Cardiovascular diseases are the leading cause of death and the main cause of disability. In the last decade, homocysteine has been found to be a risk factor or a marker for cardiovascular diseases, including myocardial infarction (MI) and heart failure (HF). There are indications that vitamin B6 plays a significant role in the process of transsulfuration in homocysteine metabolism, specifically, in a part of the reaction in which homocysteine transfers a sulfhydryl group to serine to form α-ketobutyrate and cysteine. Therefore, an elevated homocysteine concentration (hyperhomocysteinemia) could be a consequence of vitamin B6 and/or folate deficiency. Hyperhomocysteinemia in turn could damage the endothelium and the blood vessel wall and induce worsening of atherosclerotic process, having a negative impact on the mechanisms underlying MI and HF, such as oxidative stress, inflammation, and altered function of gasotransmitters. Given the importance of the vitamin B6 in homocysteine metabolism, in this paper, we review its role in reducing oxidative stress and inflammation, influencing the functions of gasotransmitters, and improving vasodilatation and coronary flow in animal models of MI and HF.

Background: Evidence regarding the performance-related effects of Actovegin is limited, despite legislated restrictions being in place for this supplement within sport settings. Objectives: Our study examined the effects of Actovegin on physiological responses and performance during maximal cardiopulmonary exercise in collegiate athletes. Methods: A randomized, double-blind, placebo-controlled experimental design was adopted. Moderately trained collegiate athletes from various sports were randomly allocated to placebo (n = 8) or Actovegin (n = 8) groups. All athletes consumed three capsules across each day for seven days of loading. Athletes underwent two separate cardiopulmonary exercise tests one week apart. Separate 2 × 2 mixed ANOVAs and effect sizes (${\eta }_p^2$) were used to assess for between- and within-group differences. Results: A significant time * group effect (p = 0.036, ${\eta }_p^2$ = 0.278) was observed in systolic blood pressure. Significant main effects were only observed for time in several variables, with increases in peak oxygen uptake (VO₂) (p < 0.001, ${\eta }_p^2$ = 0.893), peak minute ventilation (p = 0.004, ${\eta }_p^2$ = 0.456), ventilatory equivalents for carbon dioxide (p = 0.002, ${\eta }_p^2$ = 0.517), oxygen pulse (p = 0.006, ${\eta }_p^2$ = 0.434), VO₂ at first ventilatory threshold (p = 0.002, ${\eta }_p^2$ = 0.520), velocity at second ventilatory threshold (p < 0.001, ${\eta }_p^2$ = 0.997), VO₂ at second ventilatory threshold (p < 0.001, ${\eta }_p^2$ = 0.628), and peak velocity (p = 0.010, ${\eta }_p^2$ = 0.386), and a decrease in respiratory exchange ratio (p < 0.001, ${\eta }_p^2$ = 0.695). Conclusions: Our findings suggest that although physiological and performance alterations were evident with Actovegin supplementation during cardiopulmonary exercise, no further benefits beyond those obtained with a placebo were attained.