Search PubMed⌕ Search

Biomedical subjects

T E Graham

Publications and source records attributed to T E Graham.

At least 55 records · Page 3Linked to original sources

Tricarboxylic acid cycle intermediates in human muscle at rest and during prolonged cycling.

Previous studies have used the muscle concentration of citrate + malate + fumarate to estimate tricarboxylic acid (TCA) cycle pool size in humans [e.g., Am. J. Physiol. 259 (Cell Physiol. 28): C834-C841, 1990]. Our purpose was to quantify changes in individual TCA cycle intermediates (TCAI) and total pool size by measuring the concentrations of the eight TCAI in human muscle. Eight males cycled to exhaustion (Exh) at approximately 70% of their maximal oxygen uptake, and biopsies were obtained from the vastus lateralis at rest and during exercise. Succinyl-CoA was not consistently detectable, but the sum of the other seven TCAI was 1.23 +/- 0.04 mmol/kg dry wt at rest, 4.80 +/- 0.25 and 4.87 +/- 0.30 mmol/kg after 5 and 15 min of exercise, respectively, and 3.08 +/- 0.15 mmol/kg at Exh. Pool size during exercise was approximately 50% higher than that seen in rodent muscle after intense electrical stimulation (Eur. J. Biochem. 110: 371-377, 1980). Relative changes in individual TCAI were not uniform, and no one intermediate was "representative" of the changes in total pool size. We conclude that changes in specific intermediates or total pool size cannot be used as indicators of cycle flux and that the apparent species differences in total pool size may reflect differences in fiber type composition, recruitment pattern, or relative intensity of contraction.

Adult↗

Map turtle winter leech loads.

Adult common map turtles, Graptemys geographica (n = 243), were obtained in November 1995 from a hibernation site in the Lamoille River, Vermont. Of the 208 female turtles examined, 151 (72.6%) had at least 1 leech (Placobdella parasitica) attached and 10 of 35 males (28.6%) were similarly parasitized. Mean abundances were 1.49 (SD = 1.461, n = 208) for female turtles and 0.34 (SD = 0.591, n = 35) for males; the difference was significant (t = 4.558, df = 241, P < 0.001). Leech broods were found on 34 of 208 female turtles (16.3%) and 2 of 35 males (5.7%). One of the leeches was of record size (77.7 mm total length); another specimen measuring 64.4 mm had 153 brood-sized (x = 4.5 mm) young attached to its venter. Because of poor visibility and partial ice cover, only 7 turtles were recovered in March 1996. All of these turtles had attached leeches, and 4 turtles had broods of 9-52 young ranging in length from 4.58 to 5.78 mm. One Placobdella ornata was found in the March sample. Our results suggest that leeches of various size classes remain attached to hibernating adult map turtles throughout the winter.

Animals↗

Stimulation of muscle ammonia production during exercise following branched-chain amino acid supplementation in humans.

1. This study examined the effects of a large (308 mg kg-1) oral dose of branched-chain amino acids (BCAAs) on muscle amino acid and ammonia (NH3) metabolism during 90 min of dynamic knee extensor exercise (64 +/- 2% of maximum workload). 2. BCAA supplementation resulted in a 4-fold increase in the arterial BCAA level (from 373 to 1537 microM, P < 0.05) and a 1.5-fold increase in the intramuscular BCAA level (from 3.4 +/- 0.2 to 5.2 +/- 0.5 mmol (kg dry weight)-1, P < 0.05) by the onset of exercise. Over the 90 min exercise period, the exercising muscle removed a total of 7104 +/- 2572 mumol kg-1 of BCAAs. In contrast, in the control trial, there was a total release of 588 +/- 86 mumol kg-1 (P < 0.05) of BCAAs. 3. The total release of NH3 over the 90 min exercise period was 2889 +/- 317 mumol kg-1 (P < 0.05) in the control trial and 4223 +/- 552 mumol kg-1 (P < 0.05) in the BCAA trial. Similarly, the total release of alanine and glutamine was 1557 +/- 153 and 2213 +/- 270 mumol kg-1, respectively, for the control trial and 2771 +/- 178 and 3476 +/- 217 mumol kg-1, respectively, for the BCAA trial. 4. The lactate release and arterial lactate values were all consistently lower in the BCAA trial than in the control trial. The net production of lactate (intramuscular shifts + total release) was lower (P < 0.05) in the BCAA trial (49.9 +/- 11.4 mmol kg-1) than in the control trial (64.0 +/- 11.7 mmol kg-1). 5. It is concluded that: (1) the administration of BCAAs can greatly increase their concentration in plasma and subsequently their uptake by muscle during exercise, and (2) long-term exercise following BCAA administration results in significantly greater muscle NH3, alanine and glutamine production, as well as lower lactate production, than is observed during exercise without BCAA supplementation. These data strongly suggest that BCAAs are an important source of NH3 during submaximal exercise and that their contribution to NH3, alanine and glutamine production can be significantly altered by changes in BCAA availability.

Adult↗

Acute effects of caffeine ingestion at rest in humans with impaired epinephrine responses.

Caffeine ingestion has been demonstrated to increase circulating epinephrine (Epi) and norepinephrine (NE), elevate free fatty acids (FFAs), and alter heart rate, blood pressure (BP), and ventilation in humans. Whether these physiological responses are a result of caffeine acting through direct stimulation of specific tissues via adenosine receptors or secondary to Epi increases is not known. In the present experiment, six tetraplegics (level of spinal cord lesions C4-C6) were tested at rest for 3 h to investigate the effects of 6 mg/kg caffeine in capsule form on subjects with impaired Epi responses. Ventilatory, cardiovascular, metabolic, and hormonal data were collected every 15-20 min after caffeine ingestion. There were no significant (P > 0.05) increases in plasma Epi after caffeine ingestion [0.19 +/- 0.04 (SE) nM (preingestion); 0.20 +/- 0.04 nM (80 min postingestion)] or in plasma NE [0.53 +/- 0.16 nM (preingestion); 0.49 +/- 0.09 nM (80 min postingestion; P > 0.05)]. However, significant increases were found in serum FFAs [0.53 +/- 0.08 nM (preingestion); 1.03 +/- 0.20 mM (40 min postingestion; P < 0.05] and in glycerol. These concentrations remained elevated throughout the experiment. BP increased in the first hour postingestion. These data demonstrate that caffeine in physiological doses directly stimulates specific tissues, i.e., adipose and peripheral vascular tissue, and these effects are not secondary to increases in Epi after caffeine ingestion.

Adult↗

Metabolic catecholamine, and endurance responses to caffeine during intense exercise.

This study examined the possible effects of caffeine ingestion on muscle metabolism and endurance during brief intense exercise. We tested 14 subjects after they ingested placebo or caffeine (6 mg/kg) with an exercise protocol in which they cycled for 2 min, rested 6 min, cycled 2 min, rested 6 min, and then cycled to voluntary exhaustion. In each exercise the intensity required the subject's maximal O2 consumption. Eight subjects had muscle and venous blood samples taken before and after each exercise period. The caffeine ingestion resulted in a significant increase in endurance (4.12 +/- 0.36 and 4.93 +/- 0.60 min for placebo and caffeine, respectively) and resulted in a significant increase in plasma epinephrine concentration throughout the protocol but not in norepinephrine concentration. During the first two exercise bouts, the power and work output were not different; blood lactate concentrations were not affected significantly by caffeine ingestion, but during the exercise bouts muscle lactate concentration was significantly increased by caffeine. The net decrease in muscle glycogen was not different between treatments at any point in the protocol, and even at the time of fatigue there was at least 50% of the original glycogen concentration remaining. the data demonstrated that caffeine ingestion can be an effective ergogenic aid for exercise that is as brief as 4-6 min. However, the mechanism is not associated with muscle glycogen sparing. It is possible that caffeine is exerting actions directly on the active muscle and/or the neural processes that are involved in the activity.

Adult↗

Expression of the human 5-hydroxytryptamine1A receptor in Sf9 cells. Reconstitution of a coupled phenotype by co-expression of mammalian G protein subunits.

The possibility that Spodoptera frugiperda (Sf9) cells can provide an intact cell setting for reconstitution of the human 5-hydroxytryptamine1A (5-HT1A) receptor with mammalian G protein subunits was explored. The 5-HT1A receptor was found to assume an uncoupled phenotype when expressed alone in Sf9 cells at relatively high levels (5-34 pmol of receptor/mg of membrane protein), i.e. agonist-binding to the receptor was characterized by a relatively high Kd and an insensitivity to GTP. Co-expression of the receptor with members of the alpha i "family" together with various combinations of beta 1 and gamma subunits increased the affinity for agonists to that observed for the coupled form of receptor in mammalian cells, concomitant with conferrance of guanosine 5'-(beta,gamma-imino)triphosphate sensitivity. The agonists employed were [3H]8-hydroxy-N,N-dipropyl-2-aminotetralin ([3H]8-OH-DPAT) and [125I]R(+)-trans-8-hydroxy-2-[N-n-propyl-N-(3'-iodo-2'-propenyl) amino]tetralin ([125I]8-OH-PIPAT). The binding of an antagonist, [125I]4-(2'-methoxyphenyl)-1-[2'-[N-(2"- pyridinyl)-p-iodobenzamido]ethyl]piperazine ([125I]p-MPPI), was unaffected by co-expression of G protein subunits. Both alpha and beta gamma subunits were required for optimal coupling. No differences were evident among alpha i1, alpha i2, alpha i3, alpha o, and alpha z when expressed with beta 1 gamma 2 in this regard, nor among most permutations of beta 1 gamma subunits when expressed with alpha i1 (beta 1 gamma 2 approximately beta 1 gamma 3 approximately beta 1 gamma 5 > beta 1 gamma 1). Alpha s and alpha q expressed with beta 1 gamma 2 did not participate in coupling. These data support the conclusion that normal interactions between a mammalian receptor and a select array of G proteins can be established in intact Sf9 cells, and extend previous observations of 5-HT1A receptor coupling to G(o) and the pertussis toxin-insensitive G protein Gz.

8-Hydroxy-2-(di-n-propylamino)tetralin↗

Electrical stimulation and amino acid and ammonia metabolism in the canine gastrocnemius muscle.

This study examined the effects of electrical stimulation on amino acid and ammonia (NH3) metabolism in the isolated in situ canine gastrocnemius muscle preparation. Cut sciatic nerves of 10 mongrel dogs were stimulated at either 3 or 5 twitches/s (10 V, 0.2-ms duration) for 60 min. Muscle NH3 release dramatically increased on stimulation, and over 60 min the 3- and 5-Hz groups released 86.7 +/- 24.2 vs. 160.8 +/- 17.4 mumol.min-1.100 g-1 (P < 0.05) of NH3, respectively. Similarly, the intramuscular NH3 concentration was elevated (P < 0.05) above rest for both groups throughout stimulation, and it was higher (P < 0.05) at 5 min for the 5-Hz (82.7 +/- 2.4 mumol/100 g wet wt) than for the 3-Hz (67.4 +/- 7.4 mumol/100 g wet wt) group. Stimulation was also characterized by a large release of amino acids by both groups. The total amino acid release for 60 min was 415.4 +/- 64.9 vs. 193.3 +/- 56.2 (P < 0.05) mumol/100 g for the 3- and 5-Hz groups, respectively. However, there were no shifts or differences between groups in the intramuscular total amino acid pools. Glutamine (Gln) and alanine (Ala) dominated the amino acids released by muscle and together represented 35 and 46% of the total amino acids released over 60 min for the 3- and 5-Hz groups, respectively. The total release of Gln was higher (P < 0.05) for the 3-Hz (81.1 +/- 5.6 mumol/100 g) than for the 5-Hz (49.4 +/- 10.7 mumol/100 g) group, but there were no differences between groups in total Ala release. In contrast, both groups demonstrated an uptake of branched-chain amino acids (valine, isoleucine, and leucine) after 45 min of stimulation. These data show a stimulation-dependent production of NH3 and release of amino acid by the canine gastrocnemius muscle. These data further show that the degree of net muscle NH3 production is proportional to the frequency, whereas the degree of amino acid release is an inverse function of frequency.

Adenine Nucleotides↗

Training and muscle ammonia and amino acid metabolism in humans during prolonged exercise.

We studied the responses of NH3 and amino acids (AA) to prolonged exercise (3 h) in trained (Tr; n = 6) and untrained (Utr; n = 6) men. Each subject exercised the knee extensor muscles of one leg at 60% of maximum capacity. Thigh blood flow and femoral arteriovenous differences (0, 30, 60, 120, 150, and 180 min) as well as muscle biopsies (0, 120, and 180 min) were taken for NH3 and AA measurements. In both groups, muscle Glu decreased (P < 0.05) and Asp increased (P < 0.05), but the intramuscular AA pool, including the essential AA, remained constant despite a total AA efflux of 22.4 +/- 8.3 and 24.4 +/- 6.8 mmol/kg wet wt in Tr and Utr, respectively. Tr had greater (P < 0.05) muscle Tau, Phe, Ala, and Glu. Both groups had a large Glu uptake and effluxes of NH3, Gln, and Ala as well as essential AA. The latter implies that there was a net protein catabolism. The efflux of NH3 and Gln was much greater than that expected from AMP deamination, suggesting that deamination of AA was occurring. Many of the AA responses use Glu, and Tr maintained the intramuscular Glu pool at a higher concentration (P < 0.05), implying that they derived more Glu from protein catabolism and/or AA transaminations. Under these conditions, prolonged dynamic knee extensor exercise is associated with a large release of alpha-amino moieties both as NH3 and as Gln as well as a net protein catabolism; these responses are similar in Tr and Utr.

Adult↗

Metabolic, catecholamine, and exercise performance responses to various doses of caffeine.

This study examined the exercise responses of well-trained endurance athletes to various doses of caffeine to evaluate the impact of the drug on exercise metabolism and endurance capacity. Subjects (n = 8) withdrew from all dietary sources of caffeine for 48 h before each of four tests. One hour before exercise they ingested capsules of placebo or caffeine (3, 6, or 9 mg/kg), rested quietly, and then ran at 85% of maximal O2 consumption to voluntary exhaustion. Blood samples for methylxanthine, catecholamine, glucose, lactate, free fatty acid, and glycerol analyses were taken every 15 min. Plasma caffeine concentration increased with each dose (P < 0.05). Its major metabolite, paraxanthine, did not increase between the 6 and 9 mg/kg doses, suggesting that hepatic caffeine metabolism was saturated. Endurance was enhanced with both 3 and 6 mg/kg of caffeine (increases of 22 +/- 9 and 22 +/- 7%, respectively; both P < 0.05) over the placebo time of 49.4 +/- 4.2 min, whereas there was no significant effect with 9 mg/kg of caffeine. In contrast, plasma epinephrine was not increased with 3 mg/kg of caffeine but was greater with the higher doses (P < 0.05). Similarly only the highest dose of caffeine resulted in increases in glycerol and free fatty acids (P < 0.05). Thus the highest dose had the greatest effect on epinephrine and blood-borne metabolites yet had the least effect on performance. The lowest dose had little or no effect on epinephrine and metabolites but did have an ergogenic effect. These results are not compatible with the traditional theory that caffeine mediates its ergogenic effect via enhanced catecholamines.

Adult↗

Exercise causes branched-chain oxoacid dehydrogenase dephosphorylation but not AMP deaminase binding.

The responses of AMP deaminase (AMPD) and branched-chain oxoacid dehydrogenase (BCOAD) to moderate (70% maximal O2 consumption for 90 min) followed by intense (90% maximal O2 consumption to exhaustion) cycling exercise were evaluated in the active skeletal muscle of human subjects (n = 8). The exercise conditions invoke different energy demands and ammonia production rates. Active muscle and plasma ammonia concentrations continuously increased throughout moderate exercise in the absence of significant inosine 5-monophosphate accumulation. The free activity of AMPD decreased during moderate exercise (by approximately 25-35%), whereas myosin-bound activity did not change. BCOAD was significantly dephosphorylated (activated) at 5 min and was continuously dephosphorylated during moderate exercise (to a maximum of approximately 21%). Ammonia accumulation rate increased dramatically during the higher intensity exercise accompanied by inosine monophosphate accumulation of approximately 2 mmol/kg dry muscle. The higher intensity exercise caused no further changes in AMPD activity distribution or BCOAD dephosphorylation. Resting muscle percent bound AMPD was notably higher than values previously reported for rat muscle. Increases in percent bound AMPD during exercise were the result of decreases in the sum of free and bound activities and not increases in bound activity. The results of this study do not support a role for myosin binding in the activation of AMPD in human skeletal muscle.

3-Methyl-2-Oxobutanoate Dehydrogenase (Lipoamide)↗

Caffeine and exercise: metabolism and performance.

Caffeine ingestion prior to prolonged exercise delays fatigue. However, the mechanisms involved are very unclear. Caffeine is associated with elevated plasma epinephrine but the metabolic impact of this is uncertain. Glycogen sparing occurs in active muscle, at least in the first few minutes, but studies have generally failed to demonstrate enhanced fat metabolism. The demethylation of caffeine by the hepatic cytochrome P-450 oxygenases begins within minutes and dimethylxanthines (especially paraxanthine) are generated. These compounds appear in the plasma within an hour of caffeine ingestion and may have effects on tissues that have been attributed to caffeine and/or epinephrine. While the most widely supported theory is that caffeine and other methylxanthines are adenosine receptor antagonists, this action alone cannot explain all of the observed responses. Nevertheless, habituation to and withdrawal from caffeine are associated with up and down regulation of adenosine receptors. One study demonstrated marked differences in the effects of caffeine on the plasma concentrations of epinephrine and dimethylxanthines between caffeine users and nonusers. Caffeine is clearly a very active drug that has many effects on humans including increasing exercise endurance. This can be associated with muscle glycogen sparing and elevated plasma epinephrine, but the underlying mechanisms are unknown.

Caffeine↗

Branched-chain amino acids augment ammonia metabolism while attenuating protein breakdown during exercise.

In this study, five men exercised the knee extensor muscles of one leg for 60 min (71 +/- 2% maximal work capacity) with and without (control) an oral supplement (77 mg/kg) of branched-chain amino acids (BCAA). BCAA supplementation resulted in a doubling (P < 0.05) of the arterial BCAA levels before exercise (339 +/- 15 vs. 822 +/- 86 microM). During the 60 min of exercise, the total release of BCAA was 68 +/- 93 vs. 816 +/- 198 mumol/kg (P < 0.05) for the BCAA and control trials, respectively. The intramuscular BCAA concentrations were higher (P < 0.05) for the BCAA trial and remained higher (P < 0.05) throughout exercise. In both trials, substantial quantities of NH3 were released, and when NH3 production equivalent to IMP accumulation was subtracted the net NH3 production was 1,112 +/- 279 and 1,670 +/- 245 mumol/kg (P < 0.05) for the control and BCAA trials, respectively. In contrast, the release of the essential amino acids (EAA) was much lower for the BCAA than the control trial (P < 0.05). When the BCAA were subtracted from the EAA (EAA-BCAA), the total release of EAA minus BCAA was lower (P < 0.05) for the BCAA (531 +/- 70 mumol/kg) than the control (924 +/- 148 mumol/kg) trial. These data suggest that BCAA supplementation results in significantly greater muscle NH3 production during exercise. Furthermore, the increased intramuscular and arterial BCAA levels before and during exercise result in a suppression of endogenous muscle protein breakdown during exercise.

Adolescent↗

Impaired plasma FFA oxidation imposed by extreme CHO deficiency in contracting rat skeletal muscle.

The extent to which carbohydrate (CHO) availability affects free fatty acid (FFA) metabolism in contracting skeletal muscle is not well characterized. To study this question, rats were depleted of glycogen by swimming exercise and lard feeding 24 h before perfusion of their isolated hindquarters. After 20 min of preperfusion with a medium containing no glucose, palmitate (600 or 2,000 microM), and [1-14C]palmitate, flow was restricted to one hindlimb, which was electrically stimulated for 2 min to further deplete muscles of glycogen. After 2 min of recovery, glucose was added to the perfusate at final concentrations of 0, 6, or 20 mM, and after another 3 min muscles were stimulated for 30 min. At 6 and 2,000 microM palmitate, glucose uptake after 30 min of stimulation averaged 23.5 +/- 9.3 and 45.9 +/- 10.6 mumol.g-1.h-1 with 6 and 20 mM glucose, respectively. At 6 and 2,000 microM palmitate, palmitate uptake was lower (30-37%, P < 0.05) with 0 than with 6 or 20 mM glucose. At 600 microM palmitate, percent palmitate oxidation was higher (27%, P < 0.05) with 0 than with 6 or 20 mM glucose, resulting in similar total palmitate oxidation with the three glucose concentrations (0.28 +/- 0.01 mumol.g-1.h-1). At 2,000 microM palmitate, percent palmitate oxidation was not significantly different among glucose concentrations, resulting in a significantly lower rate of palmitate oxidation with 0 (0.62 +/- 0.18 mumol.g-1.h-1) than with 6 or 20 mM glucose (0.77 +/- 0.25 and 0.78 +/- 0.20 mumol.g-1.h-1, respectively).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Caffeine attenuates the exercise-induced increase in plasma [K+] in humans.

This study examined the dose-response effects of caffeine on plasma K+ balance during prolonged exercise. Two series of experiments were performed. In series A, 1 h after ingestion of 9 mg/kg dextrose (placebo) or 9 mg/kg caffeine, eight subjects cycled at 78% of peak O2 consumption until exhaustion; in series B, in four trials, 1 h after ingestion of 0, 3, 6, or 9 mg/kg caffeine, eight subjects ran on a treadmill at 85% of peak O2 consumption until exhaustion. Blood was sampled from an antecubital vein for analysis of hematocrit, plasma concentrations of epinephrine ([Epi]) and norepinephrine, and [K+]. The change in plasma volume was calculated from hematocrit. During exercise, there was a net addition of K+ to and a net loss of fluid from the plasma compartment. Caffeine had no effect on plasma volume and norepinephrine concentration during exercise. In series A and B 9 mg/kg caffeine and in series B 6 mg/kg caffeine resulted in a significant attenuation of the increase in plasma [K+] with exercise. In series A increases in plasma [Epi] were 1.4- to 2-fold greater during exercise with caffeine than with placebo. At exhaustion, plasma [Epi] was twofold higher with caffeine (10.1 +/- 2.3 nM) than with placebo (5.3 +/- 0.8 nM), whereas plasma [K+] was only 4.88 +/- 0.18 meq/l with caffeine compared with 5.37 +/- 0.14 meq/l with placebo. It is concluded that caffeine attenuates the increase in plasma [K+] during exercise by stimulation (via one of its metabolites or by increased [Epi]) of tissue Na-K pump activity.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

Branched-chain amino acid supplementation augments plasma ammonia responses during exercise in humans.

This study examined the effects of branched-chain amino acid (BCAA) supplementation on amino acid and ammonia (NH3) responses during prolonged exercise in humans. Seven men cycled for 60 min at 75% of maximal O2 uptake after 45 min of either placebo (dextrose, 77 mg/kg) or BCAA (leucine + isoleucine + valine, 77 mg/kg) supplementation. Plasma samples (antecubital vein) were collected at rest and during exercise and analyzed for plasma NH3 and amino acids, whole blood glucose and lactate, and serum free fatty acids and glycerol. After BCAA administration, plasma BCAA levels increased from 375 +/- 22 to 760 +/- 80 microM (P < 0.05) by the onset of exercise and remained elevated throughout the experiment. Plasma NH3 concentrations increased continually during exercise for both trials and were higher (P < 0.05) after BCAA supplementation than after placebo administration. The mean plasma NH3 increase from rest to 60 min was 79 +/- 10 and 53 +/- 4 microM for BCAA and placebo trials, respectively. Plasma alanine and glutamine concentrations were elevated (P < 0.05) during exercise for both treatments. However, only glutamine concentrations were greater (P < 0.05) for BCAA trial than for placebo trial during exercise. There were no significant differences between treatments for glucose, lactate, free fatty acids, and glycerol or any other plasma amino acid. These data suggest that increased BCAA availability before exercise, when initial muscle glycogen is normal, results in significantly greater plasma NH3 responses during exercise than does placebo administration.

Adenosine Monophosphate↗

Caffeine metabolism and epinephrine responses during exercise in users and nonusers.

This study compared the caffeine (CAF) metabolism and the catecholamine and metabolic responses of users and nonusers of caffeine after acute ingestion of caffeine (5 mg/kg) during 1 h of steady-state exercise (50% maximal oxygen consumption). Nonusers (n = 7) completed two exercise trials after ingesting either CAF (5 mg/kg) or placebo (PL). Users (n = 7) underwent three trials designed to control caffeine use and abstained from voluntary CAF intake for 18 days. After 4 days they had a PL trial and in the following 14 days they were given random 6 days of CAF (2 x 2.5 mg.kg-1 x day-1) or PL ingestion followed in each case on the 7th day by a CAF exercise trial identical to that of the nonusers. In nonusers CAF increased (P < 0.05) plasma epinephrine (EPI) concentration above PL values during exercise. Users did not exhibit any increased EPI with CAF, but the EPI response to exercise in all three trials was twofold greater than that of the nonusers' PL trial (P < 0.05). In all trials both groups had identical norepinephrine responses. The groups had similar plasma and urinary caffeine concentration, but plasma dimethylxanthines varied; the users had greater (P < 0.05) theophylline concentration, and the nonusers had a greater (P < 0.05) rise in paraxanthine (PX) concentration. The users and nonusers' plasma free fatty acids (FFA), glycerol and respiratory exchange ratio were similar after ingestion of CAF. Although PX may increase FFA in resting subjects, in this study PX concentrations in nonusers varied from that of the users, yet FFA data were similar.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗