Effects of plasma epinephrine on fat metabolism during exercise: interactions with exercise intensity

This study determined the effects of elevated plasma epinephrine on fat metabolism during exercise. On four occasions, seven moderately trained subjects cycled at 25% of peak oxygen consumption (VO(2 peak)) for 60 min. After 15 min of exercise, subjects were intravenously infused with low (0.96 +/- 0.10 nM), moderate (1.92 +/- 0.24 nM), or high (3.44 +/- 0.50 nM) levels (all P < 0.05) of epinephrine to increase plasma epinephrine above control (Con; 0.59 +/- 0.10 nM). During the interval between 35 and 55 min of exercise, lipolysis [i.e., rate of appearance of glycerol] increased above Con (4.9 +/- 0.5 micromol. kg(-1). min(-1)) with low, moderate, and high (6.5 +/- 0.5, 7.1 +/- 0.8, and 10.6 +/- 1.2 micromol. kg(-1). min(-1), respectively; all P < 0.05) levels of epinephrine despite simultaneous increases in plasma insulin. The release of fatty acid into plasma also increased progressively with the graded epinephrine infusions. However, fatty acid oxidation was lower than Con (11.1 +/- 0.8 micromol. kg(-1). min(-1)) during moderate and high levels (8.7 +/- 0.7 and 8.1 +/- 0.9 micromol. kg(-1). min(-1), respectively; P < 0.05). In one additional trial, the same subjects exercised at 45% VO(2 peak) without epinephrine infusion, which produced a plasma epinephrine concentration identical to low levels. However, lipolysis was lower (i.e., 5.5 +/- 0.6 vs. 6.5 +/- 0.5 micromol. kg(-1). min(-1); P < 0.05). In conclusion, elevations in plasma epinephrine concentration during exercise at 25% of VO(2 peak) progressively increase whole body lipolysis but decrease fatty acid oxidation. Last, increasing exercise intensity from 25 to 45% VO(2 peak) attenuates the lipolytic actions of epinephrine.     

Effects of adrenergic agonists and antagonists on muscle O2 uptake and lactate metabolism

To investigate adrenergic receptor-mediated responses in dog gastrocnemius-plantaris muscle, several catecholamine agonists, isoproterenol, epinephrine, norepinephrine, and phenylephrine, and two antagonists, propranolol and phenoxybenzamine, were given during repetitive, isotonic, tetanic contractions. The response variables that were measured were muscle blood flow, shortening during constant load contractions, and arterial and venous O2 and lactate concentrations. The calculated variables were O2 uptake (VO2), net lactic acid output (L), and power output. In the control experiments, the contractions increased VO2 to approximately 50 times rest by 2 min. Thereafter, shortening, work, and VO2 declined together by 17% at 30 min, indicating muscle fatigue. L increased rapidly to nearly 0.8 mumol X g-1 X min-1 by 2 min, declined to 0.3-0.4 mumol X g-1 X min-1 by 7 min, and was like rest at 15, 22.5, and 30 min. The arterial lactate concentration rose steadily from rest to 30 min of contractions. Epinephrine infusion stopped the decline of VO2 during the contractions, but this effect was not observed with the other agonists. Propranolol decreased VO2 compared with controls at 22.5 and 30 min of contractions. Phenoxybenzamine decreased VO2 compared with controls at all times during contraction, and the decline with time was present. Coinfusion of epinephrine with propranolol reduced the decline in VO2 observed with propranolol alone. Both epinephrine and isoproterenol increased L compared with controls. This epinephrine response was antagonized by propranolol but enhanced by phenoxybenzamine. Both isoproterenol and epinephrine infusions increased arterial lactate concentration.(ABSTRACT TRUNCATED AT 250 WORDS)     

Plasma free and sulfoconjugated catecholamine responses to varying exercise intensity

Plasma free catecholamines rise during exercise, but sulfoconjugated catecholamines reportedly fall. This study examined the relationship between exercise intensity and circulating levels of sulfoconjugated norepinephrine, epinephrine, and dopamine. Seven exercise-trained men biked at approximately 30, 60, and 90% of their individual maximal oxygen consumption (VO2max) for 8 min. The 90% VO2max period resulted in significantly increased plasma free norepinephrine (rest, 219 +/- 85; exercise, 2,738 +/- 1,149 pg/ml; P less than or equal to 0.01) and epinephrine (rest, 49 +/- 49; exercise, 555 +/- 516 pg/ml; P less than or equal to 0.05). These changes were accompanied by consistent increases in sulfoconjugated norepinephrine at both the 60% (rest, 852 +/- 292; exercise, 1,431 +/- 639; P less than or equal to 0.05) and 90% (rest, 859 +/- 311; exercise, 2,223 +/- 1,015; P less than or equal to 0.05) VO2max periods. Plasma sulfoconjugated epinephrine and dopamine displayed erratic changes at the three exercise intensities. These findings suggest that sulfoconjugated norepinephrine rises during high-intensity exercise.     

Effect of endurance training on possible determinants of VO2 during heavy exercise

When moderate exercise begins, O2 uptake (VO2) reaches a steady state within 3 min. However, with heavy exercise, VO2 continues to rise beyond 3 min (VO2 drift). We sought to identify factors contributing to VO2 drift. Ten young subjects performed cycle ergometer tests of 15 min duration for each of four constant work rates, corresponding to 90% of the anaerobic threshold (AT) and 25, 50, and 75% of the difference between maximum VO2 (VO2 max) and AT for that subject. Time courses of VO2, minute ventilation (VE), and rectal temperature were recorded. Blood lactate, norepinephrine, and epinephrine were measured at the end of exercise. Eight weeks of cycle ergometer endurance training improved average VO2 max by 15%. Subjects then performed four tests identical to pretraining studies. For the above AT tests, training reduced VO2 drift substantially; reduction in each of the possible mediators we measured was also demonstrated. The training-induced decrease in VO2 drift was well correlated with decreases in end exercise lactate and less well correlated with the drift in VE seen at above AT work rates. The training-induced reduction in VO2 drift was not significantly correlated with attenuation of rectal temperature rise or decrease in end-exercise level of the catecholamines. Thus the slow rise in VO2 during heavy exercise seems linked to lactate, though a component dictated by the work of breathing cannot be ruled out.     

Effect of exercise on epinephrine turnover in trained and untrained male subjects

The kinetics underlying plasma epinephrine concentrations were studied. Six athletes (T) and six sedentary males (C) were given intravenous infusions of 3H-labeled epinephrine, after which arterial blood was drawn. They rested sitting and bicycled continuously to exhaustion (60 min at 125 W, 60 min at 160 W, 40 min at 200 W, and 240 W to the end). Work time was 154 +/- 13 (SE) (T) and 75 +/- 6 (C) min. At rest, epinephrine clearance was identical [28.4 +/- 1.3 (T) vs. 29.2 +/- 1.8 (C) ml . kg-1 . min-1], but plasma concentration [1.42 +/- 0.27 (T) vs. 0.71 +/- 0.16 (C) nmol . l-1] and, accordingly, secretion [2.9 +/- 0.7 vs. 1.5 +/- 0.4 nmol . min-1] were higher (P less than 0.05) in T than C subjects. Epinephrine clearance was closely related to relative work load, decreasing from 15% above the basal level at 30% of maximal O2 uptake (VO2 max) to 22% below at 76% of VO2 max. Epinephrine concentrations increased much more with work intensity than could be accounted for by changes in clearance and were, at exhaustion, higher (P less than 0.05) in T (7.2 +/- 1.6) than in C (2.5 +/- 0.7 nmol . l-1) subjects despite similar glucose, heart rate, and hematocrit values. At a given load, epinephrine clearance rapidly became constant, whereas concentration increased continuously. Forearm extraction of epinephrine invalidated use of blood from a cubital vein or a hand vein arterialized by hot water in turnover measurements. During exercise, changes in epinephrine concentrations reflect changes in secretion rather than in clearance. Training may increase adrenal medullary secretory capacity.     

Effects of epinephrine, phenoxybenzamine, and propranolol on maximal exercise in sheep.

The mixed adrenergic agonist, epinephrine (10 micrograms/kg, i.v.), the beta-adrenergic receptor antagonist, propranolol (0.2 mg/kg, i.v.), or the alpha-adrenergic receptor antagonist, phenoxybenzamine (1 mg/kg, i.v.), were administered to sheep immediately before maximal incremental exercise. The effects of each of these drugs on hemoglobin (Hb) concentration during maximal exercise and on maximal exercise performance were investigated. The maximal incremental exercise protocol began at 4.0 km/h and 0% grade and finished at 5.6 km/h and 12% grade, with speed or grade increases every 1.5 minutes. Maximal exercise in control (untreated) sheep caused a mean 42% increase in hematocrit and 44% increase in Hb. This exercise-induced increase in Hb was unaffected by propranolol but was partially blocked by phenoxybenzamine. Epinephrine caused an immediate increase in Hb which abated during the early minutes of exercise and then subsequently increased toward the end of the exercise challenge. Maximum oxygen consumption (VO2) in control sheep was 47.6 +/- 6.7 ml/min per kilogram. Maximum VO2 after epinephrine, 51.6 +/- 8.7 ml/min per kilogram, was not significantly different from control. Maximum VO2 after propranolol and phenoxybenzamine, 35.4 +/- 15.3 and 40.8 +/- 8.2 ml/min per kilogram, respectively, were both significantly less than control exercise (P < 0.05).     

Adrenergic regulation of HSL serine phosphorylation and activity in human skeletal muscle during the onset of exercise

Skeletal muscle hormone-sensitive lipase (HSL) activity is increased by contractions and increases in blood epinephrine (EPI) concentrations and cyclic AMP activation of the adrenergic pathway during prolonged exercise. To determine the importance of hormonal stimulation of HSL activity during the onset of moderate- and high-intensity exercise, nine men [age 24.3 +/- 1.2 yr, 80.8 +/- 5.0 kg, peak oxygen consumption (VO2 peak) 43.9 +/- 3.6 ml x kg(-1) x min(-1)] cycled for 1 min at approximately 65% VO2 peak, rested for 60 min, and cycled at approximately 90% VO2 peak for 1 min. Skeletal muscle biopsies were taken pre- and postexercise, and arterial blood was sampled throughout exercise. Arterial EPI increased (P < 0.05) postexercise at 65% (0.45 +/- 0.10 to 0.78 +/- 0.27 nM) and 90% VO2 peak (0.57 +/- 0.34 to 1.09 +/- 0.50 nM). HSL activity increased (P < 0.05) following 1 min of exercise at 65% VO2 peak [1.05 +/- 0.39 to 1.78 +/- 0.54 mmol x min(-1) x kg dry muscle (dm)(-1)] and 90% VO2 peak (1.07 +/- 0.24 to 1.91 +/- 0.62 mmol x min(-1) x kg dm(-1)). Cyclic AMP content also increased (P < 0.05) at both exercise intensities (65%: 1.52 +/- 0.67 to 2.75 +/- 1.12, 90%: 1.85 +/- 0.65 to 2.64 +/- 0.93 micromol/kg dm). HSL Ser660 phosphorylation (approximately 55% increase) and ERK1/2 phosphorylation ( approximately 33% increase) were augmented following exercise at both intensities, whereas HSL Ser563 and Ser565 phosphorylation were not different from rest. The results indicate that increases in arterial EPI concentration during the onset of moderate- and high-intensity exercise increase cyclic AMP content, which results in the phosphorylation of HSL Ser660. This adrenergic stimulation contributes to the increase in HSL activity that occurs in human skeletal muscle in the first minute of exercise at 65% and 90% VO2 peak.     

Contribution of exercising legs to the slow component of oxygen uptake kinetics in humans.

Rates of performing work that engender a sustained lactic acidosis evidence a slow component of pulmonary O2 uptake (VO2) kinetics. This slow component delays or obviates the attainment of a stable VO2 and elevates VO2 above that predicted from considerations of work rate. The mechanistic basis for this slow component is obscure. Competing hypotheses depend on its origin within either the exercising limbs or the rest of the body. To resolve this question, six healthy males performed light nonfatiguing [approximately 50% maximal O2 uptake (VO2max)] and severe fatiguing cycle ergometry, and simultaneous measurements were made of pulmonary VO2 and leg blood flow by thermodilution. Blood was sampled 1) from the femoral vein for O2 and CO2 pressures and O2 content, lactate, pH, epinephrine, norepinephrine, and potassium concentrations, and temperature and 2) from the radial artery for O2 and CO2 pressures, O2 content, lactate concentration, and pH. Two-leg VO2 was thus calculated as the product of 2 X blood flow and arteriovenous O2 difference. Blood pressure was measured in the radial artery and femoral vein. During light exercise, both pulmonary and leg VO2 remained stable from minute 3 to the end of exercise (26 min). In contrast, during severe exercise [295 +/- 10 (SE) W], pulmonary VO2 increased 19.8 +/- 2.4% (P less than 0.05) from minute 3 to fatigue (occurring on average at 20.8 min). Over the same period, leg VO2 increased by 24.2 +/- 5.2% (P less than 0.05). Increases of leg and pulmonary VO2 were highly correlated (r = 0.911), and augmented leg VO2 could account for 86% of the rise in pulmonary VO2.(ABSTRACT TRUNCATED AT 250 WORDS)     

Early adaptations in blood substrates, metabolites, and hormones to prolonged exercise training in man.

This study was designed to investigate the effect of short-term, submaximal training on changes in blood substrates, metabolites, and hormonal concentrations during prolonged exercise at the same power output. Cycle training was performed daily by eight male subjects (VO2max = 53.0 +/- 2.0 mL.kg-1.min-1, mean +/- SE) for 10-12 days with each exercise session lasting for 2 h at an average intensity of 59% of VO2max. This training protocol resulted in reductions (p less than 0.05) in blood lactate concentration (mM) at 15 min (2.96 +/- 0.46 vs. 1.73 +/- 0.23), 30 min (2.92 +/- 0.46 vs. 1.70 +/- 0.22), 60 min (2.96 +/- 0.53 vs. 1.72 +/- 0.29), and 90 min (2.58 +/- 1.3 vs. 1.62 +/- 0.23) of exercise. The reduction in blood lactate was also accompanied by lower (p less than 0.05) concentrations of both ammonia and uric acid. Similarly, following training lower concentrations (p less than 0.05) were observed for blood beta-hydroxybutyrate (60 and 90 min) and serum free fatty acids (90 min). Blood glucose (15 and 30 min) and blood glycerol (30 and 60 min) were higher (p less than 0.05) following training, whereas blood alanine and pyruvate were unaffected. For the hormones insulin, glucagon, epinephrine, and norepinephrine, only epinephrine and norepinephrine were altered with training. For both of the catecholamines, the exercise-induced increase was blunted (p less than 0.05) at both 60 and 90 min. As indicated by the changes in blood lactate, ammonia, and uric acid, a depression in glycolysis and IMP formation is suggested as an early adaptive response to prolonged submaximal exercise training.     

Effect of increased central blood volume with water immersion on plasma catecholamines during exercise

To examine the influence of an increase in central blood volume with head-out water immersion (WI) on the sympathoadrenal response to graded dynamic exercise, nine healthy men underwent upright leg cycle exercise on land and with WI. Plasma norepinephrine and epinephrine concentrations were used as indexes of overall sympathoadrenal activity. Oxygen consumption (VO2), heart rate, systolic blood pressure, and plasma concentrations of norepinephrine, epinephrine, and lactate were determined at work loads corresponding to approximately 40, 60, 80, and 100% peak VO2. Peak VO2 did not differ on land and with WI. Plasma norepinephrine concentration was reduced (P less than 0.05) at 80 and 100% peak VO2 with WI and on land, respectively. Plasma epinephrine and lactate concentrations were similar on land and with WI at the three submaximal work stages, but both were reduced (P less than 0.05) at peak exertion with WI. Heart rate was lower (P less than 0.05) at the three highest work intensities with WI. These results suggest that the central shift in blood volume with WI reduces the sympathoadrenal response to high-intensity dynamic exercise.     

Prolonged exercise following diuretic-induced hypohydration: effects on cardiovascular and thermal strain

To examine the role of a reduction in plasma volume (PV) on the cardiovascular and thermoregulatory responses to submaximal exercise, ten untrained males (VO2 peak = 3.96 +/- 0.14 L x min(-1); mean +/- SE) performed 60 min of cycle exercise at -61% of VO2 peak while on a diuretic (DIU) and under control (CON) conditions. Participants consumed either Novotriamazide (100 mg triameterene + 50 mg hydrochlorothiazide, a diuretic) or a placebo, in random order, for 4 days prior to the exercise. Diuretic resulted in a calculated 14.6% reduction (P < 0.05) in resting PV. Heart rate was higher (P < 0.05) at rest and throughout exercise for DIU compared with CON. No differences were observed for cardiac output (Qc) and stroke volume (SV) at rest for the two conditions, but during exercise both Qc and SV were lower (P < 0.05) with DIU. Exercise VO2 (L x min(-1)) for CON and DIU at 30 min (2.39 +/- 0.09 vs 2.43 +/- 0.08) and 60 min (2.56 +/- 0.08 vs 2.53 +/- 0.12) were similar between conditions. Whole body a-vO2 difference was significantly greater (P < 0.05) for DIU both at rest and during exercise as compared with CON. Rectal temperature (Tre) was significantly higher (P < 0.05) during DIU from 15 min to the end of exercise. Blood concentrations of norepinephrine were higher (P < 0.05) with DIU compared to CON at 15 min of exercise and beyond. For blood epinephrine, no differences were observed between DIU and CON. These results suggest that reductions in PV led to greater circulating concentrations of norepinephrine which likely resulted from increased cardiac and thermoregulatory stresses. In addition, reductions in PV do not appear to increase cardiovascular instability during prolonged dynamic exercise.     

Plasma catecholamines and heart rate at the beginning of muscular exercise in man

The relationship between the time course of heart rate and venous blood norepinephrine (NE) and epinephrine (E) concentrations was studied in 7 sedentary young men before and during 3 bicycle exercises of 5 min each (respectively 23 +/- 2.8%, 45 +/- 2.6% and 65 +/- 2.4% VO2max, mean +/- SE). During the low level exercise the change in heart rate is monoexponential (tau = 5.7 +/- 1.2 s) and no increment above the resting level of NE (delta NE) or of E (delta E) occurs. At the medium and highest intensity of exercise: a) the change in heart rate is biexponential, tau for the fast and the slow component averaging about 3 and 80 s respectively; b) delta NE (but not delta E) increases continuously with time of exercise; c) at the 5th min of exercise heart rate increments are related to delta NE; d) between 20 s and 5 min, at corresponding sampling times, the heart rate of the slow component is linearly related to delta NE. At exercise levels higher than 33% VO2max the increase in heart rate described by the slow component of the biexponential kinetic could be due to an augmented sympathetic activity revealed by increased NE blood levels.     

Effects of nifedipine on responses to exercise in normal subjects

The responses to sublingual nifedipine (20 mg) and placebo were compared in normal subjects during two studies on cycle ergometer [progressive exercise and constant work-load exercise at approximately 60% of maximal O2 consumption (VO2max)]. The use of nifedipine did not modify maximal power, ventilation (VE), VO2, and heart rate (HR) at the end of the multistage progressive exercise (30-W increments every 3 min). Over the 45 min of the constant-load exercise and the ensuing 30-min recovery we observed with nifedipine compared with placebo 1) no differences in VO2, VE, respiratory exchange ratio, and systolic arterial blood pressure; 2) a higher HR (P less than 0.001) and lower diastolic arterial blood pressure (P less than 0.01); 3) a greater and more prolonged rise in norepinephrine (P less than 0.01) and growth hormone (P less than 0.001); 4) no significant differences in epinephrine and insulin and a lesser increase in glucagon during recovery (P less than 0.01); and 5) a lesser fall in blood glucose (P less than 0.01) and greater increase in acetoacetate (P less than 0.001), beta-hydroxybutyrate (P less than 0.05), and blood lactate (P less than 0.001). Our data do not support the hypothesis that nifedipine reduces hormonal secretions in vivo and are best explained by an enhanced secretion of catecholamines compensating for the primary vasodilator effect of nifedipine.     

Increased epinephrine response and inaccurate glucoregulation in exercising athletes

Epinephrine responses to insulin-induced hypoglycemia have indicated that athletes have a higher adrenal medullary secretory capacity than untrained subjects. This view was tested by an exercise protocol aiming at identical stimulation of the adrenal medulla in the two groups. Eight athletes (T) and eight controls (C) ran 7 min at 60% maximal O2 consumption (VO2max), 3 min at 100% VO2max, and 2 min at 110% VO2max. Plasma epinephrine both at rest and at identical relative work loads [110% VO2max: 8.73 +/- 1.51 (T) vs. 3.60 +/- 1.09 mmol X l-1 (C)] was higher [P less than 0.05) in T than in C. Norepinephrine, as well as heart rate, increased identically in the two groups, indicating identical sympathetic nervous activity. Lactate and glycerol were higher in T than in C after running. Glucose production peaked immediately after exercise and was higher in T than in C. Glucose disappearance increased less than glucose production and was identical in T and C. Accordingly plasma glucose increased, more in T than in C (P less than 0.01). In T glucose levels approached the renal threshold greater than 20 min postexercise. Glucose clearance increased less in T than in C during exercise and decreased postexercise to or below (T, P less than 0.05) basal levels, despite increased insulin levels. Long-term endurance training increases responsiveness of the adrenal medulla to exercise, indicating increased secretory capacity. During maximal exercise this may contribute to higher glucose production, lower clearance, more inaccurate glucoregulation, and higher lypolysis in T compared with C.     

Glucoregulation and hormonal responses to maximal exercise in non-insulin-dependent diabetes

Maximal dynamic exercise results in a postexercise hyperglycemia in healthy young subjects. We investigated the influence of maximal exercise on glucoregulation in non-insulin-dependent diabetic subjects (NIDDM). Seven NIDDM and seven healthy control males bicycled 7 min at 60% of their maximal O2 consumption (VO2max), 3 min at 100% VO2max, and 2 min at 110% VO2max. In both groups, glucose production (Ra) increased more with exercise than did glucose uptake (Rd) and, accordingly, plasma glucose increased. However, in NIDDM subjects the increase in Ra was hastened and Rd inhibited compared with controls, so the increase in glucose occurred earlier and was greater [147 +/- 21 to 169 +/- 19 (30 min postexercise) vs. 90 +/- 4 to 100 +/- 5 (SE) mg/dl (10 min postexercise), P less than 0.05]. Glucose levels remained elevated for greater than 60 min postexercise in both groups. Glucose clearance increased during exercise but decreased postexercise to or below (NIDDM, P less than 0.05) basal levels, despite increased insulin levels (P less than 0.05). Plasma epinephrine and glucagon responses to exercise were higher in NIDDM than in control subjects (P less than 0.05). By use of the insulin clamp technique at 40 microU.m-2.min-1 of insulin with plasma glucose maintained at basal levels, glucose disposal in NIDDM subjects, but not in controls, was enhanced 24 h after exercise. It is concluded that, because of exaggerated counter-regulatory hormonal responses, maximal dynamic exercise results in a 60-min period of postexercise hyperglycemia and hyperinsulinemia in NIDDM. However, this event is followed by a period of increased insulin effect on Rd that is present 24 h after exercise.(ABSTRACT TRUNCATED AT 250 WORDS)     

Plasma catecholamine and lactate response during graded exercise with varied glycogen conditions.

The relationships between the lactate threshold (TLa), plasma catecholamines, and ventilatory threshold (TVE) were examined under normal and glycogen-depleted conditions. Nine male subjects performed a graded exercise test on a bicycle ergometer in a normal glycogen (NG) state and in a glycogen-depleted (GD) state to determine if manipulation of muscle glycogen content would affect their ventilatory, lactate, and catecholamine responses. High correlations were found between plasma lactate and the two catecholamines, epinephrine (r = 0.964) and norepinephrine (r = 0.965) under both conditions. The GD protocol resulted in a shift in the TLa to a later work rate; inflections in epinephrine and norepinephrine shifted in a coordinated manner. TVE and TLa occurred at similar work loads under NG conditions [67.2 +/- 1.5 and 65.6 +/- 2.3% maximal oxygen consumption (VO2max), respectively], but TLa occurred at a later work load (75.3 +/- 1.9% VO2max) compared with TVE (68.3 +/- 1.6% VO2max) under GD conditions. These results suggest a causal relationship between plasma lactate and epinephrine during a graded exercise test under the glycogen conditions studied. Although an association existed between ventilation and lactate, this relationship was not as strong.     

Heredity and overfeeding-induced changes in submaximal exercise VO2

The present study investigated the role of heredity in determining changes in the energy cost of submaximal exercise in response to short-term overfeeding. Six pairs of monozygotic twins were subjected to a 1,000 kcal/day surplus for 22 days with careful experimental controls over food intake and physical activities. O2 consumption (VO2) was measured during a submaximal treadmill exercise test 165 min postprandially before and the morning after the overfeeding protocol. As expected, overfeeding induced significant increases in body weight and fat mass. No significant increase in mean exercise VO2 was observed after overfeeding. However, the interindividual variation in overfeeding-induced changes in exercise VO2 was large and not randomly distributed. When comparing intrapair variance for changes in exercise VO2 to interpair variance, a moderate to high within-pair resemblance in response, i.e., a genotype-overfeeding interaction, was observed. Changes in exercise VO2 were positively correlated with those in postexercise levels of blood catecholamines, particularly epinephrine. A negative correlation was found between changes in exercise VO2 and body fat gain. These results are consistent with the concept of a role for the sympathoadrenal system in the regulation of adaptive thermogenesis and the predisposition to store fat. Moreover, these data suggest that the sensitivity to adapt in exercise energy expenditure after overfeeding is inherited to a significant extent.     

Time required for the restoration of normal heavy exercise VO2 kinetics following prior heavy exercise.

Prior heavy exercise markedly alters the O2 uptake (VO2) response to subsequent heavy exercise. However, the time required for VO2 to return to its normal profile following prior heavy exercise is not known. Therefore, we examined the VO2 responses to repeated bouts of heavy exercise separated by five different recovery durations. On separate occasions, nine male subjects completed two 6-min bouts of heavy cycle exercise separated by 10, 20, 30, 45, or 60 min of passive recovery. The second-by-second VO2 responses were modeled using nonlinear regression. Prior heavy exercise had no effect on the primary VO2 time constant (from 25.9 +/- 4.7 s to 23.9 +/- 8.8 s after 10 min of recovery; P = 0.338), but it increased the primary VO2 amplitude (from 2.42 +/- 0.39 to 2.53 +/- 0.41 l/min after 10 min of recovery; P = 0.001) and reduced the VO2 slow component (from 0.44 +/- 0.13 to 0.21 +/- 0.12 l/min after 10 min of recovery; P < 0.001). The increased primary amplitude was also evident after 20-45 min, but not after 60 min, of recovery. The increase in the primary VO2 amplitude was accompanied by an increased baseline blood lactate concentration (to 5.1 +/- 1.0 mM after 10 min of recovery; P < 0.001). Baseline blood lactate concentration was still elevated after 20-60 min of recovery. The priming effect of prior heavy exercise on the VO2 response persists for at least 45 min, although the mechanism underpinning the effect remains obscure.     

Oxygen consumption following exercise of moderate intensity and duration.

To study the effects of exercise intensity and duration on excess postexercise oxygen consumption (EPOC), 8 men [age = 27.6 (SD 3.8) years, VO2max = 46.1 (SD 8.5) ml min-1 kg-1] performed four randomly assigned cycle-ergometer tests (20 min at 60% VO2max, 40 min at 60% VO2max, 20 min at 70% VO2max, and 40 min at 70% VO2max). O2 uptake, heart rate and rectal temperature were measured before, during, and for 1 h following the exercise tests. Blood for plasma lactate measurements was obtained via cannulae before, and at selected times, during and following exercise. VO2 rapidly declined to preexercise levels following each of the four testing sessions, and there were no differences in EPOC between the sessions. Blood lactate and rectal temperature increased (P < 0.05) with exercise, but had returned to preexercise levels by 40 min of recovery. The results indicate that VO2 returned to resting levels within 40 min after the end of exercise, regardless of the intensity (60% and 70% VO2max) or duration (20 min and 40 min) of the exercise, in men with a moderate aerobic fitness level.     

Implementing a mathematical model to compare oxygen uptake kinetics between cyclists and noncyclists during steady state

The purpose was to compare a mathematical model of oxygen uptake and bioenergetic systems to an experimental protocol. Twelve (N = 12) noncyclists (NC), age (21.8 ± 1.4 years), and 8 (N = 8) cyclists (C), age (30.5 ± 5.7 years), were subjects. All subjects signed an informed consent. Oxygen consumption (VO2, ml·kg?1·min?1) was measured with steady-state VO2 requirements and responses determined using the mathematical model from the following equation: VO2 (WR) = VO2 (rest) + VO2 (unloading pedaling) + α.WR; ΔVO2(t, WR) = ΔVO2 (WR) = [1-e[-(t-td)/tO2]. Exercise means (SD) included the following: VO2NC(WR) = 48.4 (16.6) ml?1·min?1 for NCs and VO2C(WR) = 56.4 (24.95) ml?1·min?1 for Cs ; ΔVO2C(t, WR) = 6:38 ml?1·min?1 for NCs and ΔVO2C(t, WR) = 7.44 ml?1·min?1 for Cs. The correlation between the mathematical model and actual measure was statistically significant (p < 0.01) with a coefficient of r = 0.947. The experimental protocol was significantly associated with the mathematical model. This allows for a quantitative analysis and safe prediction of steady-state oxygen uptake conditions on populations before exposure to exercising conditions. Through more precise analysis of conditions, greater specificity of training may lead to more predictable adaptation outcomes.