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The effect of caffeine consumption on creatine kinase levels following eccentric exercise.

INTRODUCTION

When an active muscle is stretched, its cells may be damaged. Research has shown that after severe eccentric contractions that are followed by muscle soreness, muscle fibrils, connective tissues around fibers, the plasma membrane of muscle fibrils, sarcomeres, sarcoplasmic reticulum, or a combination of these parts are damaged, leading to special biochemical and functional symptoms in the individual [8]. One of these symptoms is increased creatinekinasein the blood that often occurs following vigorous eccentric exercises and delayed onset muscle soreness. Creatine kinase (CK) is a key enzyme in muscle cell metabolism that can be found especially in the cells surrounding contractile filaments and has very low concentration in blood.

Vejjajiva and Teasdale were the first researchers to examine the effects of training on CK activity. Many studies have reported increased release of CK and its peak concentration 24-72 hours after exercise. Peak CK levels does not always occur simultaneously with peak DOMS. The release of CK depends on the type, intensity, and duration of exercise. Serum CK concentration increases with exercise intensity. In a research on eccentric and concentric contraction groups, increased CK was observed only in the eccentric contraction group. It was also shown that adaptation of CK is achieved with an 18-day training protocol. Other studies support the adaptation effect. In one study, for instance, increase in CK and DOMS levels was much greater after the first exercise session than the second exercise session (1-6 weeks later). Other researchers have reported peak serum CK 24-72 hours after exercise [9]. The type, intensity, and duration of daily activities, gender, heredity, age, physical fitness, individual differences, and environmental factors can increase CK activity following exercise [1].

DOMS caused by eccentric exercise can be treated to quickly restore peak muscle performance of muscles. Treatments include: caffeine, anti-inflammatory medications, massage, stretching, ultrasound and electrical stimulation, physical activity, cryotherapy, and heat therapy.

Caffeine is a water-soluble alkaloid in crystalline form. Caffeine can be found in team coffee, chocolate, and some carbonated beverages [4]. Caffeine can be effective in reducing pain by inhibiting adenosine receptors in the brain. Adenosine is amoleculein the brain that, when bound to its receptors, causes fatigue, pain, and drowsiness. This binding can also cause blood vessels in the brain to dilateto let more oxygen into this organ during sleep. When more adenosine molecules bind to the receptors in the brain, the feeling of fatigue, pain, and drowsiness become stronger [2]. Adenosine is also secreted in response to injury and activates nociceptorsin body cells [3]. The high concentration of adenosine at or near sites of damage and inflammation increases the likelihood of nociceptive afferent activation [5]. Caffeine is a competitive, nonselective adenosine receptor antagonist. A study examined the effect of caffeine consumption on DOMS in 16 female basketball players and showed that caffeine can prevent the increase in serum creatine kinase caused by DOMS [10]. The purpose of the present research is to examine the effect of caffeine consumption on creatine kinase levels following eccentric exercise.

Methodology:

This research was quasi-experimental with a pretest-posttest design. 16 female volleyball players were randomly divided into an experimental group and a control group. The subjects had no history of cardiovascular disease or musculoskeletal disorders and gave their consent to participate in the study. After selecting and grouping the subjects, the research was conducted in 2 consecutive days. It must be noted that 12 and 24 hours before the exercise each subject in the experimental group drank one cup of coffee containing 1 mg caffeine per kilogram body weight, while the control group drank a placebo. These groups were asked to drink the same materials before exercise.

The dominant leg of the subjects was determined by a dynamometers and maximum isometric strength was measured in kilograms. Isometric strength was measured by having the subjects sit on a seat with the knees bent to 90 degrees and the dynamometer attached to the ankle of the dominant leg.

After 10 minutes of warm-up, the subjects in both groups performed jumping and landing from a 1-meter high platform 50 times at 30-second intervals. It must be noted that muscle soreness from this method of exercise was tested and verified three weeks earlier. After the exercise, the subjects consumed the drinks and the serum creatine kinase (CK) levels were measured. The drinks were also injected by the subjects 12 hours after exercise. The subjects were instructed to perform their daily tasks and not to take any painkillers. 24 hours after the test, the serum CK of the subjects was once again measured. The data were analyzed using ANOVA and Tukey's test and independent t-test was used to compare the two groups.

Results:

The effect of caffeine consumption on serum creatine kinase levels after eccentric exercise was measured. The results are provided in Table 1.

The results show that, as a result of eccentric exercise, creatine kinase significantly increased only at 24 hours after exercise (68.80 percent). This observation indicates the delayed nature of muscle soreness and the emergence of its symptoms. The results of examining the experimental group are provided in Table 3.

The results show that, like the control group, caffeine consumption and eccentric exercise has led to significant increase in CK levels only at 24 hours after exercise (37.18 percent). Comparing these data with the data of the control group may suggest that consumption of caffeine has had not been effective in preventing increase in CK levels due to delayed onset muscle soreness. There was no significant difference between the control group and the experimental group in CK levels in the pretest and at 24 hours after consumption (p = 0.7831 and p = 0.995 respectively), CK changes of the two groups before exercise up to 24 hours after exercise were compared, which indicated that there is a significant difference between these groups (p = 0.029). This means that caffeine has prevented further increase in CK levels at 24 hours after exercise (37.18 percent increase in the experimental group against 68.80 percent increase in the control group). Therefore, it can be concluded that caffeine consumption has a significant effect on changes in serum creatine kinase after eccentric contractions (Figure 1).

Discussion:

Considering the limitations of sport facilities, it is necessary to find a quick and effective way to overcome the negative impacts of delayed onset muscle soreness (DOMS), including increased creatine kinase levels. In the present study, the caffeine in coffee was used to treat DOMS caused by eccentric exercise, since it was easier than other therapeutic methods (e.g., medications and electrical stimulation) and could be more easily accepted by athletes. The caffeine molecule is structurally similar to adenosine and it can bind to adenosine receptors on the surface of cells without activating them. This can inhibit the binding of adenosine to these receptors and thus reduce fatigue following muscle damage [4]. Moreover, this increases free adenosine, thus increasing blood flow to musclesand leading to faster removal of waste and inflammatory materials [11]. The results of the present research suggested the positive effect of caffeine in reducing DOMS, which is consistent with the findings of Karbaleifar et al. [10].

Conclusion:

It appears that caffeine consumption increases the removal of waste and reduces DOMS. Therefore, it is recommended that trainers or physiotherapists use coffee to quickly reduce serum creatine kinase and DOMS.

Article history:

Received 11 September 2013

Received in revised form 21 November 2013

Accepted 25 November 2013

Available online 12 January 2014

REFERENCES

[1] Omrani, A., 1996. "A study of the clinical and functional outcomes of delayed muscle soreness", Master's Thesis, Iran University of Medical Sciences.

[2] Daniels, J.W., P.A. Mole, J.D. Shaffrath, C.L. Stebbins, 1998. "Effects of caffeine on blood pressure, heart rate, and forearm blood flow during dynamic leg exercise", Journal of Applied Physiology, 85: 154-159.

[3] Kalmar, J.M., E. Cafarelli, 1999. "Effects of caffeine on neuromuscular function", Journal of Applied Physiology, 87: 801-808.

[4] Lopes, J.M., M. Aubier, J. Jardim, J.V. Aranda, P.T. Macklem, 1983. "Effect of caffeine on skeletal muscle function before and after fatigue", Journal of Applied Physiology, 87(54): 1303-1305.

[5] Maridakis, V., P.J. O'Connor, G.A. Dudley, K.K. McCully, 2006. "Caffeine attenuates delayed-onset muscle pain and force loss following eccentric exercise", Journal of Pain, 8: 237-43.

[6] Armstrong, R.B.,1990. "Initial events in exercise-induced muscular injury", Medicine and Science in Sports and Exercise, 22: 429-35.

[7] Clarkson, P.M., W.C. Byrnes, E. Gillisson, E. Harper, 1987. "Adaptation to exercise-induced muscle damage", Clinical Science, 73: 383-6.

[8] Clarkson, P.M., K. Nosaka, B. Braun, 1992. "Muscle function after exercise-induced muscle damage and rapid adaptation", Medicine and Science in Sports and Exercise, 24: 512-520.

[9] Cleak, M.J., R.G. Eston, 1992. "Delayed onset muscle soreness: mechanisms and management", Journal of Sports Science, 10: 325-341.

[10] Karbaleifar, S., M. Nasiri, M. Salehian, 2011. "The effects of caffeine on perceived pain of muscles", Annals of Biological Research, 2: 16-21.

[11] Maughan, R.J., M. Gleeson, P.L. Greenhaff, 1997. "Biochemistry of Exercise and Training", Oxford: University Press.

Masoomeh Nobahar

Department of Physical Education and Sport Science, Payamenoor University, Iran

Corresponding Author: MasoomehNobahar, Department of Physical Education and Sport Science, Payamenoor University, Iran

Mobile:+989183386440

Table 1: Analysis of variance of the CK data
of the control group.

Variance          Sum of       Mean      Observed F    Significance
                  Squares     Squares                      Level

Between-Group    10571.01    5371.291       10.17          0.001
Within-Group     10946.29     519.998
Total            21517.83

Table 2: The results of Tukey's test for the CK
data of control group.

                       24 Hours     Immediately    Immediately
                        after          after          after
                     Consumption    Consumption      Exercise

Before Exercise        -52.01 *        -14.60         -14.62
                       0.001 **        0.097          0.147

Immediately after       -67.62         -29.22
Exercise                0.049          0.178

Immediately after       -37.48
Consumption             0.037

* Difference, ** Significance

Table 3:Analysis of variance of the CK data of
the experimental group.

Variance            Sum of       Mean     Observed F    Significance
                   Squares     Squares                      Level

Between-Group      3831.00     1914.55       6.069          0.008
Within-Group       6635.655    317.780
Total             10466.655

Table 4: The results of Tukey's test for the CK data
of the experimental group.

                       24 Hours     Immediately    Immediately
                        after          after          after
                     Consumption    Consumption      Exercise

Before Exercise        -27.25 *        -36.15         -10.5
                       0.007 **        0.117          0.543

Immediately after       -17.65         -26.43
Exercise                0.073          0.334

Immediately after       -9.12
Consumption             0.187

* Difference, ** Significance
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Author:Nobahar, Masoomeh
Publication:Advances in Environmental Biology
Article Type:Report
Geographic Code:7IRAN
Date:Nov 1, 2013
Words:1738
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