Plasma asymmetric dimethylarginine concentrations are not related to differences in maximal oxygen uptake in endurance trained and untrained men

Abstract

New Findings What is the central question of this study?Is there an association of plasma concentration of asymmetric dimethylarginine, which is related to exercise capacity in patients with cardiovascular diseases, with oxygen delivery and subsequently exercise capacity in healthy subjects in the absence of the potentially confounding influence of inflammation and oxidative stress? What is the main finding and its importance?Plasma asymmetric dimethylarginine concentrations are not related to exercise capacity in healthy subjects, while O2 delivery in the working skeletal muscle during the maximal graded‐exercise test is not associated with any of the l‐arginine analogues. ADMA alone does not play a crucial role in local muscle perfusion and in maintaining exercise capacity. Abstract Asymmetric dimethylarginine (ADMA) is an endogenous inhibitor of nitric oxide (NO) synthesis that could limit oxygen (O2) delivery in the working skeletal muscles by altering endothelium‐dependent vasodilatation. Exercise capacity is associated with plasma ADMA concentrations in patients with cardiovascular diseases, but this issue has still not been investigated in healthy subjects. We aimed to determine whether plasma ADMA concentrations were negatively associated with exercise capacity in young healthy male subjects. Ten men with maximal oxygen uptake (V̇O2 max ) > 65 mL kg−1 min−1 were included in the high exercise capacity group (HI‐FIT), and 10 men with V̇O2 max < 45 mL kg−1 min−1 were included in the low exercise capacity group (LO‐FIT). Plasma ADMA and other l‐arginine analogue concentrations were measured before and after a maximal graded‐exercise test by liquid chromatography–tandem mass spectrometry. Microvascular O2 delivery during exercise was estimated through the pattern from the sigmoid model of muscle deoxygenation in the vastus lateralis measured by near infrared spectroscopy. V̇O2 max was 60% higher in the HI‐FIT group (median: 70.2 mL kg−1 min−1; IQR: 68.0–71.9 mL kg−1 min−1) than in the LO‐FIT group (median: 43.8 mL kg−1 min−1; IQR: 34.8–45.3 mL kg−1 min−1). Plasma ADMA concentrations did not differ between the LO‐FIT and HI‐FIT groups before (0.50 ± 0.06 vs. 0.54 ± 0.07 μmol L−1, respectively) and after the maximal incremental exercise test (0.49 ± 0.08 vs. 0.55 ± 0.03 μmol L−1, respectively). There was no significant association of plasma ADMA concentrations with the pattern of local muscle deoxygenation and exercise capacity. Exercise capacity and microvascular O2 delivery are not related to plasma ADMA concentrations in young healthy male subjects. Our findings show that ADMA does not play a crucial role in local muscle perfusion and in maintaining exercise capacity without pathological conditions.

L-arginine and Its Derivatives Correlate with Exercise Capacity in Patients with Advanced Heart Failure

“…Ilic et al [ 18 ] reported that after exercise stress echocardiography plasma levels of ADMA and SDMA increased both in patients with CAD and in healthy volunteers, with a higher baseline and post-exercise value in the CAD group. In contrast to that, the results of Pawlak-Chaouch et al [ 19 ] did not demonstrate any change in SDMA and ADMA after a maximal graded exercise test in healthy men independently of their physical capacity. Plasma ADMA and SDMA were not associated with the pattern of local muscle deoxygenation and exercise capacity.…”

Changes in Water Soluble Uremic Toxins and Urinary Acute Kidney Injury Biomarkers After 10- and 100-km Runs

“…The levels of ADMA and SDMA are increased in renal failure, but also in subject with cardiovascular disease (CVD) without decreased eGFR [60]. During exercise, the production of NO is increased due to the shear stress in vascular walls [57,61]. Increased levels of NO result in smooth muscle and vascular relaxation [58].…”

“…Increased levels of NO result in smooth muscle and vascular relaxation [58]. Exercise capacity is positively associated with NO-dependent endothelial function in patients with CVD [54,61]. ADMA decreases blood muscle supply during exercise [54,61].…”

“…Exercise capacity is positively associated with NO-dependent endothelial function in patients with CVD [54,61]. ADMA decreases blood muscle supply during exercise [54,61]. On the other hand increase of ADMA leads to renin-angiotensin-aldosterone system (RAAS) activation [52], decrease in sodium excretion, and increase in blood pressure [53,59], and all these changes could be beneficial during exercise.…”

“…SDMA was analyzed in four studies and its decrease was observed in two studies [53,55]. There were also four studies showing changes in ADMA and SDMA after a single short exercise [17,58,61,65]. In one study, ADMA and SDMA increased [58], in one study decreased [17] and in two studies remained unchanged.…”