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

New Findings

What is the central question of this study?

Asymmetric dimethylarginine (ADMA) is related to exercise capacity in patients with cardiovascular diseases. However, no studies have investigated whether there are associations of plasma ADMA concentrations with oxygen (O₂) delivery and subsequently exercise capacity in healthy subjects without potentially confounding influence of inflammation and oxidative stress.

What is the main finding and its importance?

Plasma ADMA concentrations are not related to exercise capacity in healthy subjects, while O₂ delivery in the working skeletal muscle during maximal graded‐exercise test is not associated with any of L‐arginine analogs. These findings demonstrate that ADMA alone does not play a crucial role in local muscle perfusion and in maintaining exercise capacity.

Abstract

Purpose

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 vasodilation. 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.

Methods

Ten men with maximal oxygen uptake (V̇O_2max) > 65 mL kg⁻¹ min⁻¹ were included in the high exercise capacity group (HI‐FIT), and ten men with V̇O_2max < 45 mL·kg⁻¹·min⁻¹ were included in the low exercise capacity group (LO‐FIT). Plasma ADMA and other L‐arginine analogs 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 (NIRS).

Results

V̇O_2max was 60% higher in the HI‐FIT group (median: 70.2; IQR: 68.0–71.9) than in the LO‐FIT group (median: 43.8; IQR: 34.8–45.3). 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 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.

Conclusion

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.

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