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BACKGROUND: Exercise-induced impairment of blood fluidity is considered to be associated with thrombosis development. However, the effects of L-arginine on blood fluidity after exercise remain unclear. OBJECTIVE: We investigated the mechanisms of impaired blood fluidity after high-intensity exercise, and examined whether L-arginine improves exercise-induced blood fluidity impairment in vitro. METHODS: Ten healthy male participants performed 15 minutes of ergometer exercise at 70% of their peak oxygen uptake levels. Blood samples were obtained before and after exercise. L-arginine and NG-monomethyl-L-arginine acetate (L-NMMA)—a nitric oxide (NO) synthase inhibitor—were added to the post-exercise blood samples. Using Kikuchi’s microchannel method, we measured the blood passage time, percentage of obstructed microchannels, and the number of adherent white blood cells (WBCs) on the microchannel terrace. RESULTS: Exercise increased the hematocrit levels. The blood passage times, percentage of obstructed microchannels, and the number of adherent WBCs on the microchannel terrace increased after exercise; however, they decreased in a dose-dependent manner after the addition of L-arginine. L-NMMA inhibited the L-arginine-induced decrease in blood passage time. CONCLUSIONS: High-intensity exercise impairs blood fluidity by inducing hemoconcentration along with increasing platelet aggregation and WBC adhesion. The L-arginine–NO pathway improves blood fluidity impairment after high-intensity exercise in vitro.

Blood fluidity is reportedly influenced by the volume and function of blood cells and plasma and is a predictor of primary cardiovascular events in patients with traditional cardiovascular risk factors. Heavy alcohol consumption was shown to be associated with a higher risk for cardiovascular diseases. Acetaldehyde (ACD), an oxidizing substance formed from ethanol, reportedly stimulates monocyte adhesion, causes abnormalities in the red blood cell (RBC) membrane, and decreases RBC deformability. In addition, it was reported that blood ACD levels are reduced in mice pretreated with L-cysteine. However, there are no studies on the effect of ACD and/or L-cysteine on blood fluidity. In the present study, we evaluated whether ACD impairs blood fluidity. In addition, the effect of L-cysteine on blood fluidity impaired by ACD was examined. Blood samples were obtained from 10 healthy, non-smoking, male volunteers (age: 23.4 ± 1.2 years, body mass index: 21.8 ± 2.6 kg/m2). ACD or ACD and L-cysteine were added to the blood samples before each experiment. We measured the passage time of 100 μL blood and RBC suspension using Kikuchi’s microchannel method. Percentage of microchannel obstruction and the number of adherent white blood cells (WBCs) on microchannel terrace were counted. The blood passage time, percentage of microchannel obstruction, and numbers of adherent WBCs on the microchannel terrace increased after adding ACD in a concentration-dependent manner, whereas they decreased after adding ACD and L-cysteine in a L-cysteine concentration-dependent manner. No significant effects were observed in passage time for 100 μL RBC suspension after adding ACD and L-cysteine. This study suggested that blood fluidity impaired by ACD might improve after adding L-cysteine.

[Purpose] This study aimed to evaluate the effect of body weight support with an assistive device on predicted locomotive physical activity measured using triaxial accelerometers in healthy young subjects. [Subjects and Methods] Sixteen healthy subjects aged 21.9 ± 1.1 years walked on a treadmill at speeds of 45 and 55 meters/min under 0%, 10%, 20%, and 30% body weight support conditions. Predicted metabolic equivalents and number of steps were evaluated using triaxial accelerometers. Measured metabolic equivalents and number of steps were evaluated using a metabolic system and observers, respectively. Raw data of synthetic accelerations were also obtained. [Results] Predicted metabolic equivalents and number of steps and raw data of synthetic accelerations decreased with increasing amounts of body weight support. [Conclusion] These findings suggest that accelerometers may underestimate locomotive physical activity with increasing amounts of body weight support using assistive devices. Thus, it is important to consider the amount of body weight support when assessing physical activities in subjects using assistive devices for mobility.

Summary Cigarette smoking increases oxidative stress, which is a risk factor for several diseases. Smoking has also been reported to enhance plasma oxidative stress during strenuous exercise. However, no prior study has examined the changes in plasma oxidative stress after single-sprint anaerobic exercise in cigarette smokers. The purpose of this study was to investigate these changes in young cigarette smokers by measuring reactive oxygen species generation and total antioxidant content. Participants were 15 male smokers (mean age: 25·9 ± 2·9 years) and 18 male non-smokers (mean age: 24·2 ± 4·3 years). Hydroperoxide concentration and biological antioxidant potential (BAP) in plasma were measured at baseline and after the Wingate anaerobic test. A significant interaction between group and time was observed for plasma hydroperoxide concentration (P = 0·037). Plasma hydroperoxide concentration was significantly increased after exercise in both smokers and non-smokers (P = 0·001 and

[Purpose] Cigarette smoking increases oxidative stress, which is a risk factor for several diseases. Moreover, strenuous exercise has been shown to induce plasma and pulmonary oxidative stress in young cigarette smokers. However, no previous reports have demonstrated whether plasma and pulmonary oxidative stress occur after moderate-intensity exercise. Therefore, the aim of this study was to clarify whether moderate-intensity exercise induces pulmonary and plasma oxidative stress in smokers. [Subjects] Ten young male smokers and 10 young male nonsmokers participated in this study. [Methods] Plasma hydroperoxide concentrations were measured at baseline and then immediately and 15 min after moderate-intensity exercise. Hydrogen peroxide concentrations in exhaled breath condensate were measured at baseline and after exercise. [Results] No significant interactions were found between smokers and nonsmokers in terms of hydroperoxide or hydrogen peroxide concentrations following moderate-intensity exercise at any time point. [Conclusion] These findings suggested that moderate-intensity exercise did not induce plasma or pulmonary oxidative stress in young cigarette smokers.