Metabolic response to green tea extract during rest and moderate-intensity exercise

BackgroundGreen tea catechins have been hypothesized to increase energy expenditure and fat oxidation by inhibiting catechol-O-methyltransferase (COMT) and thus promoting more sustained adrenergic stimulation. Metabolomics may help to clarify the mechanisms underlying their putative physiological effects.ObjectiveThe study investigated the effects of 7-day ingestion of green tea extract (GTE) on the plasma metabolite profile at rest and during exercise.MethodsIn a placebo-controlled, double-blind, randomized, parallel study, 27 healthy physically active males consumed either GTE (n=13, 1200 mg catechins, 240 mg caffeine/day) or placebo (n=14, PLA) drinks for 7 days. After consuming a final drink (day 8), they rested for 2 h and then completed 60 min of moderate-intensity cycling exercise (56%±4% VO₂max). Blood samples were collected before and during exercise. Plasma was analyzed using untargeted four-phase metabolite profiling and targeted profiling of catecholamines.ResultsUsing the metabolomic approach, we observed that GTE did not enhance adrenergic stimulation (adrenaline and noradrenaline) during rest or exercise. At rest, GTE led to changes in metabolite concentrations related to fat metabolism (3-β-hydroxybutyrate), lipolysis (glycerol) and tricarboxylic acid cycle (TCA) cycle intermediates (citrate) when compared to PLA. GTE during exercise caused reductions in 3-β-hydroxybutyrate concentrations as well as increases in pyruvate, lactate and alanine concentrations when compared to PLA.ConclusionsGTE supplementation resulted in marked metabolic differences during rest and exercise. Yet these metabolic differences were not related to the adrenergic system, which questions the in vivo relevance of the COMT inhibition mechanism of action for GTE.     

Suppressing lipolysis increases interleukin-6 at rest and during prolonged moderate-intensity exercise in humans.

IL-6 induces lipolysis when administered to humans. Consequently, it has been hypothesized that IL-6 is released from skeletal muscle during exercise to act in a "hormonelike" manner and increase lipolysis from adipose tissue to supply the muscle with substrate. In the present study, we hypothesized that suppressing lipolysis, and subsequent free fatty acid (FFA) availability, would result in a compensatory elevation in IL-6 at rest and during exercise. First, we had five healthy men ingest nicotinic acid (NA) at 30-min intervals for 120 min at rest [10 mg/kg body mass (initial dose), 5 mg/kg body mass (subsequent doses)]. Plasma was collected and analyzed for FFA and IL-6. After 120 min, plasma FFA concentration was attenuated (0 min: 0.26 +/- 0.05 mmol/l; 120 min: 0.09 +/- 0.02 mmol/l; P < 0.01), whereas plasma IL-6 was concomitantly increased approximately eightfold (0 min: 0.75 +/- 0.18 pg/ml; 120 min: 6.05 +/- 0.89 pg/ml; P < 0.001). To assess the effect of lipolytic suppression on the exercise-induced IL-6 response, seven active, but not specifically trained, men performed two experimental exercise trials with (NA) or without [control (Con)] NA ingestion 60 min before (10 mg/kg body mass) and throughout (5 mg/kg body mass every 30 min) exercise. Blood samples were obtained before ingestion, 60 min after ingestion, and throughout 180 min of cycling exercise at 62 +/- 5% of maximal oxygen consumption. IL-6 gene expression, in muscle and adipose tissue sampled at 0, 90, and 180 min, was determined by using semiquantitative real-time PCR. IL-6 mRNA increased in Con (rest vs. 180 min; P < 0.01) approximately 13-fold in muscle and approximately 42-fold in fat with exercise. NA increased (rest vs. 180 min; P < 0.01) IL-6 mRNA 34-fold in muscle, but the treatment effect was not statistically significant (Con vs. NA, P = 0.1), and 235-fold in fat (Con vs. NA, P < 0.01). Consistent with the study at rest, NA completely suppressed plasma FFA (180 min: Con, 1.42 +/- 0.07 mmol/l; NA, 0.10 +/- 0.01 mmol/l; P < 0.001) and increased plasma IL-6 (180 min: Con, 9.81 +/- 0.98 pg/ml; NA, 19.23 +/- 2.50 pg/ml; P < 0.05) during exercise. In conclusion, these data demonstrate that circulating IL-6 is markedly elevated at rest and during prolonged moderate-intensity exercise when lipolysis is suppressed.     

Norepinephrine spillover at rest and during submaximal exercise in young and old subjects

Mazzeo, Robert S., Chakravarthi Rajkumar, Garry Jennings,and Murray Esler. Norepinephrine spillover at rest and during submaximal exercise in young and old subjects. J. Appl. Physiol. 82(6): 1869-1874, 1997.Aging isassociated with elevations in plasma norepinephrineconcentrations. The purpose of this investigation was toexamine total body and regional norepinephrine spillover as anindicator of sympathetic nerve activity. Eight young (26 ± 3 yr)and seven old (69 ± 5 yr) male subjects were studied at rest andduring 20 min of submaximal cycling exercise at 50% of peak workcapacity. Norepinephrine spillover was determined by continuousintravenous infusion of[³H]norepinephrine.Arterial norepinephrine concentrations were significantly greater atrest for old vs. young subjects (280 ± 36 vs. 196 ± 27 ng/ml,respectively). Whereas total norepinephrine spillover did not differbetween groups at rest, hepatomesenteric norepinephrine spillover was50% greater in old subjects compared with their young counterparts (51 ± 7 vs. 34 ± 5 ng/min, respectively). Additionally,norepinephrine clearance rates at rest were significantly lower for theold subjects (23%). During exercise, plasmanorepinephrine concentrations increased compared with rest, with oldsubjects again demonstrating greater values than the young group.Hepatomesenteric norepinephrine spillover was significantly greater(+36%) during exercise for old subjects compared with young; however,no difference was found for whole body spillover rates between agegroups. Norepinephrine clearance rates remained depressed(30%) in the old subjects during exercise. Clearance ofepinephrine mirrored that for norepinephrine both at rest and duringexercise across age groups. It was concluded that in old subjects, areduction in norepinephrine clearance and an increase in regionalnorepinephrine spillover can account for the higher plasmanorepinephrine concentrations observed at rest. This relationship isnot exacerbated by the stress imposed during an acute bout of exercise.

     

Venous and capillary blood hematocrit at rest and following submaximal exercise.

The purpose of this study was to determine if finger tip capillary blood hematocrit is a valid estimate of anticubital venous blood hematocrit at rest and after submaximal exercise. Simultaneous samples of finger tip cpaillary and venous blood were drawn from thirty-one subjects (15 males, 16 females) before and after a 15 min submaximal exercise on a bicycle ergometer. Venous and capillary blood hcts. were 42.0% +/- 3.9 and 42.0% +/- 3.5 respectively before exercise and 43.3% +/- 3.5 and 42% +/- 3.8 after exercise (X +/- s). The regression equation for predicting venous hct. from finger tip capillary blood after exercise was: Hctv = 0.87 Hctc + 6.44 with r = 0.95 (P less than 0.05). The results indicate that the finger tip capillary microhematocrit method is a valid indicator of venous blood hct. following exercise.     

Effect of initial core temperature on hyperthermic hyperventilation during prolonged submaximal exercise in the heat

We investigated whether a core temperature threshold for hyperthermic hyperventilation is seen during prolonged submaximal exercise in the heat when core temperature before the exercise is reduced and whether the evoked hyperventilatory response is affected by altering the initial core temperature. Ten male subjects performed three exercise trials at 50% of peak oxygen uptake in the heat (37°C and 50% relative humidity) after altering their initial esophageal temperature (T(es)). Initial T(es) was manipulated by immersion for 25 min in water at 18°C (Precooling), 35°C (Control), or 40°C (Preheating). T(es) after the water immersion was significantly higher in the Preheating trial (37.5 ± 0.3°C) and lower in the Precooling trial (36.1 ± 0.3°C) than in the Control trial (36.9 ± 0.3°C). In the Precooling trial, minute ventilation (Ve) showed little change until T(es) reached 37.1 ± 0.4°C. Above this core temperature threshold, Ve increased linearly in proportion to increasing T(es). In the Control trial, Ve increased as T(es) increased from 37.0°C to 38.6°C after the onset of exercise. In the Preheating trial, Ve increased from the initially elevated levels of T(es) (from 37.6 to 38.6°C) and Ve. The sensitivity of Ve to increasing T(es) above the threshold for hyperventilation (the slope of the T(es)-Ve relation) did not significantly vary across trials (Precooling trial = 10.6 ± 5.9, Control trial = 8.7 ± 5.1, and Preheating trial = 9.2 ± 6.9 L·min(-1)·°C(-1)). These results suggest that during prolonged submaximal exercise at a constant workload in humans, there is a clear core temperature threshold for hyperthermic hyperventilation and that the evoked hyperventilatory response is unaffected by altering initial core temperature.     

Effects of prolonged bed rest on cardiovascular oxygen transport during submaximal exercise in humans

The hypothesis was tested that prolonged bed rest impairs O₂ transport during exercise, which implies a lowering of cardiac output Q˙ _c and O₂ delivery (_aO₂). The following parameters were determined in five males at rest and at the steady-state of the 100-W exercise before (B) and after (A) 42-day bed rest with head-down tilt at −6°: O₂ consumption (V˙O₂), by a standard open-circuit method; Q˙ _c, by the pressure pulse contour method, heart rate ( f _c), stroke volume (Q _h), arterial O₂ saturation, blood haemoglobin concentration ([Hb]), arterial O₂ concentration (C _aO₂), and Q˙ _aO₂. The V˙O₂ was the same in A and in B, as was the resting f _c. The f _c at 100 W was higher in A than in B (+17.5%). The Q _h was markedly reduced (−27.7% and −22.2% at rest and 100 W, respectively). The Q˙ _c was lower in A than in B [−27.6% and −7.8% (NS) at rest and 100 W, respectively]. The C _aO₂ was lower in A than in B because of the reduction in [Hb]. Thus also Q˙ _aO₂ was lower in A than in B (−32.0% and −11.9% at rest and at 100 W, respectively). The present results would suggest a down-regulation of the O₂ transport system after bed rest. Accepted: 22 April 1998     

Independence of exercise hyperpnea and acidosis during high-intensity exercise in ponies

We investigated arterial PCO2 (PaCO2) and pH (pHa) responses in ponies during 6-min periods of high-intensity treadmill exercise. Seven normal, seven carotid body-denervated (2 wk-4 yr) (CBD), and five chronic (1-2 yr) lung (hilar nerve)-denervated (HND) ponies were studied during three levels of constant load exercise (7 mph-11%, 7 mph-16%, and 7 mph-22% grade). Mean pHa for each group of ponies became alkaline in the first 60 s (between 7.45 and 7.52) (P less than 0.05) at all work loads. At 6 min pHa was at or above rest at 7 mph-11%, moderately acidic at 7 mph-16% (7.32-7.35), and markedly acidic at 7 mph-22% (7.20-7.27) for all groups of ponies. Yet with no arterial acidosis at 7 mph 11%, normal ponies decreased PaCO2 below rest (delta PaCO2) by 5.9 Torr at 90 s and 7.8 Torr by 6 min of exercise (P less than 0.05). With a progressively more acid pHa at the two higher work loads in normal ponies, delta PaCO2 was 7.3 and 7.8 Torr by 90 s and 9.9 and 11.4 Torr by 6 min, respectively (P less than 0.05). CBD ponies became more hypocapnic than the normal group at 90 s (P less than 0.01) and tended to have greater delta PaCO2 at 6 min. The delta PaCO2 responses in normal and HND ponies were not significantly different (P greater than 0.1).(ABSTRACT TRUNCATED AT 250 WORDS)     

Control of exercise hyperpnea during hypercapnia in humans

Previous studies have yielded conflicting results on the ventilatory response to CO2 during muscular exercise. To obviate possible experimental errors contributing to such variability, we have examined the CO2-exercise interaction in terms of the ventilatory response to exercise under conditions of controlled hypercapnia. Eight healthy male volunteers underwent a sequence of 5-min incremental treadmill exercise runs from rest up to a maximum CO2 output (VCO2) of approximately 1.5 l . min-1 in four successive steps. The arterial PCO2 (PaCO2) at rest was stabilized at the control level or up to 14 Torr above control by adding 0-6% CO2 to the inspired air. Arterial isocapnia (SD = 1.2 Torr) throughout each exercise run was maintained by continual adjustment of the inspired PCO2. At all PaCO2 levels the response in total ventilation (VE) was linearly related to exercise VCO2. Hypercapnia resulted in corresponding increases in both the slope (S) and zero intercept (V0) of the VE-VCO2 curve; these being directly proportional to the rise in PaCO2 (means +/- SE: delta S/ delta PaCO2, 2.73 +/- 0.28 Torr-1; delta V0/ delta PaCO2, 1.67 +/- 0.18 l . min-1 . Torr-1). Thus the ventilatory response to concomitant hypercapnia and exercise was characterized by a synergistic (additive plus multiplicative) effect, suggesting a positive interaction between these stimuli. The increased exercise sensitivity in hypercapnia is qualitatively consistent with the hypothesis that VE is controlled to minimize the conflicting challenges due to chemical drive and the mechanical work of breathing (Poon, C. S. In: Modelling and Control of Breathing, New York: Elsevier, 1983, p. 189-196).     

Peripheral chemoreceptor function after carbonic anhydrase inhibition during moderate-intensity exercise.

The effect of carbonic anhydrase inhibition with acetazolamide (Acz, 10 mg/kg) on the ventilatory response to an abrupt switch into hyperoxia (end-tidal PO2 = 450 Torr) and hypoxia (end-tidal PO2 = 50 Torr) was examined in five male subjects [30 +/- 3 (SE) yr]. Subjects exercised at a work rate chosen to elicit an O2 uptake equivalent to 80% of the ventilatory threshold. Ventilation (VE) was measured breath by breath. Arterial oxyhemoglobin saturation (%SaO2) was determined by ear oximetry. After the switch into hyperoxia, VE remained unchanged from the steady-state exercise prehyperoxic value (60.6 +/- 6.5 l/min) during Acz. During control studies (Con), VE decreased from the prehyperoxic value (52.4 +/- 5.5 l/min) by approximately 20% (VE nadir = 42.4 +/- 6.3 l/min) within 20 s after the switch into hyperoxia. VE increased during Acz and Con after the switch into hypoxia; the hypoxic ventilatory response was significantly lower after Acz compared with Con [Acz, change (Delta) in VE/DeltaSaO2 = 1.54 +/- 0.10 l. min-1. SaO2-1; Con, DeltaVE/DeltaSaO2 = 2.22 +/- 0.28 l. min-1. SaO2-1]. The peripheral chemoreceptor contribution to the ventilatory drive after acute Acz-induced carbonic anhydrase inhibition is not apparent in the steady state of moderate-intensity exercise. However, Acz administration did not completely attenuate the peripheral chemoreceptor response to hypoxia.     

Prior heavy-intensity exercise speeds VO2 kinetics during moderate-intensity exercise in young adults.

The effect of prior heavy-intensity warm-up exercise on subsequent moderate-intensity phase 2 pulmonary O2 uptake kinetics (tauVO2) was examined in young adults exhibiting relatively fast (FK; tauVO2 < 30 s; n = 6) and slow (SK; tauVO2 > 30 s; n = 6) VO2 kinetics in moderate-intensity exercise without prior warm up. Subjects performed four repetitions of a moderate (Mod1)-heavy-moderate (Mod2) protocol on a cycle ergometer with work rates corresponding to 80% estimated lactate threshold (moderate intensity) and 50% difference between lactate threshold and peak VO2 (heavy intensity); each transition lasted 6 min, and each was preceded by 6 min of cycling at 20 W. VO2 and heart rate (HR) were measured breath-by-breath and beat-by-beat, respectively; concentration changes of muscle deoxyhemoglobin (HHb), oxyhemoglobin, and total hemoglobin were measured by near-infrared spectroscopy (Hamamatsu NIRO 300). tauVO2 was lower (P < 0.05) in Mod2 than in Mod1 in both FK (20 +/- 5 s vs. 26 +/- 5 s, respectively) and SK (30 +/- 8 s vs. 45 +/- 11 s, respectively); linear regression analysis showed a greater "speeding" of VO2 kinetics in subjects exhibiting a greater Mod1 tauVO2. HR, oxyhemoglobin, and total hemoglobin were elevated (P < 0.05) in Mod2 compared with Mod1. The delay before the increase in HHb was reduced (P <0.05) in Mod2, whereas the HHb mean response time was reduced (P <0.05) in FK (Mod2, 22 +/- 3 s; Mod1, 32 +/- 11 s) but not different in SK (Mod2, 36 +/- 13 s; Mod1, 34 +/- 15 s). We conclude that improved muscle perfusion in Mod2 may have contributed to the faster adaptation of VO2, especially in SK; however, a possible role for metabolic inertia in some subjects cannot be overlooked.     

Recruitment of single muscle fibers during submaximal cycling exercise.

In literature, an inconsistency exists in the submaximal exercise intensity at which type II fibers are activated. In the present study, the recruitment of type I and II fibers was investigated from the very beginning and throughout a 45-min cycle exercise at 75% of the maximal oxygen uptake, which corresponded to 38% of the maximal dynamic muscle force. Biopsies of the vastus lateralis muscle were taken from six subjects at rest and during the exercise, two at each time point. From the first biopsy single fibers were isolated and characterized as type I and II, and phosphocreatine-to-creatine (PCr/Cr) ratios and periodic acid-Schiff (PAS) stain intensities were measured. Cross sections were cut from the second biopsy, individual fibers were characterized as type I and II, and PAS stain intensities were measured. A decline in PCr/Cr ratio and in PAS stain intensity was used as indication of fiber recruitment. Within 1 min of exercise both type I and, although to a lesser extent, type II fibers were recruited. Furthermore, the PCr/Cr ratio revealed that the same proportion of fibers was recruited during the whole 45 min of exercise, indicating a rather constant recruitment. The PAS staining, however, proved inadequate to fully demonstrate fiber recruitment even after 45 min of exercise. We conclude that during cycling exercise a greater proportion of type II fibers is recruited than previously reported for isometric contractions, probably because of the dynamic character of the exercise. Furthermore, the PCr/Cr ratio method is more sensitive in determining fiber activation than the PAS stain intensity method.     

Substrate turnover and oxidation during moderate-intensity exercise following acute plasma volume expansion.

In previous work using prolonged, light cycle exercise, we were unable to demonstrate an effect of acute plasma volume (PV) expansion on glucose kinetics or substrate oxidation, despite a decline in whole-body lipolysis (Phillips et al., 1997). However, PV is known to decrease arterial O2 content. The purpose of this study was to examine whether substrate turnover and oxidation would be altered with heavier exercise where the challenge to O2 delivery is increased. Eight untrained males (VO2max = 3.52 +/- 0.12 l/min) twice performed 90 min of cycle ergometry at 62 % VO2peak, both prior to (CON) and following induced plasma volume expansion (Dextran [6 %] or Pentaspan [10 %]) (6.7 ml/kg) (PVX). Glucose and glycerol kinetics were determined with primed constant infusions of [6.6-(2)H2] glucose and [(2)H5] glycerol, respectively. PVX resulted in a 15.8 +/- 2.2 % increase (p < 0.05) in PV. Glucose and glycerol appearance (Ra) and utilization (Rd), although increasing progressively (p < 0.05) with exercise, were not different between conditions. Similarly, no differences in substrate oxidation, either fat or carbohydrate, were observed between the two conditions. Prolonged exercise resulted in an increase (p < 0.05) in plasma glucagon and a decrease (p < 0.05) in plasma insulin during both conditions. With PVX, the exercise-induced increase in glucagon was diminished (p < 0.05). We conclude that impairment in O2 content mediated by an elevated PV does not alter glucose, and glycerol kinetics or substrate oxidation even at moderate exercise intensity.     

Oxygen cost of exercise hyperpnea: measurement.

To quantitate the O2 cost of maximal exercise hyperpnea, we required eight healthy adult subjects to mimic, at rest, the important mechanical components of submaximal and maximal exercise hyperpnea. Expired minute ventilation (VE), transpulmonary and transdiaphragmatic (Pdi) pressures, and end-expiratory lung volume (EELV) were measured during exercise at 70 and 100% of maximal O2 uptake. At rest, subjects were given visual feedback of their exercise transpulmonary pressure-tidal volume loop (WV), breathing frequency, and EELV, which they mimicked repeatedly for 5 min per trial over several trials, while hypocapnia was prevented. The change in total body O2 uptake (VO2) was measured and presumed to represent the O2 cost of the hyperpnea. In 61 mimicking trials with VE of 115-167 l/min and WV of 124-544 J/min, VE, WV, duty cycle of the breath, and expiratory gastric pressure (Pga) integrated with respect to time (integral of Pga.dt/min) were not different from those observed during maximum exercise. integral of Pdi.dt/min was 14% less and EELV was 6% greater during maximum exercise than during mimicking. The O2 cost measurements within a subject were reproducible over 3-12 trials (coefficient of variation +/- 10% range 5-16%). The O2 costs of hyperpnea correlated highly and positively with VE and WV and less, but significantly, with integral of Pdi.dt and integral of Pga.dt. The O2 cost of VE rose out of proportion to the increasing hyperpnea, so that between 70 and 100% of maximal VO2 delta VO2/delta VE increased 40-60% (1.8 +/- 0.2 to 2.9 +/- 0.1 ml O2/l VE) as VE doubled.(ABSTRACT TRUNCATED AT 250 WORDS)     

Sweat ammonia excretion during submaximal cycling exercise

This study was undertaken to investigate whether part of the ammonia formed during muscular exercise was excreted with the sweat. Male medical students volunteered for the experiment. They exercised 30 min on a bicycle ergometer at 80 and 40% of the predetermined maximal O2 uptake (VO2max). Exercise at 80% VO2max was performed twice, at room temperature (20 degrees C) and in a cold room (0 degrees C), whereas exercise at 40% was performed only at room temperature (20 degrees C). Blood was collected from the antecubital vein immediately before and after exercise. Sweat was collected from the hypogastric region by use of gauze pads. It was shown that the plasma ammonia level was elevated after exercise at 80% VO2max and remained stable after exercise at 40% VO2max. The volume of sweat produced during exercise at 80% VO2max at 20 degrees C was 428 +/- 138 ml and at 0 degrees C 245 +/- 86 ml and during exercise at 40% VO2max was 183 +/- 69 ml. The ammonia concentration in the sweat after exercise at 80% VO2max at 20 degrees C was 7,140 mumol/l and at 0 degrees C 11,816 mumol/l. After exercise at 40% VO2max, it was 2,076 mumol/l. The total ammonia lost through the sweat during exercise at 80% VO2max was similar at both temperatures, despite the difference in the sweat volume (at 20 degrees C, 3,360 +/- 2,080 mumol; at 0 degrees C, 3,310 +/- 1,250 mumol). During exercise at 40% VO2max, it was 350 +/- 230 mumol. These results show that part of ammonia formed during exercise is lost with sweat. The amount lost increases with increased work rate and the plasma ammonia concentration.