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Plasma Oxytocin during Intense Exercise in Professional Cyclists
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| Horrn Res 2001;55:155-159 |
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Autores: José L. Chicharro a,b Jesús Hoyos b,e Fernando Bandrés d
Felix Gomez Gallego d Margarita Pérez b,e Alejandro Lucía b,e
a Departamento de Enfermería, and b Unidad de Investigación Fisiología del Ejercito, Universidad Complutense de Madrid;
c Agrupación Deportiva Banesto; d Departamento de Toxicología y Legislación Sanitaria Universidad Complutense
de Madrid; and e Departamento de Ciencias Morfológicas y Fisiología. Grupo de Investigación I+D+i, Spain |
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Key Words
Cycling -Oxytocin - Exercise
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Abstract:
Aims: This study was designed to explore the plasma oxytocin (OT) response to exercise until exhaustion in trained male cyclists. Methods: Twelve professional cyclists (EXP group; age: 26 ± 2 years; VO2max: 4,804 ± 549 ml) and 10 sedentary young men (CONT group; age: 23 ± 2 years; VO2max: 3,146 ± 602 ml) performed a maximal incremental exercise test on a cycle ergometer. Evaluation was made of the oxygen uptake (VO2) and concentrations of blood lactate and plasma OT immediately before, during and immediately after the tests, respectlvely. Results: Significant Increases (p < 0.01) related to exercise were recorded in V02 and lactate concentration within each group, while no such changes were observed in OT levels. OT values, on the other hand, were significantly lower (p < 0.01) in EXP than in CONT throughout the tests. Conclusion: It was concluded that plasma OT shows no response to graded exercise until exhaustion in professional cyclists. |
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Introduction:
Oxytocin (OT) is produced mainly by the hypothalamo-neurohypophysial axis [1]. The release of OT is regulated by neurons in the paraventricular
and the supraoptic nuclei of the hypothalamus. This hormone is also found in several other brain regions (e.g. limbic system, brain stem), suggesting a role in neurotransmission [2]. and in several organs outside
the central nervous system such as the ovary, adrenal gland, thymus and pancreas [1]. The complete physiological role of OT is far from clear. Apart from its obvious implication in reproductive processes, OT is thought to contribute to the neuroendocrine response to stress [3].
It is well documented that exhaustive exercise can lead to an activation of several “stress hormones”, i. e. ACTH, cortisol, catecholamines, prolactin or vasopressin. The magnitudes of the responses are modulated by both the relative intensity and the duration of exercise: in general, the greater the intensity, and the duration of exercise, the greater the hormonal release [4]. Prolonged exercise can stimulate the pituitaty-adrenal axis maximally. During intense prolonged exercise, indeed, ACTH concentrations show a marked increase, which in turn results in a significant release of cortisol [4]. Such response is exaggerated under some conditions, e.g. hypoglycemia, increases in body temperature, or
psychological stresses [5]. The svmpathetic-adrenal-medullary system is even more sensitive lo exertion [6]. Its response, indeed, is evident during low intensity exercise [6,7] and increases dramatically with increasing intensities [8]. For a given workload. The activity of this neuroendocrine system also increases with exercise duration. For instance, rises in epinephrime and norepinephrine concentrations of as much as 300-400% and 600-900%, respectively, have been reported during 50-min protocols [9]. Such high increase in catecholamine release during prolonged and/or intense exercise supports the higher need for glucose and free fatty acid uptake in muscle cells, improves cardiac function and ventilatory flow, and helps in blood redistribution and heat dissipation [4]. Although the phisiological significance of the phenomenon is not clearly established, prolactin has been shown to increase with exertion [10], particularly at high, workloads [5]. The secretion of vasopressin can also rise during physical acticity, especially in dehydrated humans and during prolonged exercise bouts [11,12]. The cause of this response is probably related to exercise-induced shifts in plasma volume and osmolality rises [11,13,14]. In contrast, data concerning the OT response lo exercise are scarce. To date, only two reports [15,16] ] have focussed on the behavior of this hormone during intense physical activity in humans. Altemus el al. [15] described no change in 0T levels during exercise in a group of women and Landgraf et al. [16] demonstrated changes in plasma levels of OT (a marked increase or even decrease) in response to running exercise until exhaustion.
To our knowledge, there are no data available on, the response of plasma OT lo incremental exercise until exhaustion in male endurance athletes of high functional capacity. Professional road cycling is an extremely demanding sport, both in terms of training volume and intensity, and is known to induce considerable phisiological adaptations [17]. Thus, the aim of this study, was to evaluate the behavior, of plasma. OT during incremental exercise performed lo exhaustion in professional cyclists. Based on the results of previous research with not highlv trained humans [15,16], we hypothesized that OT does not increase during maximal excrcise in these top-level cyclists. |
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Methods:
Subjects
Twelve professional male road cyclists (experimental or EXP group; age 26 ± 2 years; height 177,5 ± 4,41cm; body mass 70,8 ± 5.0 kg) and 10 sedentary, healthy young men (control or CONT age 23 ± 2 years; height 179,6 ± 4,4 cm; body mass 77,2 ± 5,7 kg) participated in this study. Subject of the EXP group had a minimun competition experience of three years and covered approximately 30,000 – 35,000 km per year in training and competition. Some of them are among the best cyclists in the world and had won major proffesional races (i.e. World Championships). Written informed consent was given before participation in the study, in accordance with our institution´s (Complutense University of Madrid) guidelines for human subjects.
Study Protocol
Subjects were instructed to refrain from intense training the day before testing and were familiarized with the equipment, and procedures to be followed before each exercise testing session.
Each subject performed a single exercise test on a bicycle ergometer (Ergometrics 900; Ergoline, Barcelona Spain) following a ramp protocol until exhaustion. Starting at 0 W, the workload was increased by 25 W/min and pedalling cadence was kept constant at 70 – 90 rpm. In all cases, the exercise test was terminated either (1) voluntary by the subject: (2) when pedalling cadence could not be maintained, at least 70 rpm, or (3) when established criteria of test termination were met [18]. Each test was performed under similar conditions (21 to 24 º C, and 45 to 55% relative humidity).
Determination of Heart Rate. Expired Gas and Blood Lactate
During the test, heart rate (HR) was monitored using modified 12-lead ECG tracings (EK56: Hellige; Freiburg, Germany) and gas exchange data obtained using an automated breath-by-breath system (CPX; Medical Graphics; St. Paul. Minn., USA). Measuring instruments were calibrated before each test and the necesary enviromental adjusments made. Capillary blood samples (25 µl) were obtained via fingersticks before warm-up, every 2 min during the tests, and immediately after termination of exercise for the estimation of lactate using an electro-enzymatic analyser (YSI 1500; Yellow Springs Instruments. Ohio. USA). The lactate threshold (LT) was determinated by examining the “lactate concentration –workload (W)” relationship during the tests according to the methodology described by Weltman et al. [19]. This method defines the workload corresponding to LT as the highest workload not associated with a rise in lactate levels above baseline. This always occurred just before the curvilinear increase in blood lactate observed at subsequent exercise intensities. An increase of at least 0.2 M in blood lactate was required for the determination of LT.
The variables heart rate (HR in beats/min), VO 2 (ml/min) and lactate (m M ) were expressed according to the time exercise, i.e. Rest (just before the start of execise). Below-LT (at a workload below the occurrence of the LT). Above-LT (at a workload above the LT) and Max (immediately after the end of exercise). The workloads corresponding to Below-LT and Above-LT were 200 and 400 W in EXP, respectively, and 100 and 200 W in CONT, respectively.
Plasma Oxytocin
Some 30 min prior to the exercise test, a Teflon catheter was inserted into antecubital vein and blood samples obtained at Rest, Below-LT, Above_LT and Max. The plasma OT concentration was determinated by radioimmunoassay using the kit provided by Phoenix Pharmaceuticals (Mountain View, Calif., USA), wich is based in an antiserum raised against a synthetic form of the peptide. Plasma samples were extracted on Sep-Pack C18 cartridges for the assay, as suggest in the manufacturer's protocol. Intraassay coefficients of variation were less than 5%. In order to correct exercise OT data (those corresponding to Below-OT, Above-OT and Max) for hemoconcentration in comparison with pre-exercise conditions (Rest). Loss of plasma volume (5) during exercise was estimated in each subject by a method described elsewhere [20]. This method requires determination of hematocrit (%) and hemoglobin concentration (g/dl) for each blood sample.
Statistical Analysis
Results were expressed as mean ± SD. Once a normal distribution of data was established by application of Kolmogorov-Smirnov test, repeated-measures ANOVA was used to compare OT, HR, VO 2 and lactate at Rest, Below-LT, Above-LT and Max within each of EXP and CONT groups. A Student's t test for unpaired data was also used to compare OT levels between both groups at Rest. Below-LT, Above-LT and Max. The level of significance was set at p < 0.05. |
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Results:
Table 1 lists the performance variables recorded. Both HR and VO 2 increased significantly (p < 0.01) with increasing exercise intensity in each of both groups. There were no differences between lactate levels observed at Rest and Below-LT, while a significant increase was shown by levels recorded at Above-LT and Max (p < 0.01).
The levels of OT during exercise are shown in figure 1. No significant differences were found throughout the tests within any of both groups (p > 0.05), whereas OT levels were significantly lower (p < 0.01) in EXP at Rest, Below-LT, Above-LT, and Max. |
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Fig 1: Plasma oxytocin (OT) levels in both experimental (EXP) and (CONT) groups. In all the subjects. blood samples were collected before exercise (Rest), at a workload below and above the LT (Below-LT and Above-LT, respectively), and inmediately after the end of exercise (Max). Hormone data corresponding to Below-LT, Above-LT and Max were corrected for exercise-induced hemoconcentration according to a method described elsewhere [20]. * Significant difference between EXP and CONT (p<0.01). No significant differences existed within each of both groups.
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Table 1: Performance variables durinf incremental exercise
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Rest |
Below-LT |
Avove-LT |
Max |
| EXP group |
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| HR, beats/min |
51±3 |
129±13* |
170±7** |
191±8** |
| VO2 ml/min |
257±50 |
2.714±185 |
4.142±312* |
4.804±549*** |
| Lactate, mM |
1.4±0.2 |
1.6±0.3 |
3.5±1.5** |
11.9±1.2 |
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| CONT group |
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| HR, beats/min |
88±6 |
128±12* |
164±10** |
185±12*** |
| VO2 ml/min |
432±86.1 |
1.400±128* |
2.327±318** |
3.146±602*** |
| Lactate, mM |
1.5±0.5 |
1.5±0.2 |
3.0±0.6** |
7.1±1.6 |
Data are expressed as means± SD. EXP group = Experimental group of 12 professional cyclists; CONT group = control group of 10 sedentary young males: HR = heart rate; VO2 = oxygen uptake.
* Significantly different (P<0.01) from Rest; ** significantly different (p<0.01) from both Rest and Below-LT; *** significantly different (p<0.01) from each of Rest, Below-LT and Above-LT. |
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Discussion:
The present findings show a lack of significant change in plasma OT levels in top level endurance athletes during incremental exercise until exhaustion. Despite the proposed relationship with the neuroendocrine response to stress [3], these results suggests a role of title relevance for OT in both trained and untrained humans, at least in the present exercise model. An additional finding was that OT levels were consistently lower in the cyclists compared with the sedentary controls. This is in line with previous studies which have shown that the release of other pituitary hormones (i.e. vasopresin) is attenuated by endurance training [21,22].
Incremental exercise protocols have been shown to lead to an increase in plasma concentrations of several hormones [6,12,23]. We used cycling exercise as a stimulus since it is a reproducible an quantifiable stressor that elicits neuro endocrine and metabolic responses proportional to intensity and duration of the exercise [15]. The involvement of anaerobic metabolism in this type of protocol is reflected by the significant increase in blood lactate (at Above-LT and Max), also implying greater sympathetic adrenal activity at these high workloads [24].
Only two previous investigations have explored the OT response to exercisein humans. Altemus et al. [15] examined a variety of physiological responses to treadmill exercise in untrained women (VO2max ˜ 30 ml/Kg/min) and found no change in plasma OT levels attributable to incremental exercise performed to exhaustion. Landgraf et al. [16] conducted a study on the OT reponse to prolonged (60 min), high intensity (80% VO2max) exercise in five subjects, of wich three were well-trainded runners. These authors reported contradictory results; OT levels rose in 2 of the subjects and fell in 1 subject. Contribution of our findings to the present body of knowledge in the field is twofold. First, the study population was formed by highly trained subjects, or professional cyclists, wich contrasts with the untrained female subjects [15] and moderately trained male athletes [16] of these previous studies. Secondly, the number of subjects in the present, highly homogeneus series serves to emphasize the lack of change in OT levels in response to exercise wich was questionable in Landgraf's investigation performed on very few subjects undergoing exercise at a relative intensity of exercise (80% VO2max) known to lead to different metabolic stress in trained and untrainned subjects.
It has been suggested that OT way may be involved in the reflex pressor response to muscle contraction since intrathecal injection of the hormone in to the spinal cord attenuates this response [25,26]. Further, the administration of OT in untrained men has been found to reduce the ACTH-cortisol response to exercise acting at the pituitary level or in the hypothalamus [27]. The results obtained here do not appear to support a significant role for physiologically produced OT in the neuroendocrine response to stress, at least in intense short-term exercise. On the other hand, ithas also been suggested that OT may play a further role in certain immune [28] and metabolic responses [29] and even exert effects on the cardiovascular system [30]. The present findings raise doubts as to such possible effects in both highly trained and sedentary subjects performing this type of exercise test. It is proposed that future research efforts center on the possible role of OT in intense, prolonged exercise such as during several weeks of competition.
A major drawback of our design comes from the fact that we did not measure the levels of other hormones (i.e. cathecholamines, ACTH, etc) in order to show the occurence of significant neuroendocrine activation during the present exercise protocol. Such limitation is partly compensated, nevertheless, by the fact that we measured OT levels at exercise intensities (Above-LT and Max) above the LT. As previously mentioned, it has been clearly documented that one of the neuroendocrine system most heavily involved in the control of bodily functions during exercise, i.e. the sympathetic-adrenal-medullary system, is significantly activated at exercise intensities above the LT during incremental exercise protocols [24]. Finally, we could not determine if OT could have exhibited a delayed response to exertion since the last samples were collected immediately after cessation of exercise. In this regard, we hypothesize that circulating levels of most hormones significantly involved in the neuroendocrine response to exertion would have shown a response during the present study, given the duration of the exercise protocol (20-25 min in each of the cyclists).
In conclusion, our findings suggest no change in oxytocin levels during incremental exercise to exhaustion in this highly trained group of athletes. Further, the release of this hormone seems to be attenuated by high-level endurance training.
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Acknowledgements:
The authors are indebted to the participating cylists for their generous collaboration, to Ana Carnero and Alberto González of the Instituto Cajal del Consejo Superior de Investigaciones Científicas for their help and usefull suggestions, and to Ana Burton for her help in translating and copy editing the manuscript.
This study was financed by the Agrupación Deportiva Banesto. Spain |
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References:
- Jenkins JS, Nussey SS: The role of oxytocin: Present concepts. Clin Endocrinol 1991;34:515-525.
- Bijis RM: Vasopresin and oxytocin: Their role in neurotransmission. Pharmacol Ther 1983;22:141.
- Jezova D. Skultetyova I, Tokarev DI, Bakos P, Vigas M: Vasopresin and oxytocin in stress Ann NY Acad Sci 1995;771P:192-203.
- Murray RG, Hackney AC: Endocrine responses to exercise and training; in Garret WE Jr, Kirkendall DT (eds): Exercise and Sport Science. Philadelphia. Lippincott Williams & Wilkins. 2000, pp 135-161.
- Viru A: Plasma hormones and physical exercise. Int J Sports Med 1992;13:201-209.
- Deuster PA, Chrousos GP, Luger A, De Bolt JE, Bernier LL, Trostman UH, Kyle SB, Montgomery LC, Loriaux DL: Hormonal and metabolic responses of untrained, moderately trained, and highly trained men to three exercise intensities. Metabolism 1989;38:141-148.
- Christensen NJ, Galbo H, Hamsen JF, Hesse B, Richter EA, Trap-Jensen J: Catecholamines and execise. Diabetes 1979;28:58-62
- McMurray RG. Forsythe WA, Mar MH. Hardy CJ: Exercise intesity-related responses of beta-endorphins abd catecholamines. Med Sci Sports Exerc 1987;19:570-574.
- Kinderman W, Schmabel A, Schmitt WM, Biro G, Cassens J, Weber F: Catecholamines growth hormone, cortisol, insulin, and sex hormones in anaerobic and aerobic exercise. Eur J Appl Physiol 1982;49:389-399.
- Hale RW, Kosana T, Krieger J, Pepper S: A marathon: The immediate effect on female runners' luteinizing hormone, follicle-stimulating hormoe, prolactin, testosterone, and cortisol levels. Am J Obstet Gynecol 1983;146:550-556.
- Montain SJ, Laird JE, Latza WA, Sawaka MN: Aldosterone and vasopresin responses in the heat: Hydration level and exercise intensity effects. Med Sci Sports Exerc 1997;29:661-668.
- Convertino VA, Keil LE, Bernauer EM, Greenleaf JE: Plasma Volume, Osmolality, vasopresin and renin activity during graded exercise in man. J Appl Physiol 1981;50:123-128
- Grant SM, Green HJ, Phillips SM, Enns DL, Sutton JR: Fluid and electrolyte hormonal responses to exercise and acute plasma volume expansion, J Appl Physiol 1996;;81:2386-2392
- Greenleaf JE, Brock PJ, Keil LC, Morse JT: Drinking and water balance during exercise and heat acclimation. J Appl Physiol 1983;54:414-419.
- Altemus M, Deuster Pa, Galliven E, Carter CS, Gold W: Suppression of hypothalamic-pituitary-adrenal axis responses to stress in lactating women. J Clin Endocrinol Metab 1995:802954-2959.
- Landgraf R, Häcker R, Buhl H: Plasma vasopressin and oxytocin in response to exercise and during a cay-night cycle in man. Endokrinologie 1882;79:281-291.
- Lucia A, Pardo J, Durantez A, Hoyos J, Chicharro JL: Physiological deifferences between proffesional and elite road cyclists. Int J Sports Med 1998;19:342-348.
- American College of Sports Medicine (ACSM): Guidelines for Exercise Testing and Prescription. Philadelphia, Lea & Febiger, 1986,pp 95-96.
- Weltman AD, Snead D, Seip R, Schurrer R, Levine S, Rutt R: Reliability and validity of a continuous incremental treadmill protocol for the determination of lactate threshold, fixed blood lactate concentration, and VO2max. Int J Sports Med 1990;11:26-32.
- Dill DB, Costill DL: Calculation of percentage changes in volume of blood plasma and red cells in dehydration. J Appl Physiol 1974;37:247-248.
- Convertino VA, Keil LC, Greenleaf JE: Plasma volume, renin, and vasopresin responses to graded exercise after training. J Appl Physiol 1983;54:508-514.
- Melin B, Eclache JP, Geelen G, Annat G, Allevard AM, Jarsaillon E, Zebidi A, Legros JJ, Gharib C: Plasma AVP, neurophysin, renin avtivity, and aldosterone during submaximal exercise performed until exaustion in trainned and untrained men. Eur J Appl Physiol 1980;44:141-151.
- Luger A, Deuster P, Kyle SB, Galluci WT, Montgomery LC, Gold PW, Loriaux DL, Chrousos GP; Acute hypotalamic-pituitary-adrenal responses to the stress of treadmill exercise. N Engl J Med 1987;316:1309-1315.
- Mazzeo RS, Marshall P: Influence of plasma catecholamines on the lactate threshold during graded exercise. J Appl Physiol 1989;67:1319-1322.
- Li J, Hand GA, Potts JT, Mitchell JH: Identification of hipothalamic vasopresin and oxytocin neurons activated during the exercise pressor reflex in cats. Brain Res 1997;752:45-51.
- Stebbins ChL, Ortiz-Acebedo A: The exercise pressor reflex is attenuated by intrathecal oxytocin. Am J Physiol 1994;267:45-51.
- Coiro V, Passeri M, Davoli C, Bacchi-Modena A, Bianconi L, Volpi R, Chiodera P: Oxytocin reduces exercise-inducted ACTH and cortisol rise in man. Acta Endocrinol (Copenh) 1988;119:405-412.
- Johnson HM, Torres BA: Regulation of linphokine production by arginine vasopressin and oxytocin: Modulation of lynphocyte function by neurohypophyseal hormones. J Immunol 1985;135:773-775.
- Whitton PD, Rodrigues LM, Hems DA: Stimulation by vasopresin, angiotensin, and oxytocin of gluconeogenesis in hepatocyte suspensions. Biochem J 1978;176:893-898.
- Nakano J, Fisher RD: Studies on the cardiovascular effects of synthetic oxytocin. J Pharmmacol Exp Ther 1963;142;142:206-214.
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