Biomedical subjects

S M Phillips

Publications and source records attributed to S M Phillips.

At least 55 records · Page 3Linked to original sources

PubMed1997

Mixed muscle protein synthesis and breakdown after resistance exercise in humans.

Mixed muscle protein fractional synthesis rate (FSR) and fractional breakdown rate (FBR) were examined after an isolated bout of either concentric or eccentric resistance exercise. Subjects were eight untrained volunteers (4 males, 4 females). Mixed muscle protein FSR and FBR were determined using primed constant infusions of [2H5]phenylalanine and 15N-phenylalanine, respectively. Subjects were studied in the fasted state on four occasions: at rest and 3, 24, and 48 h after a resistance exercise bout. Exercise was eight sets of eight concentric or eccentric repetitions at 80% of each subject's concentric 1 repetition maximum. There was no significant difference between contraction types for either FSR, FBR, or net balance (FSR minus FBR). Exercise resulted in significant increases above rest in muscle FSR at all times: 3 h = 112%, 24 h = 65%, 48 h = 34% (P < 0.01). Muscle FBR was also increased by exercise at 3 h (31%; P < 0.05) and 24 h (18%; P < 0.05) postexercise but returned to resting levels by 48 h. Muscle net balance was significantly increased after exercise at all time points [(in %/h) rest = -0.0573 +/- 0.003 (SE), 3 h = -0.0298 +/- 0.003, 24 h = -0.0413 +/- 0.004, and 48 h = -0.0440 +/- 0.005], and was significantly different from zero at all time points (P < 0.05). There was also a significant correlation between FSR and FBR (r = 0.88, P < 0.001). We conclude that exercise resulted in an increase in muscle net protein balance that persisted for up to 48 h after the exercise bout and was unrelated to the type of muscle contraction performed.

Adult↗

PubMed1997

Effect of acute plasma volume expansion on substrate turnover during prolonged low-intensity exercise.

We investigated the effect of acute, graded increases in plasma volume (PV) by use of dextran on substrate turnover and oxidation during exercise. Eight untrained males [peak aerobic power (VO2peak) = 45.2 +/- 2.2 (SE) ml.kg-1.min-1] performed 2 h of cycle ergometry at 46 +/- 4% of VO2peak on three occasions in a randomized order: 0% PV expansion (CON) and after 14% (LOW) and 21% (HIGH) PV expansion. Glucose and glycerol turnover were measured using primed continuous infusions of [6,6-2H2]glucose and [2H5]glycerol, respectively. Glycerol rate of appearance (Ra) was taken as a relative index of whole body lipolysis. Increases in PV had no effect on glucose Ra or disappearance (Rd) either at rest or during exercise. At the onset of exercise, both glucose Ra and Rd increased approximately 100% (P < 0.01). Glucose Ra and Rd continued to increase with exercise duration (P < 0.05) so that, at 120 min of exercise, they were > 330% higher than at rest (P < 0.01). Glycerol Ra also increased with exercise duration (P < 0.05). Total lipolysis during exercise, calculated as the area under the glycerol Ra vs. time curve, was reduced during LOW vs. CON (P < 0.01). Further expansion of PV (HIGH) had no additional effect on whole body lipolysis. No effect of hypervolemia was observed on whole body fat or carbohydrate oxidation. These results indicate that acute PV expansion can alter whole body lipolysis, possibly via a reduction in catecholamine secretion.

Adult↗

PubMed1997

Reductions in sarcoplasmic reticulum Ca2+ ATPase activity in rat skeletal muscles of different fibre composition with ischemia and reperfusion.

To investigate the significance of fibre type and the duration of ischemia on changes in sarcoplasmic reticulum Ca2+ ATPase activity (SR Ca2+ ATPase), blood flow was occluded to the rat hind limb for 1, 2, or 3 h (n = 10 per group) and the soleus and extensor digitorum longus (EDL) muscles were examined following 2 h of reperfusion. When compared with the contralateral control muscles, calcium-dependent (total tau basal) SR Ca2+ ATPase activity in soleus was reduced (p < 0.05) to 75.9% by 1 h of ischemia and 2 h of reperfusion (13.1 +/- 0.6 vs. 9.95 +/- 0.85 mumol.mg-1 wet weight.min-1; X +/- SE) with no further reduction (p > 0.05) observed at either 2 h (9.75 +/- 0.57) or 3 h (9.40 +/- 0.64) of ischemia and 2 h of reperfusion. For the EDL muscles, SR Ca2+ ATPase activity with 2 h reperfusion was not reduced (p > 0.05) with 1 h of ischemia (80.4 +/- 3.0 vs. 70.7 +/- 2.9 mumol.mg-1 wet weight.min-1) but was reduced (66.7 +/- 2.3 mumol.mg-1 wet weight.min-1; p < 0.05) in the 2-h ischemia group, with further reductions (53.2 +/- 3.4 mumol.mg-1 wet weight.min-1; p < 0.05) in the 3-h ischemia group. No changes (p > 0.05) in basal or SR Mg2+ ATPase were found for either muscle group with ischemia and reperfusion, regardless of the duration of ischemia. When these results are interpreted in the context of the increases in SR Ca2+ ATPase activity that occur with ischemia, it appears that two components are involved in the reductions in SR Ca2+ ATPase activity noted during reperfusion: one that reduces the SR Ca2+ ATPase activity to below normal and one that simply reverses the ischemic-induced increase in SR Ca2+ ATPase activity. The former component appears to be more pronounced in the EDL muscle.

Animals↗

PubMed1997

Genetic alterations in incidentally diagnosed, transitional zone prostate cancer: a seven year follow-up.

PURPOSE: To investigate the frequency and prognostic significance of genetic alterations in incidentally diagnosed, transitional zone prostate cancer. MATERIALS AND METHODS: Twenty-six incidentally diagnosed, transitional zone cancers were examined by the PCR for genetic alterations on chromosomes 8p and 13q and by immunohistochemistry for alterations of the expression of the cell-cycle regulatory proteins RB1 and p53 and of the cell adhesion molecules E-cadherin and alpha-catenin. RESULTS: All of the tumors had at least one molecular abnormality (median 2.0 range 1 to 4). Allelic loss on 8p occurred in 37% and on 13q in 50% of informative tumors. Abnormal expression of pRb was found in 67%, of p53 in 33%, of E-cadherin in 36% and of alpha-catenin in 43%. In addition microsatellite instability was found in 23% of tumors. Only loss of expression of alpha-catenin was found to have prognostic importance. CONCLUSIONS: Genetic alterations were common, but, apart from alpha-catenin, did not appear to be related to tumor progression. The lack of prognostic significance is likely to be due to the multifocal nature of prostate cancer, but may also relate to qualitative differences between transitional zone and peripheral zone prostate cancers.

Aged↗

PubMed1997

Reduced muscle lactate during prolonged exercise following induced plasma volume expansion.

To examine the effects of a dilutional mediated decrease in arterial O2 content on muscle metabolic and substrate behaviour during exercise, plasma volume was acutely expanded by either 14% (LOW) or 21% (HIGH) using a 6% dextran solution dissolved in saline (Macrodex) and compared with a control (CON) condition. The exercise protocol, performed by eight untrained males (VO2max = 45.2 +/- 2.2 mL.kg-1.min-1, X +/- SE) and with the conditions randomized, was conducted for 120 min at 46 +/- 4% VO2max. The content of inosine monophosphate determined on muscle tissue extracted from the vastus lateralis increased (p < 0.05) by 120 min of exercise (0.119 +/- 0.02 vs 0.493 +/- 0.19 mmol/kg dry weight) in CON. No effect of either LOW or HIGH expansion of plasma volume was found. Similarly, phosphocreatine content (mmol/kg dry weight), although reduced (p < 0.05) with exercise, was not different between the conditions at either 3 min (61.9 +/- 3.5, 66.2 +/- 3.5, 64.3 +/- 2.1) or 120 min (52.5 +/- 6.3, 53.8 +/- 5.8, 59.4 +/- 5.5) of exercise. In contrast, both pyruvate and lactate were reduced (p < 0.05) by 3 min of exercise in both LOW and HIGH compared with CON. The reduction in these metabolites with plasma volume expansion was not accompanied by an alteration in glycogen depletion rates. Steady-state VO2 was unaffected by acute hypervolemia. These results suggest that moderate exercise following an approximate 10% reduction in arterial O2 content can be performed without increasing the imbalance between ATP production and utilization rates. Since high energy phosphate transfer and glycolysis appeared not to be increased, mitochondrial respiration was apparently preserved by mechanisms as yet undetermined.

Adult↗

PubMed1996

Allelic loss on chromosomes 8p, 22q and 18q (DCC) in human prostate cancer.

Previous studies have suggested the involvement of tumour-suppressor genes on chromosomes 8p, 22q and 18q (DCC) in prostate cancer. The aim of this study was to further characterize these regions. We investigated 20 polymorphic regions on the 3 chromosome arms in 43 cancers and 10 cases of benign prostatic hyperplasia (BPH). Allelic loss was observed in 72% of cancers on 8p, 16% on 22q and 24% at DCC. For BPH, loss was observed in 20% on 8p and in 12% at DCC. The low incidence of LOH on 22q implies that this locus has no significant role in prostate carcinogenesis. At DCC, although the overall incidence was low, tumours with LOH were mostly of high grade or had metastases, suggesting a role for this gene in prostate cancer progression. On chromosome 8p, 29% of cancers had deletions at the LPL locus on 8p22 and 60% had deletions within a region flanked by the markers D8S339 and ANKI on 8p 11.1-p21.1. Within this region, 2 distinct areas of allelic loss were observed, at one or both ANKI and D8S255, and in the region defined by the markers D8S259-D8S505. For the regions 8p22 and ANKI-D8S255, tumours with metastases had a greater frequency of LOH compared to non-metastasizing tumours, suggesting the presence of putative metastasis-suppressor genes in these regions.

Aged↗

PubMed1996

Progressive effect of endurance training on metabolic adaptations in working skeletal muscle.

We investigated the hypothesis that a program of prolonged endurance training, previously shown to decrease metabolic perturbations to acute exercise within 5 days of training, would result in greater metabolic adaptations after a longer training duration. Seven healthy male volunteers [O2 consumption = 3.52 +/- 0.20 (SE) l/min] engaged in a training program consisting of 2 h of cycle exercise at 59% of pretraining peak O2 consumption (VO2peak) 5-6 times/wk. Responses to a 90-min submaximal exercise challenge were assessed pretraining (PRE) and after 5 and 31 days of training. On the basis of biopsies obtained from the vastus lateralis muscle, it was found that, after 5 days of training, muscle lactate concentration, phosphocreatine (PCr) hydrolysis, and glycogen depletion were reduced vs. PRE (all P < 0.01). Further training (26 days) showed that, at 31 days, the reduction in PCr and the accumulation of muscle lactate was even less than at 5 days (P < 0.01). Muscle oxidative potential, estimated from the maximal activity of succinate dehydrogenase, was increased only after 31 days of training (+41%; P < 0.01). In addition, VO2peak was only increased (10%) by 31 days (P < 0.05). The results show that a period of short-term training results in many characteristic training adaptations but that these adaptations occurred before increases in mitochondrial potential. However, a further period of training resulted in further adaptations in muscle metabolism and muscle phosphorylation potential, which were linked to the increase in muscle mitochondrial capacity.

Adaptation, Physiological↗

PubMed1996

Increments in skeletal muscle GLUT-1 and GLUT-4 after endurance training in humans.

We investigated the time course of training-induced changes in the expression of GLUT-1 and GLUT-4 in human skeletal muscle. Seven healthy males trained for 2 h/day (approximately 60% pretraining VO2peak) for 31 days (31D). Muscle biopsies were obtained before training (PRE) and after 5 (5D) and 31 days (31D) of training. Training resulted in progressive increases in muscle GLUT-4 with increasing training duration (PRE<5D<31D; P<0.01). Muscle GLUT-1 content was also increased (P<0.05) after training; however, the increase was not observed until 31D (131%). Increases in muscle hexokinase (HK) activity were complete by 5D (P<0.01). Muscle malate dehydrogenase activity was not elevated after 5D of training but was increased (+35%; P<0.01) at 31D. Results from this study show that increases in both GLUT-4 and HK represent early training-induced adaptations to prolonged exercise training. As training progresses, further increases in GLUT-4, but not HK, occur in conjunction with an increase in muscle mitochondrial potential and GLUT-1.

Adult↗

PubMed1996

Effects of training duration on substrate turnover and oxidation during exercise.

Adaptations in fat and carbohydrates metabolism after a prolonged endurance training program were examined using stable isotope tracers of glucose ([6,6-2H2]glucose), glycerol ([2H5]glycerol), and palmitate ([2H2]palmitate). Active, but untrained, males exercised on a cycle for 2 h/day [60% pretraining peak O2 consumption (VO2peak) = 44.3 +/- 2.4 ml.kg-1.min-1] for a total of 31 days. Three cycle tests (90 min at 60% pretraining VO2peak) were administered before training (PRE) and after 5 (5D) and 31 (31D) days of training. Exercise increased the rate of glucose production (Ra) and utilization (Rd) as well as the rate of lipolysis (glycerol Ra) and free fatty acid turnover (FFARa/Rd). At 5D, training induced a 10% (P < 0.05) increase in total fat oxidation because of an increase in intramuscular triglyceride oxidation (+63%, P < 0.05) and a decreased glycogen oxidation (-16%, P < 0.05). At 31D, total fat oxidation during exercise increased a further 58% (P < 0.01). The pattern of fat utilization during exercise at 31D showed a reduced reliance on plasma FFA oxidation (FFA Rd) and a greater dependence on oxidation of intramuscular triglyceride, which increased more than twofold (P < 0.001). In addition, glucose Ra and Rd were reduced at all time points during exercise at 31D compared with PRE and 5D. We conclude that long-term training induces a progressive increase in fat utilization mediated by a greater oxidation of fats from intramuscular sources and a reduction in glucose oxidation. Initial changes are present as early as 5D and occur before increases in muscle maximal mitochondrial enzyme activity.

Adult↗

PubMed1996

Fluid and electrolyte hormonal responses to exercise and acute plasma volume expansion.

To investigate the effect of acute graded increases in plasma volume (PV) on fluid and regulatory hormone levels, eight untrained men (peak aerobic power 45.2 +/- 2.2 ml.kg-1.min-1) performed prolonged cycle exercise (46 +/- 4% maximal aerobic power on three occasions, namely, with no PV expansion (Con) and after 14% (Low) and 21% (High) expansions, respectively. The exercise plasma levels of aldosterone (Aldo), arginine vasopressin (AVP), and atrial natriuretic peptide (ANP) were all altered by acute PV increases. A pronounced blunting (P < 0.05) of the Aldo response during exercise was observed, the magnitude of which was directly related to the amount of hypervolemia (Con < Low < High). At 120 min of exercise, Aldo concentrations were 660 +/- 71, 490 +/- 85, and 365 +/- 78 pg/ml for Con, Low, and High conditions, respectively. In contrast, the lower AVP and the higher ANP observed during exercise appeared to be due to the effect of PV expansion on resting concentrations. Because osmolality did not vary among conditions, the results indicate that PV represents an important primary stimulus in the response of Aldo to exercise. The lower exercise blood concentrations of both epinephrine and norepinephrine observed with PV expansion would suggest that a lower sympathetic drive may be implicated at least in the lower Aldo responses.

Adult↗

PubMed1996

Faster femoral artery blood velocity kinetics at the onset of exercise following short-term training.

OBJECTIVE: The hypothesis that the adaptation to endurance exercise training included a faster increase in blood flow at the onset of exercise was tested in 12 healthy young men who endurance-trained (ET) 2 h/day, for 10 days at 65% VO2 peak on a cycle ergometer, and in 11 non-training control (C) subjects. METHODS: Blood flow was estimated from changes in femoral artery mean blood velocity (MBV) by pulsed Doppler. Beat-by-beat changes in cardiac output (CO) and mean arterial pressure (MAP) were obtained by impedance cardiography and a Finapres finger cuff, respectively. MBV, MAP and CO were measured at rest and during 5 min of dynamic knee extension exercise. Both legs worked alternately with 2 s raising and lowering a weight (15% maximal voluntary contraction) followed by 2 s rest while the other leg raised and lowered the weight. RESULTS: In the ET group the time to 63% (T63%) of the approximately exponential increase in MBV following 10 days of training (8.6 +/- 1.2 s, mean +/- s.e.) was significantly faster than the Day 0 response (14.2 +/- 2.1 s, P < 0.05). The T63% of femoral artery vascular conductance (VCfa) was also faster following 10 days of ET (9.4 +/- 0.9 s) versus Day 0 (16.0 +/- 2.5 s) (0.05). There was no change in the T63% of both MBV and VCfa for the C group. The kinetics of CO were not significantly affected by ET, but the amplitude of CO in the adaptive phase, and at steady state, were significantly greater (P < 0.05) at Day 10 compared to Day 0 for the ET group with no change in the C group. CONCLUSIONS: These data supported the hypothesis that endurance training resulted in faster adaptation of blood flow to exercising muscle, and further showed that this response occurred early in the training program.

Adult↗

PubMed1995

Loss of the chromosomal region 10q23-25 in prostate cancer.

Loss of the chromosomal region 10q23-25 is a frequent event in the progression of prostate adenocarcinoma. A candidate tumor suppressor gene from this region, Mxi1 at 10q25, has recently been shown to be mutated in a small number of prostate tumors. To more strictly define those regions of 10q loss that are likely to be involved in tumor advancement, we have constructed a detailed deletion map spanning 10q23-25 that incorporates Mxi1. Sixty-two % (23 of 37) of tumors analyzed exhibited some degree of 10q23-25 loss. Our data suggest the presence of a prostate tumor suppressor gene(s) near the 10q23-24 boundary, which was deleted in the overwhelming majority (22 of 23) of tumors showing loss. In contrast, specific loss of Mxi1, as opposed to loss of other 10q23-25 regions or of the entire region, was observed in only 1 of 23 tumors and was accompanied by loss of markers at the 10q23-24 boundary. Furthermore, we failed to detect any mutations in Mxi1 in those tumors showing Mxi1-associated marker loss by either single-strand conformation polymorphism analysis or direct DNA sequencing.

Aged↗

PubMed1995

Abnormalities of the RB1 and DCC tumor suppressor genes: uncommon in human pancreatic adenocarcinoma.

Evidence of RB1 allele loss was found in only 6% of pancreatic cancers, and we found no significant sequence abnormalities nor loss of RB protein expression in a panel of tumors and cell lines. Using reverse transcription-polymerase chain reaction and Southern blot analysis, we found no evidence for loss of DCC expression in pancreatic cancer cell lines, and allele loss only rarely in tumor biopsies. These findings suggest that abnormalities of RB1 and DCC are unlikely to play a major role in pancreatic carcinogenesis.

Adenocarcinoma↗

PubMed1995

Suppression of immunopathology in schistosomiasis by interleukin-2-targeted fusion toxin, DAB389IL-2. I. Studies of in vitro and in vivo efficacy.

Schistosomiasis causes pathology in an estimated 200 million individuals. Clinical disease is caused by a complex immunopathologic response to the parasite ova, which are deposited in the host tissues. This immunopathologic response is caused by T lymphocytes which express the high-affinity IL-2 receptor (IL-2R). DAB389IL-2 is a diphtheria toxin-IL-2 fusion toxin protein which functionally inactivates or kills cells which bear the high-affinity IL-2R. DAB389IL-2 has been used in man to suppress IL-2R-dependent immune reactivity. Therefore, we reasoned that DAB389IL-2 might suppress immunopathology in schistosomiasis. In these studies we assessed the in vitro and in vivo effects of DAB389IL-2 on the development of immunopathology in murine schistosomiasis. DAB389IL-2 suppressed IL-2, lectin mitogen (Con A), and soluble Schistosoma mansoni egg antigen-induced lymphocyte proliferation and in vitro granuloma formation. In addition, DA-B389IL-2 suppressed in vitro IL-2R expression. DA-B389IL-2 also suppressed the development of granulomas and collagen deposition in vivo in the livers of infected animals. Therefore, DAB389IL-2 may have potential for the targeted reduction of immunopathology due to schistosomiasis in man.

Animals↗

PubMed1995

Surgical treatment of intramedullary spinal cord neoplasia in two dogs.

An area of intramedullary spinal cord enlargement at the thoracolumbar junction was identified by myelography in each of two dogs. Exploratory laminectomy followed by durotomy and myelotomy permitted removal of an intramedullary neoplasm in each dog. In one animal the tumour was diagnosed to be an ependymoma, in the other the tumour had the characteristics of a nephroblastoma. Following surgery each dog recovered quickly to pre-operative status or better. In one dog there was long term resolution of neurological deficits, while the other was euthanased because of persistent faecal incontinence.

Animals↗

PubMed1995

Decreased glucose turnover after short-term training is unaccompanied by changes in muscle oxidative potential.

This study investigated the hypothesis that training-induced reductions in exercise blood glucose utilization can occur independently of increases in muscle mitochondrial potential. To induce a training adaptation, eight active participants (23 +/- 1 yr, 80.6 +/- 3.7 kg, mean +/- SE) with a maximal oxygen consumption (VO2max) of 45.5 +/- 2.4 ml.kg-1.min-1, cycled at 59% VO2max for 2 h per day for 10 consecutive days. Measurements of blood glucose appearance (Ra) and disappearance (Rd), using a primed continuous infusion of [6,6-2H2]glucose, were made during 90 min of cycle exercise (59% VO2max) performance before and after training. Training resulted in a 25% decrease (P < 0.01) in mean glucose Ra during exercise (43.0 +/- 3.7 to 34.4 +/- 2.8 mumol.kg-1.min-1). Since blood glucose concentration was not different between training conditions, glucose metabolic clearance rate was also depressed (P < 0.05). Exercise-induced glycogen depletion in vastus lateralis muscle was reduced (P < 0.05) with training. Calculation of carbohydrate and fat oxidation based on the respiratory exchange ratio supported a shift toward greater preference for fat. Because training did not elicit changes in the maximal activities of citrate synthase and malate dehydrogenase, two enzymes of the citric acid cycle, it would appear that increases in mitochondrial potential are not necessary for the adaptations that occurred.

Adult↗

PubMed1995

Carbohydrate loading and metabolism during exercise in men and women.

During endurance exercise at approximately 65% maximal O2 consumption, women oxidize more lipids, and therefore decrease carbohydrate and protein oxidation, compared with men (L.J. Tarnopolsky, M.A. Tarnopolsky, S.A. Atkinson, and J.D. MacDougall. J. Appl. Physiol. 68: 302-308, 1990; S.M. Phillips, S.A. Atkinson, M.A. Tarnopolsky, and J.D. MacDougall. J. Appl. Physiol. 75: 2134-2141, 1993). The main purpose of this study was to examine the ability of similarly trained male (n = 7) and female (n = 8) endurance athletes to increase muscle glycogen concentrations in response to an increase in dietary carbohydrate from 55-60 to 75% of energy intake for a period of 4 days (carbohydrate loading). In addition, we sought to examine whether gender differences existed in metabolism during submaximal endurance cycling at 75% peak O2 consumption (VO2 peak) for 60 min. The men increased muscle glycogen concentration by 41% in response to the dietary manipulation and had a corresponding increase in performance time during an 85% VO2 peak trial (45%), whereas the women did not increase glycogen concentration (0%) or performance time (5%). The women oxidized significantly more lipid and less carbohydrate and protein compared with the men during exercise at 75% VO2-peak. We conclude that women did not increase muscle glycogen in response to the 4-day regimen of carbohydrate loading described. In addition, these data support previous observations of greater lipid and lower carbohydrate and protein oxidation by women vs. men during submaximal endurance exercise.

Adult↗

PubMed1995

Increased clearance of lactate after short-term training in men.

A short-term training model previously shown to result in a tighter metabolic control in working muscle in the absence of an increase in mitochondrial potential was used to examine changes in lactate turnover. Lactate flux was studied before and after 10 days of cycle training [2 h/day at 59% maximal oxygen consumption (VO2max)] in untrained men [VO2max = 45.5 +/- 2.4 (SE) ml.kg-1.min-1). A primed constant infusion of L-[1-13C]lactate was used to examine lactate kinetics during a prolonged exercise protocol (90 min at 59% VO2max). Rate of appearance of lactate increased with exercise (P < 0.01), both pretraining (rest = 30.3 +/- 4.9 ml.kg-1.min-1, exercise = 115 +/- 14 ml.kg-1.min-1) and posttraining (rest = 28.4 +/- 4.7 ml.kg-1.min-1, exercise = 112 +/- 13 ml.kg-1.min-1). Despite a lower blood lactate concentration (P < 0.05) during exercise after training, there was no difference in the rate of appearance of lactate. Training increased (P < 0.05) the metabolic clearance rate of lactate during exercise from 36.8 +/- 4.8 to 51.4 +/- 6.8 ml.kg-1.min-1. These findings indicate that at least part of the lower exercising blood lactate observed after training is due to an increase in metabolic clearance rate. In addition, the lower intramuscular lactate levels suggest a decreased recruitment of glycolysis particularly early in exercise.

Adenosine Triphosphate↗