Effects of L-arginine on impaired blood fluidity after high-intensity exercise: An in vitro evaluation.

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.

L-cysteine improves blood fluidity impaired by acetaldehyde: In vitro evaluation.

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.

The effect of exercise on blood fluidity: Use of the capillary model to assess the clogginess of blood.

AIM: The goal was to evaluate the effects of exercise on the clogginess of blood as well as the effect of increased blood cell count and hematocrit levels after exercise. We also investigated the mechanisms underlying the clogginess of blood. METHODS: The time required for blood to pass through microchannels was measured. We focused on assessing the consecutive passage times for serial 20 µL volumes. We used heparinized peripheral blood obtained from subjects after exercise conducted at three intensity levels. Blood samples were also adjusted to achieve specific hematocrit levels or supplemented by addition of adenosine diphosphate (ADP). RESULTS: The sequential blood passage times of consecutive 20 µL volumes increased with platelet aggregation and adhesion of white blood cells (WBC). We also observed an increase with blood cell counts and hematocrit levels. These changes occurred after high intensity exercise but not after low or medium intensity exercise. Furthermore, the sequential blood passage times of 20 µL volumes increased with platelet aggregation and adhesion of WBC at an ADP concentration at the threshold of aggregation but not at higher levels of hematocrit. CONCLUSIONS: These findings suggested that high intensity exercise might induce the clogginess of blood by enhanced platelet aggregation and adhesion of WBC.

Cigarette Smoking does not Induce Plasma or Pulmonary Oxidative Stress after Moderate-intensity Exercise.

[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.

Plasma oxidative stress is induced by single-sprint anaerobic exercise in young cigarette smokers.

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 <0·001, respectively). However, no significant interaction was observed between groups by time on plasma BAP (P = 0·574), and a main effect of time was observed (P<0·001). Plasma BAP was significantly increased after exercise in both groups (both, P<0·001). These findings indicate that plasma oxidative stress is higher in cigarette smokers than in non-smokers after single-sprint anaerobic exercise, which may increase the risk of oxidative damage.

Pulmonary oxidative stress is induced by maximal exercise in young cigarette smokers.

INTRODUCTION: Oxidative stress is induced by both cigarette smoking and acute exercise. It has also been reported that exercise can induce plasma oxidative stress in young cigarette smokers. However, no previous report has demonstrated that exercise induces pulmonary oxidative stress in cigarette smokers. The aim of this study was to determine whether pulmonary oxidative stress is induced by maximal exercise in cigarette smokers as measured by reactive oxygen species generation and total antioxidant content. METHODS: Fifteen male smokers (mean age: 25.9 ± 2.9 years) and 18 male nonsmokers (mean age: 24.2 ± 4.3 years) participated in this study. Hydrogen peroxide (H(2)O(2)) concentration and biological antioxidant potential (BAP) in exhaled breath condensate (EBC) were measured at baseline and after maximal exercise in the Wingate anaerobic test. RESULTS: A significant interaction of group by time was observed for EBC H2O2 concentration (p = .015). After exercise, EBC H(2)O(2) concentrations were significantly increased in the smoking group (p = .030) but not in the nonsmoking group. There were no significant changes in EBC BAP in either group. CONCLUSIONS: These findings indicate that in cigarette smokers, maximal exercise induces pulmonary oxidative stress, which may lead to oxidative damage in the lungs.

Determinants of the daily rhythm of blood fluidity.

BACKGROUND: Numerous processes in the living body exhibit daily rhythmicity. In this study, we characterized a daily rhythm of blood fluidity and identified its determinants. METHODS: The subjects were nine young males. We measured the physiological parameters and performed hematological and biochemical analyses. We repeated the measurements six times during the day at 7:30 (just after getting up and before breakfast), 10:00, 13:30 (after lunch), 16:30, 19:30 (after dinner), and 21:30. The subjects performed sedentary work all day, and the contents and time of the meals were uniform. Investigation of blood rheology was based on Kikuchi's microchannel method. RESULTS: Blood passage time varied significantly with time of day. Stepwise regression analysis was used to determine the significant factors affecting blood passage time. Body temperature, heartbeat, hematocrit, white blood cell and total cholesterol were significant determinants of blood passage time. CONCLUSION: We confirmed that blood fluidity has a daily rhythm. In addition, we found that the determinants of blood fluidity included physiological parameters such as body temperature and heartbeat, hematological parameters such as hematocrit, and white blood cell and total cholesterol.