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J Appl Physiol 98: 1272-1279, 2005. First published December 3, 2004; doi:10.1152/japplphysiol.00875.2004
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Effect of antioxidant vitamin treatment on the time course of hematological and hemorheological alterations after an exhausting exercise episode in human subjects

Umit K. Senturk,1 Ozlem Yalcin,1 Filiz Gunduz,1 Oktay Kuru,1 Herbert J. Meiselman,2 and Oguz K. Baskurt1,2

1Department of Physiology, Akdeniz University Faculty of Medicine, Antalya, Turkey; and 2Department of Physiology and Biophysics, Keck School of Medicine, University of Southern California, Los Angeles, California

Submitted 12 August 2004 ; accepted in final form 29 November 2004


   ABSTRACT
TOP
 ABSTRACT
MATERIALS AND METHODS
 RESULTS
 DISCUSSION
 GRANTS
 REFERENCES
 
This study examined the effects of a 2-mo antioxidant vitamin treatment on acute hematological and hemorheological alterations induced by exhausting exercise; both sedentary and trained individuals were employed. Eighteen young male, human subjects (9 sedentary, 9 trained by regular exercise) participated in the study and performed an initial maximal aerobic cycle ergometer exercise with frequent blood sampling over a 24-h period and analysis of hematological and hemorheological parameters. All subjects were treated with an antioxidant vitamin A, C, and E regimen, supplemented orally for 2 mo, and then subjected to a second exercise test and blood sampling at the end of this period. In the sedentary group during the first testing period (before vitamin treatment), white blood cell counts and granulocyte percentages were increased at 2 h after the exercise test and remained elevated for 4–12 h. Red blood cell (RBC) deformability and aggregation were also altered by exercise in the sedentary group before vitamin treatment. However, none of these parameters in the sedentary group were altered by exercise after the 2-mo period of antioxidant vitamin treatment. With the exception of a transient rise in granulocyte percentage, these parameters were also not affected in the trained subjects before the vitamin treatment. Significant increases of RBC lipid peroxidation observed 12 h after the exercise test in both sedentary and trained subjects were also totally prevented by vitamin treatment. Our results indicate that antioxidant vitamin treatment is effective in preventing the inflammation-like response and coincident adverse hemorheological changes after an episode of exhausting exercise, and suggest that such changes may be related to exercise-induced death events.

erythrocyte deformability; erythrocyte aggregation; inflammatory response; exercise-related mortality

THE ACUTE EFFECTS OF HEAVY physical exercise on blood and its formed elements have been documented (2, 22, 37, 54), and various hematological and physical properties of blood are altered after strenuous exercise (15, 20, 53, 54). We have previously described the time course of these alterations, including hematocrit, red blood cell (RBC), and white blood cell (WBC) counts (54). Granulocyte percentages (i.e., number of granulocytes as a percentage of the total WBC count) were found to be increased after the exhausting exercise episode and were accompanied by enhanced WBC activation (54), suggesting an inflammation-like response (16, 42, 50). Blood viscosity and RBC mechanical properties are altered as a result of exhausting exercise (15, 20, 54), and heavy exercise is known to induce alterations of plasma composition (24, 26). Some of the alterations were observed during the strenuous exercise (i.e., hematocrit, RBC and WBC counts, RBC deformability), with some returning to resting levels shortly after cessation of exercise (i.e., hematocrit and RBC counts); conversely, other changes (i.e., RBC deformability) persisted up to 12 h postexercise (54).

The alterations in blood composition and properties induced by heavy exercise may affect the flow properties of blood (9, 44), with altered RBC mechanical properties expected to interfere with microcirculatory blood flow (17). The hemorheological challenge due to acute alterations may be compensated by enhanced hemodynamics as a physiological response to heavy exercise (52); blood is a shear-thinning, non-Newtonian fluid, and increased flow velocity would tend to reduce its apparent viscosity (9). However, the hemodynamic enhancements of shear rates are rapidly reversed after the cessation of exercise, and thus prolonged hemorheological alterations that continue to exist may have deleterious effects on tissue perfusion, especially if the blood vessels of a given organ are geometrically challenged (7). Such a series of events may lead to exercise-related morbidity and mortality that is well documented in the literature (3, 5).

It has been demonstrated that exercise-related hematological and hemorheological alterations can be reduced by exercise training (53). The beneficial effects of antioxidant vitamin supplementation have also been considered, because increased oxidant stress is usually coincident with these exercise-induced alterations (25, 41, 51) and antioxidants have been shown to be effective in a rat model of exhausting exercise (41). Reactive O2 species generated during exercise due to increased O2 consumption cause oxidant stress in muscle and other tissues (2, 39). In addition to mitochondrial leakage due to enhanced O2 consumption, ischemia-reperfusion events and leukocyte activation may also contribute to oxidative stress, especially in RBC and extramuscular tissues (e.g., heart, liver, brain) (37). The present study was designed to investigate the effects of antioxidant multivitamins on the time course of hematological, hemorheological, and oxidative alterations after aerobic, exhaustive exercise in sedentary and trained human subjects.


   MATERIALS AND METHODS
TOP
 ABSTRACT
 MATERIALS AND METHODS
RESULTS
 DISCUSSION
 GRANTS
 REFERENCES
 
Subjects

Eighteen young male students of the Faculty of Medicine and the School of Physical Education and Sports, Akdeniz University, Antalya, Turkey, participated in this study. None of the subjects had obvious health problems, and all were nonsmokers. All subjects were fully informed about the purpose of the study before giving their written consent: the study was approved by the Ethical Committee of the Akdeniz University Faculty of Medicine.

Nine students of the Faculty of Medicine were selected as the sedentary group. Students in this group were not engaged in any regular exercise activity, either personally or as group activity. Nine students of the School of Physical Education and Sports were members of the University handball team and were selected as the trained group; mean training time for this group was 8 ± 0.33 h/wk. Maximal aerobic capacity (O2 max) of these subjects was assessed by a computerized, breath-by-breath analyzing system (Vmax Spectra 29 LV, Sensormedics, Loma Linda, CA). The subjects performed Bruce protocol on a motorized treadmill ergometer. O2 max corresponded to the plateau in O2 consumption, despite the increment in the workload. O2 max values together with age, height, and weight for these groups are shown in Table 1. O2 max values of the trained subjects were significantly higher than the sedentary subjects.


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  		Table 1. Age, height, weight, and O2 max of subjects in sedentary and trained groups

 
Exercise Model

The subjects performed a O2 max cycle ergometer exercise test. The test workload was started at 50 W and increased by 50 W every 2 min while the subjects maintained a pedal frequency of 50 revolutions/min. The exercise tests lasted ~8–12 min and terminated when the subjects indicated exhaustion or when the heart rate reached to maximal heart rate calculated as 220 – age. All experiments were conducted in an exercise laboratory where room temperature varied between 20 and 23°C and humidity was 40 ± 10%.

Experimental Protocol

All subjects performed the exercise test at the initial phase of their participation in the study. After this first test, they were asked to take vitamin A ({beta}-carotene; 50 mg/day), vitamin C (ascorbic acid; 1,000 mg/day), and vitamin E ({alpha}-tocopherol; 800 mg/day) orally for 2 mo. All subjects then performed another aerobic exercise test as described above at the end of this 2-mo period.

Venous blood samples were obtained from an antecubital vein before and after the aerobic exercise episode and anticoagulated with sodium heparin (15 IU/ml). The first sample was obtained 10 min before the start of the exercise episode and then at 1, 2, 4, 8, 12, and 24 h after the exercise episode. The blood samples were used to study RBC deformability and aggregation, oxidant stress parameters, and the antioxidant status of the subjects as described below; a complete peripheral blood count was also performed by using an electronic hematology analyzer (ABX Micros OT, ABX Diagnostics, Montepellier, France).

Evaluation of RBC Deformability

RBC deformability was measured at various fluid shear stresses by laser diffraction analysis by using an ektacytometer (LORCA, RR Mechatronics, Hoorn, The Netherlands). The principle of the system has been described elsewhere in detail (23). Briefly, a low-hematocrit RBC suspension in an isotonic solution of polyvinylpyrrolidone (6% in isotonic buffer, viscosity of 25.3 mPa·s) is sheared in a Couette system composed of a glass cup and a precisely fitting bob, with a gap of 0.3 mm between the cylinders. A laser beam is directed through the sheared sample, and the diffraction pattern produced by the deformed cells is analyzed by microcomputer. On the basis of the geometry of the elliptical diffraction pattern, an elongation index (EI) is calculated as: EI = (L – W)/(L + W), where L and W are the length and width of the diffraction pattern, respectively. All measurements were performed at 37°C.

EI values were determined for nine shear stresses between 0.5 and 50 Pa, and the shear stress required for half-maximal deformation (SS1/2) was calculated from the data for each sample by using a Lineweaver-Burk analysis procedure (10): increased SS1/2 values indicate decreased RBC deformability. SS1/2 parameter derived by Lineweaver-Burk procedure is characterized by a superior power compared with the maximum EI (EImax), which can also be derived by the same procedure (10). This is mainly due to the fact that RBCs deform to a maximum extent at shear stresses within the range used in this study. Therefore, EImax values approach a certain value in all group of measurements, which is determined mostly by the configuration of the ektacytometer and the measurement conditions, and this value does not reflect any differences in RBC deformability (10).

Determination of RBC Aggregation Indexes

RBC aggregation was assessed using a photometric aggregometer interfaced to a digital computer (11). This custom-built system is based on the measurement of the increase of light transmission through a RBC suspension consequent to aggregation and reports a dimensionless aggregation index (AI): increased AI values indicate enhanced RBC aggregation. All aggregation measurements were carried out at 37°C for cells in autologous plasma at a hematocrit adjusted to 0.4 l/l.

Oxidant Stress Parameters

Lipid peroxidation.   RBC lipid peroxidation was estimated by the measurement of thiobarbituric acid-reactive substance (TBARS) as described by Stocks and Dormandy (45) with 1,1,3,3-tetraethoxyprophane used as the standard. TBARS levels were determinedby measuring absorbance at 532 nm after reaction with thiobarbituric acid in RBC extracts. Results are expressed as nanomoles per gram of hemoglobin.

H2O2-induced oxidative stress and hemolysis (41).   A 5% suspension of washed RBC in buffered saline was mixed with an equal volume of 1% H2O2 solution, and the mixture was incubated at 37°C for 2 h. At the end of the incubation, the extent of hemolysis was determined by measuring hemoglobin released into the supernatant (optical absorption at 540 nm) and expressed relative to the maximum absorbance (100%) in samples completely hemolyzed in distilled water.

Antioxidant Status

The activities of three antioxidant enzymes and the levels of antioxidant vitamins were evaluated before and after antioxidant vitamin treatment. Catalase (CAT; EC 1.11.1.6 [EC] ), superoxide dismutase (SOD; EC 1.15.1.1 [EC] ), and glutathione peroxidase (GPX; EC 1.11.1.9 [EC] ) activities were assessed by using the methods of Aebi (1), Misra and Fridovich (30), and Paglia and Valentine (34), respectively. Vitamin A and C levels were analyzed by using the methods of McCormic (29), and levels of vitamin E were determined as described by Desai (19).

Statistics

Values are expressed as means ± SE. Multiple comparisons were done by one-way ANOVA followed by Newman-Keuls post hoc test. Statistical significance was accepted at values of P < 0.05.


   RESULTS
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 ABSTRACT
 MATERIALS AND METHODS
 RESULTS
DISCUSSION
 GRANTS
 REFERENCES
 
Although all subjects in the sedentary and trained groups completed the exercise protocol without problems, the exercise duration for the trained subjects was significantly longer than the sedentary subjects (Table 2). Exercise duration after the vitamin treatment regimen was also significantly greater for the trained group (629.3 ± 24.8 vs. 555.2 ± 17.2 s; P < 0.01). Although resting pulse rate of trained subjects was significantly lower than the sedentary group, maximal pulse rates in the two groups were not different (Table 2); maximal pulse rates were unaffected by vitamin treatment (188.4 ± 4.6 vs. 187.0 ± 4.3 beats/min; P > 0.05).


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  		Table 2. Resting and maximal pulse rate and exercise duration in sedentary and trained groups

 
A comparison of before and after vitamin treatment results indicated that RBC counts and hematocrit values were significantly increased (P < 0.001) after vitamin treatment in both groups, whereas MCHC values were found to be decreased in the trained group after the treatment (Table 3). However, exhausting exercise bout did not significantly affect these hematological parameters both in sedentary and trained groups (Table 4). RBC count, hematocrit, hemoglobin, mean corpuscular volume (MCV), and mean corpuscular hemoglobin concentration (MCHC) were not affected significantly by the exercise bout, although a slight decrement in RBC counts, hematocrit values, and hemoglobin values was observed in both groups (Table 4). The results were similar after the vitamin treatment in both groups (data not shown).


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  		Table 3. Hematologic parameters in sedentary and trained groups before and after vitamin treatment

 

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  		Table 4. Hematologic parameters in sedentary and trained groups before and after exercise bout

 
In the sedentary group, WBC counts increased significantly at 2 h after exercise and remained elevated at 4, 8, and 12 h (Fig. 1A). A similar trend was also observed in the trained group; however, the differences in WBC counts after the exercise episode compared with preexercise value did not reach to the level of statistical significance (Fig. 1A). There were no significant postexercise alterations of WBC counts in groups after vitamin treatment (Fig. 1B). In the sedentary group, granulocyte percentages were significantly increased at 2 h and returned to the preexercise level at 8 h, with granulocyte percentage enhanced only at 2 h in the trained group (Fig. 2A). Again, no significant postexercise alterations in granulocyte percentages were observed in either group after vitamin treatment (Fig. 2B).



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  		Fig. 1. Time course of peripheral blood white blood cell (WBC) counts during the 24-h period after exhausting exercise. A: before vitamin treatment. B: after vitamin treatment. Values are means ± SE. Differences from the value at time 0 (i.e., 10 min before exercise) were only significant in the sedentary group (F = 7.07, P < 0.0001 by 1-way ANOVA) at 2, 4, 8, and 12 h after exercise: *P < 0.05; ** P < 0.01.

 


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  		Fig. 2. Time course of granulocyte percentages in the peripheral blood during the 24-h period after exhausting exercise. A: before vitamin treatment. B: after vitamin treatment. Values are means ± SE. Differences from the value at time 0 (i.e., 10 min before exercise) were statistically significant both in sedentary (F = 4.01, P < 0.005 by 1-way ANOVA) and trained (F = 3.55, P < 0.01 by 1-way ANOVA) groups before vitamin treatment: *P < 0.05; **P < 0.01.

 
Lipid peroxidation was enhanced in both groups at 12 h after exercise and returned to preexercise levels at 24 h; there were no significant alterations in RBC lipid peroxidation in either group after the vitamin treatment (Fig. 3).



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  		Fig. 3. Time course of lipid peroxidation measured as thiobarbituric acid-reactive substance (TBARS) in peripheral blood during the 24-h period after exercise. A: before vitamin treatment. B: after vitamin treatment. Values are means ± SE. Differences from the value at time 0 (i.e., 10 min before exercise) were statistically significant both in sedentary (F = 4.17, P < 0.005 by 1-way ANOVA) and trained (F = 3.42, P < 0.01 by 1-way ANOVA) groups before vitamin treatment: **P < 0.01.

 
Plasma levels of the three vitamins that were included in the treatment protocol (i.e., A, C, and E) were found to be enhanced in both sedentary and trained subjects (Table 5). SOD and CAT activities were unaffected by the vitamin treatment, whereas GPX activity was increased in both groups (Table 6). H2O2-induced RBC hemolysis was found to be decreased after the vitamin treatment (Table 6).


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  		Table 5. Vitamin A, C, and E levels before and after vitamin treatment

 

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  		Table 6. Antioxidant enzyme activities and H2O2-induced RBC hemolysis

 
Figure 4 presents the alterations in the RBC deformability parameter SS1/2 after the exercise episode. There was a significant increment in SS1/2 2 h after the exercise period in the sedentary group, thus indicating decreased RBC deformability (Fig. 4A). However, this increase was transient, and the value returned to normal at 4 h after exercise. The SS1/2 value also slightly increased in the trained group (P > 0.05); therefore, there was no significant alteration of this parameter in the trained group either before or after the vitamin treatment. Vitamin treatment also eliminated the exercise-induced increase of SS1/2 in the sedentary group (Fig. 4B).



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  		Fig. 4. Time course of the red blood cell deformability parameter of the shear stress required for half-maximal deformation during the 24-h period after exercise (SS1/2). A: before vitamin treatment. B: after vitamin treatment. Values are means ± SE. Differences from the value at time 0 (i.e., 10 min before exercise) were only significant in the sedentary group (F = 2.55, P < 0.05 by 1-way ANOVA): *P < 0.05.

 
A significant increase of RBC aggregation was observed only in the sedentary group before the vitamin treatment; RBC AIs remained elevated for at least 24 h, although the differences from the preexercise value reach to the level of statistical significance only at the 8- and 24-h time points (Fig. 5A). Vitamin treatment eliminated these increases (Fig. 5B). It is of interest to note that the time course of deformability changes (Fig. 4) and aggregation changes (Fig. 5) differ, with aggregation increases occurring later.



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  		Fig. 5. Time course of the red blood cell aggregation index (AI) during the 24-h period after exercise. A: before vitamin treatment. B: after vitamin treatment. Values are means ± SE. Differences from the value at time 0 (i.e., 10 min before exercise) were only significant in the sedentary group (F = 2.47, P < 0.05 by 1-way ANOVA): **P < 0.01.

 

   DISCUSSION
TOP
 ABSTRACT
 MATERIALS AND METHODS
 RESULTS
 DISCUSSION
GRANTS
 REFERENCES
 
The results of the present study indicate that a period of exhausting, aerobic exercise can induce an inflammation-like response as indicated by increased WBC counts and granulocyte percentages (Figs. 1 and 2). Inasmuch as these increases occur only at 2 h or more postexercise, it is highly unlikely that they represent the rapid recruitment of WBC from marginated pools that occurs with exercise, but this increment should represent a true leukocytosis due to an inflammation-like response (16, 25, 42, 47). These findings thus confirm earlier observations (32, 54) that also included an enhanced respiratory burst of granulocytes in the 4-h period after strenuous exercise bout (54). This inflammation-like response to strenuous exercise, therefore, has features common with serious pathophysiological conditions such as sepsis syndrome (16, 42, 47). However, the inflammation-like response to exercise is not progressive and usually has a time course that is completed within 8 h after the exercise episode (54). It is interesting to note that, in contrast with the previous findings of our group (54), Turton et al. (50) reported that the neutrophil response to exhaustive exercise in healthy individuals did not include activation (50). It is clear that WBC activation is closely related to the type and level of the exercise (32, 46) as well as to the athletic capacity of the subjects: the WBC alterations in the trained group of this study were less pronounced and shorter lasting (Figs. 1 and 2).

Components and consequences of the exercise-related inflammation-like response have been well documented in the literature (e.g., 16, 21, 27, 33, 37, 43, 46, 54), with the response to strenuous exercise usually including increased oxidative stress (25, 39, 41, 48, 54). The time course of significant hematological and hemorheological alterations observed in this study are summarized in Fig. 6. Our results indicate that lipid peroxidation of RBC from both sedentary and trained subjects is enhanced 12 h after exhaustive exercise (Fig. 3). This onset of enhanced lipid peroxidation occurs after the WBC response (Figs. 1 and 3), thereby suggesting a causal relationship. However, it is interesting to note that a similar degree of oxidative damage was observed in both the sedentary and trained groups even though the WBC response at the 12-h time point is significantly blunted in the trained group.



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  		Fig. 6. Summary of the time courses of significant hematological and hemorheological alterations after an exhausting exercise episode, before the vitamin treatment. Note that significant alterations were only observed for granulocyte percentage and TBARS, indicating lipid peroxidation in the trained group. There were no significant alterations after the vitamin treatment.

 
The temporal pattern of RBC mechanical changes also differed from that observed for lipid peroxidation, with the timing of RBC deformability impairment corresponding to the WBC response (Fig. 4): SS1/2 was significantly higher at the second hour following exercise as were WBC count and granulocyte percentage. Conversely, RBC aggregation peaked at the eighth hour after the exercise (Fig. 5); thus after the WBC and granulocyte percentage peaks but before the point at which lipid peroxidation reached its postexercise peak. Oxidant stress is a well-documented cause of RBC mechanical deterioration (12, 14) and can be induced by activated neutrophils affecting neighboring RBCs (6, 8). However, lipid peroxidation is only one indicator of RBC oxidant damage, and other components of RBC (e.g., proteins) may also be damaged by oxidants (14). In fact, it has been previously shown that correlations between lipid peroxidation and other oxidant-related RBC damage indicators (e.g., RBC mechanical properties) may not always exist (12). RBC deformability is very sensitive to alterations of RBC membrane skeletal proteins (e.g., cross-linking) that may occur before lipid peroxidation can be detected (6, 12). Furthermore, the mechanisms or sites for the effects for alterations in RBC deformability and RBC aggregation due to oxidant attack may differ (12); RBC aggregation is altered due to the changes in membrane surface properties, whereas RBC deformability is determined by the properties of spectrin-based protein network underlying the lipid bilayer of the membrane (31).

Exercise-related alterations observed in the present study (i.e., increased WBC and granulocyte counts, enhanced lipid peroxidation, RBC mechanical changes) tended to be lessened by exercise training and essentially eliminated by antioxidant vitamin treatment. Exercise training induces various alterations such as cardiac and vascular changes (52), metabolic adaptations (38, 49), and increased effectiveness of antioxidant defense (4). These mechanisms increase the exercise tolerance in trained individuals as manifested by their prolonged exercise duration (Table 2). The inflammation-like response in the trained individuals was also less intense (Figs. 1 and 2). The antioxidant enzyme activities (i.e., SOD, CAT, and GPX) were higher in the trained individuals before vitamin supplementation and continued to be higher after the treatment period. It is notable that antioxidant multivitamin supplementation for 2 mo before exercise was found to be more effective than exercise training alone. Although the level and duration of the response was diminished, WBC counts and granulocyte percentages of the trained subjects were affected by exercise, whereas these parameters were not affected in sedentary subjects after the vitamin supplementation. Reinforcement of normal antioxidant defense levels by antioxidant multivitamin supplementation thus appears to be of major value in preventing oxidative stress changes of hemorheological parameters consequent to exhausting exercise (48, 53, 54).

Vitamin supplementation to prevent exercise-related oxidant damage is a common concept and has been employed to prevent muscle damage in competing athletes (18, 27, 28, 35, 36, 40, 51). The present study demonstrated the effectiveness of antioxidant multivitamin supplementation in preventing hemorheological alterations that might be encountered during and/or after an exhausting exercise episode, especially in untrained individuals. Such an episode may or may not be related to purely voluntary activity. Any individual may face such physical exertion during everyday life, and alterations similar to those demonstrated in this study may occur. In turn, changes of hemorheological parameters may affect vascular hemodynamics, resulting in impaired tissue perfusion (9), especially if blood vessels have limited vasodilatory reserve (7, 13). Such exercise-related hemorheological alterations may underlie exertion-related death events (3, 5); antioxidant multivitamin supplementation in individuals that are not regularly exercising might be useful in preventing such adverse exercise-related events.


   GRANTS
TOP
 ABSTRACT
 MATERIALS AND METHODS
 RESULTS
 DISCUSSION
 GRANTS
REFERENCES
 
This study was supported by National Heart, Lung, and Blood Institute Research Grants HL-15722 and HL-48484, Fogarty International Center IR03 TW01295, and Akdeniz University Research Projects Unit (project no. 2002.01.0103012).


   FOOTNOTES
 

Address for reprint requests and other correspondence: O. K. Baskurt, Dept. of Physiology, Akdeniz Univ., Faculty of Medicine, Kampus, Antalya, Turkey (E-mail: baskurt{at}akdeniz.edu.tr)

The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.


   REFERENCES
TOP
 ABSTRACT
 MATERIALS AND METHODS
 RESULTS
 DISCUSSION
 GRANTS
 REFERENCES
 

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