Role of creatine supplementation on exercise-induced cardiovascular function and oxidative stress

Abstract

Many degenerative diseases are associated with increased oxidative stress. Creatine has the potential to act as an indirect and direct antioxidant; however, limited data exist to evaluate the antioxidant capabilities of creatine supplementation within in-vivo human systems. This study aimed to investigate the effects of oral creatine supplementation on markers of oxidative stress and antioxidant defenses following exhaustive cycling exercise. Following preliminary testing and two additional familiarization sessions, 18 active males repeated two exhaustive incremental cycling trials (T1 and T2) separated by exactly 7 days. The subjects were assigned, in a double-blind manner, to receive either 20 g of creatine (Cr) or a placebo (P) for the 5 days preceding T2. Breath-by-breath respiratory data and heart rate were continually recorded throughout the exercise protocol and blood samples were obtained at rest (preexercise), at the end of exercise (postexercise), and the day following exercise (post24 h). Serum hypdroperoxide concentrations were elevated at postexercise by 17 +/- 5% above pre-exercise values (P = 0.030). However, supplementation did not influence lipid peroxidation (serum hypdroperoxide concentrations), resistance of low density lipoprotein to oxidative stress (t1/2max LDL oxidation) and plasma concentrations of non-enzymatic antioxidants (retinol, alpha-carotene, beta-carotene, alpha-tocopherol, gamma-tocopherol, lycopene, and vitamin C). Heart rate and oxygen uptake responses to exercise were not affected by supplementation. These findings suggest that short-term creatine supplementation does not enhance non-enzymatic antioxidant defence or protect against lipid peroxidation induced by exhaustive cycling in healthy males.

Figure 1

Exercise-induced lipid peroxidation as measured by serum hydroperoxide concentrations. Exhaustive cycling caused increases in lipid peroxidation (time of sample effect, p = 0.030), with serum hydroperoxide concentrations being elevated after exercise (ost-exercise) when compared with values before (Pre-exercise) and 24 hours after exercise (Post-24 h). The pattern of response was similar following supplementation with creatine (Cr) and placebo (P) (trial × timing of sample × group effect, p = 0.205). Values represent mean ± SEM (N = 9).

Figure 2

Schematic diagram representing the experimental design that was used to evaluate the role of creatine supplementation on exercise-induced cardiovascular function and oxidative stress. After repeated familiarization, the subjects performed two main exercise trials that consisted of exhaustive incremental cycling. Two days after completing the first main exercise trial (T1) the subjects were assigned, in a randomised double-blind fashion, to either a creatine (Cr) group or a placebo (P) group and instructed to take supplements for 5 d, which included 4 d prior to and the day of trial two (T2).