Normoxic and Hypobaric, Hypoxic Environments: A Pilot Study

“…The results of this study showed that the levels of plasma fibrinogen and serum IL-6 significantly increased after exercise in all groups, but there was no significant difference between the exercise environments (NN vs. HH). These results are consistent with previous studies [ 6 , 27 ] that demonstrated that acute exercise significantly increased the levels of fibrinogen and IL-6 in the blood by causing an inflammatory response, and suggest that exercising in an HH environment, which corresponds to conditions at an altitude of about 3000 m, did not lead to additional inflammatory responses compared to exercising in an NN environment. Liakos et al [ 6 ] reported that the levels of fibrinogen and IL-6 were significantly increased after maximal treadmill exercise testing using the Bruce protocol, and in Stelzer et al’s study [ 27 ], the levels of fibrinogen and IL-6 were analyzed to verify changes in the inflammatory response with ultra-endurance exercise.…”

“…Even though it is a necessary defensive reaction that helps damaged tissue to recover, it can also cause other diseases like cardiovascular disease [ 23 ] and is closely related to musculoskeletal damage and muscle fatigue [ 24 , 25 ]. In some previous studies [ 6 , 26 ], the levels of fibrinogen, IL-6, and TNF-α in the blood have been reported to be indices reflecting the inflammatory response induced by acute exercise. This study analyzed the levels of plasma fibrinogen, serum IL-6, and TNF-α to verify changes in the inflammatory response depending upon the exercise performed in NN and HH environments and investigated the effect of HBOT on recovery.…”

“…The body exhibits decreased muscular function and/or inflammatory response due to excessive muscle fatigue without proper recovery from the damage, and this can lead to exercise impairment as well as a reduction in the ability to perform exercise [ 3 , 5 ]. Previous studies suggested that inflammatory cytokines, such as interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α), and fibrinogen could be blood biomarkers for the inflammatory response induced by exercise [ 6 ]. Serum creatine kinase (CK) and lactate dehydrogenase (LDH) levels are typical indices that reflect exercise-induced muscle damage [ 7 ].…”

The renin–angiotensin system and prevention of age-related functional decline: where are we now?

“…To date, data regarding an interaction between ARBs and exercise in humans is sparse. One trial comparing ARBs to calcium channel blockers in hypertensive patients found ARBs to attenuate indicators of exerciseinduced inflammatory response and thrombogenic factor activation (Liakos et al 2012). However, similar interactions are not universal.…”

Associations of suPAR with lifestyle and cardiometabolic risk factors

“…Evidence from Caucasian populations show that inflammation associates with unhealthy lifestyle factors such as smoking [19,20], excessive alcohol consumption [16], physical inactivity [20,21], malnutrition [22] and psychological conditions [23].…”