Assessment of right and left ventricular volumes during upright exercise in normal men

Ventricular volumes were measured in 10 normal subjects by usingtwo independent methods: the stroke volume was obtained by theFick principle and the ejection fraction by multigated radionuclideangiography. Data were collected at rest in the supine and uprightpositions and during an upright exercise test, which includedthree levels of increasing severity. The left and right ventricular end-diastolic volumes (EDV) weremaximal in the supine posture (respectively 183 and 260 ml);at rest both were significantly lower in the upright position(158 and 220 ml). At maximal exercise, the ventricular end-diastolicvolumes were similar (left EDV=147 ml) or slightly lower (rightEDV= 178 ml) than at rest in the upright position. During uprightexercise, the end-systolic volumes (ESV) gradually decreased(P<0.001) from 56 to 34 ml (left ESV) and from 118 to 64ml (right ESV); simultaneously, the left ventricular ejectionfraction (EF) increased from 64 to 77% (P<0.001) and theright ventricular EF increased from 47 to 64% (P<0.001). Since during exercise in the upright position, the end-diastolicvolumes are unchanged or tend to decrease, a Frank-Starlingmechanism cannot be called upon; the cardiac response to uprightexercise is thus mainly based on an increased venous returnand on an increase in myocardial contractility reflected bythe increase in ejection fraction and the decrease in end-systolicvolumes. The methods used in the present study can provide referencevalues for the measurement of absolute ventricular volumes duringexercise by gated equilibrium radionuclide angiography.     

Left ventricular dimensions and function during exercise in dogs with chronic right ventricular pressure overload

Left ventricular (LV) dimensions and shortening at rest and during treadmill exercise were examined before and after 4 weeks of pulmonary artery (PA) constriction in 6 conscious dogs. The dogs were preinstrumented with LV and right ventricular (RV) catheters, an LV micromanometer, a PA inflatable cuff occluder and ultrasonic crystals to measure an LV anteroposterior, a septal-lateral, an apex-base and a free wall segment chord. With PA constriction, RV pressures increased from $\text{49 ±}\text{4}\text{2}\text{± 1 mm}$ Hg (systolic/end-diastolic) to $\text{104 ±}\text{5}\text{2}\text{± 1}$ at rest and from $\text{71 ±}\text{9}\text{2}\text{± 1}\text{to}\text{133 ±}\text{8}\text{14}\text{± 2}$ at peak exercise (mean ± standard error of the mean). Heart rate, LV pressure and LV dP/dt were similar before and after RV pressure overload at rest and with exercise. During exercise at control, systolic shortening increased significantly in all chords. With chronic PA constriction at rest, shortening of all chords also remained normal despite decreases in end-diastolic dimensions, which were most marked in the septal-lateral chord (23% decrease, p <0.01). However, during exercise in the presence of RV pressure overload, septal-lateral shortening decreased 46% (p <0.01) despite increases in systolic shortening in the other chords similar to the control response. Therefore, although LV function at rest in chronic RV pressure overload is normal, exercise may induce regional abnormalities of LV contraction that appear to be mediated by a reduced contribution of the ventricular septum to LV ejection.     

Left ventricular function during and after right ventricular pacing

OBJECTIVES: The aim of this research was to evaluate right ventricular pacing effects on left ventricular function. BACKGROUND: Right ventricular pacing alters the ventricular activation sequence and reduces left ventricular ejection fraction (EF). It is unclear whether the observed reduction in EF can be completely attributed to the alteration in activation sequence. METHODS: Twelve subjects (eight women), mean age 68 +/- 12 years, with transvenous dual-chamber pacemakers, normal left ventricular function, and intact atrioventricular (AV) conduction were studied with serial-gated blood pool studies. Left ventricular EF was measured at a fixed rate after at least 1 week of atrial pacing only (baseline), during short-term (2 h) and mid-term (1 week) AV sequential pacing with a short AV delay, and after short- and mid-term AV pacing. RESULTS: Baseline EF was 66.5 +/- 4.5%. Short-term AV pacing resulted in a decrease in EF to 60.3 +/- 5.2% (p < 0.0002). After one week of AV pacing, there was a further decline in EF to 52.9 +/- 8.3% (p < 0.0001). After cessation of mid-term pacing, EF was 57.3 +/- 5.9% (p < 0.0001 vs. baseline). A total of 2, 5, 8, and 24 h later, EF remained depressed (59% to 60%, p < 0.007). At 32 h, EF was 62.9 +/- 7.6% (p < 0.11 compared with baseline). CONCLUSIONS: The abnormal activation sequence resulting from right ventricular pacing accounts for only part of the reduction in EF as mid-term pacing is associated with a lower EF than short-term pacing, and EF remains depressed after cessation of AV pacing. Changes in ventricular function induced by right ventricular pacing may account for some of its associated adverse effects.     

Left and right ventricular function during symptom-limited exercise in patients with isolated mitral stenosis

Ventricular function during exercise in patients with mitral stenosis has not been widely studied. Accordingly, 20 patients with isolated mitral stenosis were assessed during supine, symptom-limited equilibrium radionuclide ventriculographic studies. All patients had a normal left ventricular (LV) ejection fraction at rest (greater than or equal to 50 percent), and all were in sinus rhythm. Left ventricular ejection fraction rose (p less than 0.001) from 64 +/- 9 percent at rest to 74 +/- 11 percent during exercise. This normal response was due solely to a decrease (p less than 0.01) in exercise LV end-systolic volume. A significant (p less than 0.01) decrease in end-diastolic volume during exercise limited the increase in ejection fraction during exercise. The decrease in end-diastolic volume during exercise caused stroke volume to remain unchanged; cardiac output rose according to heart rate alone. Right ventricular (RV) ejection fraction did not rise with exercise due to an increase in end-systolic volume. With exercise, LV end-diastolic volume was smaller (p less than 0.05) with severe mitral stenosis compared to mild mitral stenosis. With exercise, RV ejection fraction was decreased (p less than 0.05) with severe compared to mild mitral stenosis. In conclusion, LV function during exercise is normal in patients with normal resting LV ejection fraction. A decrease in LV diastolic filling with exercise prevents a rise in stroke volume, and cardiac output increases by heart rate alone. With, exercise, RV ejection fraction does not rise, due to an increase in RV end-systolic volume.     

Effects of age on ventricular performance during graded supine exercise

To assess the effects of age on ventricular performance, graded supine exercise tests with equilibrium radionuclide ventriculography were performed in six normal subjects of mean age 37 +/- 4 years and in eight normal subjects with a mean age of 59 +/- 2 years. At a standard submaximal work load, older subjects had a similar heart rate (older: 126 +/- 10, younger: 128 +/- 5 bpm) and systolic blood pressure responses (older: 198 +/- 24, younger: 202 +/- 24 mm Hg). Cardiac output counts increased appropriately in both groups during submaximal exercise. However, when expressed as percent change from resting values, the increases in cardiac output (older: 125 +/- 14, younger: 75 +/- 10 L/min; p less than 0.05) were greater for the older subjects. The percent change in end-diastolic counts (older: 8.4 +/- 5, younger: -2.8 +/- 4), stroke counts (older: 26 +/- 6, younger: 8.6 +/- 4), and ejection fraction (older: 18 +/- 3, younger: 11 +/- 1%) in proceeding from rest to exercise Stage III (600 kg-m/min) was greater for the older subjects. Age-related differences in each of these measurements were significant at p less than 0.05. These findings suggest that cardiac output during exercise is maintained by an increased heart rate in younger subjects, and by a combination of increased heart rate and the Frank-Starling mechanism in older individuals. Since the heart rate and mean blood pressure response to exercise were similar in both groups, the use of the Frank-Starling mechanism during exercise in older subjects suggests that age-related differences in ventricular preload are important in modulating the performance of the aging left ventricle.     

Augmented forearm vasoconstriction during dynamic exercise in healthy older men.

BACKGROUND. We tested the hypothesis that the nonactive limb vasoconstriction evoked during large-muscle dynamic exercise becomes augmented with aging in humans. METHODS AND RESULTS. Sixteen young control subjects (age, 26 +/- 1 year) and twelve older (65 +/- 1 year) healthy men with similar chronic physical activity levels were studied during supine leg cycling exercise. Both peak work load (1,100 +/- 60 versus 1,400 +/- 40 kpm/min) and peak O2 uptake (1.85 +/- 0.10 versus 2.38 +/- 0.07 l/min) were lower in the older men (p < 0.05). There were no differences in the two groups under conditions of quiet supine (basal) rest. During cycling for 5 minutes each at mild, moderate, and heavy submaximal intensities (approximately 45%, 65%, and 85% of peak O2 uptake), the increases in arterial blood pressure generally were similar in the young and older subjects; however, heart rate rose less in the older men (p < 0.05). Whole forearm blood flow (venous occlusion plethysmography) was lower and vascular resistance was higher (approximately 55-90%) in the older men at all loads (p < 0.05), but the steady-state forearm skin blood flow responses (laser Doppler velocimetry) were not different in the two groups. The increases in antecubital venous norepinephrine concentrations were greater in the older men at each work load (p < 0.05), although the plasma epinephrine responses were similar in the two groups. In other studies, 1) peak whole forearm reactive hyperemia and vascular conductance after sustained circulatory arrest (ischemia) were slightly (approximately 20%) but not significantly lower in the older men and 2) the forearm vasoconstrictor and plasma norepinephrine responses to a nonexercise sympathoexcitatory stimulus (limb immersion in ice water) tended to be blunted in the older men. CONCLUSIONS. During brief, submaximal, large-muscle dynamic exercise, healthy older men demonstrate augmented forearm vasoconstriction that is probably caused by greater constriction of skeletal muscle resistance vessels; this appears to be mediated, at least in part, by increased sympathetic outflow. These altered sympathetic vasoconstrictor adjustments do not represent a nonspecific hyperresponsiveness to acute stress with human aging. Finally, the regulation of arterial blood pressure appears to be normal in these healthy older men.     

Hemodynamically important right ventricular infarction: follow-up evaluation of right ventricular systolic function at rest and during exercise with radionuclide ventriculography and respiratory gas exchange

The prognosis and recovery of right ventricular systolic function in patients with hemodynamically documented right ventricular myocardial infarction (RVMI) is unclear. Therefore 27 patients who met hemodynamic criteria for RVMI were followed for at least 1 year. Four patients died within 1 year and 23 survived. Postmortem examination performed in three of the four patients showed extensive infarction of the right and left ventricles. Survivors underwent early and late follow-up resting radionuclide ventriculograms and late exercise studies. During long-term follow-up (1 to 4 years) resting radionuclide ventriculography demonstrated a significant improvement in right ventricular ejection fraction (30 +/- 7% to 43 +/- 8%; p less than .001) and right ventricular wall motion index (2.2 +/- 0.4 to 1.5 +/- 0.5; p less than .001) in 18 patients who survived longer than 1 year. Fourteen of these patients underwent upright bicycle exercise while off beta-blocking drugs and peak radionuclide ejection fraction was acquired after anaerobic threshold was achieved. Right ventricular ejection fraction increased significantly from 41 +/- 10% to 47 +/- 12% (p less than .001), as did the left ventricular ejection fraction (55 +/- 15% to 60 +/- 12%; p less than .05). The direction and magnitude of change of the right ventricular ejection fraction correlated significantly with the left ventricular ejection fraction (r = .82, p less than .02). Deviations from this correlation occurred in patients who had a decreased forced expiratory volume in 1 sec and an abnormal ventilatory reserve during exercise.(ABSTRACT TRUNCATED AT 250 WORDS)     

Importance of left ventricular function and systolic ventricular interaction to right ventricular performance during acute right heart ischemia.

To determine whether modulation of systolic ventricular interaction influences right ventricular performance during right heart ischemia, the effects of septal ischemia and inotropic stimulation were studied in 15 dogs in an open chest preparation. Right coronary branch occlusions led to right ventricular dilation and free wall dyskinesia, reversed septal curvature and reduced left ventricular diastolic volume. In systole, the septum thickened but bulged paradoxically into the right ventricle generating an active but depressed right ventricular systolic pressure (28.9 +/- 5.5 to 22.1 +/- 4.5 mm Hg), with associated decreases in right ventricular stroke work (5.66 +/- 0.94 to 1.92 +/- 0.53 g.m/m2) and left ventricular systolic pressure (123 +/- 11 to 80 +/- 10 mm Hg). Septal ischemia induced systolic septal thinning, left ventricular dilation and decreased left ventricular systolic pressure (80 +/- 10 to 55 +/- 10 mm Hg) and stroke work. Although the extent of paradoxic septal displacement increased, there were further decrements in right ventricular systolic pressure (22.1 +/- 4.5 to 18.7 +/- 4.3 mm Hg) and stroke work (1.92 +/- 0.53 to 0.7 +/- 0.2 g.m/m2). Dopamine infusion augmented left ventricular free wall contraction and increased left ventricular systolic pressure (55 +/- 10 to 172 +/- 17 mm Hg) and stroke work. Although systolic septal thinning persisted, the extent of paradoxic septal displacement increased strikingly and, despite continued right ventricular free wall dyskinesia, right ventricular systolic pressure increased (18.7 +/- 4.3 to 39.6 +/- 6.2 mm Hg) as did right ventricular stroke work (0.7 +/- 0.2 to 7 +/- 1.6 g.m/m2).(ABSTRACT TRUNCATED AT 250 WORDS)     

Left ventricular function after exercise training in young men

The effects of endurance training have been extensively studied in athletes, but longitudinal studies of exercise-induced cardiac changes in normal patients are limited. To assess the effects of 6 months of moderate-intensity aerobic training (1 hour/day, 3 times/week) on normal hearts, 23 sedentary men aged 31.1 +/- 3.5 years were studied by standard and tissue Doppler echocardiography. Left ventricular (LV) systolic function was assessed by the ejection fraction and Doppler-measured stroke volume, and diastolic function was assessed by transmitral and pulmonary venous flow. Tissue Doppler systolic (Sm), early (Em), and late (Am) myocardial velocities were obtained at the septal and lateral mitral annulus. After training, there was a 14.5% increase in peak oxygen consumption (p = 0.000002) and a decrease in heart rate (60 +/- 7 to 56 +/- 8 beats/min, p = 0.01). Septal and posterior wall thickness increased (8.7 +/- 1.0 to 9.4 +/- 1.3 mm, p = 0.002, and 8.2 +/- 0.7 to 8.8 +/- 1.1 mm, p = 0.0009, respectively), with a 15% increase in LV mass index (p = 0.0002). LV diameters, stroke volumes, and ejection fractions were unchanged. Mitral inflow showed a decrease in late-wave velocity (p = 0.00004), thus increasing the early (E)/A ratio. Septal and lateral Sm (p = 0.02) and Em velocities (p <0.05) increased after training. In conclusion, the physiologic increase in LV mass in response to regular exercise in healthy young men occurs in parallel with a decrease in atrial contribution to flow. LV function estimated by tissue Doppler is improved despite the lack of changes in standard echocardiographic indexes.     

Changes in plasma proenkephalin peptide F and catecholamine levels during graded exercise in men.

Proenkephalin peptide F immunoreactivity, epinephrine, and norepinephrine were measured in the plasma of endurance-trained and untrained male subjects riding on a bicycle ergometer at 28%, 54%, 83%, and 100% of maximum oxygen consumption (VO2). At rest the trained group had peptide F levels almost twice the level of the untrained group, whereas all other variables measured were the same. The maximum epinephrine and norepinephrine levels were found at 100% exercise intensity, with a precipitous drop in the levels at 5 min of recovery. In contrast, the peptide F immunoreactivity reached a maximum at 5 min of recovery and was still substantially above the initial level after 15 min of rest. In addition, the trained subjects showed another peak of peptide F immunoreactivity at 54% VO2max. Possible explanations for the different patterns of catecholamine and peptide F levels are presented.     

Left ventricular diastolic function during positive end-expiratory pressure. Impact of right ventricular ischemia and ventricular interaction.

The individual and additive effects of positive end-expiratory pressure (PEEP) and right coronary artery (RCA) occlusion on left ventricular end-diastolic pressure-volume relations (LVEDPVR) were examined in six anesthetized dogs. Right ventricular (RV) and left ventricular (LV) ejection fractions (EF), end-diastolic volume (EDV) and end-systolic volumes (ESV) were measured by thermodilution as PEEP was added before and after RCA occlusion. PEEP alone caused a decline in cardiac output, transmural left atrial pressure (LAP) (6.0 +/- 0.6 to 3.2 +/- 1.4 mm Hg, p less than 0.05), and LVEDV (49 +/- 3 to 36 +/- 4 ml, p less than 0.05). RVEDV, the mean slope (+/- SD) of the LVEDPVR (0.37 +/- 0.16 to 0.30 +/- 0.19) and LAP at a common LV volume (35 ml, V35) did not change with PEEP. RCA occlusion caused cardiac output and RVEF (38 +/- 5 to 27 +/- 5%, p less than 0.05) to decline and RVESV (25 +/- 4 to 33 +/- 6 ml, p less than 0.05) to increase. RVEDV, the slope of the LVEDPVR, and LAP at V35 were unchanged from baseline. The addition of PEEP after RCA occlusion caused cardiac output to decline further. However, unlike before occlusion, there was no change in LAP (6.5 +/- 1.3 to 5.0 +/- 1.4 mm Hg) despite a decline in LVEDV (47 +/- 3 to 29 +/- 6 ml, p less than 0.05). RVESV and RVEDV increased with PEEP after RCA occlusion as did LAP at V35. The slope of the mean LVEDPVR tended to increase (0.98 +/- 1.03).(ABSTRACT TRUNCATED AT 250 WORDS)     

Comparison of right and left ventricular function in obese and nonobese men

We studied systolic and diastolic function of the left and right ventricles in obese male subjects. Obese subjects had increased left ventricular mass and normal left ventricular systolic and diastolic function. They also had impaired right ventricular relaxation and right ventricular filling.     

Left ventricular size and performance during graded supine exercise in normal subjects

To investigate left ventricular size and performance during graded submaximal exercise, 14 normal subjects with a mean age of 21 years exercised in a supine position to achieve the target heart rate. Using two-dimensional echocardiography, we recorded and analysed the left ventricular (LV) cross-sectional area and internal dimension at the level of the tips of the mitral valve at rest and during mild, moderate and severe exercise. The heart rate and systolic blood pressure increased substantially from rest to peak exercise (71 +/- 11 to 162 +/- 10 beats/min, 122 +/- 10 to 204 +/- 22 mmHg). The end-diastolic cross-sectional area and internal dimension (EDA & EDD) increased by 1.1-2.2 cm2 (7-13%) and 0.2-0.3 cm (4-7%), respectively, from mild to moderate exercise, (p less than 0.05-0.001). At peak exercise, however, these decreased and showed no statistically significant difference from the values at rest. The end-systolic cross-sectional area and internal dimension (ESA & ESD) decreased by 1.1 to 1.6 cm2 (14-20%) and 0.2-0.3 cm (7-10%), respectively, from moderate to severe exercise (p less than 0.01-0.001). However, the end-systolic values during mild exercise were not significantly different from those at rest. The stroke area (EDA-ESA) and dimension (EDD-ESD) increased by 1.6-2.6 cm2 (19-31%) and 0.2-0.6 cm (25-38%), respectively, during all levels of graded exercise (p less than 0.05-0.001). The percent change of LV cross-sectional area and internal dimension during systole increased gradually from rest to moderate exercise (51.0 +/- 7.1 to 61.9 +/- 4.4%, 35.4 +/- 3.9 to 45.0 +/- 3.7%), respectively, and showed no further increase during peak exercise. The mean circumferential fiber shortening velocity increased sharply from rest to peak exercise (1.27 +/- 0.14 to 2.25 +/- 0.21 circ/sec). These results suggest that the Frank-Starling mechanism operates during mild to moderate exercise, and contractility increases markedly at moderate to severe exercise levels as cardiac performance is augmented during graded submaximal exercise.     

Effects of severity of mitral stenosis on left and right ventricular function at rest and during exercise

Few studies have assessed the effect of severity of mitral stenosis (MS) on ventricular function. Using equilibrium radionuclide ventriculography to measure ejection fraction and volume changes, 63 patients were studied during supine, symptom-limited exercise. To more carefully assess the 12 patients with MS and impaired left ventricular function, 2 groups of patients were formed. Group I (n = 51) had a normal (less than 50%) resting left ventricular (LV) ejection fraction (EF) and group II (n = 12) had an abnormally low (less than 50%) resting LVEF. Both groups were divided into mild (greater than 1.4 cm2), moderate (1.1-1.4 cm2) and severe (less than 1.0 cm2) MS. There were no differences in mean rest or exercise LVEF for group I. Exercise LVEF increased significantly (p less than 0.05) from rest with mild MS, but not with moderate or severe MS. The decrease in exercise LVEF was due to a decrease in exercise end-diastolic volume of 9 +/- 23% and 15 +/- 18% for moderate and severe MS, respectively. Exercise end-systolic volume decreased normally for all degrees of MS severity. Exercise right ventricular (RV)EF did not increase for any degree of MS severity due to an increase in end-systolic volume. All patients in group II had an RVEF of less than 40%. For this group, severity of MS had no effect on resting LVEF and the response to exercise was similar to group I. We conclude that in patients with MS, resting LVEF is unaffected by MS severity whereas exercise LVEF decreases with increased severity of MS due to impaired diastolic filling.(ABSTRACT TRUNCATED AT 250 WORDS)     

Intermittent coronary spasm during graded exercise.

We report a patient with Prinzmetal's angina with nearly normal coronary angiogram who not only developed severe myocardial ischemia during exercise, documented both electrocardiographically (ST elevation) and scintigraphically (with thallium-201), but also did so intermittently as the graded exercise progressed. Diagnostic coronary angiography showed spontaneous focal spasm of the proximal left anterior descending coronary artery. This unique response to exercise in a patient with variant angina suggests that factors other than catecholamine stimulation alone are active and rapidly attenuated in some patients. This phenomenon could be overlooked without appropriate electrocardiographic monitoring.     

Right ventricular diastolic function during exercise: effect of ischemia

The effects of exercise on right ventricular diastolic function were evaluated in 14 patients who underwent supine rest and exercise right ventricular angiography. On the basis of coronary anatomy and exercise left ventricular regional wall motion analysis, these patients were classified into two groups: Group 1 (n = 7) had no or only mild coronary artery disease and Group 2 (n = 7) had significant coronary disease and exercise-induced left ventricular wall motion abnormalities suggesting ischemia. Chamber stiffness at rest was higher in Group 2 (48 x 10(-3) ml-1/m2) than in Group 1 (18 x 10(-3) ml-1/m2, p = 0.006). During exercise, right ventricular filling rate in the second half of diastole was significantly lower in Group 2 (126 versus 276 ml/m2 per s, p less than 0.03). The time constant of right ventricular pressure decay decreased significantly in both groups with exercise; however, both groups displayed a parallel upward shift of the pressure-volume curve with exercise. Because ischemia could not be demonstrated in Group 1, it is an unlikely explanation for this shift. Septal shifting was not a significant factor with exercise. Because of an increase in left ventricular end-diastolic volume with exercise and a close correlation between right and left ventricular end-diastolic pressures (r = 0.96 for Group 1 and r = 0.76 for Group 2), pericardial constraint is the most likely cause for this upward shift of the pressure-volume curve. Therefore, an increase in right ventricular end-diastolic pressure may not be a reliable indicator of ischemia during exercise because this pressure is coupled to changes in left ventricular volume and pericardial constraint.     

Fat metabolism during high-intensity exercise in endurance-trained and untrained men

To determine whether trained individuals rely more on fat than untrained persons during high-intensity exercise, six endurance-trained men and six untrained men were studied during 30 minutes of exercise at 75% to 80% maximal oxygen consumption (VO2max). The rates of appearance (Ra) and disappearance (Rd) of glycerol and free fatty acids (FFAs) were determined using [1,1,2,3,3-2H]glycerol and [1-13C]palmitate, respectively, whereas the overall rate of fatty acid oxidation was determined using indirect calorimetry. During exercise, the whole-body rate of lipolysis (ie, glycerol Ra) was higher in the trained group (7.1 +/- 1.2 v 4.5 +/- 0.7 micromol x min(-1) x kg(-1), P < .05), as was the Ra (approximately Rd) of FFA (9.0 +/- 0.9 v 5.0 +/- 1.0 micromol x min(-1) x kg(-1), P < .001). FFA utilization was higher in trained subjects even when expressed as a percentage of total energy expenditure (10% +/- 1% v 7% +/- 1%, P < .05). However, this difference in plasma FFA flux could not account for all of the difference in fatty acid oxidation between trained and untrained subjects (20.8 +/- 3.3 v 7.9 +/- 1.6 micromol x min(-1) x kg(-1), or 23% +/- 3% v 13% +/- 2% of total energy expenditure, both P < .05). Thus, the oxidation of fatty acids derived from some other source also must have been greater in the trained men. We conclude that trained athletes use more fat than untrained individuals even during intense exercise performed at the same percentage of VO2max. The additional fatty acids appear to be derived from both adipose tissue and, presumably, intramuscular triglyceride stores.