The application of soccer performance testing protocols to the non-elite player.

AIM: The application of performance testing for the evaluation of non-elite soccer players has received little attention. The purpose of this investigation was to use tests developed for elite soccer players to evaluate performance in non-elite soccer players and compare performance test results between elite (literature) and non-elite (data) players. METHODS: Thirteen male soccer players volunteered to participate. The tests included a treadmill VO2max test, 20 m sprint, vertical jump (VJ), 30 s Wingate cycle ergometer test, the Loughborough Intermittent Shuttle Test (LIST), and 2 20-m multi-stage shuttle runs to exhaustion (fatigue test). Actual VO2max (absolute and relative) scores were correlated with the estimated VO2max scores (fatigue test), 20 m sprint, VJ, and 30 s Wingate using a Pearson's product-moment correlation. A paired t-test was conducted on the fatigue test trials. RESULTS: Non-significant relationships were observed between actual VO2max scores and estimated VO2max from the fatigue test (absolute and relative terms). Non-significant relationships were also observed between peak and average power output (Wingate), 20 m sprint, and VJ. Mean heart rates (HRs) throughout the LIST was 165+/-7 bpm, which represented 88% of HRmax. CONCLUSIONS: The results of this study demonstrate that to elicit physiological differences between elite and non-elite players, assessment must include both an aerobic and anaerobic component.

A review of the stroke volume response to upright exercise in healthy subjects.

Traditionally, it has been accepted that, during incremental exercise, stroke volume plateaus at 40% of Vo(2)max. However, recent research has documented that stroke volume progressively increases to Vo(2)max in both trained and untrained subjects. The stroke volume response to incremental exercise to Vo(2)max may be influenced by training status, age, and sex. For endurance trained subjects, the proposed mechanisms for the progressive increase in stroke volume to Vo(2)max are enhanced diastolic filling, enhanced contractility, larger blood volume, and decreased cardiac afterload. For untrained subjects, it has been proposed that continued increases in stroke volume may result from a naturally occurring high blood volume. However, additional research is needed to evaluate the importance of blood volume, or other mechanisms, that influence the stroke volume response to exercise in untrained subjects.

Non-linear relationships between central cardiovascular variables and VO2 during incremental cycling exercise in endurance-trained individuals.

AIM: The purpose of this study was to examine the relationships between the central cardiovascular variables (cardiac output, stroke volume and heart rate) and oxygen uptake (VO2) during continuous, incremental cycle exercise to maximal aerobic capacity (VO2max). METHODS: Twenty-one moderately to highly trained males (n=19) and females (n=2) participated in the study. A baseline maximal exercise test was performed to measure VO2max. Following the initial VO2max test, cardiac output was measured (CO2 rebreathing technique) at rest and 3 times during each of 4 exercise trials (2 submaximal tests to 90% VO2max and 2 maximal tests). Stroke volume and arteriovenous O2 difference were calculated using standard equations. RESULTS: Significant non-linear relationships were found between all central cardiovascular variables and VO2 (P<0.01). A plateau in cardiac output at VO2max was identified in 3 subjects. Stroke volume plateaued at an average of 37+/-12.5% of VO2max in 18 subjects and increased continuously to VO2max in 3 subjects. The arteriovenous O2 difference progressively increased to VO2max in 17 subjects and revealed a plateau response in 4 subjects. CONCLUSIONS: Our data suggest that there is a significant non-linear relationship between the central cardiovascular variables and VO2 during incremental exercise to VO2max. Furthermore, depending on the person, VO2max may be limited by cardiac output (evidence of cardiac output[Q] plateau) or peripheral factors (continued increase in Q).

Acute and persistent effects of a 46-kilometer wilderness trail run at altitude: cardiovascular autonomic modulation and baroreflexes.

OBJECTIVE: To test the hypothesis that prolonged physical exercise induces long-lasting effects on blood pressure and heart rate we studied 17 endurance runners before and after the 1995 Sandia Wilderness Crossing Research Run (46 km of rocky trails, average altitude 2500 m). METHODS: We evaluated the response of the cardiovascular system to sympathetic stimulation by orthostatism and to sympathetic and parasympathetic carotid baroreceptor stimulations by sinusoidal neck suction at different frequencies (sympathetic activity on blood pressure by low-frequency stimulation, parasympathetic activity on RR interval by high-frequency stimulation). We used power spectral analysis of beat-to-beat RR interval, systolic and diastolic non-invasive blood pressure, in order to quantify the respiratory fluctuations (depending on vagal activity on the RR interval) and the slower non-respiratory fluctuations, depending on sympathetic activity on the blood pressure. Recordings were performed 24 h before, and 30 min, 24 h and 48 h after the run. RESULTS: Thirty minutes after the race we found reduced blood pressure, signs of relative sympathetic predominance (increased RR interval low-frequency/high-frequency ratio from 0.65 +/- 0.15 to 1.63 +/- 0.37, P < 0.05), reduced effect of parasympathetic baroreceptor stimulation (decrease in RR interval high-frequency neck-suction synchronous oscillations, from 5.33 +/- 0.34 to 3.55 +/- 0.37 ln-ms2, P < 0.005), unchanged blood pressure responses to sympathetic stimulations; 24 h after the race, the response to parasympathetic stimulation was increased (to 6.44 +/- 0.32 ln-ms2, P < 0.0005) compared to baseline (24 h before the race), whereas sympathetic stimulation by neck suction had no longer an effect on blood pressure. CONCLUSION: The acute effects of prolonged exertion are associated with a relative increase in sympathetic activity. Twenty-four hours after this race an increased sensitivity to vagal and reduced sensitivity to sympathetic baroreflex stimulation was found. In this field study at altitude we found long-lasting effects on cardiovascular autonomic modulation after physical exertion.

Breathing patterns and cardiovascular autonomic modulation during hypoxia induced by simulated altitude.

OBJECTIVE: To assess the influence of different breathing patterns on autonomic cardiovascular modulation during acute exposure to altitude-induced hypoxia. DESIGN: We measured relative changes in minute ventilation (VE), oxygen saturation (%SaO2), spectral analysis of RR interval and blood pressure, and response to stimulation of carotid baroreceptors (neck suction) at baseline and after acute (1 h) hypobaric hypoxia (equivalent to 5,000 m, in a hypobaric chamber). METHODS: We studied 19 human subjects: nine controls and 10 Western yoga trainees of similar age, while breathing spontaneously, at 15 breaths/min (controlled breathing) and during 'complete yogic breathing' (slow diaphragmatic + thoracic breathing, approximately 5 breaths/min) in yoga trainees, or simple slow breathing in controls. RESULTS: At baseline %SaO2, VE and autonomic pattern were similar in both groups; simulated altitude increased VE in controls but not in yoga trainees; %SaO2 decreased in all subjects (P< 0.0001), but more in controls than in yoga trainees (17 versus 12%, 14 versus 9%, 14 versus 8%, all P< 0.05 or better, during spontaneous breathing, controlled breathing and yogic or slow breathing, respectively). Simulated altitude decreased RR interval (from 879 +/- 45 to 770 +/- 39, P < 0.01) and increased indices deducted from spectral analysis of heart rate variability (low frequency/high frequency (LF/HF) ratio from 1.6 +/- 0.5 to 3.2 +/- 1.1, P < 0.05) and systolic blood pressure (low-frequency fluctuations from 2.30 +/- 0.31 to 3.07 +/- 0.24 In-mmHg2, P< 0.05) in controls, indicating sympathetic activation; these changes were blunted in yoga trainees, and in both groups during slow or yogic breathing. No effect of altitude was seen on stimulation of carotid baroreceptors in both groups. CONCLUSIONS: Well-performed slow yogic breathing maintains better blood oxygenation without increasing VE (i.e. seems to be a more efficient breathing) and reduces sympathetic activation during altitude-induced hypoxia.

Increased endothelin and creatine kinase after electrical stimulation of paraplegic muscle.

The purpose of this study was to assess changes in creatine kinase (CK) and endothelin (ET) in individuals with spinal cord injury (SCI) after computerized functional electrical stimulation leg ergometry (CFES LE). Eight subjects (7 male and 1 female) with complete spinal cord lesions (C7 to L1) completed zero-loaded CFES LE tests at baseline, after 3, 6, and 12 wk of CFES LE training (30 min, 3 times/wk), and also after detraining (DT) (n = 5). Venous blood samples were drawn 24, 48, and 72 h after CFES LE for measurement of ET and CK. The CK response was largest (peak CK) 72 h after baseline tests (28.2 +/- 6.0 to 895.7 +/- 345.9 ktals/l) and was no different from baseline by weeks 3, 6, and 12. After DT, CK was similar before and after CFES LE (153.8 +/- 19.0 and 189.7 +/- 34.5 ktals/l, respectively). CFES LE also significantly increased peak ET after baseline (from 11.7 +/- 1.5 to 18.0 +/- 2.5 pg/ml). During the subsequent training, peak ET remained significantly higher than the baseline value at weeks 3, 6, and 12 (20.2 +/- 1.8, 18.0 +/- 1.1, and 16.9 +/- 2.2 pg/ml, respectively). After DT, peak ET increased significant relationship (r = 0.44) existed between ln peak CK activity and peak ET. In summary, the increase in circulating ET in spinal cord-injured individuals may have implications for baroreceptor function and therefore blood pressure control in SCI. Further research into CFES LE, ET, and baroreceptor function in SCI is warranted.

Threshold for muscle lactate accumulation during progressive exercise.

The purpose of this study was to investigate the relationship between muscle and blood lactate concentrations during progressive exercise. Seven endurance-trained male college students performed three incremental bicycle ergometer exercise tests. The first two tests (tests I and II) were identical and consisted of 3-min stage durations with 2-min rest intervals and increased by 50-W increments until exhaustion. During these tests, blood was sampled from a hyperemized earlobe for lactate and pH measurement (and from an antecubital vein during test I), and the exercise intensities corresponding to the lactate threshold (LT), individual anaerobic threshold (IAT), and onset of blood lactate accumulation (OBLA) were determined. The test III was performed at predetermined work loads (50 W below OBLA, at OBLA, and 50 W above OBLA), with the same stage and rest interval durations of tests I and II. Muscle biopsies for lactate and pH determination were taken at rest and immediately after the completion of the three exercise intensities. Blood samples were drawn simultaneously with each biopsy. Muscle lactate concentrations increased abruptly at exercise intensities greater than the "below-OBLA" stage [50.5% maximal O2 uptake (VO2 max)] and resembled a threshold. An increase in blood lactate and [H+] also occurred at the below-OBLA stage; however, no significant change in muscle [H+] was observed. Muscle lactate concentrations were highly correlated to blood lactate (r = 0.91), and muscle-to-blood lactate ratios at below-OBLA, at-OBLA, and above-OBLA stages were 0.74, 0.63, 0.96, and 0.95, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Muscle glycogenolysis during differing intensities of weight-resistance exercise.

Skeletal muscle glycogen metabolism was investigated in eight male subjects during and after six sets of 70% one repetition maximum (1 RM, I-70) and 35% 1 RM (I-35) intensity weight-resistance leg extension exercise. Total force application to the machine lever arm was determined via a strain gauge and computer interfaced system and was equated between trials. Compared with the I-70 trial, the I-35 trial was characterized by almost double the repetitions (13 +/- 1 vs. 6 +/- 0) and half the peak concentric torque for each repetition (12.4 +/- 0.5 vs. 24.2 +/- 1.0 Nm). After the sixth set, muscle glycogen degradation was similar between I-70 and I-35 trials (47.0 +/- 6.6 and 46.6 +/- 6.0 mmol/kg wet wt, respectively), as was muscle lactate accumulation (13.8 +/- 0.7 and 16.7 +/- 4.2 mmol/kg wet wt, respectively). After 2 h of passive recovery without caloric intake, muscle glycogen increased by 22.2 +/- 6.8 and 14.2 +/- 2.5 mmol/kg wet wt in the I-70 and I-35 trials, respectively. Optical absorbance measurement of periodic acid-Schiff-stained muscle sections after the 2 h of recovery revealed larger absorbance increases in fast-twitch than in slow-twitch fibers (0.119 +/- 0.024 and 0.055 +/- 0.024, P = 0.02). Data indicated that when external work was constant, the absolute amount of muscle glycogenolysis was the same regardless of the intensity of resistance exercise. Nevertheless the rate of glycogenolysis during the I-70 trial was approximately double that of the I-35 trial.

Changes in muscle proton transverse relaxation times and acidosis during exercise and recovery.

We studied changes in muscle proton (1H) transverse relaxation times (T2) by magnetic resonance imaging during exercise and compared these changes with alterations in muscle metabolism measured by phosphorus-31 magnetic resonance spectroscopy (31P-MRS). Eleven subjects completed two trials of intermittent incremental forearm wrist flexion exercise requiring 30 contractions/min for 5 min, 7 min of recovery between stages, and 5-N load increments/stage. Between stages of the first trial, T2 images of muscle 1H were obtained. Muscle T2 increased from 27.3 +/- 1.1 (SD) ms at rest to 35.8 +/- 3.6 ms after volitional fatigue (P < 0.05), whereas less active wrist extensor muscle T2 remained unchanged (26.8 +/- 0.9 to 28.8 +/- 1.6 ms; P > 0.05). After localizing the predominant muscle recruited from the T2 images, subjects completed an identical trial at least 1 wk later but involving surface coil 31P-MRS of the T2-enhanced muscle to measure the H+ concentration ([H+]). Intramuscular [H+] of T2-enhancing muscle increased from 1.1 +/- 0.1 x 10(-7) M at rest to 4.1 +/- 2.0 x 10(-7) M after volitional fatigue. Both muscle T2 and intramuscular [H+] increased in a bimodal manner, with T2 increasing before muscle [H+] (P < 0.05). The correlation coefficient between the percent change in T2 and muscle [H+] during exercise was +0.74 (range 0.48-0.98; P < 0.05) and +0.47 during recovery. After 12 min of recovery, muscle [H+] decreased to 1.4 +/- 0.3 x 10(-7) M (P < 0.05), and T2 remained close to postexercise values (32.2 +/- 3.1 ms, P > 0.05). The data indicate that 1) the T2 increases during increases in exercise intensity are nonlinear, 2) the T2 increases during exercise are significantly correlated with increases in [H+], and 3) the slow recovery of T2 compared with [H+] indicates that [H+] has a minor contribution to the recovery in T2.

Exercise exacerbates acute mountain sickness at simulated high altitude.

We hypothesized that exercise would cause greater severity and incidence of acute mountain sickness (AMS) in the early hours of exposure to altitude. After passive ascent to simulated high altitude in a decompression chamber [barometric pressure = 429 Torr, approximately 4,800 m (J. B. West, J. Appl. Physiol. 81: 1850-1854, 1996)], seven men exercised (Ex) at 50% of their altitude-specific maximal workload four times for 30 min in the first 6 h of a 10-h exposure. On another day they completed the same protocol but were sedentary (Sed). Measurements included an AMS symptom score, resting minute ventilation (VE), pulmonary function, arterial oxygen saturation (Sa(O(2))), fluid input, and urine volume. Symptoms of AMS were worse in Ex than Sed, with peak AMS scores of 4.4 +/- 1.0 and 1.3 +/- 0.4 in Ex and Sed, respectively (P < 0.01); but resting VE and Sa(O(2)) were not different between trials. However, Sa(O(2)) during the exercise bouts in Ex was at 76.3 +/- 1.7%, lower than during either Sed or at rest in Ex (81.4 +/- 1.8 and 82.2 +/- 2.6%, respectively, P < 0.01). Fluid intake-urine volume shifted to slightly positive values in Ex at 3-6 h (P = 0.06). The mechanism(s) responsible for the rise in severity and incidence of AMS in Ex may be sought in the observed exercise-induced exaggeration of arterial hypoxemia, in the minor fluid shift, or in a combination of these factors.

Impaired muscle glycogen resynthesis after eccentric exercise.

Eight men performed 10 sets of 10 eccentric contractions of the knee extensor muscles with one leg [eccentrically exercised leg (EL)]. The weight used for this exercise was 120% of the maximal extension strength. After 30 min of rest the subjects performed two-legged cycling [concentrically exercised leg (CL)] at 74% of maximal O2 uptake for 1 h. In the 3 days after this exercise four subjects consumed diets containing 4.25 g CHO/kg body wt, and the remainder were fed 8.5 g CHO/kg. All subjects experienced severe muscle soreness and edema in the quadriceps muscles of the eccentrically exercised leg. Mean (+/- SE) resting serum creatine kinase increased from a preexercise level of 57 +/- 3 to 6,988 +/- 1,913 U/l on the 3rd day of recovery. The glycogen content (mmol/kg dry wt) in the vastus lateralis of CL muscles averaged 90, 395, and 592 mmol/kg dry wt at 0, 24, and 72 h of recovery. The EL muscle, on the other hand, averaged 168, 329, and 435 mmol/kg dry wt at these same intervals. Subjects receiving 8.5 g CHO/kg stored significantly more glycogen than those who were fed 4.3 g CHO/kg. In both groups, however, significantly less glycogen was stored in the EL than in the CL.

Gender differences in substrate utilisation during exercise.

The selection and utilisation of metabolic substrates during endurance exercise are regulated by a complex array of effectors. These factors include, but are not limited to, endurance training and cardiorespiratory fitness, exercise intensity and duration, muscle morphology and histology, hormonal factors and diet. Although the effects of these factors on substrate utilisation patterns are well understood, the variation in substrate utilisation during endurance exercise between males and females is not. Because of the extreme heterogeneity in exercise protocols and individuals studied, the differences in substrate utilisation between males and females remain somewhat inconclusive. Regardless of heterogeneity, if the results from studies are interpreted collectively, an apparent gender difference in the selection and metabolism of substrates can be seen in sedentary individuals. However, this difference between genders diminishes as the level of cardiorespiratory fitness is increased to that of highly trained individuals. During rest and lower intensity exercise, the preferential metabolism of lipid occurs with a concomitant sparing of muscle glycogen. However, as the intensity of exercise is increased, the relative contribution of carbohydrate also increases. The exercise intensity at which the shift from lipid to carbohydrate is determined and regulated by the previously mentioned factors. Because the intensity and duration of exercise play a predominant role, the variation in exercise protocols poses a methodological concern when interpreting previous research. When attempting to compare the metabolism of substrates during endurance exercise, appropriate selection and interpretation of measurement techniques are necessary. Measurement techniques include the nonprotein respiratory exchange ratio, muscle and fat biopsies and the measurement of various blood metabolites, such as free fatty acids and glycerol. Similarly, in vitro analysis of lipolytic activity has also been demonstrated in males and females in response to varying levels of female gonadotrophic hormones. When comparing the substrate utilisation patterns between males and females, the area of hormonal regulation has received less attention. Often the catecholamine response to endurance exercise is measured; however, the gonadotrophic hormones, particularly those of the female, have received less attention when comparing genders. Indeed, the regulatory nature of the female gonadotrophic hormones has been demonstrated. Collectively, the effects of elevated estrogen, as in the luteal phase of menstruation, appear to promote lipolytic activity. Estrogen-mediated lipolytic activation occurs by apparently altering the sensitivity to lipoprotein lipase and by increasing the levels of human growth hormone (somatotropin), an activator of lipolysis.(ABSTRACT TRUNCATED AT 400 WORDS)

Glycerol. Biochemistry, pharmacokinetics and clinical and practical applications.

Glycerol is a naturally occurring 3-carbon alcohol in the human body. It is the structural backbone of triacylglycerol molecules, and can also be converted to a glycolytic substrate for subsequent metabolism. Serum glycerol concentrations approximate 0.05 mmol/L at rest, and can increase to 0.30 mmol/L during increased lipolysis associated with prolonged exercise or caloric restriction. When glycerol is ingested or infused at doses greater than 1.0 g/kg bodyweight, serum concentrations can increase to approximately 20 mmol/L, resulting in more than a 10 mOsmol/kg increase in serum osmolality. Glycerol infusion and ingestion have been used in research settings for almost 60 years, with widespread clinical use between 1961 and 1980 in the treatment of cerebral oedema resulting from acute ischaemic stroke, intraocular hypertension (glaucoma), intracranial hypertension, postural syncope and improved rehydration during acute gastrointestinal disease. Since 1987, glycerol ingestion with added fluid has been used to increase total body water (glycerol hyperhydration) by up to 700 ml, thereby providing benefits of improved thermoregulation and endurance during exercise or exposure to hot environments. Despite the small number of studies on glycerol hyperhydration and exercise, it appears to be an effective method of improving tolerance to exercise and other heat-related stressors.

Blood pressure measurement during exercise: a review.

This review summarizes research dealing with the validity of commonly used methods for measuring systemic blood pressure during exercise. Arterial blood pressures measured from within peripheral arteries exaggerate systolic blood pressures because of wave form reflection but provide representative mean and diastolic pressures of the central arterial circulation. Manual and automated sphygmomanometry are the best noninvasive indirect methods of blood pressure measurement to estimate ascending aorta systolic pressures; however, both methods significantly underestimate diastolic pressures at rest and during exercise. The error in diastolic pressure measurement increases with increasing exercise intensity. The accuracy of many indirect noninvasive devices for blood pressure measurement at rest and during exercise can be questioned because of the use of unsuitable criterion methods. Ascending aorta pressures should ideally be used as a gold standard or criterion method for blood pressure measurement during exercise and instrument/method validation. However, given the constraints of varied criterion standards and current recommendations for blood pressure measurement, the following units were found to be acceptable devices for measuring systolic blood pressure during exercise: Accutracker II, A&D TM 2421, Colin 630 (auscultation), Critikon 1165, and possibly the Paramed 9350.

Multiple variables explain the variability in the decrement in VO2max during acute hypobaric hypoxia.

PURPOSE: We used multiple regression analyses to determine the relationships between the decrement in sea level (SL, 760 Torr) VO2max during hypobaric hypoxia (HH) and variables that could alter or be related to the decrement in VO2max. METHODS: HH conditions consisted of 682 Torr, 632 Torr, and 566 Torr, and the measured independent variables were SL-VO2max, SL lactate threshold (SL-LT), the change in hemoglobin saturation at VO2max between 760 and 566 Torr (delta SaO2max), lean body mass (LBM), and gender. Male (N = 14) and female (N = 14) subjects of varied fitness, training status, and residential altitude (1,640-2,460 m) completed cycle ergometry tests of VO2max at each HH condition under randomized and single-blinded conditions. RESULTS: VO2max decreased significantly from 760 Torr after 682 Torr (approximately 915 m) (3.5 +/- 0.9 to 3.4 +/- 0.8 L.min-1, P = 0.0003). Across all HH conditions, the slope of the relative decrement in VO2max (%VO2max) during HH was -9.2%/100 mm Hg (-8.1%/1000 m) with an initial decrease from 100% estimated to occur below 705 Torr (610 m). Step-wise multiple regression revealed that SL-VO2max, SL-LT, delta SaO2max, LBM, and gender each significantly combined to account for 89.03% of the variance in the decrement in VO2max (760-566 Torr) (P < 0.001). CONCLUSIONS: Individuals who have a combination of a large SL-VO2max, a small SL-LT (VO2, L.min-1), greater reductions in delta SaO2max, a large LBM, and are male have the greatest decrement in VO2max during HH. The unique variance explanation afforded by SL-LT, LBM, and gender suggests that issues pertaining to oxygen diffusion within skeletal muscle may add to the explanation of between subjects variability in the decrement in VO2max during HH.

Glycogen resynthesis in skeletal muscle following resistive exercise.

The purpose of this investigation was to determine the influence of post-exercise carbohydrate (CHO) intake on the rate of muscle glycogen resynthesis after high intensity weight resistance exercise in subjects not currently weight training. In a cross-over design, eight male subjects performed sets (mean = 8.8) of six single leg knee extensions at 70% of one repetition max until 50% of full knee extension was no longer possible. Total force application was equated between trials using a strain gauge interfaced to a computer. The subjects exercised in the fasted state. Post-exercise feedings were administered at 0 and 1 h consisting of either a 23% CHO solution (1.5 g.kg-1) or an equal volume of water (H2O). Total force production, preexercise muscle glycogen content, and degree of depletion (-40.6 and -44.3 mmol.kg-1 wet weight) were not significantly different between H2O and CHO trials. As anticipated during the initial 2-h recovery, the CHO trial had a significantly greater rate of muscle glycogen resynthesis as compared with the H2O trial. The muscle glycogen content was restored to 91% and 75% of preexercise levels when water and CHO were provided after 6 h, respectively.

Influence of muscle glycogen depletion on the rate of resynthesis.

In an effort to determine what effect the degree of muscle glycogen depletion has on the rate of resynthesis, six male cyclists completed an exercise protocol that involved both one- and two-legged cycling. One leg completed 30 min of single-leg cycling, ten one-min sprints, and 30 min cycling with both legs. This resulted in a large degree of depletion (LD). The contralateral leg completed only 30 min of double-leg cycling and experienced a small amount of depletion (SD). Following the exercise, the subjects rested quietly for 6 h and were fed a 24% carbohydrate (CHO) solution every 20 min in order to achieve a CHO intake of 0.7 g.kg-1.h-1. Biopsies taken from the vastus lateralis muscle immediately after exercise revealed that the glycogen content of the LD leg decreased 93.9 (+/- 11.6) mmol.kg-1 w.w., whereas the SD leg used 49.3 (+/- 5.7) mmol.kg-1 w.w. (P less than 0.01). Subsequent biopsies taken at 2 and 6 h of recovery demonstrated that the rate of muscle glycogen resynthesis was significantly greater in the LD leg, averaging 8.8 (+/- 2.4) mmol.kg-1.h1 w.w, while the SD leg restored glycogen at a rate of 3.0 (+/- 1.0) mmol.kg-1.h-1 w.w. (P less than 0.05). Glycogen synthase activity, expressed as its activity ratio (I/D), was also greater (P less than 0.01) in the LD leg both immediately after exercise (0.45 +/- 0.05 vs 0.24 +/- 0.04) and at 2 h of recovery (0.54 +/- 0.06 vs 0.27 +/- 0.06).(ABSTRACT TRUNCATED AT 250 WORDS)

Effects of estradiol on substrate turnover during exercise in amenorrheic females.

The purpose of this investigation was to determine the effects of transdermal estradiol (E2) replacement on substrate utilization during exercise. Amenorrheic females (N = 6) performed three exercise trials following 72 h of placebo (C 72) and 72 and 144 h of medicated transdermal estradiol (E2) treatment (E2 72 and E2 144). Exercise involved 90 min of treadmill running at 65% VO2max followed by timed exercise to exhaustion at 85% VO2max. Resting blood samples were obtained for glucose, insulin, free fatty acids (FFA), and E2. Exercise blood samples were obtained for E2, lactate, epinephrine, and norepinephrine. Rates of appearance and disposal were calculated for glucose and glycerol using a primed, continuous infusion of [6,6-2H] glucose and [2H5] glycerol. Medicated transdermal placement increased E2 significantly at rest, before exercise (35.03 +/- 12.3, 69.5 +/- 20.1, and 73.1 +/- 31.6 pg.mL-1 for the C 72, E2 72, and E2 144 trials, respectively, P < 0.05). Resting FFA increased significantly following E2 treatment (0.28 +/- 0.16, 0.41 +/- 0.27, and 0.40 +/- 0.21 mmol.L-1 for the C 72, E2 72, and E2 144 trials, respectively, P < 0.05). Glucose Ra was significantly decreased during exercise as a result of E2 replacement (21.9 +/- 7.7, 18.9 +/- 6.2, and 18.9 +/- 5.6 mumol.kg-1.min-1 for the C 72, E2 72, and E2 144 trials, respectively, P < 0.05). Average glucose Rd also decreased during exercise as a result of E2 replacement (21.3 +/- 7.8, 18.5 +/- 6.4, and 18.6 +/- 5.8 mumol.kg-1.min-1 for the C 72, E2 72, and E2 144 trials, respectively, P < 0.05). However, the estimated relative contribution of plasma glucose and muscle glycogen to total carbohydrate oxidation was similar among the trials. Epinephrine values were significantly lower late in exercise during the E2 72 and E2 144 trials, compared with the C 72 trial (P < 0.05). These results indicate that elevated E2 levels can alter glucose metabolism at rest and during moderate intensity exercise as a result of decreased gluconeogenesis, epinephrine secretion, and/or glucose transport.

Temporal inhomogeneity in brachial artery blood flow during forearm exercise.

The purpose of this study was to measure the influences of muscle contraction and exercise intensity on brachial artery blood flow during incremental forearm wrist flexion exercise to fatigue. Twelve subjects performed incremental forearm exercise (increments of 0.1 W every 5 min) with their nondominant arms. Doppler waveforms and two-dimensional images of the brachial artery were recorded during the last 2 min of each stage. Exercise intensities were expressed as a percent of the maximal workload achieved (%WLmax). Blood flow was calculated during each of the concentric (CP), eccentric (EP), and recovery phases (RP) of the contraction cycle. Blood flow during the CP of the contraction did not increase above resting values (25.0 +/- 10.5 mL.min-1) at any intensity (100%WLmax = 21.6 +/- 6.5 mL.min-1). Conversely, blood flow during the EP and RP increased from 25.6 +/- 3.0 to 169.1 +/- 12.8 (P < 0.05), and from 24.7 +/- 3.1 to 137.9 +/- 19.5 mL.min-1 (P < 0.05), respectively from rest to maximal exercise. Time averaged blood flow increased linearly from rest to maximal exercise (75.3 +/- 26.3 to 334.6 +/- 141.6 mL.min-1, P < 0.05). Thus, a significant impairment in blood flow occurs with concentric contractions during forearm dynamic exercise. The implications of a temporal disparity in blood flow to oxygen delivery and skeletal metabolism during exercise are discussed.

Exercise mode and gender comparisons of energy expenditure at self-selected intensities.

The purpose of this study was to compare oxygen consumption (VO2) and energy expenditure after 20 min of self-selected submaximal exercise for four modes of exercise. Eighteen subjects (9 male and 9 female) first completed a test of VO2max during treadmill running. On separate days, subjects then completed 20 min submaximal treadmill running (TR), simulated cross-country skiing (XC), cycle ergometry (CE), and aerobic riding (AR) exercise. Total VO2 and energy expenditure were significantly higher for TR than all other modes for both males and females (43.6 +/- 10.4, 39.1 +/- 9.7, 36.1 +/- 7.6, 28.4 +/- 6.1 LO2, for TR, XC, CE, and AR, respectively, P < 0.0001). For males and females, heart rate was similar during TR and XC and lower during CE and AR (154.8 +/- 14.2, 152 +/- 13.1, 143.4 +/- 14.9, and 126.2 +/- 12.0 beats.min-1 for TR, XC, CE, and AR, respectively, P < 0.0001). Compared with females, males had significantly greater VO2 (P < 0.005) and energy expenditure (P < 0.004), while females had higher heart rates (P < 0.003). Ratings of perceived exertion (RPE) were not different between TR, XC, and CE, but were significantly lower during AR (13.4 +/- 1.3, 13.6 +/- 0.8, 13.2 +/- 0.9, and 12.6 +/- 1.0 for TR, XC, CE, and AR, respectively, P < 0.003). TR elicited the greatest VO2 and energy expenditure during self-selected exercise despite and RPE similar to XC and CE. Therefore, treadmill exercise may be the modality of choice for individuals seeking to improve cardiorespiratory endurance and expend a larger number of kjoules.