Plasma beta-endorphin concentration: response to intensity and duration of exercise

Twelve college-age men exercised on a bicycle ergometer to VO2max and at 60, 70, and 80% VO2max for 30 min to determine the effects of exercise intensity on plasma beta-endorphin (B-EP). The time course for alterations in B-EP and the relationship to lactate were also examined. Following the VO2max test, the three submaximal intensities were completed on separate days using a counter-balanced design. Blood was sampled from an indwelling venous catheter at rest during exercise and recovery to assess the time course response. B-EP content was determined by radioimmunoassay (Immunonuclear) with less than 5% cross-reactivity to B-LPH. At rest, B-EP content was similar across visits, 4.34 +/- 0.36 pmol.l-1. The 60% intensity did not elevate B-EP at any time measured. B-EP content increased by 15 min at 70% VO2max with a further increase at 30 min. B-EP remained elevated during the 20 min recovery. At 80% VO2max B-EP content increased by 5 min. B-EP continued to increase during the exercise and peaked at 21.91 +/- 2.03 pmol.l-1 5 min into the recovery. Lactate showed a mild correlation with B-EP (r = 0.43) at 80% VO2max. A significant correlation (r = 0.78) between lactate and B-EP did occur with the VO2max test. It is concluded that an exercise intensity of at least 70% VO2max for 15 min is needed to increase plasma B-EP. Furthermore, the higher the exercise intensity the more rapid the onset for increases in plasma B-EP.     

Exercise intensity-related responses of beta-endorphin and catecholamines

Ten men and 10 women exercised on a bicycle ergometer for 20 min at 40, 60, and 80% maximal oxygen uptake (VO2max) to determine the relationship between plasma beta-endorphin, catecholamines, and exercise intensity. Compared to rest, plasma beta-endorphins were not significantly elevated during the 40 and 60% workloads (4.8 +/- 1.0 pmol.l-1 vs 3.8 +/- 0.7 and 6.3 +/- 0.9, respectively). In contrast, the 80% exercise significantly elevated endorphins to 16.1 +/- 4.0 pmol.l-1. Plasma norepinephrine concentrations were 0.30 +/- 0.04 ng.ml-1 at rest and increased with exercise intensity (40% = 0.60 +/- 0.05, 60% = 0.93 +/- 0.07, 80% = 2.00 +/- 0.14, VO2max = 2.55 +/- 0.14 ng.ml-1). Plasma epinephrine followed the same trend (rest = 0.07 +/- 0.01, 40% = 0.33 +/- 0.03, 60% = 0.49 +/- 0.02, 80% = 0.88 +/- 0.07, VO2max = 0.95 +/- 0.06 ng.ml-1). Norepinephrine was found to significantly correlate to endorphins (r = 0.499; P less than 0.02). Conversely, epinephrine was not correlated with beta-endorphin (r = 0.309; P greater than 0.05). The low correlation suggests a weak relationship between beta-endorphin and catecholamine responses during exercise. The results of this investigation suggest that the relationship between beta-endorphin and exercise intensity is curvilinear, with anaerobic activity producing the most significant endorphin response. It was also noted that the beta-endorphin response was not related to gender, but the amine response to exercise was gender-related, being greater for the men.     

Effects of phosphatidylserine on exercise capacity during cycling in active males

PURPOSE: The purpose of the study was to investigate the effects of 750 mg of soybean-derived phosphatidylserine, administered daily for 10 d, on exercise capacity, oxygen uptake kinetic response, neuroendocrine function, and feeling states during exhaustive intermittent exercise. METHODS: Following preliminary testing, fourteen active males completed a staged intermittent exercise protocol on two further occasions (T1 and T2) separated by 16 +/- 1 d. The protocol consisted of three 10-min stages of cycling at 45, 55, and 65% VO2max, followed by a final bout at 85% VO2max that was continued until exhaustion. Approximately 5 d after T1 the subjects were assigned, in a double-blind manner, to either phosphatidylserine (PS) or placebo (P). Breath-by-breath respiratory data and heart rate were continually recorded throughout the exercise protocol, and blood samples were obtained at rest, during the rest periods within the protocol (Post-55, Post-65), at the end of exercise (Post-85), 20 min after the completion of exercise (postexercise), and the day following exercise (Post-24 h). RESULTS: The main finding of this study was that supplementation had a significant effect on exercise time to exhaustion at 85% VO2max (P = 0.005). The exercise time to exhaustion in PS increased following supplementation (7:51 +/- 1:36 to 9:51 +/- 1:42 min:s, P = 0.001), whereas P remained unchanged (8:09 +/- 0:54 to 8:02 +/- 0:54 min:s, P = 0.670). Supplementation did not significantly affect oxygen kinetic mean response times (MRT(on) and MRT(off)), serum cortisol concentrations, substrate oxidation, and feeling states during the trial. CONCLUSION: This is the first study to report improved exercise capacity following phosphatidylserine supplementation. These findings suggest that phosphatidylserine might possess potential ergogenic properties.     

Passive versus active recovery during high-intensity intermittent exercises

PURPOSE: To compare the effects of passive versus active recovery on muscle oxygenation and on the time to exhaustion for high-intensity intermittent exercises. METHODS: Twelve male subjects performed a graded test and two intermittent exercises to exhaustion. The intermittent exercises (15 s) were alternated with recovery periods (15 s), which were either passive or active recovery at 40% of .VO2max. Oxyhemoglobin was evaluated by near-infrared spectroscopy during the two intermittent exercises. RESULTS: Time to exhaustion for intermittent exercise alternated with passive recovery (962 +/- 314 s) was significantly longer (P < 0.001) than with active recovery (427 +/- 118 s). The mean metabolic power during intermittent exercise alternated with passive recovery (48.9 +/- 4.9 mL.kg-1.min-1) was significantly lower (P < 0.001) than during intermittent exercise alternated with active recovery (52.6 +/- 4.6 mL.kg-1.min-1). The mean rate of decrease in oxyhemoglobin during intermittent exercises alternated with passive recovery (2.9 +/- 2.4%.s-1) was significantly slower (P < 0.001) than during intermittent exercises alternated with active recovery (7.8 +/- 3.4%.s-1), and both were negatively correlated with the times to exhaustion (r = 0.67, P < 0.05 and r = 0.81, P < 0.05, respectively). CONCLUSION: The longer time to exhaustion for intermittent exercise alternated with passive recovery could be linked to lower metabolic power. As intermittent exercise alternated with passive recovery is characterized by a slower decline in oxyhemoglobin than during intermittent exercise alternated with active recovery at 40% of .VO2max, it may also allow a higher reoxygenation of myoglobin and a higher phosphorylcreatine resynthesis, and thus contribute to a longer time to exhaustion.     

Effect of mild dehydration on the lactate threshold in women

PURPOSE: The purpose of this investigation was to examine the effects of dehydration on the lactate threshold and performance time to exhaustion in women. METHODS: Seven moderately trained women (age = 23.6 +/- 1.6 yr) performed two graded exercise tests on separate occasions, once in a normally hydrated state (HY) and once in a dehydrated state (DE). Dehydration was achieved by a 45-min submaximal exercise the evening before testing, followed by a 12-h period of fluid restriction. VO2, VCO2, V(E), R-values, blood lactate, and catecholamine concentrations were measured at baseline and during each workload. Plasma volume and plasma osmolality were also determined. Body weight dropped significantly for the dehydrated trial (2.6 +/- 0.7%). RESULTS: There was a corresponding decrease in plasma volume measured (3.5 +/- 2.6%). The VO2max (3.1 +/- 0.3 L x min(-1) HY; 3.0 +/- 0.1 L x min(-1) DE) obtained was not significantly different between the hydration and dehydration trial. Plasma norepinephrine, epinephrine, and lactate concentrations were not significantly different at baseline or maximum intensity although epinephrine concentrations were higher for the dehydrated trial during submaximal workloads. Lactate concentrations were highly correlated with epinephrine (r = 0.95 HY; r = 0.97 DE). The lactate threshold occurred at a significantly lower relative percent of VO2max for the dehydrated trial (72.2 +/- 1.1% HY; 65.5 +/- 1.8% DE) as well as a lower absolute power output when compared with that in the hydrated trial. There was a significant decrease in time to exhaustion for the dehydrated trial (17.3 +/- 0.7 min HY; 16.3 + 0.7 min DE). Time to exhaustion for the dehydrated trial was correlated with the % VOmax at which the lactate threshold occurred (r = 0.74). CONCLUSIONS: These data indicate that low levels of dehydration induced a shift in the lactate threshold, in part because of elevated epinephrine concentrations. This shift may have been one cause for the decrease in time to exhaustion for the dehydrated trial.     

The effect of training on exercise-induced R-wave amplitude changes in young females

The effects of an exercise training program on R-wave amplitude (Ramp) changes during graded exercise were investigated in 14 adolescent females. The experimental group (EG) (N = 6) underwent a 20-wk aerobic exercise program. Eight subjects served as controls (CG). Oxygen uptake (VO2), heart rate (HR), and Ramp were determined during incremental exercise to exhaustion, pre- and post-program. The Ramp was calculated by using the average of 10 electrocardiographic complexes to provide a stable criterion. Pre-training, EG and CG were not significantly different for VO2max and HRmax; Ramp decreased significantly between rest and 5 min prior to exhaustion for both groups (P less than 0.05). Ramp changes were significant between the first min of exercise and 2 min prior to exhaustion for EG (P less than 0.05) and between the first min of exercise and 1 min prior to exhaustion for CG (P less than 0.05). These changes occurred at 87% of VO2max and 95% of HRmax for EG and at 93% of VO2max and 97% of HRmax for CG. CG showed no change in these variables post-program except for Ramp exhibiting a significant change between rest and the first min of exercise (P less than 0.05). EG showed a significant increase in VO2max (P less than 0.05), and Ramp changes during exercise were delayed. The first significant change occurred between rest and 3 min prior to exhaustion (P less than 0.05), and the second change occurred between the first min of exercise and exhaustion (P less than 0.05). Thus the latter Ramp change was delayed to 100% of VO2max and HRmax post-training.(ABSTRACT TRUNCATED AT 250 WORDS)     

Effect of prolonged exercise on arterial oxygen saturation in athletes susceptible to exercise-induced hypoxemia

This study examined the effect of prolonged endurance exercise on the development of exercise-induced hypoxemia (EIH) in athletes who had previously displayed EIH during an incremental maximal exercise test. Five male and three female endurance-trained athletes participated. Susceptibility to EIH was confirmed through a maximal incremental exercise test and defined as a reduction in the saturation of arterial oxygen (SpO(2)) of >/=4% from rest. Sixty minutes of running was conducted, on a separate day, at an oxygen consumption corresponding to 95% of ventilatory threshold. Immediately following the 60 min exercise bout, athletes commenced a time trial to exhaustion at 95% maximal oxygen consumption (VO(2max)). The reduction in SpO(2) was significantly greater during the maximal incremental test, than during the 60 min, or time trial to exhaustion (-8.8+/-1.4%, -3.3+/-1.1%, and -4.1+/-2.3%, P<0.05, respectively). The degree of desaturation during the 60 min was significantly related to the relative intensity of exercise at 95% ventilatory threshold (adjusted r(2)=0.54, P=0.02). In conclusion, athletes who did not exercise at greater than 73% VO(2max) during 60 min of endurance exercise did not display EIH, despite being previously susceptible during an incremental maximal test.     

Effect of simulated weightlessness on exercise-induced anaerobic threshold

Ventilation (VE), CO2 output (VCO2), oxygen uptake (VO2), respiratory exchange ratio (R), and the ventilatory equivalents for VO2 and VCO2 were measured during graded exercise before and after 10 d of continuous bed rest (BR) in the -6 degrees head-down position to determine the effect of deconditioning on the anaerobic threshold (AT), i.e., the highest workrate or VO2 which was achieved without evidence of lactic acidosis, as judged from the profile of ventilatory and gas exchange responses. Ten healthy male subjects performed a supine graded cycle ergometer test before (pre) and after (post) BR which consisted of 4 min of unloaded pedaling at 60 rpm followed by an increased workrate of 15 W X min-1 until volitional fatigue (max). VE, VCO2, VO2, R, VE/VO2 and VE/VCO2 were measured every 30 s and used collectively to identify the AT. Plasma (PV) and blood (BV) volumes were measured pre- and post-BR by T-1824. Following BR, VO2max decreased from 2.42 +/- 0.17 to 2.25 +/- 0.13 L X min-1 (7.0%, p less than 0.05). BR significantly (p less than 0.05) reduced the AT from 1.26 +/- 0.09 to 0.95 +/- 0.05 L X min-1 VO2; from 52.2 +/- 2.0 to 42.6 +/- 1.6% VO2max; and from 93 +/- 9 to 65 +/- 6 W. A correlation coefficient (r) of -0.11 (NS) was found between the change in VO2max and change in AT. A decrease in BV of 8.8% (p less than 0.05) was due to the 11.0% reduction in PV; red cell volume remained constant.(ABSTRACT TRUNCATED AT 250 WORDS)     

Effects of acute modafinil ingestion on exercise time to exhaustion

PURPOSE: The purpose of this study was to investigate the effect of acute ingestion of modafinil (M) on time to exhaustion during high-intensity exercise. Modafinil (M) is a psychostimulant developed to treat narcolepsy, with "arousal" properties attributed to an increased release of dopamine in the CNS. Because other stimulants with similar properties have ergogenic effects, it was hypothesized that acute treatment with M would enhance physical performance. METHODS: Fifteen healthy male subjects, with a maximal aerobic power (VO2max) of 47 +/- SD 8 mL x kg x min, exercised on a cycle ergometer for 5 min at 50% VO2max and then at approximately 85% VO2max to exhaustion. They did this weekly for 3 wk: a control trial (C) the first week, and then 3 h after ingesting either placebo (P) or M (4 mg x kg) during the remaining 2 wk. The P and M trials were conducted with a balanced order, double-blind design. RESULTS:: Mean +/- SD times to exhaustion at 85% VO2max (TE) were 14.3 +/- 2.8, 15.6 +/- 3.8 and 18.3 +/- 3.5 min for the C, P, and M trials, respectively. TE for M was significantly longer than for the C and P trials. Oxygen uptake at exhaustion was slightly but significantly greater for M compared with P and C. HR increased with time and was further elevated by M. Subjective ratings of perceived exertion (RPE) were significantly lower for M compared with C and P but only after 10 min of exercise at 85% VO2max. CONCLUSION: Acute ingestion of modafinil prolonged exercise time to exhaustion at 85% VO2max and reduced RPE. The RPE results suggest that the dampening of the sensation of fatigue was likely a factor responsible for the enhanced performance.     

Comparison of physiological strain and muscular performance of athletes during two intermittent running exercises at the velocity associated with VO2max

The purpose of this study was to examine physiological strain and muscular performance responses of well trained athletes during two intermittent running exercise protocols at the velocity associated with VO2max. Ten national level middle-distance runners (VO2max 69.4+/-5.1; mean+/-SD) performed in random order two 28 min treadmill running exercises: 14 bouts of 60 s runs with 60 s rest (IR60) and 7 bouts of 120 s runs with 120 s rest between each run (IR120). During IR120 peak oxygen uptake (12%), peak heart rate (3%) and peak blood lactate (79%) were significantly higher than during IR60 (P< 0.001) and almost the same as in the VO2max test. In IR120 the relative aerobic energy release calculated on the basis of the accumulated oxygen deficit during the running bouts was significantly higher than in IR60 (81.5+/-2.7 vs. 70.2+/-2.6%, P<0.001) likewise the sum oxygen consumption during the 14 min running (P< 0.001), while during the 14 min recovery it was as much lower (P < 0.001). There were no changes either during or between the IR60 and IR120 protocols with regard to the muscular performance parameters, stride length or height of maximal vertical jumps. In conclusion, during intermittent running at the velocity associated with VO2max doubling the duration of work and rest bouts from 60 s to 120s increased the physiological strain of well trained athletes to the same level as at exhaustion in the VO2max test but the muscular performance variables were not influenced.     

Hormonal responses during prolonged exercise are influenced by a selective DA/NA reuptake inhibitor

OBJECTIVE: A decrease in dopamine activity is thought to lead to a reduction in motivation and arousal and therefore to the "central" component of fatigue. The purpose of the present study was to investigate the effects of a dopamine (DA) noradrenaline (NA) reuptake inhibitor, bupropion (Zyban), on exercise performance and on the hormonal response to exercise. METHODS: Eight healthy well trained male cyclists (Watt(max) 397+/-15 W) participated in the study. Subjects completed one maximal exercise test (to determine maximal power output Watt(max)), and two endurance performance tests (time trials) in a double blind randomised cross-over design. Subjects took either placebo capsules (lactose) or 2 x 300 mg bupropion (BUP). Blood samples were collected for adrenocorticotropin (ACTH), prolactin, cortisol, growth hormone, beta-endorphins, and catecholamines. RESULTS: Performance was not influenced by BUP (placebo: 89+/-1 min; BUP 2 x 300 mg: 89+/-0.7 min). All hormones increased during exercise in all trials. Cortisol plasma concentrations were significantly higher in the BUP trial at rest, at min 60, and at the end of exercise, while beta-endorphins were higher in the BUP trial at the end of exercise and during recovery, and ACTH at the end of exercise. CONCLUSION: From the present results, we can conclude that bupropion had a more marked central noradrenergic effect (compared to dopaminergic) on the hormonal response to exercise, but no effect on the outcome of performance.     

Short-term overtraining: effects on performance, circulatory responses, and heart rate variability

PURPOSE AND METHODS: Nine elite canoeists were investigated concerning changes in performance, heart rate variability (HRV), and blood-chemical parameters over a 6-d training camp. The training regimen consisted of cross-country skiing and strength training, in total 13.0+/-1.6 h, corresponding to a 50% increase in training load. RESULTS: Time to exhaustion (RunT) decreased from 19.1+/-1.0 to 18.0+/-1.2 min (P < 0.05). VO2max and max lactate (La(max)) both decreased significantly (P < 0.05) over the training period (4.99+/-0.97 to 4.74+/-0.98 L x min(-1) and from 10.08+/-1.25 to 8.98+/-1.03 mmol x L(-1) respectively). Heart rates (HR) decreased significantly at all workloads. Plasma volume increased by 7+/-7% (P < 0.05). Resting cortisol, decreased from 677+/-244 to 492+/-222 nmol x L(-1) (P < 0.05), whereas resting levels of adrenaline and noradrenaline remained unchanged. The change between tests in RunT correlated significantly with the change in HRmax (r = 0.79; P = 0.01). There were no group changes in high or low frequency HRV, neither at rest nor following a tilt. CONCLUSIONS: The reduced maximal performance indicates a state of fatigue/overreaching and peripheral factors are suggested to limit performance even though HRmax and La(max) both were reduced. The reduced submaximal heart rates are probably a result of increased plasma volume. HRV in this group didn't seem to be affected by short-term overtraining.     

Acute reduction in maximal oxygen uptake after long-distance running

Nine male marathon runners, 24 to 39 years of age, were studied during steady state and maximal graded treadmill exercise under control conditions (C) and immediately after a paced outdoor 21.1-km run averaging 89.5 min (E). The half-marathon run and both treadmill trials were performed at 239 +/- 33 m/min. Oxygen uptake (VO2), respiratory exchange ratio (RER), heart rate (HR), plasma lactate concentration (PLa), and rating of perceived exertion (RPE) were measured in the steady state at 0% grade and at the fatigue end point. Compared to C, mean values in E were significantly lower (p less than 0.05) for time to exhaustion (6.0 vs 4.1 min), VO2max (60.0 vs 56.3 ml/kg/min), peak RER (1.18 vs 1.06), and PLa (9.7 vs 7.8 mM/L), whereas maximal HR (184 vs 184 b/min) and peak RPE (19.6 vs 19.9) were not significantly different between trials. Submaximal VO2 during steady-state runs was similar between C and E (44.4 vs 45.0 ml/kg/min; p = NS). Since the attainable VO2max decreased after E, the percentage of VO2max utilized during steady-state runs was higher, averaging 74% in C and 80% in E (p less than 0.05). In the steady state during E, HR (153 vs 161 b/min) and RPE (13.2 vs 14.8) were higher (p less than 0.05), and the increase in PLa from rest (2.7 vs 1.9 mM/L) was lower (p less than 0.05). Submaximal HR during graded exercise in E was 7 to 8 b/min higher (p less than 0.05) at a given VO2, indicating reduced heart rate reserve.(ABSTRACT TRUNCATED AT 250 WORDS)     

Effects of endurance training on the androgenic response to exercise in man

Six healthy subjects, aged 35.8 +/- 4.4 years, volunteered to participate in a 40-week training program on a bicycle ergometer [three 60-min sessions per week at 80%-85% of maximal oxygen uptake (VO2 max)]. Before training and at the 10th, 20th, 30th, and 40th weeks of the training program, plasma testosterone, cortisol, and androstenedione concentrations were measured at rest (t0) and at the end (t60) of a 1-h endurance exercise requiring 85%-90% of VO2 max. Training resulted in significant increases of anaerobic threshold (12.6%) and VO2 max (7.3%). The training program did not significantly alter the resting values of plasma testosterone, androstenedione, and cortisol; in contrast, the exercise responses (delta = t60-t0) of testosterone, androstenedione, and cortisol were increased. The highest amplitude of these responses was reached at the 30th week for cortisol and androstenedione and at the 40th for testosterone. These results suggest that long-term training enhances both testicular adrenal and responses to endurance exercise. The possible role of hormonal changes in the mobilization of energy substrates during exercise is discussed.     

Gonadotropin decrease induced by prolonged exercise at about 55% of the VO2max in different phases of the menstrual cycle

In order to evaluate the influence of physical exercise on the hypothalamic-pituitary-ovarian axis, we studied ten women in the early follicular phase (EFP), twelve in the late follicular phase (LEP) and nine in the luteal phase (LP). The test consisted of a 90-minute physical exercise on a motor driven treadmill at 55-60% of VO2max. Blood samples were taken before, during and after the test. Prolactin and cortisol did not increase in any phase. Estradiol showed a significant increase in LFP (from 361.5 +/- 110.6 to 472.7 +/- 138.9 pmol/L) and in LP (from 457.2 +/- 94.6 to 555.3 +/- 96.9 pmol/L) but not in EFP. Progesterone levels increased significantly only in LP (from 28.2 +/- 6.7 to 33.5 +/- 6.7 mmol/L): Luteinizing hormone (LH) levels decreased significantly in all phases: from 13.7 +/- 2.0 to 10.5 +/- 1.1 IU/L in EFP; from 14.6 +/- 2.1 to 11.5 +/- 1.9 IU/L in LFP and from 7.5 +/- 1.3 to 5.7 +/- 1.0 IU/L in LP, while follicle stimulating hormone (FSH) levels decreased only in LFP (from 8.1 +/- 0.5 to 6.7 +/- 0.6 IU/L). Our exercise protocol (prolonged, continuous and moderate) was able to cause a decrease in gonadotropins levels, and this phenomenon is not due to changes in the other tested hormones.     

Maximal physiological responses between aquatic and land exercise in overweight women

PURPOSE: To investigate the maximal physiological responses between aquatic and land-based graded exercise tests in overweight women. METHODS: Twenty healthy, overweight (body mass index (BMI) > or = 25 kg.m(-2)), Caucasian women (mean +/- SD; age 48 +/- 7 yr, BMI 30 +/- 4 kg.m(-2)) completed a deep water running (DWR) and treadmill walking (TMW) graded exercise test. Maximal responses during the DWR and TMW graded exercise tests were compared using paired t-tests. Comparisons were made in the incidence of achievement of maximal oxygen consumption (VO2max) criteria between DWR and TMW protocols. Criteria were a plateau in VO2 (change < 2.1 mL.kg.min(-1)), heart rate (HR) equal to or above the age-adjusted maximum, and respiratory exchange ratio (RER) > or = 1.15. RESULTS: Maximal responses for VO2max (22.5 +/- 4.86 vs 27.7 +/- 4.73 mL.kg.min(-1)), HRmax (159 +/- 16 vs 170 +/- 12 bpm), and RER (1.03 +/- 0.06 vs 1.10 +/- 0.06) were significantly lower (P < 0.01) for the DWR test compared with the TMW test, respectively. Achievement of various VO2max criteria was demonstrated more consistently during the TMW test than the DWR test. CONCLUSION: Maximal physiological responses of overweight women to DWR and TMW are significantly different but are comparable with other populations. As the maximal responses for DWR compared with TMW differ, the use of land-based criteria for VO2max is not recommended for a graded DWR exercise test.     

Whole‐body fat oxidation determined by graded exercise and indirect calorimetry: a role for muscle oxidative capacity?

During whole-body exercise, peak fat oxidation occurs at a moderate intensity. This study investigated whole-body peak fat oxidation in untrained and trained subjects, and the presence of a relation between skeletal muscle oxidative enzyme activity and whole-body peak fat oxidation. Healthy male subjects were recruited and categorized into an untrained (N=8, VO(2max) 3.5+/-0.1 L/min) and a trained (N=8, VO(2max) 4.6+/-0.2 L/min) group. Subjects performed a graded exercise test commencing at 60 W for 8 min followed by 35 W increments every 3 min. On a separate day, muscle biopsies were obtained from vastus lateralis and a 3 h bicycle exercise test was performed at 58% of VO(2max). Whole-body fat oxidation was calculated during prolonged and graded exercise from the respiratory exchange ratio using standard indirect calorimetry equations. Based on the graded exercise test, whole-body peak fat oxidation was determined. The body composition was determined by DEXA. Whole-body peak fat oxidation (250+/-25 and 462+/-33 mg/min) was higher (P<0.05) and occurred at a higher (P<0.05) relative workload (43.5+/-1.8% and 49.9+/-1.2% VO(2max)) in trained compared with untrained subjects, respectively. Muscle citrate synthase activity and beta-hydroxy-acyl-CoA-dehydrogenase activity were higher (49% and 35%, respectively, P<0.05) in trained compared with untrained subjects. Both lean body mass and maximal oxygen uptake were significantly correlated to whole-body peak fat oxidation (r(2)=0.57, P<0.001), but leg muscle oxidative capacity was not correlated to whole-body peak fat oxidation. In conclusion, whole-body peak fat oxidation occurred at a higher relative exercise load in trained compared with untrained subjects. Whole-body peak fat oxidation was not significantly related to leg muscle oxidative capacity, but was related to lean body mass and maximal oxygen uptake. This may suggest that leg muscle oxidative activity is not the main determinant of whole-body peak fat oxidation.     

Effects of high-intensity interval training on the response during severe exercise

This study examined the effect of high-intensity interval training on the VO2 response during severe, constant-load exercise. Prior to, and following training, 10 females (V O2 peak 37.4+/-6.0 mL kg-1 min-1) performed a graded exercise test to determine VO2 peak and lactate threshold (LT) and a 6 min cycle test (CT) at the pre-training VO2 peak intensity. Training involved high-intensity intervals (2 min work, 1 min rest) performed 3x week for 8 weeks. Breath-by-breath data from 0 to 6 min during the CT were smoothed using 5s averages and fit to a bi-exponential model starting from 20s. Training resulted in significant improvements in VO2 max (2.34+/-0.37-2.78+/-0.30 L min-1), power at VO2 max (170+/-26-204+/-25 W) and power at LT (113+/-17-136+/-20 W) (p<0.05). Following training, the VO2 response showed a significant increase in the amplitude of the primary phase (A1) (1396+/-103-1695+/-100 mL min-1; p<0.05) and end-exercise VO2 (VO2 EE), with no difference (p>0.05) in the time constants of either phase or the amplitude of the slow component (318+/-67-380+/-48 mL; p=0.15). In conjunction, accumulated oxygen deficit (AOD) (43.7+/-9.8-17.2+/-2.8 mL O2 eq kg-1) and anaerobic contribution to the CT (19.4+/-4.4-7.2+/-1.2%) were significantly reduced. In contrast to previous moderate-intensity research, a high-intensity interval training program increased A1 and VO2 EE for the same absolute exercise intensity, decreasing the AOD during a severe-intensity CT.     

Aerobic exercise adaptations in trained adolescent runners following a season of cross-country training

Adaptations in aerobic exercise responses as well as the relationship between aerobic exercise responses and running performance were examined in a group of previously trained adolescent runners (n = 9; 15.9 +/- 1.0 years) over the course of a competitive cross-country season. Running economy (RE), submaximal blood lactate concentration [BLa] and VO2max were assessed before and immediately after the season. Five-km race time improved (P < 0.05) from 18.68 +/- 1.10 min at the beginning of the season to 18.16 +/- 1.11 min at the end of the season. Significant increases were observed in peak VO2 (61.6 +/- 3.5 to 65.3 +/- 2.9 mL x kg(-1) x min(-1)) and graded exercise test time (11.32 +/- 1.56 to 12.22 +/- 0.79 min). There was a tendency for RE (P = 0.051) to worsen slightly and for [BLa] (P = 0. 057) to decline as a result of training. At the beginning of the season submaximal [BLa] at 14 km x hr(-1) (r = 0.86) and graded exercise test time (r = -0.87) were significantly related to 5-km time. At the end of the season, RE (r = 0.78) and [BLa] (r = 0.77) at 14 km x hr(-1) and graded exercise test time (r = -0.69) were significantly related to race time. In this well-trained group of runners, further training during the cross-country season increased peak VO2 and improved race time. Submaximal [BLa] and graded exercise test time appear to be the most robust predictors of performance, while RE became a significant predictor of race time at the end of the season.     

Effects of acute prednisolone intake during intense submaximal exercise

To study the effects of a therapeutical dose of corticosteroid alone or associated with beta-2 agonist on performance and substrate response during intense submaximal exercise, seven healthy moderately trained male volunteers participated in the double-blind randomized cross-over study. An intense endurance exercise test to exhaustion was performed after ingestion of placebo (Pla), 20 mg prednisolone (Pred), and 20 mg prednisolone plus 4 mg salbutamol (Pred-Sal). Blood samples were collected at rest, after 5, 10 min of exercise, at exhaustion, and after 5 (r5), 10 (r10), and 20 (r20) min of passive recovery for ACTH, growth hormone, insulin, blood glucose, and lactate measurements. There were no significant differences in exercise time to exhaustion between the three treatments (Pla: 21.5 +/- 2.9; Pred: 22.0 +/- 2.5; Pred-Sal: 24.2 +/- 2.8 min). ACTH was significantly lowered after Pred and Pred-Sal vs. Pla from the start of exercise to the end of the experiment (p < 0.05). Pred and Pred-Sal increased resting and recovery (r10 and r20) significantly but not exercise blood glucose values. There were no significant differences in growth hormone concentrations between the three treatments whereas insulin was significantly higher at rest, during exercise, and at r20 after Pred-Sal administration vs. Pred and Pla (p < 0.05). Pred and Pred-Sal showed no significant effect on blood lactate compared with Pla treatment. These preliminary results do not support the hypothesis that acute oral therapeutic corticosteroid intake alone or associated with beta-2 mimetic improves performance during intense submaximal exercise, but further studies are necessary with tests of longer duration.