β-endorphin and adrenocorticotropic hormone production during marathon and incremental exercise

Summary To evaluate the increases in concentration of -endorphin and adrenocorticotropic hormone (ACTH) 16 healthy athletes, well-trained for endurance exercise, volunteered for an exhausting incremental graded treadmill exercise and a marathon run. Maximum oxygen uptake was determined during the treadmill exercise. Venous blood samples were drawn before and after exercise, and at 30, 60 and 120 min during the recovery phase. For the marathon race venous blood was collected before, after 1 and 2 h of running and at the end, as well as at 0.5, 1, 2 and 24 h during the recovery phase. Lactate concentration, heart rate and perceived exertion were also determined at all points of blood collection. Both types of exercise led to significant increases in concentration of -endorphin and ACTH of similar magnitude, with -endorphin tending to be higher after the marathon run. The decrease of both was slower during the recovery from the marathon than after the incremental test. Concentrations of both hormones increased exponentially during the marathon run. Positive correlations between -endorphin and ACTH concentrations were determined at the end of both runs. It was found that incremental exhausting and prolonged exhausting endurance exercise such as marathon running induced an increase of similar magnitude in both -endorphin and ACTH concentration.     

β-Endorphin and adrenocorticotrophin after incremental exercise and marathon running-female responses

Investigations of exercise-induced increases in -endorphin, adrenocorticotropic hormone (ACTH) and cortisol concentration have been carried out mainly in men. Data concerning the female reaction are sparse and less clear. In a comparison between incremental exercise and marathon running 14 experienced female marathon runners volunteered to run to exhaustion according to an incremental treadmill protocol. They ran a marathon 4 weeks later. Blood was analysed for -endorphin, ACTH and cortisol concentration immediately prior to the laboratory treadmill test, 3, 30 and 60 min later, as well as prior to the marathon, after 60 min and 120 min of running and 3, 30 min, and 24 h after completion of the run. At each blood collection, lactate concentration, heart frequency and perceived exertion were determined. The mean marathon running time was 3.22 h. Baseline concentrations for -endorphin of 22 pmol · l^–1 before the marathon and 19 pmol · l^–1 before the treadmill exercise increased 1.4-fold 30 min after the marathon and 1.9-fold after the treadmill exercise; for ACTH the baseline of 4.7 and 4.0 pmol · l^–1 t was increased by 8.3- and 10.3-fold, respectively. Cortisol concentration rose exponentially from a baseline 17 g · dl^–1 and peaked at 2.2-fold 30 min after the run, when the maximal concentration also had been reached after the treadmill test, increasing 1.3-fold from a baseline of 21 g · dl^–1. The maximal values for cortisol concentration after both exercises differed from each other, while the maxima of ACTH and -endorphin concentrations were similar. The ACTH and -endorphin concentration declined more slowly during the recovery after the marathon than after the treadmill. Cortisol concentration was below baseline 24 h later. In comparison with men studied earlier, female marathon runners showed higher baseline concentrations and lesser increases in -endorphin and lower baseline concentrations and larger increases in ACTH concentration after both types of exercise. The delayed decrease in concentration of the hormones after the marathon was similar in male and female runners.     

Does gender affect pulmonary function and exercise capacity?

It is well established that women exhibit several anatomic and physiologic characteristics that distinguish their responses to exercise from those of men. These factors have been shown to influence the training response and contribute to lower maximal aerobic power in women. Additionally, the reproductive hormones, estrogen and progesterone, can influence ventilation, substrate metabolism, thermoregulation, and pulmonary function during exercise. Pulmonary structural and morphologic differences between genders include smaller vital capacity and maximal expiratory flow rates, reduced airway diameter, and a smaller diffusion surface than age- and height-matched men. These differences may have an effect on the integrated ventilatory response, respiratory muscle work, and in pulmonary gas exchange during exercise. Specifically, recent evidence suggests that during heavy exercise, women demonstrate greater expiratory flow limitation, an increased work of breathing, and perhaps greater exercise induced arterial hypoxemia compared to men. The consequence of these pulmonary effects has the potential to adversely affect aerobic capacity and exercise tolerance in women.     

Ventilatory response to moderate incremental exercise performed 24 h after resistance exercise with concentric and eccentric contractions

In order to test our hypothesis that muscle condition has an effect on the cognition of self-motion and consequently on the ventilatory response during exercise, six healthy subjects performed a moderate incremental exercise test (IET) on a cycle ergometer under two conditions [resistance exercise condition (REC) and control condition (CC)]. In the REC, resistance exercise (30 incline leg presses) was conducted during two sessions scheduled at 48 and then 24 h prior to the IET. For the CC, the subjects were instructed to refrain from participating in strenuous exercise for a period of 2 days prior to the IET. In the IET, the workload was increased from 78 to 118 watts in steps of 8 watts every 3 min. Although the ventilatory response during the IET was significantly higher in the REC than in the CC, there were no significant differences in cognitive indexes (RPE and awareness of change in workload) between the two conditions. In addition, the magnitude of muscle soreness was significantly higher in the REC than in the CC. However, the level of soreness in the REC was very low, and there were no significant differences in blood lactate concentration and integrated EMG between the two conditions. These results suggest that a change in peripheral neural reflex is the primary cause of increased ventilatory response to moderate exercise after resistance exercise, although the role of a cognitive element cannot be absolutely excluded.     

The role of exercise dependence for the relationship between exercise behavior and eating pathology: mediator or moderator?

Our study examined the potential mediating or moderating effect of exercise dependence on the exercise-eating pathology relationship. Female university students (N = 330) completed Internet-based self-report measures of exercise behavior, exercise dependence, and eating pathology. Exercise dependence served as a mediator for the relationship between exercise and eating pathology. This unidirectional causal model suggests that an individual's pathological motivation or compulsion to exercise is the critical mediating component in the exercise-eating pathology relationship. The best target for removing the link between exercise behavior and eating pathology may be reformulating exercise dependence symptoms.     

β-Endorphin,adrenocorticotropic hormone,cortisol and catecholamines during aerobic and anaerobic exercise

Summary Twelve non-specifically trained volunteers (aged 26.5 years, SD 3.6) performed exhausting incremental graded exercise (ST) and 1-min anaerobic cycle ergometer exercise (AnT) at 2-h intervals for the purpose of investigating -endorphin (-E) behaviour dependent on exercise intensity and anaerobic metabolism. In order to determine [-E], adrenocorticotropic hormone [ACTH], cortisol [C], adrenaline [A] and noradrenaline [NA] concentrations, venous blood samples were collected prior and subsequent to exercise until the 20th min of the recovery period, as well as in ST before and after exceeding the individual anaerobic threshold (TH_{an, i}). Before, during and after ST, lactate concentration, heart rate and perceived degree of exertion were also determined; after AnT maximum lactate concentration was measured. Both types of exercise led to significant increases in [-E], [ACTH], [A] and [NA], with levels of [-E] and [ACTH] approximately twice as high after ST as after AnT. The [C] increased significantly only after ST. During ST significant changes in [-E] and [ACTH] were measured only after exceeding TH_{an, i}. At all measuring times before and after ST and AnT both hormones correlated positively. In AnT the increases of [-E] and [A] demonstrated a correlation (r= 0.65; P< 0.05). Both in AnT and ST there was a relationship between the maximum concentrations of -E and lactate (r=0.63 and 0.71; each P<0.05). We therefore conclude that physical exercise with increasing or mostly anaerobic components leads to an increase in [-E], the extent correlating with the degree of lactate concentration. The similar behaviour of [-E] and [A] after AnT might suggest mutual influences of endogenous opioids and catecholamines.     

Synchronous whole-body vibration increases VO₂ during and following acute exercise

Single bout whole-body vibration (WBV) exercise has been shown to produce small but significant increases in oxygen consumption (VO₂). How much more a complete whole-body exercise session (multiple dynamic exercises targeting both upper and lower body muscles) can increase VO₂ is unknown. The purpose of this study was to quantify VO₂ during and for an extended time period (24 h) following a multiple exercise WBV exercise session versus the same session without vibration (NoV). VO₂ of healthy males (n = 8) was measured over 24 h on a day that included a WBV exercise session versus a day with the same exercise session without vibration (NoV), and versus a control day (no exercise). Upper and lower body exercises were studied (five, 30 s, 15 repetition sets of six exercises; 1:1 exercise:recovery ratio over 30 min). Diet was controlled. VO₂ was 23% greater (P = 0.002) during the WBV exercise session versus the NoV session (62.5 ± 12.0 vs. 50.7 ± 8.2 L O₂) and elicited a higher (P = 0.033) exercise heart rate versus NoV (139 ± 6 vs. 126 ± 11 bpm). Total O₂ consumed over 8 and 24 h following the WBV exercise was also increased (P < 0.010) (240.5 ± 28.3 and 518.9 ± 61.2 L O₂) versus both NoV (209.7 ± 22.9 and 471.1 ± 51.6 L O₂) and control (151.4 ± 20.7 and 415.2 ± 51.6 L O₂). NoV was also increased versus control (P < 0.003). A day with a 30-min multiple exercise, WBV session increased 24 h VO₂ versus a day that included the same exercise session without vibration, and versus a non-exercise day by 10 and 25%, respectively.     

Cardiac vagal withdrawal and reactivation during repeated rest–exercise transitions

It is not known whether subjects that have higher cardiac vagal reactivation (CVR) during repeated exercise transitions also have higher cardiac vagal withdrawal (CVW) at the onset of exercise, which would lead to better heart rate (HR) regulation during exercise transitions. Therefore, our aims were to investigate: (a) the influence of CVR on CVW during repeated rest–exercise transitions; and (b) the influence of the sympathetic activity on CVR and CVW. Fifty-eight healthy men (22 ± 4 years) performed 20 rest–exercise transitions interspaced by 30 s. In addition, nine healthy men (24 ± 3 years) ingested either 25 mg of atenolol or placebo, on a crossover, double-blind, randomized design, then performed 20 rest–exercise transitions interspaced by 30 s. Cardiac vagal reactivation was assessed by a HR variability index (RMSSD) and CVW by the HR increase at the onset of a valid and reliable cycling protocol. The CVR and CVW responses were associated (partial r ranged from 0.60 to 0.66; p < 0.05). Participants with higher CVR over transitions maintained their CVW over repeated transitions [first transition (mean ± SEM) = 1.59 ± 0.04 vs. 20th = 1.50 ± 0.03 (a.u.), p = 0.24], while participants with lower CVR had a CVW decrease over repeated transitions [first transition (mean ± SEM) = 1.38 ± 0.04 vs. 20th = 1.19 ± 0.03 (a.u.), p < 0.01). In addition, the CVR and CVW over the rest–exercise transitions were similar during atenolol and placebo (ANCOVA interaction p = 0.12 and p = 0.48, respectively). In conclusion, the CVR among repeated rest–exercise transitions influenced the CVW at the onset of exercise, which was not affected by a partial β₁ cardioselective adrenoceptor blockade.     

Metabolic and cardioventilatory responses during a graded exercise test before and 24 h after a triathlon

Previous studies have reported respiratory, cardiac and muscle changes at rest in triathletes 24?h after completion of the event. To examine the effects of these changes on metabolic and cardioventilatory variables during exercise, eight male triathletes of mean age 21.1 (SD 2.5) years (range 17–26 years) performed an incremental cycle exercise test (IET) before (pre) and the day after (post) an official classic triathlon (1.5-km swimming, 40-km cycling and 10-km running). The IET was performed using an electromagnetic cycle ergometer. Ventilatory data were collected every minute using a breath-by-breath automated system and included minute ventilation (V˙ _E), oxygen uptake (V˙O₂), carbon dioxide production (V˙CO₂), respiratory exchange ratio, ventilatory equivalent for oxygen (V˙ _E/V˙O₂) and for carbon dioxide (V˙ _E/V˙CO₂), breathing frequency and tidal volume. Heart rate (HR) was monitored using an electrocardiogram. The oxygen pulse was calculated as V˙O₂/HR. Arterialized blood was collected every 2 min throughout IET and the recovery period, and lactate concentration was measured using an enzymatic method. Maximal oxygen uptake (V˙O_{2 max} ) was determined using conventional criteria. Ventilatory threshold (VT) was determined using the V-slope method formulated earlier. Cardioventilatory variables were studied during the test, at the point when the subject felt exhausted and during recovery. Results indicated no significant differences (P>0.05) in V˙O_{2 max} [62.6 (SD 5.9) vs 64.6 (SD 4.8) ml?·?kg^?1?·?min^?1], VT [2368 (SD 258) vs 2477 (SD 352) ml?·?min^?1] and time courses of V˙O₂ between the pre- versus post-triathlon sessions. In contrast, the time courses of HR and blood lactate concentration reached significantly higher values (P<0.05) in the pre-triathlon session. We concluded that these triathletes when tested 24?h after a classic triathlon displayed their pre-event aerobic exercise capacity, bud did not recover pre-triathlon time courses in HR or blood lactate concentration.     

Human thermoregulatory function during exercise and immersion after 35 days of horizontal bed-rest and recovery

The present study evaluated the effect of 35 days of experimental horizontal bed-rest on exercise and immersion thermoregulatory function. Fifteen healthy male volunteers were assigned to either a Control (n=5) or Bed-rest (n=10) group. Thermoregulatory function was evaluated during a 30-min bout of submaximal exercise on a cycle ergometer, followed immediately by a 100-min immersion in 28°C water. For the Bed-rest group, exercise and immersion thermoregulatory responses observed post-bed-rest were compared with those after a 5 week supervised active recovery period. In both trials, the absolute work load during the exercise portion of the test was identical. During the exercise and immersion, we recorded skin temperature, rectal temperature, the difference in temperature between the forearm and third digit of the right hand (T_{forearm-fingertip})— an index of skin blood flow, sweating rate from the forehead, oxygen uptake and heart rate at minute intervals. Subjects provided ratings of temperature perception and thermal comfort at 5-min intervals. Exercise thermoregulatory responses after bed-rest and recovery were similar. Subjective ratings of temperature perception and thermal comfort during immersion indicated that subjects perceived similar combinations of Tsk and Tre to be warmer and thermally less uncomfortable after bed-rest. The average (SD) exercise-induced increase in Tre relative to resting values was not significantly different between the Post-bed-rest (0.4 (0.2)°C) and Recovery (0.5 (0.2)°C) trials. During the post-exercise immersion, the decrease in Tre, relative to resting values, was significantly (P<0.05) greater in the Post-bed-rest trial (0.9 (0.5)°C) than after recovery (0.4 (0.3)°C). T_{forearm-fingertip} was 5.2 (0.9)°C and 5.8 (1.0)°C at the end of the post-bed-rest and recovery immersions, respectively. The gain of the shivering response (increase in O₂ relative to the decrease in Tre; O₂/Tre) was 1.19 l min^–1°C^–1 in the Recovery trial, and was significantly attenuated to 0.51 l min^–1°C^–1 in the Post-bed-rest trial. The greater cooling rate observed in the post-bed-rest trial is attributed to the greater heat loss and reduced heat production. The former is the result of attenuated cold-induced vasoconstriction and enhanced sweating rate, and the latter a result of a lower shivering O₂ response.     

Do sauna therapy and exercise act by raising the availability of tetrahydrobiopterin?

Sauna therapy has been used to treat a number of different diseases known or thought to have a tetrahydrobiopterin (BH4) deficiency. It has been interpreted to act in multiple chemical sensitivity by increasing chemical detoxification and excretion but there is no evidence that this is its main mode of action. Sauna therapy may act to increase BH4 availability via two distinct pathways. Increased blood flow in heated surface tissues leads to increased vascular shear stress, inducing increased activity of GTP cyclohydrolase I (GTPCH-I) in those vascular tissues which will lead to increasing BH4 synthesis. A second mechanism involves the heat shock protein Hsp90, which is induced by even modest heating of mammalian tissues. Sauna heating of these surface tissues may act via Hsp90, which interacts with the GTPCH-I complex and is reported to produce increased GTPCH-I activity by lowering its degradation. The increased consequent availability of BH4 may lead to lowered nitric oxide synthase uncoupling, such as has been reported for the eNOS enzyme. Increased BH4 synthesis in surface tissues of the body will produce increased circulating BH4 which will feed BH4 to other body tissues that may have been BH4 deficient. Similar mechanisms may act in vigorous exercise due to the increased blood shear stresses and possibly also heating of the exercising tissues and heart. There is a large and rapidly increasing number of diseases that are associated with BH4 depletion and these may be candidates for sauna therapy. Such diseases as hypertension, vascular endothelial dysfunction, multiple chemical sensitivity and heart failure are thought to be helped by sauna therapy and chronic fatigue syndrome and fibromyalgia may also be helped and there are others that may be good candidates for sauna therapy.     

Kinetics of cardiorespiratory response to dynamic and rhythmic — static exercise in men

Summary Kinetics of cardiorespiratory response to dynamic (DE) and then to rhythmic-static exercise (RSE) was compared in nine male subjects exercising in an upright position on a cycle ergometer at an intensity of about 50 % O_2max and a mean pedalling frequency of 60 rpm over 5 min. Respiratory frequency (f _R), tidal volume (V _T), minute ventilation ( _E), heart rate (f _c), stroke volume (SV), and cardiac output (Q _t) were measured continuously. The RSE caused a greater increase in f _R than DE, whereas V _T increased more during DE. The effect of reciprocal changes in f _R and V _T was that _E and its kinetics, expressed as a time constant (), did not differ between experimental situations. The ventilatory equivalent for O₂ ( _E: O₂) was greater for RSE (31.3) than for DE (23.0, P<0.01). Elevation of f _c was similar for both types of exercise. The SV increased suddenly at the beginning of DE from 54 ml to 74 ml and then decreased to the end of exercise. At the onset of RSE only a moderate increase in SV was observed, from 56 ml to 62 ml, and then SV remained stable. The DE caused a greater and faster increase in Q _t (4.20 l · min^–1, for equal to 16.1s) than RSE (3.25 l · min^–1, for equal to 57.0s, P<0.05 and P<0.002, respectively). Total peripheral resistance was almost 40% greater for RSE than for DE. No relationship was found between Q _t and V_E at the first 15 s of both types of exercise. It is concluded that the kinetics of _E did not depend on to kinetics of Q _t in the exercising subjects. This finding contradicts the hypothesis of cardiodynamic hyperpnoea indicating an importance of neurogenic factors, mediated either centrally or peripherally, in fast cardiorespiratory responses to exercise.     

Met-enkephalin, β-endorphin and cortisol responses to sub-maximal exercise after sleep disturbances

Summary The present study compared the effects of partial sleep deprivation and the effects of an intake of a hypnotic compound (zolpidem) prior to bedtime, on sleep and on hormonal and metabolic adaptations to subsequent exercise. Sleep deprivation consisted of a delayed bedtime and an early getting-up time. Eight young subjects, who slept well and were highly trained athletes, were enrolled in this study. Sleep was recorded polygraphically and the following afternoon exercise was performed on a cycle ergometer for 30 min at 75% of maximal oxygen consumption (VO_2max) after a 10-min warm up. Met-enkephalin, -endorphin, cortisol, and lactate concentrations were measured at rest and during exercise. The data obtained after experimental sleep, with and without medication were compared with those obtained in the reference condition with normal sleep. Both types of sleep reduction decreased the total sleep time, stage 2 sleep, and rapid eye movement sleep, whereas zolpidem administration did not modify either the duration of sleep or the sleep stages. After the reference night, plasma met-enkephalin did not show any significant change at the end of the submaximal exercise, whereas -endorphin, cortisol, and lactic acid concentrations increased significantly in all subjects. The changes in concentration in -endorphin were significantly related to the changes in cortisol (r=0.78;P<0.01) and to the changes in plasma lactic acid (r=0.58;P<0.05). Cortisol concentrations were also related to lactic acid values (r=0.94;P<0.01). Partial sleep loss altered lactate concentrations during submaximal exercise but did not affect the hormonal levels of met-enkephalin, -endorphin and cortisol in the blood. Zolpidem administration failed to change lactate and hormone concentrations. These results suggested that partial sleep deprivation may have contributed to the changes in metabolic responses without significantly altering the hormonal response to exercise. Zolpidem intake did not impair the response of different variables to exercise the following day.     

Acute and 2?days delayed effects of exhaustive stretch-shortening cycle exercise on barefoot walking and running patterns

This study investigated the acute and 2?days delayed influences of exhaustive stretch-shortening cycle exercise (SSC) on barefoot walking and running gait patterns. The SSC exercise was performed on a sledge apparatus, on which the subjects (N?=?10) repeated until exhaustion intermittent series of 25 bilateral submaximal rebounds. Maximal drop-jumps and submaximal barefoot treadmill walking and running were performed before (PRE) and after (POST) the exhaustive exercise and repeated 48?h (D2) later. Electromyographic activity and 3D kinematics of the right lower limb and foot were recorded for 15?s at gait initiation (BEG) and at the end (END: at 3?min of walk and 5?min of run). The exhaustive SSC exercise resulted in 6% reductions in maximal drop jump performance at POST and D2, and affected mostly both gait patterns at D2. The walking pattern presented compensatory neural adjustments within the triceps surae muscle group. This expected pain-induced protective strategy of the soleus muscle was sufficient to preserve the kinematics pattern. The running condition revealed a major knee strategy, which might support the concept of pain protective strategy of knee extensor muscles at the expense of impact cushioning. Regardless the testing session, most parameters showed fatigue-induced changes at gait initiation (BEG), which were opposite to subsequent BEG to END adjustments. This is likely to support anticipatory strategies rather than progressive adjustments during the exercise.     

The reproducibility of closed-pouch sweat collection and thermoregulatory responses to exercise–heat stress

Seven active male subjects cycled for 60 min at 29.5 (0.8)% peak work rate on three separate occasions in a hot environmental condition [36.0 (0.1)°C, 60 (1)% relative humidity] in order to determine the reproducibility of a closed-pouch sweat collection technique for sweat composition at the scapula, forearm and thigh. To confirm that sweat composition was not influenced by between-trial variations in sudomotor drive, local sweat rate, whole-body sweat rate, heart rate (HR), rectal temperature (T_re) and mean skin temperature (T_sk) responses were also measured, consequently reproducibility was also established for these variables. Sweat composition did not differ among trials, with the mean coefficients of variation (CVs) for sweat [Na⁺], [K⁺] and pH being 10.4 (7.4)%, 8.1 (6.5)% and 1.3 (1.1)%, respectively. Local sweat rates did not differ among the three trials (P>0.05) although whole-body sweat rate was reduced in the third trial (P<0.05). The mean CVs were 11.0 (7.8)% and 4.7 (1.6)% for local and whole-body sweat rates, respectively. Between-trial differences were not evident for T_re, T_sk or HR with mean CVs of 0.3 (0.2)%, 0.7 (0.6)% and 3.9 (1.7)%, respectively, although HR tended to be greater in the first trial (P=0.08). It is proposed that moderate variations in sweat composition were influenced by variations in the local sweat rate, which were induced by application of the pouch.     

Physical activity and plasma interleukin-6 in humans – effect of intensity of exercise

The present study included data from three marathon races to investigate the hypothesis that a relationship exists between running intensity and elevated concentrations of interleukin (IL)-6 in plasma. The study included a total of 53 subjects whose mean age was 30.6 [95% confidence interval (CI) 1.4] years, mean body mass 77.7 (95%CI 2.0) kg, mean maximal oxygen uptake (V˙O_2max) 59.3 (95%CI 1.4) ml · min⁻¹ · kg⁻¹, and who had participated in the Copenhagen Marathons of 1996, 1997 or 1998, achieving a mean running time of 206 (95%CI 7) min. Running intensity was calculated as running speed divided by V˙O_2max. The concentration of IL-6 in plasma peaked immediately after the run. There was a negative correlation between peak IL-6 concentration and running time (r=−0.30, P < 0.05) and a positive correlation between peak IL-6 concentration and running intensity (r=0.32, P < 0.05). The IL-1 receptor antagonist (IL-1ra) plasma concentration peaked 1.5 h after the run and there was a positive correlation between the peak plasma concentrations of IL-6 and IL-1ra (r=0.39, P < 0.01). Creatine kinase (CK) plasma concentration peaked on the 1st day after the run, but no association was found between peak concentrations of IL-6 and CK. In conclusion, the results confirmed the hypothesized association between plasma IL-6 concentration and running intensity, but did not confirm the previous finding of a connection between IL-6 plasma concentration and muscle damage. Accepted: 6 August 2000