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Diferencias interindividuales en las concentraciones de cortisol plasmático tras una de ejercicio mixto aeróbico-anaeróbico.
Abstract
Introducción y objetivos: El objetivo del estudio fue evaluar las diferencias en la concentración plasmática de cortisol tras la realización de un esfuerzo mixto, aeróbicoanaeróbico, en un grupo de jóvenes físicamente activos. Métodos: Catorce voluntarios realizaron, en un cicloergómetro, 40 min de ejercicio a la intensidad correspondiente al 50% del pico individual de consumo de oxígeno, manteniendo el ritmo de pedaleo a 60 revoluciones/min. Durante el mismo, se intercalaron 4 fases de 30 s con una carga de 0,04 kg por kilo de masa corporal en los minutos 10, 20, 30 y 40. Tras estos primeros minutos, pedaleaban durante 20 min a la máxima velocidad posible frente a una carga constante correspondiente al 50% del consumo de oxígeno. Se controlaron los parámetros cardiorrespiratorios y se recogieron muestras sanguíneas al inicio de la prueba, cada 10 min durante el ejercicio y a los 15 min de la recuperación. Resultados: Las respuestas cardiopulmonar y metabólica fueron muy homogéneas, con un aumento de los valores de cortisol a lo largo de la prueba (F = 5,16; p < 0,001) que presentó diferencias entre los sujetos (F = 6,74; p < 0,001). En 8 participantes (57,1% de la muestra) se observó un aumento, y en 6 (42,9%) los cambios fueron pequeños con respecto a los valores previos al inicio de la prueba. Conclusión: A pesar de haber evaluado un grupo homogéneo, se observaron diferencias interindividuales en la concentración plasmática de cortisol tras la realización de un esfuerzo mixto, lo que puede tener implicaciones en la adaptación provocada por el ejercicio.
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The present study investigated cortisol responses to three different stimulation procedures, with a focus on the contribution of genetic factors. Thirteen monozygotic (MZ) twin pairs and 11 dizygotic (DZ) twin pairs performed bicycle ergometry until exhaustion and were exposed to the psychological stress of public speaking and mental arithmetic in front of an audience. Furthermore, 9 MZ pairs and 10 DZ pairs were injected with 100 micrograms synthetic human CRH (hCRH). The adrenocortical response to these challenges was monitored by determination of cortisol in saliva. Significant intraindividual stability of baseline cortisol levels was found in females, but was less in males. Maximum cortisol responses to all three stimulation procedures were significantly intercorrelated in males, but in females only the cortisol responses to hCRH and ergometer exercise showed a significant correlation. While a decided influence of genetic factors was observed for all three baseline cortisol levels as well as for the response to hCRH, heredity appeared to be play a minor role in the adrenocortical response to psychological stress. Cortisol changes after bicycle ergometry revealed no impact of genetic factors on the secretion of cortisol in response to strenuous physical exercise.
We previously described a syndrome of congestive heart failure occurring in healthy young men at extreme altitude (Anand et al. Lancet 335: 561-565, 1990). The pathogenesis of this condition is unclear. We therefore measured body fluid compartments, renal blood flow, and a variety of plasma hormones in 10 asymptomatic young men staying above 6,000 m for > 10 wk and compared the results with controls at sea level. Body compartments were measured with isotope dilution techniques and renal blood flow with o-[125I]iodohippurate sodium. There was a marked expansion of all the fluid spaces: total body sodium was 14% above normal (P < 0.05), total body water was 18% above normal (P < 0.05), plasma volume was 33% above normal (P < 0.05), and blood volume was 84.5% above normal (P < 0.001). The effective renal plasma flow was lower than normal by 55% (P < 0.001), but the reduction in the effective renal blood flow was 37% below normal (P < 0.001) because the hematocrit was high (41.6% above normal). Plasma norepinephrine was nearly 3 times normal (P < 0.01), cortisol 3 times normal (P < 0.001), and growth hormone 18 times normal (P < 0.01). Aldosterone was twice normal (P < 0.03). Plasma epinephrine, atrial natriuretic peptide, and plasma renin activity were unchanged. The degree of fluid retention in these normal subjects was similar to that in patients with severe untreated congestive heart failure (Anand et al. Circulation 80: 299-305, 1989), whereas sodium retention and reduction in effective renal blood flow were less.(ABSTRACT TRUNCATED AT 250 WORDS)
The hypothalamo-pituitary-adrenal axis is involved throughout the exercise-recovery cycle. Nevertheless, differences in hormone responses during early recovery between sedentary and endurance trained subjects are not well known. The aim of this preliminary study was to monitor plasma cortisol and adrenocorticotropic hormone (ACTH) concentrations both during and after the end of running exercise performed by four endurance trained adults (marathon men) compared to four sedentary subjects. Two parameters, i.e. intensity and duration, were changed on 4 consecutive days. The 1st day (D0) was spent in the laboratory: all blood samples were obtained at rest to determine diurnal variations of each hormone. On the following days (D1-D4) the subjects exercised: D1 and D2 brief (20 min), light (50% maximal heart rate HRmax, D1) or strenuous (80% HRmax, D2), D3 and D4 prolonged (120 min), light (D3) or strenuous (D4). In both groups, neither brief (D1, D2) nor prolonged light exercise (D3) induced any significant variation in plasma ACTH or cortisol concentrations. Plasma ACTH and cortisol concentrations increased only if the exercise was intense and prolonged (D4). The training factor did not modify the intensity or duration thresholds for the activation of the pituitary-adrenocortical response to exercise in the conditions of our experiment. However, during immediate recovery from the four exercise regimens, the plasma ACTH concentrations of the marathon men were constantly above the values of the sedentary subjects, although plasma cortisol concentration remained similar in both groups. As an indirect means of evaluating the relationships between ACTH and cortisol we compared the areas under the cortisol and ACTH curves (AUC) from 0.5 to 3.5 h during recovery from D1 to D4 compared to D0 at the same time. Cortisol AUC were similar in the sedentary subjects and marathon men although the ACTH AUC were different in the sedentary subjects and marathon men, suggesting a change in the pituitary-adrenal relationship at some yet indeterminate level. During the immediate recovery from exercise whatever its intensity, the magnitude of the ACTH response was increased in the trained subjects but with a reduced effect upon its target, the adrenal glands. This phenomenon has not been described in the literature. Two non-exclusive phenomena may be involved, i.e. a decreased adrenal sensitivity to ACTH stimulation, and/or a decreased hypothalamo-pituitary axis sensitivity to cortisol negative feedback.
To compare profiles of hypothalamic-pituitary-adrenal (HPA) responsiveness, healthy, moderately trained men (n = 15) were classified as high (n = 7) or low responders (n = 8) on the basis of plasma adrenocorticotropic hormone (ACTH) responses to strenuous treadmill exercise 4 h after 4 mg of dexamethasone (Dex). These groups were then evaluated to compare 1) HPA and growth hormone responses to exercise at 90% maximal oxygen uptake 4 h after placebo, Dex (4 mg), and hydrocortisone (100 mg); 2) pituitary-adrenal responses to infusion of arginine vasopressin (AVP); 3) plasma cortisol after a Dex suppression test (1 mg); and 4) behavioral characteristics. In comparison to low responders, high responders exhibited significantly 1) higher plasma ACTH responses to exercise after placebo and Dex; 2) higher plasma AVP secretion with exercise after placebo and marked Dex- and hydrocortisone-induced enhancement of exercise-induced AVP secretion; 3) lower Dex-induced increases in basal and stimulated growth hormone secretion; 4) higher plasma ACTH responses to infusion of AVP; and 5) a trend (P = 0.09) for higher trait anxiety ratings. Similar suppression of plasma cortisol was noted after 1 mg Dex. We conclude that subgroups of healthy male volunteers exhibit unique profiles of HPA responsiveness. We also believe that glucocorticoid pretreatment combined with strenuous exercise allows functional HPA responsiveness to be distinguished between subgroups of healthy controls and may be useful in the determination of susceptibility to disorders characterized by hyper- and hypo-HPA activation.
The aim of this study was to evaluate the acute responses of blood hormone concentrations and neuromuscular performance following whole-body vibration (WBV) treatment. Fourteen male subjects [mean (SD) age 25 (4.6) years] were exposed to vertical sinusoidal WBV, 10 times for 60 s, with 60 s rest between the vibration sets (a rest period lasting 6 min was allowed after 5 vibration sets). Neuromuscular performance tests consisting of counter-movement jumps and maximal dynamic leg presses on a slide machine, performed with an extra load of 160% of the subjects body mass, and with both legs were administered before and immediately after the WBV treatment. The average velocity, acceleration, average force, and power were calculated and the root mean square electromyogram (EMGrms) were recorded from the vastus lateralis and rectus femoris muscles simultaneously during the leg-press measurement. Blood samples were also collected, and plasma concentrations of testosterone (T), growth hormone (GH) and cortisol (C) were measured. The results showed a significant increase in the plasma concentration of T and GH, whereas C levels decreased. An increase in the mechanical power output of the leg extensor muscles was observed together with a reduction in EMGrms activity. Neuromuscular efficiency improved, as indicated by the decrease in the ratio between EMGrms and power. Jumping performance, which was measured using the counter-movement jump test, was also enhanced. Thus, it can be argued that the biological mechanism produced by vibration is similar to the effect produced by explosive power training (jumping and bouncing). The enhancement of explosive power could have been induced by an increase in the synchronisation activity of the motor units, and/or improved co-ordination of the synergistic muscles and increased inhibition of the antagonists. These results suggest that WBV treatment leads to acute responses of hormonal profile and neuromuscular performance. It is therefore likely that the effect of WBV treatment elicited a biological adaptation that is connected to a neural potentiation effect, similar to those reported to occur following resistance and explosive power training. In conclusion, it is suggested that WBV influences proprioceptive feedback mechanisms and specific neural components, leading to an improvement of neuromuscular performance. Moreover, since the hormonal responses, characterised by an increase in T and GH concentration and a decrease in C concentration, and the increase in neuromuscular effectiveness were simultaneous but independent, it is speculated that the two phenomena might have common underlying mechanisms.
The aim of this study was to compare hormonal changes in plasma total testosterone (T), cortisol (C), luteinizing hormone (LH), follicle-stimulating hormone (FSH) and prolactin (P) in two world-class teams, both consisting of 9 top male pro-cyclists, during a real sports situation (the 1998 "Vuelta a España", a 3-week multi-stage international cycling competition). Venous blood samples were taken the day before the race (S0), after 1 week (S1), after 2 weeks (S2) and at the end of the race (S3). The S0 T level was significantly lower in the team with more racing days in the previous month. There was a significant basal T decrease (p < 0.05) during the race in comparison with the initial value, in spite of the difference in S0 T level between teams. However, there was no difference between teams in the mean decrease in T level. C decreased significantly between S0 and S1 and between S1 and S2, but not between S2 and S3. There were no differences in P concentration between teams or throughout the study, except for a significant increase between S2 and S3. There were no initial differences in LH nor FSH concentration between the teams, nor at any of the study follow-up times. We conclude that in professional top-level athletes S0 T values depend on the number of competition days of the previous month. We observed a similar decrease in the T levels in both teams, independent of the absolute S0 values. In both teams C decreased during long-lasting cycling competition.
The aim of this study was to examine the acute responses of serum growth hormone, testosterone, and cortisol to three training protocols in rowing. Six young rowers, members of the national team, carried out three frequently used protocols in rowing, i.e., an endurance, a moderate interval, and a resistance protocol, on separate days in a counterbalanced design. Blood samples were collected before, immediately after, and 4 h after exercise for the determination of growth hormone, testosterone, cortisol, and creatine kinase. All three protocols caused marked increases in growth hormone, the most spectacular being that immediately after the endurance protocol. The change in testosterone concentration immediately after the endurance protocol was significantly higher than the changes after the other two protocols. Cortisol concentration was significantly higher immediately after the endurance protocol than after the other two protocols, but remained relatively low in all cases, suggesting that these protocols did not considerably promote catabolism in muscle tissue. Based on these data, endurance training caused greater responses of the three hormones studied compared to interval or resistance training. In fact, resistance training (at intensities above 85% of 1RM) did not cause any significant changes in the three hormones. We therefore propose that evaluation of training programmes designed for elite athletes should include measurements of hormonal changes in order to ascertain that the programmes do cause the expected adaptations.
Previous pharmacological and pathological studies have reported negative relationships between circulating testosterone and certain stress hormones (i.e., cortisol and prolactin) in humans. These relationships have subsequently been used in hypotheses explaining the subclinical resting testosterone levels often found in some endurance-trained males, but as of yet no one has specifically examined these relationships as they relate to exercise. Thus, we examined the relationship between total and free testosterone levels and cortisol, and between total and free testosterone and prolactin following prolonged endurance exercise in trained males. Twenty-two endurance-trained males volunteered to run at 100% of their ventilatory threshold (VT) on a treadmill until volitional fatigue. Blood samples were taken at pre-exercise baseline (B0); volitional fatigue (F0); 30 min (F30), 60 min (F60), and 90 min (F90) into recovery; and at 24 h post-baseline (P24 h). At F0 [mean running time = 84.8 (3.8) min], exercise induced significant changes (P<0.05) from B0 in total testosterone, cortisol and prolactin. All three of these hormones were still significantly elevated at F30; but at F60 only cortisol and prolactin were greater than their respective B0 values. Free testosterone displayed no significant changes from B0 at F0, F30, or the F60 time point. At F90, neither cortisol nor prolactin was significantly different from their B0 values, but total and free testosterone were reduced significantly from B0. Cortisol, total testosterone and free testosterone at P24 h were significantly lower than their respective B0 levels. Negative relationships existed between peak cortisol response (at time F30) versus total testosterone (at F90, r=-0.53, P<0.05; and at P24 h, r=-0.60, P<0.01). There were no significant relationships between prolactin and total or free testosterone. In conclusion, the present findings give credence to the hypothesis suggesting a linkage between the low resting testosterone found in endurance-trained runners and stress hormones, with respect to cortisol.
KRAEMER, W. J., S. J. FLECK, R. CALLISTER, M. SHEALY, G. A. DUDLEY, C. M. MARESH, L. MARCHITELLI, C. CRUTHIRDS, T. MURRAY, and J. E. FALKEL. Training responses of plasma beta-endorphin, adrenocorticotropin, and cortisol. Med. Sci. Sports Exerc, Vol. 21, No. 2, pp. 146-153, 1989. The purpose of this study was to examine the effects of three different run training programs on plasma responses of beta-endorphin ([beta]-EP), adrenocorticotropin (ACTH), and cortisol to maximal treadmill exercise. Subjects were randomly assigned to one of three training groups: sprint intervals (SI) (N = 8), endurance (E) (N = 10), or combination (C) (N= 7). Training was monitored for 10 wk, and maximal treadmill exercise tests were administered pre-training and after 2, 4, 6, 8, and 10 wk of training. Blood samples were obtained (pre-training and after 10 wk) before, immediately after, and 5 and 15 min following the maximal exercise tests. All groups significantly (P < 0.05) increased maximal oxygen consumption values at 8 and 10 wk of the training period. Significant exercise-induced increase in plasma [beta]-EP, ACTH, cortisol, and blood lactate were observed for both pre- and post-training tests in all training groups. The SI group demonstrated significant post-training increases in [beta]-EP, ACTH, cortisol, and 5 min post-exercise blood lactate concentrations in response to maximal exercise. No training-induced hormonal changes were observed for the E group. While exercise-induced increases were observed, the C group exhibited significant post-training reductions in plasma responses of[beta]-EP, ACTH, and blood lactate concentrations in response to maximal exercise. Still, resting and post-exercise increases in plasma cortisol concentrations were significantly higher in magnitude in the post-training test. Lactate was significantly correlated with [beta]-EP (r = 0.72), ACTH (r = 0.70), and cortisol (r = 0.64). These data suggest that different run training programs produce differential effects on plasma [beta]-EP, ACTH, and cortisol in response to maximal exercise and that these responses may be linked to anaerobic metabolic factors.
(C)1989The American College of Sports Medicine
To study the dynamics of alterations in blood hormones and their individual variability during prolonged exercise, changes in plasma levels of corticotropin, cortisol, aldosterone, testosterone, progesterone, somatotropin, insulin and C-peptide were recorded in 32 endurance athletes and 50 untrained persons during a 2-hour exercise on a cycle ergometer at 60% VO2max. Common changes were activation of the pituitary corticotropin function, mostly at the end of exercise, rises in aldosterone and somatotropin concentrations and decreases in insulin and C-peptide levels during exercise. The activation of pituitary-adrenocortical system and the decrease of insulin but not C-peptide levels were more pronounced in athletes than in untrained persons. A large inter-individual variability existed in changes of cortisol, testosterone and progesterone in both groups. Five variants were found in the dynamics of cortisol concentration. Whereas the alterations of corticotropin were characterized mainly by a biphasic increase, the dynamics of corticotropin and cortisol coincided only in one variant out of five. Most characteristic for the postexercise recovery period were decreased activity of the pituitary-adrenocortical system and delayed normalization of aldosterone level.
The purpose of this study was to examine the effects of three different run training programs on plasma responses of beta-endorphin (beta-EP), adrenocorticotropin (ACTH), and cortisol to maximal treadmill exercise. Subjects were randomly assigned to one of three training groups: sprint intervals (SI) (N = 8), endurance (E) (N = 10), or combination (C) (N = 7). Training was monitored for 10 wk, and maximal treadmill exercise tests were administered pre-training and after 2, 4, 6, 8, and 10 wk of training. Blood samples were obtained (pre-training and after 10 wk) before, immediately after, and 5 and 15 min following the maximal exercise tests. All groups significantly (P less than 0.05) increased maximal oxygen consumption values at 8 and 10 wk of the training period. Significant exercise-induced increase in plasma beta-EP, ACTH, cortisol, and blood lactate were observed for both pre- and post-training tests in all training groups. The SI group demonstrated significant post-training increases in beta-EP, ACTH, cortisol, and 5 min post-exercise blood lactate concentrations in response to maximal exercise. No training-induced hormonal changes were observed for the E group. While exercise-induced increases were observed, the C group exhibited significant post-training reductions in plasma responses of beta-EP, ACTH, and blood lactate concentrations in response to maximal exercise. Still, resting and post-exercise increases in plasma cortisol concentrations were significantly higher in magnitude in the post-training test. Lactate was significantly correlated with beta-EP (r = 0.72), ACTH (r = 0.70), and cortisol (r = 0.64).(ABSTRACT TRUNCATED AT 250 WORDS)
Beta-endorphin (beta-End) and adrenocorticotrophic hormone (ACTH) were determined in the peripheral blood of 14 human volunteers exercising on a bicycle ergometer. After 1 h of submaximal work below anaerobic threshold (AT), defined as the 4 mmol X l-1 lactic acid level in arteriolar blood (Kindermann 1979; Mader 1980), beta-End and ACTH levels did not change from control conditions. Eleven of the same 14 subjects performed an uninterrupted graded exercise test on the same bicycle ergometer until exhaustion. This time beta-End and ACTH levels increased concomitantly with exercise of high intensity: at each moment, during and after this maximal test, a highly significant correlation (P less than 0.0001) was noted between the levels of beta-End and ACTH. The peak values of these hormones were reached within 10 min after stopping maximal exercise, and coincided with lactic acid peak levels. A rise in lactic acid levels above the anaerobic threshold always preceded the exercise-induced rise in beta-End and ACTH. Within the population tested, two subgroups could be distinguished: one comprising individuals whose hormonal response nearly coincided with the rise in lactic acid (rapid responders) and a second group composed of subjects whose normal response appeared delayed with respect to the lactic acid rise (slow responders). These results support the view that beta-End and ACTH are secreted in equimolar quantities into the blood circulation in response to exercise, and suggest that metabolic changes of anaerobiosis play a key role in the regulation of stress-hormone release.(ABSTRACT TRUNCATED AT 250 WORDS)
Blood levels of cortisol, prolactin, somatotropin, dopamine, noradrenaline, adrenaline, and lactate were analyzed in 18 healthy men in good physical condition in four repeated bicycle exercise tests. Profiles of pituitary hormone secretion into blood varied intra- and interindividually from one test to another, even though the work load remained unchanged. Catecholamine and lactate levels regularly increased during each exercise test. A factor analysis of the endocrine responses supports the assumption that pituitary hormones respond to psychological state factors while catecholamines and lactate increases are related to physical load.
To investigate whether measurements of cortisol responses to exercise are confounded by neglect of the hormone's circadian rhythm, we measured the serum and salivary cortisol responses of eight women to 40 min of 70% maximal oxygen consumption treadmill exercise beginning at 0800 and 2000. Responses were calculated relative to the usually employed preexercise concentrations and also to concentrations at the same times of another day while subjects were at rest. Compared with areas under response curves (AUCs) calculated relative to their circadian baselines, AUCs for serum and salivary cortisol calculated by reference to preexercise concentrations were underestimated (serum, P < 0.001; salivary, P < 0.01) by 93 and 84% in the morning and by 37 and 35% in the evening, respectively. Calculated by the usual preexercise baseline method, rises in serum and salivary cortisol were similarly underestimated. More accurately calculated relative to their circadian baselines, serum and salivary cortisol AUCs were similar (P = 0.63 and P = 0.37, respectively) in the morning and evening, as were their rises (P = 0.23 and P = 0.70, respectively). In future investigations of the existence and magnitude of cortisol responses, those responses must be calculated relative to the hormone's circadian baseline.
Treadmill exercise activates the hypothalamic-pituitary-adrenal axis and evokes metabolic responses proportional to exercise intensity and duration. To determine whether glucocorticoid administration would alter humoral and metabolic regulation during exercise, we administered 4 mg dexamethasone (DEX) or placebo to 11 normal, moderately trained men (19-42 yr old) in a double blinded random fashion 4 h before high intensity intermittent treadmill running. Plasma levels of ACTH, cortisol, arginine vasopressin (AVP), lactate, and glucose were measured before, during, and after exercise. A wide range of ACTH responses were seen in the DEX-treated group and arbitrarily defined as two subsets of individuals according to their responses to dexamethasone: DEX nonsuppressors and DEX suppressors. Exercise-induced increases in heart rate and circulating concentrations of cortisol, AVP, lactate, and glucose were all significantly greater (P < 0.05) in nonsuppressors (n = 4) compared to suppressors (n = 7) after both placebo and DEX administration. Interestingly, heart rate, AVP, and lactate responses were unaltered by DEX alone in both groups. In summary, this study demonstrates that normal individuals exhibit differential neuroendocrine and metabolic responses to exercise and pituitary/adrenal suppression after pretreatment with DEX. These findings reflect marked individual differences in the stress response to exercise that may derive from or lead to differential glucocorticoid negative feedback sensitivity in humans.
The aim of this study was to test the hypothesis that individual differences in the response of maximal O(2) uptake (VO(2max)) to a standardized training program are characterized by familial aggregation. A total of 481 sedentary adult Caucasians from 98 two-generation families was exercise trained for 20 wk and was tested for VO(2max) on a cycle ergometer twice before and twice after the training program. The mean increase in VO(2max) reached approximately 400 ml/min, but there was considerable heterogeneity in responsiveness, with some individuals experiencing little or no gain, whereas others gained >1.0 l/min. An ANOVA revealed that there was 2.5 times more variance between families than within families in the VO(2max) response variance. With the use of a model-fitting procedure, the most parsimonious models yielded a maximal heritability estimate of 47% for the VO(2max) response, which was adjusted for age and sex with a maternal transmission of 28% in one of the models. We conclude that the trainability of VO(2max) is highly familial and includes a significant genetic component.
The aim of this study was to investigate whether there are familial influences on cortisol levels at baseline and in response to endurance exercise training and, if so, whether there is evidence for a major gene effect. There were 476 white individuals in 99 nuclear families and 247 black individuals in 105 families with valid cortisol data in the HERITAGE Family Study. Data adjustments were carried out separately in each of 8 sex by generation by race groups, using stepwise multiple regression procedures. The familial factors underling the variability in baseline cortisol (log-transformed and adjusted for age and baseline body mass index [BMI]) and its training response (post-training minus baseline, adjusted for age, baseline BMI, and the baseline cortisol value) were assessed by estimating familial correlations and carrying out segregation analysis. In the white sample, significant familial resemblance was detected for both baseline cortisol and the training response, with maximal heritabilities of 38% and 32%, respectively. However, significant familial correlations were not detected for either cortisol phenotype in the black sample, perhaps owing, in part, to the much smaller family sizes. Results of segregation analysis of the white sample provided evidence for Mendelian additive genes influencing baseline cortisol and its training response. The major genes accounted for 33% and 31% of the variance for baseline cortisol and the training response with 48% and 5% of the sample homozygous for the genotype leading to high values, respectively. In conclusion, we found significant familial effects influencing levels of baseline cortisol and its training response in the white sample. The putative major gene effects appear to explain most of the observed familial resemblance, this will motivate further linkage and association studies.
According to the central fatigue hypothesis, serotonin (5-HT) is related to fatigue, whereas the noradrenergic system is primarily concerned with arousal and motivation, and therefore hypothesized to enhance performance. The purpose of the present study was to examine the effects of a selective noradrenergic reuptake inhibitor (reboxetine 2 x 4 mg REB-NARI) on exercise performance.
Seven healthy well-trained male cyclists (age: 23 +/- 1.7 yr, height: 182 +/- 5.8 cm, weight: 73.5 +/- 8.5 kg, VO2max: 73.5 +/- 6.4 mL x kg(-1) x min(-1), Watt(max): 376 +/- 11.7 W) participated to the study. Subjects completed two endurance tests (time trials) starting at 65% Wmax in a double-blind randomized cross-over design. Blood samples were collected for adrenocorticotropin, prolactin, cortisol, growth hormone (GH), beta-endorphins, and catecholamines and were taken at 30-min time intervals until the end of exercise. Performance was analyzed with a paired t-test, whereas data for hormonal and metabolic differences during the trials were analyzed using an ANOVA repeated measures design and an LSD-planned comparisons test. Significance level was set at P < 0.05.
Performance was not influenced by the NARI (REB: 97 min +/- 3 min, placebo (PLAC): 92 min +/- 1 min). All hormones increased during exercise except for GH in the REB trial, which was significantly lower than PLAC. The other hormones were significantly higher in the REB trial versus the PLAC trial at the end of exercise and during recovery.
In conclusion, the results demonstrate that the drug had a central effect. In particular, the higher resting GH concentrations indicated a marked and selective noradrenergic effect of REB. However, performance was not influenced by a selective NARI in well-trained endurance athletes.
The purposes of this study were 1) to evaluate gender differences in back extensor endurance capacity during isometric and isotonic muscular contractions, 2) to determine the relation between absolute load and endurance time, and 3) to compare men [n = 10, age 22.4 +/- 0.69 (SE) yr] and women (n = 10, age 21.7 +/- 1.07 yr) in terms of neuromuscular activation patterns and median frequency (MF) shifts in the electromyogram (EMG) power spectrum of the lumbar and hip extensor muscles during fatiguing submaximal isometric trunk extension exercise. Subjects performed isotonic and isometric trunk extension exercise to muscular failure at 50% of maximum voluntary contraction force. Women exhibited a longer endurance time than men during the isometric task (146.0 +/- 10.9 vs. 105.4 +/- 7.9 s), but there was no difference in endurance performance during the isotonic exercise (24.3 +/- 3.4 vs. 24.0 +/- 2.8 repetitions). Absolute load was significantly related to isometric endurance time in the pooled sample (R(2) = 0.34) but not when men and women were analyzed separately (R(2) = 0.05 and 0.04, respectively). EMG data showed no differences in neuromuscular activation patterns; however, gender differences in MF shifts were observed. Women demonstrated a similar fatigability in the biceps femoris and lumbar extensors, whereas in men, the fatigability was more pronounced in the lumbar musculature than in the biceps femoris. Additionally, the MF of the lumbar extensors demonstrated a greater association with endurance time in men than in women (R(2) = 0.45 vs. 0.19). These findings suggest that gender differences in muscle fatigue are influenced by muscle contraction type and frequency shifts in the EMG signal but not by alterations in the synergistic activation patterns.
The differences in attentional style among subjects of different ages and the influence of emotionality on the attentional components were studied for a limited experimental period. Variation in the hormonal data and its relation to behavioural parameters were also evaluated. The subjects enrolled in the study were divided into four age groups (A 18-29, B 30-45, C 46-59, D 60-77 years). The attentional tests involved different types of attention: alert, go/no-go, divided attention and working memory. Emotionality was assessed on the basis of skin conductance, heart rate and frontalis muscle tone. Testosterone (T), free testosterone (fT), non-specifically bound testosterone (NST), sex hormone binding globulin (sHBG), oestradiol, cortisol and adrenocorticotrophic hormone were determined in the plasma. The data were analysed to identify endocrine and behavioural differences related to sex and age. The results showed an influence of age on reaction time (RT) and RT variability. This was particularly evident for groups C and D with respect to A in the simple (alert) and complex RT tests (go/no-go and working memory). Divided attention, with the highest RT, showed a clear distinction between group A and the other groups. The difference in frontalis electromyography (EMG) (test vs control) increased with age, while the autonomic responses (skin conductance and heart rate) did not vary. In most attentional tests, the age-related reduction of RT was associated with increased T, fT and NST and decreased cortisol.
The purpose of the study was to investigate whether severe fatigue, possibly leading to overreaching, could be diagnosed at an early stage by a combination of parameters. Seven well-trained male subjects (age [mean +/- SD]: 25.3 +/- 4.7 yr; body mass: 76 +/- 6.6 kg; VO2max: 61.1 +/- 7 ml.kg(-1).min(-1)) increased their training load by doubling their training volume and increasing the intensity by 15 % over a period of two weeks. Before and after this intensified training period subjects underwent a series of tests including a maximal incremental cycle ergometer test (Wmax) with continuous ventilatory measurements and blood lactate values, time trial, basal blood parameter tests (red and white blood profile), hormones [growth hormone (GH), insulin-like growth factor 1(IGF-1), adreno-corticotropic hormone (ACTH), cortisol], neuro-endocrine stress test [short insulin tolerance test (SITT), combined anterior pituitary test (CAPT) and exercise], a shortened Profile of Mood State (POMS), the estimated rate of perceived exertion (RPE) and a cognitive reaction time test. The intensified training period resulted in a significant increase of the training load (p <0.01), training monotony (p <0.01) and training strain (p <0.01). The RPE during training increased significantly (p <0.01) during the intensified training period. Total mood score obtained from the POMS tended to increase (p=0.06), reflecting an increase in worse mood state. A novel finding was that reaction times increased significantly, indicating that overreaching might adversely affect speed of information processing by the brain, especially for the most difficult conditions. After the intensified training period, neither changes in exercise-induced plasma hormone values, nor SITT values were observed. During the CAPT only cortisol showed a significant decrease after the intensified training period. Hemoglobin showed a significant decrease after the intensified training period whereas hematocrit, red blood cell count (RBC) and MCV tended to decrease. The intensified training had no effect on physical performance (Wmax or time trial), maximal blood lactate, maximal heart rate and white blood cell profile. The most sensitive parameters for detecting overreaching are reaction time performance (indicative for cognitive brain functioning), RPE and to a lesser extend the shortened POMS. This strongly suggests, that central fatigue precedes peripheral fatigue. All other systems,including the neuro-endocrine, are more robust and react most likely at a later stage in exhaustive training periods.
Familial aggregation of VO 2max response to exercise training: results from the HERITAGE Family Study Documento descargado de http://www.apunts.org el 01/02 Copia para uso personal, se prohíbe la transmisión de este documento por cualquier medio o formato
- C Bouchard
- P An
- T Rice
- Js Skinner
- Jh Wilmore
- J Gagnon
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