Prediction of blood lactate accumulation from excess CO2 output during constant exercise

To determine the predictability of blood lactate accumulation from excess CO2 output derived from bicarbonate buffering of lactic acid during constant exercise, eight normal active volunteers were studied during three stages of constant exercise on a cycle ergometer. Three work rates consisted of 100% (stage I), 120% (stage II) and 150% (stage III) of each subject's anaerobic threshold (AT), each of which was lasted for 4 min. Excess CO2 output (Ex CO2, ml) at each stage of constant exercise was estimated form the integral of difference between total VCO2 and aerobic VCO2 (from regression line for VCO2 and VO2 at exercise intensities below the AT obtained in incremental exercise test). Ex CO2 per body mass (Ex CO2-mass-1) was increased progressively with blood lactate (La) accumulation from rest to each stage of constant exercise. Mean values (+/-SD) in the measured La accumulation (delta La,measured) and predicted La accumulation (delta La,predicted) at three stages of constant exercise were 1.82 +/- 0.83 vs 3.19 +/- 1.70 for stage 1, 5.58 +/- 3.47 vs 7.09 +/- 3.28 for stage II and 12.19 +/- 2.36 vs 12.74 +/- 1.83 mmol.l-1 for stage III, respectively. There was a significant difference between delta La,measured and delta La,predicted at stage I (p < 0.05), but no significant differences between these two variables at stage II and III. The averaged difference from delta La,predicted to delta La,measured at stage III (0.55 mmol.l-1) showed a tendency to be smaller than stage I (1.38 mmol.l-1) and II (1.50 mmol.l-1). On the other hand, delta La,predicted was found to correlate very closely with delta La,measured (r = 0.954, P < 0.001, n = 20). The results of this study suggest that the changes of La accumulation could be predicted from excess CO2 output generated in constant exercises above the AT.     

Oral glucose ingestion increases endurance capacity in normal and diabetic (type I) humans

The effects of an oral glucose administration (1 g/kg) 30 min before exercise on endurance capacity and metabolic responses were studied in 21 type I diabetic patients [insulin-dependent diabetes mellitus (IDDM)] and 23 normal controls (Con). Cycle ergometer exercise (55-60% of maximal O2 uptake) was performed until exhaustion. Glucose administration significantly increased endurance capacity in Con (112 +/- 7 vs. 125 +/- 6 min, P < 0.05) but only in IDDM patients whose blood glucose decreased during exercise (70.8 +/- 8.2 vs. 82.8 +/- 9.4 min, P < 0.05). Hyperglycemia was normalized at 15 min of exercise in Con (7.4 +/- 0.2 vs. 4.8 +/- 0.2 mM) but not in IDDM patients (12.4 +/- 0.7 vs. 15.6 +/- 0.9 mM). In Con, insulin and C-peptide levels were normalized during exercise. Glucose administration decreased growth hormone levels in both groups. In conclusion, oral glucose ingestion 30 min before exercise increases endurance capacity in Con and in some IDDM patients. In IDDM patients, in contrast with Con, exercise to exhaustion attenuates hyperglycemia but does not bring blood glucose levels to preglucose levels.     

Determination of aspartame and its major decomposition products in foods

When exercise to exhaustion is performed using at least two different intensities, work to fatigue (Wlim) can be expressed as a linear function of time to fatigue (Tlim). Whereas the slope of this function is related to endurance ability, the y-intercept is associated with the potential to perform high intensity interval exercise. The purpose of the present investigation was to determine the influence of 8-wk intermittent high-intensity exercise training on the y-intercept derived from the Wlim-Tlim relationship. Eight healthy, untrained male students (19.1 +/- 0.6 yr) completed five 60-s bouts of maximal exercise on the cycle ergometer, three times a week, for 8 wk. Seven controls avoided regular activity for the same period. Prior to and immediately following the training period, the Wlim-Tlim relationship, VO2max, and total work completed in five 60-s exercise bouts on the cycle ergometer were determined. Correlational analysis established relationships between the y-intercept and total work accomplished in the interval test pre- (r = 0.90; P < 0.01; N = 15) and post-training (r = 0.92; P < 0.01; N = 15), confirming that the y-intercept is related to the ability to perform exercise of this nature. Moreover, the "anaerobic" energy yield, calculated from total work and oxygen consumed during the interval exercise, was also related to the y-intercept (r = 0.78; P < 0.01). Interval training significantly increased both the y-intercept (P = 0.0015) and total work accomplished in the interval test (P = 0.001), while the slope of the Wlim-Tlim relationship (critical power) remained unchanged.(ABSTRACT TRUNCATED AT 250 WORDS)     

Effects of ambient temperature on the capacity to perform prolonged cycle exercise in man

Eight healthy males performed four rides to exhaustion at approximately 70% of their VO2max obtained in a neutral environment. Subjects cycled at ambient temperatures (Ta) of 3.6 +/- 0.3 (SD), 10.5 +/- 0.5, 20.6 +/- 0.2, and 30.5 +/- 0.2 degrees C with a relative humidity of 70 +/- 2% and an air velocity of approximately 0.7 m.s-1. Weighted mean skin temperature (Tsk), rectal temperature (Tre), and heart rate (HR) were recorded at rest, during exercise and at exhaustion. Venous samples were drawn before and during exercise and at exhaustion for determination of hemoglobin, hematocrit, blood metabolites, and serum electrolytes and osmolality. Expired air was collected for calculation of VO2 and R which were used to estimate rates of fuel oxidation. Ratings of perceived exertion (RPE) were also obtained. Time to exhaustion was significantly influenced by Ta (P = 0.001): exercise duration was shortest at 30.5 degrees C (51.6 +/- 3.7 min) and longest at 10.5 degrees C (93.5 +/- 6.2 min). Significant effects of Ta were also observed on VE, VO2, R, estimated fuel oxidation, HR, Tre, Tsk, sweat rate, and RPE. This study demonstrates that there is a clear effect of temperature on exercise capacity which appears to follow an inverted U relationship.     

Lactate distribution in the blood during steady-state exercise

PURPOSE: The purpose of this investigation was to examine the plasma to red blood cell (RBC) lactate concentration ([La]) gradient and RBC:plasma [La] ratio during 30 min of steady-state cycle ergometer exercise at work rates below lactate threshold ( LT. Blood samples were taken from a heated forearm vein, immediately cooled to 4 degrees C in a dry-ice ethanol slurry, and centrifuged at 4 degrees C to separate plasma and RBCs. RESULTS: During >LT, plasma [La] rose to 8.8+/-1.1 mM after 10 min and remained above 6 mM. RBC [La] (4.9+/-0.7 mM) was significantly lower than plasma [La] at 10 min and remained lower throughout exercise. As a result, there was a sizable [La] gradient (approximately 3.5 mM) from plasma to RBC during most of >LT. In LT, the ratio of RBC [La]:plasma [La] was the same for both (0.58+/-0.02) and not significantly different from rest. CONCLUSIONS: These results refuted our hypothesis that the RBC:plasma [La] ratio would decrease at the onset of >LT exercise because of muscle lactate release exceeding the ability of RBCs to take up the lactate. Instead, there appears to be an equilibrium between plasma [La] and RBC [La] in arterialized venous blood from a resting muscle group as evidenced by the constant RBC [La]:plasma [La] ratio.     

Left ventricular function during dynamic exercise in untrained and moderately trained subjects

The influence of exercise training on left ventricular function at rest (R), at anaerobic threshold (AT), and during peak exercise (PE) was evaluated in 12 healthy untrained and 13 trained (T) subjects who underwent Doppler echocardiography at R and radionuclide ventriculography at R and during exercise. The end-diastolic volume and stroke volume were significantly higher in the T group than in the untrained group at R. The ejection fraction rose significantly from R to AT and from AT to PE (80.0 +/- 0.84 vs. 83.6 +/- 0.91%), but no significant difference was observed between groups. The peak diastolic filling rate rose significantly during exercise, with a further significant increase observed in the T group (AT, 6.38 +/- 0.40 vs. 5.01 +/- 0.16 end-diastolic counts/s; PE, 8.24 +/- 0.42 vs. 7.15 +/- 0.35 end-diastolic counts/s). The percent variation of minimal systolic counts fell significantly at AT and PE in relation to R. Our data demonstrate that exercise training produces a significant increase in peak diastolic filling rate but no change in systolic function during exercise and that metabolic acidosis caused by exercise does not limit systolic function.     

Pre-exercise branched-chain amino acid administration increases endurance performance in rats

This study investigated the effects of pre-exercise branched-chain amino acid (BCAA) administration on blood ammonia levels and on time to exhaustion during treadmill exercise in rats. Adult female Wistar rats were trained on a motor driven treadmill. After a 24-h fast, rats were injected intraperitoneally (i.p.) with 1 mL of placebo or BCAA (30 mg), 5 min before performing 30 min of submaximal exercise (N = 18) or running to exhaustion (N = 12). In both cases, rats were sacrificed immediately following exercise, and blood was collected for the measurement of glucose, nonesterified fatty acid (NEFA), lactic acid, BCAA, ammonia, and free-tryptophan (free-TRP) levels. Control values were obtained from sedentary rats that were subjected to identical treatments and procedures (N = 30). Plasma BCAA levels increased threefold within 5 min after BCAA administration. Mean run time to exhaustion was significantly longer (P < 0.01) after BCAA administration (99 +/- 9 min) compared with placebo (76 +/- 4 min). During exercise, blood ammonia levels were significantly higher (P < 0.01) in the BCAA treated compared with those in the placebo treated rats both in the 30-min exercise bout (113 +/- 25 mumol.L-1 (BCAA) vs 89 +/- 16 mumol.L-1) and following exercise to exhaustion (186 +/- 44 mumol.L-1 (BCAA) vs 123 +/- 19 mumol.L-1). These data demonstrate that BCAA administration in rats results in enhanced endurance performance and an increase in blood ammonia during exercise.     

Effects of a low-dose amino acid supplement on adaptations to cycling training in untrained individuals

The purpose of this study was to determine if amino acid supplementation influences blood and muscle lactate response to exercise and the time course of the metabolic adaptations to training. Two groups of untrained males (n = 7 each) were given (double-blind) a daily supplement (2.9 g.day-1) containing a mixture of leucine, isoleucine, valine, glutamine, and carnitine (EXP) or 3 g.day-1 of lactose (CON). Following 7 days of supplementation there was no significant change in VO2peak, time to exhaustion (TTX) at 120% VO2peak, or muscle and blood lactate in either EXP or CON. Subjects then initiated 6 weeks of combined aerobic and anaerobic training on a Monark cycle ergometer. It was found that amino acid supplementation had no effect on either blood or muscle lactate accumulation during exercise, while supplementation resulted in a faster adaptation in buffer capacity. Performance during intense exercise was not improved with amino acid supplementation.     

Ratings of perceived exertion (RPE) during cycling exercises at constant power output

The purpose of the present investigation was to study the overall rating of perceived exertion (RPEov) according to the 6-20 scale proposed by Borg (1970) and muscular RPE (RPEmu) in exercises at constant load. The relationship between RPE and heart rate for three different loads was studied during exhausting exercises in 10 participants. Whether the drift of RPE during a 20 min exercise at constant load could be an index of the endurance time during long-lasting exercises at constant load was also investigated. At 1-week intervals, the participants performed cycling exercises up to exhaustion at 60, 73, and 86% maximal aerobic power (MAP) measured during an incremental test. Heart rate, RPEov, RPEmu and exhaustion time (tlim) were measured. The upward shift of the HRmax-RPE regressions was significant between 86, 73 and 60% MAP (p < 0.001) for RPEov and RPEmu. This result suggests that the equation HR = 10 x RPE proposed by Borg (1973) for incremental exercise is not valid for long-lasting exercise at constant load until exhaustion because the heart rate corresponding to a given RPE depends on load and time. Mean RPE increased linearly with time up to exhaustion. Unexpectedly, the relationships between RPEmu or RPEov and percentage of exhaustion time were similar for exercises at 60 and 73% MAP although the exhaustion times were very different (79.40 +/- 30.64 min versus 36.19 +/- 15.99 min, respectively) (p < 0.001). Consequently, it is likely that RPE was a subjective estimation of the hardness of exercise rather than the intensity of exercise. The RPE pattern at the beginning of long-lasting exercises at constant load (60 and 73% MAP) cannot be considered as a sensitive predictor of the point of self-imposed exhaustion for individuals. Indeed, the errors in the estimation of exhaustion time from extrapolation of RPE at the beginning of exercise were very large. Moreover, at 60% MAP, a steady-state in RPE was observed during 20 min in five subjects whose tlim were not longer than tlim of the other subjects. In addition, the data of the present study indicate that RPEmu could be more useful than RPEov in cycling.     

First-pass radionuclide angiography during bicycle and treadmill exercise

BACKGROUND: Treadmill testing is usually preferred over cycle ergometry because of the greater sensitivity in diagnosing coronary artery disease. Treadmill testing has only recently been used with radionuclide angiography (RNA) because patient motion makes RNA imaging difficult. In this study we evaluate the comparability of treadmill and cycle exercise RNA with a dual isotope motion correction technique. METHODS AND RESULTS: Volunteer patients (n = 27) performed first-pass RNA during maximal exercise using both cycle ergometer and treadmill. Exercise capacity was greater during treadmill exercise (8.1 +/- 2.4 vs 7.5 +/- 2.2 METs). Twenty-three of 27 treadmill and all cycle ergometer exercise studies were technically adequate. Maximal heart rate was greater during treadmill exercise (150 +/- 24 vs 143 +/- 25 beats * min-l), however, systolic blood pressure was greater during cycle ergometry (174 +/- 23 vs 188 +/- 25 mmHg), resulting in no difference in heart rate times systolic blood pressure (25.7 +/- 7.2 vs 26.9 +/- 6.0). There were no differences between treadmill and cycle ergometer for peak exercise left ventricular ejection fraction (56% +/- 13% vs 57% +/- 14%) (r = 0.89). Calculated left ventricular end-diastolic volume was not different at rest (183 +/- 42 ml vs 176 +/- 44 ml) but differed significantly at peak exercise (282 +/- 75 ml vs 231 +/- 60 ml). The clinical impression, based on wall motion and left ventricular ejection fraction was very similar between treadmill and cycle ergometer. CONCLUSION: Treadmill exercise RNA is feasible, with about 85% of studies likely to be technically adequate. The overall clinical results are very similar to cycle exercise RNA, although the ordinarily expected advantages of treadmill exercise were largely absent.     

The V(O2) slow component for severe exercise depends on type of exercise and is not correlated with time to fatigue

The purpose of this study was to examine the influence of the type of exercise (running vs. cycling) on the O2 uptake V(O2) slow component. Ten triathletes performed exhaustive exercise on a treadmill and on a cycloergometer at a work rate corresponding to 90% of maximal VO2 (90% work rate maximal V(O2)). The duration of the tests before exhaustion was superimposable for both type of exercises (10 min 37 s +/- 4 min 11 s vs. 10 min 54 s +/- 4 min 47 s for running and cycling, respectively). The V(O2) slow component (difference between V(O2) at the last minute and minute 3 of exercise) was significantly lower during running compared with cycling (20.9 +/- 2 vs. 268.8 +/- 24 ml/min). Consequently, there was no relationship between the magnitude of the V(O2) slow component and the time to fatigue. Finally, because blood lactate levels at the end of the tests were similar for both running (7.2 +/- 1.9 mmol/l) and cycling (7.3 +/- 2.4 mmol/l), there was a clear dissociation between blood lactate and the V(O2) slow component during running. These data demonstrate that 1) the V(O2) slow component depends on the type of exercise in a group of triathletes and 2) the time to fatigue is independent of the magnitude of the V(O2) slow component and blood lactate concentration. It is speculated that the difference in muscular contraction regimen between running and cycling could account for the difference in the V(O2) slow component.     

Post-exercise changes in blood pressure, heart rate and rate pressure product at different exercise intensities in normotensive humans

To evaluate the effect of exercise intensity on post-exercise cardiovascular responses, 12 young normotensive subjects performed in a randomized order three cycle ergometer exercise bouts of 45 min at 30, 50 and 80% of VO2peak, and 12 subjects rested for 45 min in a non-exercise control trial. Blood pressure (BP) and heart rate (HR) were measured for 20 min prior to exercise (baseline) and at intervals of 5 to 30 (R5-30), 35 to 60 (R35-60) and 65 to 90 (R65-90) min after exercise. Systolic, mean, and diastolic BP after exercise were significantly lower than baseline, and there was no difference between the three exercise intensities. After exercise at 30% of VO2peak, HR was significantly decreased at R35-60 and R65-90. In contrast, after exercise at 50 and 80% of VO2peak, HR was significantly increased at R5-30 and R35-60, respectively. Exercise at 30% of VO2peak significantly decreased rate pressure (RP) product (RP = HR x systolic BP) during the entire recovery period (baseline = 7930 +/- 314 vs R5-30 = 7150 +/- 326, R35-60 = 6794 +/- 349, and R65-90 = 6628 +/- 311, P < 0.05), while exercise at 50% of VO2peak caused no change, and exercise at 80% of VO2peak produced a significant increase at R5-30 (7468 +/- 267 vs 9818 +/- 366, P < 0.05) and no change at R35-60 or R65-90. Cardiovascular responses were not altered during the control trial. In conclusion, varying exercise intensity from 30 to 80% of VO2peak in young normotensive humans did not influence the magnitude of post-exercise hypotension. However, in contrast to exercise at 50 and 80% of VO2peak, exercise at 30% of VO2peak decreased post-exercise HR and RP.     

Young and old subjects matched for aerobic capacity have similar noradrenergic responses to exercise

Sympathetic nervous system activity as indicated by circulating norepinephrine has been demonstrated to increase with advancing chronological age both at rest and during submaximal exercise. Much of the earlier work investigating this aging phenomenon used a younger group that had a higher peak oxygen consumption (VO2) than did the older group, which made comparisons difficult. In the present study, young [n = 7, 36 +/- 1.0 (SE) yr] and old subjects (n = 8, 61 +/- 1.2 yr) were matched on peak VO2 and then exercised at approximately the same relative submaximal VO2 (75%) and power output on a cycle ergometer for 21 min. Blood samples were collected at rest and in the 7th, 14th, and last minute of a 21-min exercise bout via an indwelling catheter in an antecubital vein. The norepinephrine responses for the young and old groups, respectively, were as follows: rest, 486 +/- 111 vs. 673 +/- 108; 7 min, 1,258 +/- 255 vs. 1,185 +/- 172; 14 min, 1,639 +/- 316 vs. 1,528 +/- 288; and 21 min, 2,038 +/- 488 vs. 1,936 +/- 453 pg/ml. These responses were not significantly different between the groups at any time period. The epinephrine values for the age groups were not statistically different: rest, 115 +/- 60 vs 88 +/- 51; 7 min, 140 +/- 18 vs. 326 +/- 88; 14 min, 216 +/- 33 vs. 366 +/- 104; and 21 min, 324 +/- 100 vs. 447 +/- 113 pg/ml.(ABSTRACT TRUNCATED AT 250 WORDS)     

Okadaic acid induces appearance of the mitotic epitope MPM-2 in SV40-infected CV-1 cells with a >G2-phase DNA content

Previous results from endurance training in women have been discrepant in regard to influences on basal and maximum adrenocorticotropin (ACTH) and beta-endorphin (beta-EP) concentrations before and after exhaustive exercise. A group of 23 untrained young women ran 3 times a week for 30 min at an individual specific intensity corresponding to their respective anaerobic threshold, derived from the lactate performance curve obtained from prior treadmill testing. ACTH and beta-EP were measured at rest, as well as 5 and 30 min after exhaustive progressive spiroergometric treadmill running, both before and after the 8 week endurance training program. Basal beta-EP did not change after training, but less elevated concentrations were measured both 5 (p < 0.05) and 30 min (p < 0.05) after exercise, after the training program. In contrast, the resting concentration of ACTH increased significantly; the respective maximum concentration was less elevated after 5 min and much less elevated 30 min after the exercise (p < 0.05). Positive correlations were found after the exhaustive exercise between beta-EP and ACTH, as well as between maximum lactate and ACTH. Training was associated with significant changes in maximum running speed (p < 0.01), maximum oxygen uptake (p < 0.01) and the running speed at the anaerobic threshold (p < 0.05). Maximum lactate and the level of perceived exertion remained unchanged, showing a similar level of exhaustion. Our results indicate that endurance training modulates the hormonal responses of beta-EP and ACTH to comparable workloads of high intensity. After the training program the maximum concentrations are significantly lower during the recovery period. The tendency to elevated basal ACTH, and thus elevated cortisol, might be a new factor to consider in evaluation of endurance training induced hormonal disturbances in women.     

Effects of a single bout of exercise on glucose effectiveness

The effects of a single bout of exercise on glucose effectiveness (SG) and insulin sensitivity (SI) in 22 sedentary subjects were estimated with a minimal model approach. The intravenous glucose tolerance test (IVGTT) was performed 1) 11 h after an exercise bout on a cycle ergometer at the lactate threshold level (mild exercise) for 60 min, 2) 11 h after an exercise bout at the 4 mM lactate level (hard exercise) for 36 +/- 1 min, 3) 11 h after an exhaustive-exercise bout (exhaustive exercise) for 96 +/- 7 min, or 4) without any prior exercise (control). Only the exhaustive exercise increased the glucose disappearance constant (2.69 +/- 0.28 vs. 2.05 +/- 0.13%/min; P < 0.05) and SI (15.0 +/- 2.0 vs. 10.3 +/- 0.9 x 10(-5) min/pM: P < 0.05) in comparison with the control condition. The SG and SG at zero insulin (GEZI) were not affected by any exercise condition. However, a marked individual difference in GEZI emerged after the exhaustive exercise and could be divided into two subgroups: one decreased in GEZI (0.014 +/- 0.001 vs. 0.007 +/- 0.001 min-1) and the other increased in GEZI (0.014 +/- 0.001 vs. 0.021 +/- 0.003 min-1). The former subgroup was accompanied by elevated levels of plasma creatine kinase (100 +/- 16 vs. 598 +/- 315 IU/l; P < 0.05) and myoglobin (Mb; 46 +/- 4 vs. 126 +/- 47 ng/ml; P < 0.05), whereas the latter subgroup showed no significant change in creatinine kinase (99 +/- 10 vs. 128 +/- 9 IU/l; P > 0.05) and Mb (50 +/- 7 vs. 51 +/- 4 ng/ml; P > 0.05). In both subgroups, SI was similarly increased after the exhaustive exercise. These results thus suggest that a single bout of exercise that results in muscle damage or changes in muscle permeability, as reflected in the increased creatine kinase and Mb levels, decreases GEZI, whereas exhaustive exercise without such alterations increases GEZI.     

Effect of creatine supplementation on sprint exercise performance and muscle metabolism

The aim of the present study was to examine the effect of creatine supplementation (CrS) on sprint exercise performance and skeletal muscle anaerobic metabolism during and after sprint exercise. Eight active, untrained men performed a 20-s maximal sprint on an air-braked cycle ergometer after 5 days of CrS [30 g creatine (Cr) + 30 g dextrose per day] or placebo (30 g dextrose per day). The trials were separated by 4 wk, and a double-blind crossover design was used. Muscle and blood samples were obtained at rest, immediately after exercise, and after 2 min of passive recovery. CrS increased the muscle total Cr content (9.5 +/- 2.0%, P < 0.05, mean +/- SE); however, 20-s sprint performance was not improved by CrS. Similarly, the magnitude of the degradation or accumulation of muscle (e.g., adenine nucleotides, phosphocreatine, inosine 5'-monophosphate, lactate, and glycogen) and plasma metabolites (e.g. , lactate, hypoxanthine, and ammonia/ammonium) were also unaffected by CrS during exercise or recovery. These data demonstrated that CrS increased muscle total Cr content, but the increase did not induce an improved sprint exercise performance or alterations in anaerobic muscle metabolism.     

Hypogastric arterial aneurysms associated with abdominal aortic aneurysms

The purpose of this study was to compare the physiological responses of professional and elite road cyclists during an incremental cycle ergometer test. Twenty-five elite cyclists (EC; 23+/-1 yr) and 25 professional cyclists (PC; 25+/-2yr) performed a ramp protocol (increases of 25 W x min(-1)) during which the following parameters were measured: oxygen consumption (VO2), pulmonary ventilation (VE), ventilatory equivalents for oxygen and carbon dioxide (VE x VO2(-1) and VE x VCO2(-1), respectively), respiratory exchange ratio (RER), ventilatory thresholds 1 and 2 (VT1 and VT2, respectively), blood lactate, and electromyographic activity (EMG) of the vastus lateralis. Significant differences existed between the two groups mainly at submaximal intensities, since both VT1 and VT2 occurred at a higher exercise intensity (p<0.001) in PC than in EC (VT2: 80.4+/-6.6 vs 87.0+/- 5.9% VO2max in EC and PC, respectively). Lactate levels showed a similar response in both groups at low-to-moderate intensities (< 300 W), and thereafter blood lactate was significantly higher in EC. Finally, the "electromyographic threshold" (EMGT) occurred at a significantly higher intensity (p < 0.05) in PC when compared to EC (64.7+/-14.2 vs 56.0+/-14.9% VO2max, respectively). It was concluded that, in comparison with EC, PC exhibit some remarkable physiological characteristics such as a high VT2, an important reliance on fat metabolism even at high power outputs, and several neuromuscular adaptations.     

Effect of anaesthetizing the region of the paraventricular hypothalamic nuclei on energy metabolism during exercise in the rat

The ventromedial and posterior hypothalamic nuclei are known to influence glucoregulation during exercise. The extensive projections of the paraventricular hypothalamic nucleus (PVN) to the sympathetic nervous system suggest that the PVN also may be involved in glucoregulation during exercise. The region of the PVN was anaesthetized with bupivacaine before running (26 m min-1) or continued rest, via previously implanted bilateral brain cannulas aimed at the dorsal aspect of the PVN. Control rats were treated identically to PVN-anaesthetized rats, but were not infused. Blood, for determination of plasma concentrations of metabolites and hormones, was drawn from a tail artery, and 3H-glucose was infused in a tail vein for glucose turnover determinations. At rest, no significant changes in plasma concentrations of metabolites or hormones were induced by anaesthesia of the region of the PVN. During exercise, glucose production and utilization and plasma concentrations of glucose, lactate, glycerol, noradrenaline, adrenaline, corticosterone, and glucagon increased (P < 0.02) and plasma insulin decreased (P < 0.02) in all rats. However, initially in exercise, adrenaline (4.3 +/- 0.8 vs. 7.9 +/- 1.0 nmol l-1 in controls, P < 0.05, t = 6 min) and later corticosterone levels (1.37 +/- 0.06 vs. 1.69 +/- 0.10 nmol l-1 in controls, P < 0.05, t = 20 min) were attenuated by PVN anaesthesia. Initially during exercise, glucose utilization was higher and plasma glucose lower in PVN-anaesthetized rats compared to controls (16.6 +/- 0.8 vs. 12.7 +/- 0.6 mumol min-1 100 g-1 and 7.1 +/- 0.2 vs. 8.1 +/- 0.2 mmol l-1, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)     

Improved oxygen utilization during mild exercise in heart failure

In heart failure with low cardiac output, exercise tolerance is reduced despite modulated regional blood distribution and oxygen extraction. However, low cardiac output does not necessarily lead to reduced exercise tolerance especially during mild exercise. In the present study, in order to understand the mechanisms regulating exercise tolerance in heart failure, we measured oxygen consumption (VO2) and cardiac output (CO) during both mild and intense exercise. Patients with heart failure were divided into 2 groups; group L (n = 8) consists of patients with low anaerobic threshold (AT) < 13 ml/min per kg and group H (n = 7) consisting of patients with AT > 13 ml/min per kg. At rest, VO2 was similar between groups L and H, whereas CO was lower in group L than in group H (3.5 + 0.3 vs 4.8 + 1.4 ml/min, p < 0.01). Increase in VO2 during warm-up exercise was not significant between the 2 groups (7.4 +/- 0.5 (group L) vs 6.2 +/- 0.3 ml/min per kg (group H), ns), but increase in CO was lower in group L than in group H (2.5 +/- 0.6 vs 3.4 +/- 0.4 ml/min, p < 0.01). After warm-up to the AT point, however, the increase in not only VO2 but also CO was markedly reduced in group L than in group H (VO2: 0.5 +/- 0.4 vs 3.7 +/- 0.8 ml/min per kg, p < 0.01, CO: 0.2 +/- 0.3 vs 1.1 +/- 0.3 L/min, p < 0.01). Based on these measurements, we calculated the arteriovenous oxygen difference (c(A-V)O2 difference) during exercise in individual patients using Fick's equation. The c(A-V)O2 difference was markedly increased in severe heart failure during the warm-up stage, but between the end of warm-up and the AT point, it remained at the same level as that of group H. These results suggest the presence of a unique mechanism regulating the c(A-V)O2 difference in severe heart failure patients, activation of which may, at least during mild exercise, contribute to efficient oxygen delivery to the peripheral tissues thus compensating for the jeopardized exercise tolerance in those patients.     

Evaluation of right ventricular systolic pressure during incremental exercise by Doppler echocardiography in adults with atrial septal defect

STUDY OBJECTIVES: Pulmonary hypertension is the most important complication in patients with atrial septal defect (ASD), but its role in limiting exercise has not been examined. This study sought to evaluate exercise performance in adults with ASD and determine the contribution of elevated pulmonary artery pressure in limiting exercise capacity. DESIGN: We used Doppler echocardiography during exercise in 10 adults (aged 34 to 70 years) with isolated ASD (New York Heart Association class I, II) and an equal number of matched control subjects. Incremental exercise was performed on an electrically braked upright cycle ergometer. Expired gases and VE were measured breath-by-breath. Two-dimensional and Doppler echocardiographic images were obtained at rest prior to exercise to determine ASD size, stroke volume (SV), shunt ratio (Qp:Qs), right ventricular outflow tract (RVOT) size, and right ventricular systolic pressure at rest (RVSPr). Doppler echocardiography was repeated at peak exercise to measure right ventricular systolic pressure during exercise (RVSPex). RESULTS: Resting echocardiography revealed that RVOT was larger (21+/-4 vs 35+/-8 mm, mean+/-SD; p=0.0009) and RVSPr tended to be higher (17+/-8 vs 31+/-8 mm Hg; p=0.08) in ASD; however, left ventricular SV was not different (64+/-23 vs 58+/-23 mL; p>0.05), compared with control subjects. Despite normal resting left ventricular function, ASD patients had a significant reduction in maximum oxygen uptake (VO2max) (22.9+/-5.4 vs 17.3+/-4.2 mL/kg/min; p=0.005). RVSPex was higher (19+/-8 vs 51+/-10 mm Hg; p=0.001) and the mean RVSP-VO2 slope (1+/-2 vs 18+/-3 mm Hg/L/min; p=0.003) and intercept (17+/-4 vs 27+/-4 mm Hg; p=0.05) were higher in the ASD group. VO2max correlated inversely with both RVSPr (r=-0.69; p=0.007) and RVSPex (r=-0.67; p=0.01). CONCLUSION: These findings suggest that adults with ASD have reduced exercise performance, which may be associated with an abnormal increase in pulmonary artery pressure during exercise.