Biomedical subjects

J A Hawley

Publications and source records attributed to J A Hawley.

At least 19 recordsLinked to original sources

PubMed2006

Interspersed normoxia during live high, train low interventions reverses an early reduction in muscle Na+, K +ATPase activity in well-trained athletes.

Hypoxia and exercise each modulate muscle Na(+), K(+)ATPase activity. We investigated the effects on muscle Na(+), K(+)ATPase activity of only 5 nights of live high, train low hypoxia (LHTL), 20 nights consecutive (LHTLc) versus intermittent LHTL (LHTLi), and acute sprint exercise. Thirty-three athletes were assigned to control (CON, n = 11), 20-nights LHTLc (n = 12) or 20-nights LHTLi (4 x 5-nights LHTL interspersed with 2-nights CON, n = 10) groups. LHTLc and LHTLi slept at a simulated altitude of 2,650 m (F(I)O(2) 0.1627) and lived and trained by day under normoxic conditions; CON lived, trained, and slept in normoxia. A quadriceps muscle biopsy was taken at rest and immediately after standardised sprint exercise, before (Pre) and after 5-nights (d5) and 20-nights (Post) LHTL interventions and analysed for Na(+), K(+)ATPase maximal activity (3-O-MFPase) and content ([(3)H]-ouabain binding). After only 5-nights LHTLc, muscle 3-O-MFPase activity declined by 2% (P < 0.05). In LHTLc, 3-O-MFPase activity remained below Pre after 20 nights. In contrast, in LHTLi, this small initial decrease was reversed after 20 nights, with restoration of 3-O-MFPase activity to Pre-intervention levels. Plasma [K(+)] was unaltered by any LHTL. After acute sprint exercise 3-O-MFPase activity was reduced (12.9 +/- 4.0%, P < 0.05), but [(3)H]-ouabain binding was unchanged. In conclusion, maximal Na(+), K(+)ATPase activity declined after only 5-nights LHTL, but the inclusion of additional interspersed normoxic nights reversed this effect, despite athletes receiving the same amount of hypoxic exposure. There were no effects of consecutive or intermittent nightly LHTL on the acute decrease in Na(+), K(+)ATPase activity with sprint exercise effects or on plasma [K(+)] during exercise.

Adult↗

PubMed2006

Discordant gene expression in skeletal muscle and adipose tissue of patients with type 2 diabetes: effect of interleukin-6 infusion.

AIMS/HYPOTHESIS: We compared metabolic gene expression in adipose tissue and skeletal muscle from patients with type 2 diabetes and from well-matched healthy control subjects. We hypothesised that gene expression would be discordantly regulated when comparing the two groups. Our secondary aim was to determine the effect of Interleukin-6 (IL6) infusion on circulating adipokines and on gene expression in human adipose tissue. To do this we used real-time RT-PCR. METHODS: Both diabetic and control subjects underwent basal skeletal muscle and subcutaneous adipose tissue biopsies. A subset of these individuals underwent a 3-h infusion of recombinant human IL6 and had adipose tissue samples taken before and after infusion. RESULTS: The mRNA gene expression of suppressor of cytokine signalling (SOCS) 3, peroxisome proliferative activated receptor (PPAR) alpha/delta, PPAR gamma, coactivator 1, alpha (PPARGC1A), carnitine palmitoyltransferase 1B and solute carrier family 2 (facilitated glucose transporter), member 4 (formerly known as glucose transporter 4/GLUT4), was higher in adipose tissue, but lower in skeletal muscle of diabetic patients than in that of control subjects. In addition, uncoupling protein 1 (UCP1) gene was detected in the adipose tissue of some of the diabetic patients, but not in the control subjects. The following genes were increased by infusion of recombinant human IL6 in both groups: SOCS1/3, resistin, adiponectin, AMP-activated protein kinase-alpha-1 and PPARA. Plasma tumour necrosis factor alpha, adiponectin and resistin were all unaffected by IL6 infusion, but plasma resistin was lower in the diabetic subjects than in control subjects. CONCLUSIONS/INTERPRETATION: The observation that PPARGC1A and the PPARs were upregulated in the adipose tissue of type 2 diabetic patients, along with the finding that adipose tissue from some patients with type 2 diabetes can express UCP1 mRNA, suggests that in these patients white adipose tissue may move towards a brown adipose tissue phenotype.

Adiponectin↗

PubMed2006

The effect of exercise and training status on platelet activation: do cocoa polyphenols play a role?

Sedentary and trained men respond differently to the same intensity of exercise, this is probably related to their platelet reactivity and antioxidant capacity. There is growing interest in the utilization of antioxidant-rich plant extracts as dietary food supplements. The aim of this study was to investigate the effect of an acute bout of sub maximal exercise on platelet count and differential response of platelet activation in trained and sedentary subjects and to observe if cocoa polyphenols reverse the effect of exercise on platelet function. The practical significance of this study was that many sedentary people engage in occasional strenuous exercise that may predispose them to risk of heart disease. Fasting blood samples were collected from 16 male subjects, pre and post 1-h cycling exercise at 70% of maximal aerobic power (VO2max) before and after consumption of cocoa or placebo. Agonist stimulated citrated whole blood was utilized for measuring platelet aggregation, adenosine triphosphate (ATP) release and platelet activation. Baseline platelet count (221 +/- 33 x 10(9)/L) and ATP release (1.4 +/- 0.6 nmol) increased significantly (P < 0.05) after exercise in all subjects. Baseline platelet numbers in the trained were higher (P < 0.05) than in the sedentary (235 +/- 37 vs. 208 +/- 34 x 10(9)/L), where as platelet activation in trained was lower (P < 0.05) than sedentary (51 +/- 6 vs. 59 +/- 5%). Seven days of cocoa polyphenol supplementation had little effect on any of the parameters measured. We conclude that trained subjects show decreased activation of stimulated platelets when compared to the sedentary subjects and short-term cocoa polyphenol supplementation did not decrease platelet activity in response to exercise independent of prior training status.

Adolescent↗

PubMed2005

Sleep in athletes undertaking protocols of exposure to nocturnal simulated altitude at 2650 m.

A popular method to attempt to enhance performance is for athletes to sleep at natural or simulated moderate altitude (SMA) when training daily near sea level. Based on our previous observation of periodic breathing in athletes sleeping at SMA, we hypothesised that athletes' sleep quality would also suffer with hypoxia. Using two typical protocols of nocturnal SMA (2650 m), we examined the effect on the sleep physiology of 14 male endurance-trained athletes. The selected protocols were Consecutive (15 successive exposure nights) and Intermittent (3x 5 successive exposure nights, interspersed with 2 normoxic nights) and athletes were randomly assigned to follow either one. We monitored sleep for two successive nights under baseline conditions (B; normoxia, 600 m) and then at weekly intervals (nights 1, 8 and 15 (N1, N8 and N15, respectively)) of the protocols. Since there was no significant difference in response between the protocols being followed (based on n=7, for each group) we are unable to support a preference for either one, although the likelihood of a Type II error must be acknowledged. For all athletes (n=14), respiratory disturbance and arousal responses between B and N1, although large in magnitude, were highly individual and not statistically significant. However, SpO2 decreased at N1 versus B (p<0.001) and remained lower on N8 (p<0.001) and N15 (p<0.001), not returning to baseline level. Compared to B, arousals were more frequent on N8 (p=0.02) and N15 (p=0.01). The percent of rapid eye movement sleep (REM) increased from N1 to N8 (p=0.03) and N15 (p=0.01). Overall, sleeping at 2650 m causes sleep disturbance in susceptible athletes, yet there was some improvement in REM sleep over the study duration.

Adult↗

PubMed2004

Interleukin-6 and tumor necrosis factor-alpha are not increased in patients with Type 2 diabetes: evidence that plasma interleukin-6 is related to fat mass and not insulin responsiveness.

AIMS/HYPOTHESIS: Our aim was to examine the possible direct relationship of interleukin-6 and TNFalpha with insulin sensitivity in humans. METHODS: We carried out two series of euglycaemic-hyperinsulinaemic clamp experiments. In the first (CLAMP1), skeletal muscle mRNA expression and plasma concentrations of IL-6 and TNFalpha were examined in patients with Type 2 diabetes ( n=6), subjects matched for age (n=6), and young healthy (n=11) control subjects during a 120-min supra-physiological hyperinsulinaemic (40 mU.m(-2).min(-1)) euglycaemic clamp. In the second series of experiments (CLAMP2), patients with Type 2 diabetes (n=6) and subjects matched for age (n=7) were studied during a 240-min high-physiological hyperinsulinaemic (7 mU.m(-2).min(-1)) euglycaemic clamp, during which arterial and venous (femoral and subclavian) blood samples were measured for IL-6 and TNFalpha flux. RESULTS: In both experiments the glucose infusion rate in the patients was markedly lower than that in the other groups. In CLAMP1, basal skeletal muscle IL-6 and TNFalpha mRNA were the same in all groups. They were not affected by insulin and they were not related to the glucose infusion rate. In CLAMP2, neither cytokine was released from the arm or leg during insulin stimulation in either group. In both experiments plasma concentrations of these cytokines were similar in the patients and in the control subjects, although in CLAMP1 the young healthy control group had lower (p<0.05) plasma IL-6 concentrations. Using data from all subjects, a strong positive correlation (r=0.85; p<0.00001) was observed between basal plasma IL-6 and BMI. Conversely, a negative relationship (r=-0.345; p<0.05) was found between basal plasma TNFalpha and BMI, although this was not significant when corrected for BMI. When corrected for BMI, no relationship was observed between either basal plasma IL-6 or TNFalpha and GIR. CONCLUSIONS/INTERPRETATION: These data show that the increased circulating IL-6 concentrations seen in patients with Type 2 diabetes are strongly related to fat mass and not insulin responsiveness, and suggest that neither IL-6 nor TNFalpha are indicative of insulin resistance.

Adipose Tissue↗

PubMed2004

The effect of insulin and exercise on c-Cbl protein abundance and phosphorylation in insulin-resistant skeletal muscle in lean and obese Zucker rats.

AIMS/HYPOTHESIS: Recruitment of the protein c-Cbl to the insulin receptor (IR) and its tyrosine phosphorylation via a pathway that is independent from phosphatidylinositol 3'-kinase is necessary for insulin-stimulated GLUT4 translocation in 3T3-L1 adipocytes. The activation of this pathway by insulin or exercise has yet to be reported in skeletal muscle. METHODS: Lean and obese Zucker rats were randomly assigned to one of three treatment groups: (i). control, (ii). insulin-stimulated or (iii). acute, exhaustive exercise. Hind limb skeletal muscle was removed and the phosphorylation state of IR, Akt and c-Cbl measured. RESULTS: Insulin receptor phosphorylation was increased 12-fold after insulin stimulation ( p<0.0001) in lean rats and threefold in obese rats. Acute exercise had no effect on IR tyrosine phosphorylation. Similar results were found for serine phosphorylation of Akt. Exercise did not alter c-Cbl tyrosine phosphorylation in skeletal muscle of lean or obese rats. However, in contrast to previous studies in adipocytes, c-Cbl tyrosine phosphorylation was reduced after insulin treatment ( p<0.001). CONCLUSIONS/INTERPRETATION: We also found that c-Cbl associating protein expression is relatively low in skeletal muscle of Zucker rats compared to 3T3-L1 adipocytes and this could account for the reduced c-Cbl tyrosine phosphorylation after insulin treatment. Interestingly, basal levels of c-Cbl tyrosine phosphorylation were higher in skeletal muscle from insulin-resistant Zucker rats ( p<0.05), but the physiological relevance is not clear. We conclude that the regulation of c-Cbl phosphorylation in skeletal muscle differs from that previously reported in adipocytes.

Animals↗

PubMed2003

Intensified exercise training does not alter AMPK signaling in human skeletal muscle.

The AMP-activated protein kinase (AMPK) cascade has been linked to many of the acute effects of exercise on skeletal muscle substrate metabolism, as well as to some of the chronic training-induced adaptations. We determined the effect of 3 wk of intensified training (HIT; 7 sessions of 8 x 5 min at 85% Vo2 peak) in skeletal muscle from well-trained athletes on AMPK responsiveness to exercise. Rates of whole body substrate oxidation were determined during a 90-min steady-state ride (SS) pre- and post-HIT. Muscle metabolites and AMPK signaling were determined from biopsies taken at rest and immediately after exercise during the first and seventh HIT sessions, performed at the same (absolute) pre-HIT work rate. HIT decreased rates of whole body carbohydrate oxidation (P < 0.05) and increased rates of fat oxidation (P < 0.05) during SS. Resting muscle glycogen and its utilization during intense exercise were unaffected by HIT. However, HIT induced a twofold decrease in muscle [lactate] (P < 0.05) and resulted in tighter metabolic regulation, i.e., attenuation of the decrease in the PCr/(PCr + Cr) ratio and of the increase in [AMPfree]/ATP. Resting activities of AMPKalpha1 and -alpha2 were similar post-HIT, with the magnitude of the rise in response to exercise similar pre- and post-HIT. AMPK phosphorylation at Thr172 on both the alpha1 and alpha2 subunits increased in response to exercise, with the magnitude of this rise being similar post-HIT. Acetyl-coenzyme A carboxylase-beta phosphorylation was similar at rest and, despite HIT-induced increases in whole body rates of fat oxidation, did not increase post-HIT. Our results indicate that, in well-trained individuals, short-term HIT improves metabolic control but does not blunt AMPK signaling in response to intense exercise.

AMP-Activated Protein Kinases↗

PubMed2003

Disassociation of muscle triglyceride content and insulin sensitivity after exercise training in patients with Type 2 diabetes.

AIM/HYPOTHESIS: We determined the effect of exercise training on insulin sensitivity and muscle lipids (triglyceride [TG(m)] and long-chain fatty acyl CoA [LCACoA] concentration) in patients with Type 2 diabetes. METHODS: Seven patients with Type 2 diabetes and six healthy control subjects who were matched for age, BMI, % body fat and VO(2)peak participated in a 3 days per week training program for 8 weeks. Insulin sensitivity was determined pre- and post-training during a 120 min euglycaemic-hyperinsulinaemic clamp and muscle biopsies were obtained before and after each clamp. Oxidative enzyme activities [citrate synthase (CS), beta-hydroxy-acyl-CoA (beta-HAD)] and TG(m) were determined from basal muscle samples pre- and post training, while total LCACoA content was measured in samples obtained before and after insulin-stimulation, pre- and post training. RESULTS: The training-induced increase in VO(2)peak (approximately 20%, p<0.01) was similar in both groups. Compared with control subjects, insulin sensitivity was lower in the diabetic patients before and after training (approximately 60%; p<0.05), but was increased to the same extent in both groups with training (approximately 30%; p<0.01). TG(m) was increased in patients with Type 2 diabetes (170%; p<0.05) before, but was normalized to levels observed in control subjects after training. Basal LCACoA content was similar between groups and was unaltered by training. Insulin-stimulation had no detectable effect on LCACoA content. CS and beta-HAD activity were increased to the same extent in both groups in response to training ( p<0.001). CONCLUSION/INTERPRETATION: We conclude that the enhanced insulin sensitivity observed after short-term exercise training was associated with a marked decrease in TG(m) content in patients with Type 2 diabetes. However, despite the normalization of TG(m )to levels observed in healthy individuals, insulin resistance was not completely reversed in the diabetic patients.

3-Hydroxyacyl CoA Dehydrogenases↗

PubMed2003

Improved running economy in elite runners after 20 days of simulated moderate-altitude exposure.

To investigate the effect of altitude exposure on running economy (RE), 22 elite distance runners [maximal O(2) consumption (Vo(2)) 72.8 +/- 4.4 ml x kg(-1) x min(-1); training volume 128 +/- 27 km/wk], who were homogenous for maximal Vo(2) and training, were assigned to one of three groups: live high (simulated altitude of 2,000-3,100 m)-train low (LHTL; natural altitude of 600 m), live moderate-train moderate (LMTM; natural altitude of 1,500-2,000 m), or live low-train low (LLTL; natural altitude of 600 m) for a period of 20 days. RE was assessed during three submaximal treadmill runs at 14, 16, and 18 km/h before and at the completion of each intervention. Vo(2), minute ventilation (Ve), respiratory exchange ratio, heart rate, and blood lactate concentration were determined during the final 60 s of each run, whereas hemoglobin mass (Hb(mass)) was measured on a separate occasion. All testing was performed under normoxic conditions at approximately 600 m. Vo(2) (l/min) averaged across the three submaximal running speeds was 3.3% lower (P = 0.005) after LHTL compared with either LMTM or LLTL. Ve, respiratory exchange ratio, heart rate, and Hb(mass) were not significantly different after the three interventions. There was no evidence of an increase in lactate concentration after the LHTL intervention, suggesting that the lower aerobic cost of running was not attributable to an increased anaerobic energy contribution. Furthermore, the improved RE could not be explained by a decrease in Ve or by preferential use of carbohydrate as a metabolic substrate, nor was it related to any change in Hb(mass). We conclude that 20 days of LHTL at simulated altitude improved the RE of elite distance runners.

Acclimatization↗

PubMed2002

Interaction of exercise and diet on GLUT-4 protein and gene expression in Type I and Type II rat skeletal muscle.

We determined the interaction of exercise and diet on glucose transporter (GLUT-4) protein and mRNA expression in type I (soleus) and type II [extensor digitorum longus (EDL)] skeletal muscle. Forty-eight Sprague Dawley rats were randomly assigned to one of two dietary conditions: high-fat (FAT, n=24) or high-carbohydrate (CHO, n=24). Animals in each dietary condition were allocated to one of two groups: control (NT, n=8) or a group that performed 8 weeks of treadmill running (4 sessions week-1 of 1000 m @ 28 m min-1, RUN, n=16). Eight trained rats were killed after their final exercise bout for determination of GLUT-4 protein and mRNA expression: the remainder were killed 48 h after their last session for measurement of muscle glycogen and triacylglycerol concentration. GLUT-4 protein expression in NT rats was similar in both muscles after 8 weeks of either diet. However, there was a main effect of training such that GLUT-4 protein was increased in the soleus of rats fed with either diet (P < 0.05) and in the EDL in animals fed with CHO (P < 0.05). There was a significant diet-training interaction on GLUT-4 mRNA, such that expression was increased in both the soleus (100% upward arrowP < 0.05) and EDL (142% upward arrowP < 0.01) in CHO-fed animals. Trained rats fed with FAT decreased mRNA expression in the EDL ( downward arrow 45%, P < 0.05) but not the soleus ( downward arrow 14%, NS). We conclude that exercise training in CHO-fed rats increased both GLUT-4 protein and mRNA expression in type I and type II skeletal muscle. Despite lower GLUT-4 mRNA in muscles from fat-fed animals, exercise-induced increases in GLUT-4 protein were largely preserved, suggesting that control of GLUT-4 protein and gene expression are modified independently by exercise and diet.

Animals↗

PubMed2001

Carbohydrate ingestion attenuates the increase in plasma interleukin-6, but not skeletal muscle interleukin-6 mRNA, during exercise in humans.

1. The present study was undertaken to examine the effects of exercise and carbohydrate (CHO) ingestion on interleukin-6 (IL-6) gene expression in skeletal muscle and plasma IL-6 concentration. 2. Seven moderately trained men completed 60 min of exercise at a workload corresponding to each individual's lactate threshold on four randomised occasions. Two trials were conducted on a bicycle ergometer (Cyc) and two on a running treadmill (Run) either with (CHO) or without (Con) the ingestion of a CHO beverage throughout the exercise. Muscle biopsies were obtained from the vastus lateralis before and immediately after exercise and IL-6 gene expression in these samples was determined using real-time PCR. In addition, venous blood samples were collected at rest, and after 30 min during and at the cessation of exercise. These samples were analysed for plasma IL-6. 3. Irrespective of exercise mode or CHO ingestion, exercise resulted in a 21 +/- 4-fold increase (P < 0.01; main exercise effect) in IL-6 mRNA expression. In contrast, while the mode of exercise did not affect the exercise-induced increase in plasma IL-6, CHO ingestion blunted (P < 0.01) this response. 4. These data demonstrate that CHO ingestion attenuates the plasma IL-6 concentration during both cycling and running exercise. However, because IL-6 mRNA expression was unaffected by CHO ingestion, it is likely that the ingestion of CHO during exercise attenuates IL-6 production by tissues other than skeletal muscle.

Adult↗

PubMed2001

Moderate levels of hypohydration impairs bowling accuracy but not bowling velocity in skilled cricket players.

The effects of exercise-induced hypohydration on the motor skill performance of cricket bowling was examined in seven medium-fast bowlers who performed a random order of two experimental trials. Trials consisted of a bowling test (36 deliveries; PREBOWL) in a thermoneutral (16+/-2 degrees C) environment followed by approximately 1 hr of intermittent exercise in a heated environment (28+/-2 degrees C) and a further thermoneutral bowling test (36 deliveries; POSTBOWL). During one trial fluid intake was restricted (HYPO) whereas in the other, subjects were forced to drink in an effort to maintain euhydration (EUH). During all bowling tests subjects were provided with a fixed target on a cricket pitch and the line, length, and velocity of each delivery was determined. Pre-trial hydration status was confirmed by similar body mass (BM; 89.5+/-13.7 vs. 88.9+/-13.4 kg) and haemoglobin concentration (15.0+/-0.8 vs. 14.8+/-0.8 g.100 ml(-1) for EUH and HYPO, respectively). BM loss was greater in HYPO than EUH (2.48+/-0.58 vs. 0.46+/-0.45 kg). Accordingly, the resultant hypohydration was higher after HYPO than EUH (2.78+/-0.49 vs. 0.47+/-0.41% of BM). Whereas HYPO had no effect on bowling velocity (102+/-4 vs. 105+/-8 km x h(-1)), univariate analyses revealed independent differences for both bowling line (2.9+/-0.5 vs 3.4+/-0.6, P<0.01) and length (2.9+/-0.5 vs 3.4+/-0.6, P<0.01) of delivery after HYPO. We conclude that moderate (-2.8% of BM) exercise-induced hypohydration has minimal effect on maximal bowling velocity, but there is a detrimental effect on skilled motor performance in well-trained subjects.

Adult↗

PubMed2001

Pacing strategy in simulated cycle time-trials is based on perceived rather than actual distance.

This study determined the pacing strategies and performance responses of six well-trained cyclists/triathletes (peak O2 uptake 66.4+/-3.7 ml x kg(-1) x min(-1), mean+/-SD) during seven simulated time-trials (TT) conducted on a wind-braked cycle ergometer. All subjects first performed a 40 km familiarisation ride (TT1). They were then informed they would be riding a further four 40 km TT for the purpose of a reliability study. Instead, the actual distances ridden for the next three TT were a random order of 34 (TT2), 40 (TT3) and 46 km (TT4). The only feedback given to subjects during TT1-4 was the percentage distance of that ride remaining. During a further 40 km TT (TT5) subjects were allowed to view their heart rate (HR) responses throughout the ride. Despite the significantly different performance times across the three distances (47:23+/-4:23 vs 55:57+/-3:24 vs 65:41+/-3:56 min for the 34, 40 and 46 km respectively, P<0.001), average power output (296+/-48 vs 294+/-48 vs 286+/-40 W) and HR (173+/-11 vs 174+/-12 vs 173+/-12 beats x min(-1)) were similar. The true nature of the first part of the study was then revealed to subjects who subsequently completed an additional 34 km and 46 km TT TT6-7) in which the actual and perceived distance ridden was the same. Power output and HR responses were similar for both unknown (TT2 and TT6) and known (TT4 and TT7) rides for both distances: 296+/-48 vs 300+/-55 W and 173+/-11 vs 177+/-11 beats x min(-1) (34 km) and 286+/-40 vs 273+/-42 W and 173+/-12 vs 174+/-12 beats x min(-1) (46 km). In conclusion, well-trained cyclists rode at similar power outputs and HR during time trials they perceived to be the same distance, but which varied in actual distance from 34 to 46 km.

Adult↗

PubMed2001

Metabolic demands of intense aerobic interval training in competitive cyclists.

PURPOSE: To investigate the metabolic demands of a single session of intense aerobic interval training in highly trained competitive endurance cyclists. METHODS: Seven cyclists (peak O2 uptake [VO2 peak] 5.14 +/- 0.23 L x min(-1), mean +/-SD) performed 8 x 5 min work bouts at 86 +/- 2% of VO2 peak with 60-s recovery. Muscle biopsies were taken from the vastus lateralis immediately before and after the training session, whereas pulmonary gas exchange and venous blood were sampled at regular intervals throughout exercise. RESULTS: Muscle glycogen concentration decreased from 501 +/- 91 to 243 +/- 51 mmol x kg (-1) dry mass (P < 0.01). High rates of total carbohydrate oxidation were maintained throughout exercise (340 micromol.kg(-1).min(-1)), whereas fat oxidation increased from 16 +/- 8 during the first to 25 +/- 13 micromol x kg(-1) x min(-1) during the seventh work bout (P < 0.05). Blood lactate concentration remained between 5 and 6 mM throughout exercise, whereas muscle lactate increased from 6 +/- 1 at rest to 32 +/- 12 mmol x kg(-1) d.m. immediately after the training session (P < 0.01). Although muscle pH decreased from 7.09 +/- 0.06 at rest to 7.01 +/- 0.03 at the end of the session (P < 0.01), blood pH was similar after the first and seventh work bouts (7.34). Arterial oxygen saturation (% S(P)O2) fell to 95.6 +/- 1% during the first work bout and remained at 94% throughout exercise: the 60-s rest intervals were adequate to restore % S(P)O2) to 97%. CONCLUSION: Highly trained cyclists are able to sustain high steady state aerobic power outputs that are associated with high rates of glycogenolysis and total energy expenditure similar to those experienced during a 60-min competitive ride.

Acid-Base Equilibrium↗

PubMed2001

Effect of caffeine co-ingested with carbohydrate or fat on metabolism and performance in endurance-trained men.

We examined the effect of caffeine co-ingested with either carbohydrate or fat on metabolism and performance in eight endurance-trained subjects who performed a random order of four experimental trials consisting of 120 min of steady-state ergometer cycling at 70 % of maximal O(2) uptake (SS) followed by a time trial in which subjects completed a set amount of work (7 kJ kg-1) as quickly as possible. One hour before SS subjects ingested either 2.6 g kg-1 carbohydrate (CHO); 2.6 g kg-1 CHO + 6 mg kg-1 caffeine (CHO + CAF); 1.2 g kg-1 fat with 2000 U I.V. heparin (FAT); or 1.2 g kg-1 fat with 2000 U I.V. heparin + 6 mg kg-1 caffeine (FAT + CAF). The rate of carbohydrate oxidation was higher (micromol kg-1 min-1: CHO, 243 +/- 39 and CHO + CAF, 239 +/- 30 vs. FAT, 196 +/- 48 and FAT + CAF, 191 +/- 55; P < 0.05, values are means +/- S.D.) and the rate of fat oxidation lower (micromol kg-1 min-1: CHO, 19 +/- 8 and CHO + CAF, 22 +/- 7 vs. FAT, 35 +/- 19 and FAT + CAF, 37 +/- 17; P < 0.05) with carbohydrate than fat ingestion. Yet despite lower carbohydrate use with fat feeding, the time taken to complete the time trial was less after carbohydrate than after fat ingestion (min: CHO, 30.37 +/- 7.42 and CHO + CAF, 29.12 +/- 5.62 vs. FAT, 33.02 +/- 8.50 and FAT + CAF, 32.78 +/- 7.70; P < 0.05). We conclude that (1) caffeine co-ingested with either carbohydrate or fat meals has no additive effect on substrate utilization or exercise performance and (2) carbohydrate ingestion before exercise improves subsequent time trial performance compared with fat ingestion. Experimental Physiology (2001) 86.1, 137-144.

Adult↗

PubMed2001

Interaction of diet and training on endurance performance in rats.

We determined the interaction of diet and training on metabolic adaptations in skeletal muscle and liver, and the consequences of these adaptations for endurance. Eighty rats performed a baseline treadmill run to exhaustion at 16 m min(-1) (RUN1) and were then divided into two groups and given one of two diets: high carbohydrate (CHO) or high fat (FAT). Each dietary group was then divided into one of four subgroups: sedentary control that performed no training (NT); low-intensity running (8 m min(-1); LOW) and two groups who trained at their maximal voluntary running speed without electrical stimulation (28 m min(-1); VMAX). Training volume was identical for LOW and VMAX (1000 m session(-1)) and animals ran 4 days week(-1) for 8 weeks. To assess the interaction of the higher intensity exercise with diet, a second endurance test (RUN2) was undertaken after 6 weeks at either 16 m min(-1) or 28 m min(-1). The NT group ran for a longer duration (increase of 77 %) after FAT than CHO (239 +/- 28 vs. 135 +/- 30 min, P < 0.05) at 16 m min(-1). There were no differences in RUN2 for the LOW group when rats ran at 16 m min(-1) (454 +/- 86 vs. 427 +/- 75 min for CHO and FAT groups, respectively), but rats in the VMAX group fed FAT ran longer than rats fed CHO at 28 m min(-1) (100 +/- 28 vs. 58 +/- 11 min, respectively, P < 0.05). FAT increased the activities of the enzymes citrate synthase, beta-hydroxyacyl-CoA dehydrogenase and carnitine palmitoyl-transferase compared to CHO (P < 0.01), but there was no systematic effect of training. We conclude: (1) there was no additive effect of a high-fat diet on endurance performance when rats performed low-intensity training; (2) running performance at 28 m min(-1) was only enhanced by a high-fat diet after more intense training; (3) diet-induced and training-induced adaptations that increase exercise capacity may be under independent control. Experimental Physiology (2001) 86.4, 499-508.

3-Hydroxyacyl CoA Dehydrogenases↗

PubMed2001

High-fat diet versus habitual diet prior to carbohydrate loading: effects of exercise metabolism and cycling performance.

We examined the effects of a high-fat diet (HFD-CHO) versus a habitual diet, prior to carbohydrate (CHO)-loading on fuel metabolism and cycling time-trial (TT) performance. Five endurance-trained cyclists participated in two 14-day randomized cross-over trials during which subjects consumed either a HFD (> 65% MJ from fat) or their habitual diet (CTL) (30 +/- 5% MJ from fat) for 10 day, before ingesting a high-CHO diet (CHO-loading, CHO > 70% MJ) for 3 days. Trials consisted of a 150-min cycle at 70% of peak oxygen uptake (VáO2peak), followed immediately by a 20-km TT. One hour before each trial, cyclists ingested 400 ml of a 3.44% medium-chain triacylglycerol (MCT) solution, and during the trial, ingested 600 ml/hour of a 10% 14C-glucose + 3.44% MCT solution. The dietary treatments did not alter the subjects' weight, body fat, or lipid profile. There were also no changes in circulating glucose, lactate, free fatty acid (FFA), and b-hydroxybutyrate concentrations during exercise. However, mean serum glycerol concentrations were significantly higher (p < .01) in the HFD-CHO trial. The HFD-CHO diet increased total fat oxidation and reduced total CHO oxidation but did not alter plasma glucose oxidation during exercise. By contrast, the estimated rates of muscle glycogen and lactate oxidation were lower after the HFD-CHO diet. The HFD-CHO treatment was also associated with improved TT times (29.5 +/- 2.9 min vs. 30.9 +/- 3.4 min for HFD-CHO and CTL-CHO, p <.05). High-fat feeding for 10 days prior to CHO-loading was associated with an increased reliance on fat, a decreased reliance on muscle glycogen, and improved time trial performance after prolonged exercise.

Adult↗

PubMed2001

Short-term high-fat diet alters substrate utilization during exercise but not glucose tolerance in highly trained athletes.

We determined the effect of a high-fat diet and carbohydrate (CHO) restoration on substrate oxidation and glucose tolerance in 7 competitive ultra-endurance athletes (peak oxygen uptake [VO(2peak)] 68 +/- 1 ml x kg(-1) x min(-1); mean +/- SEM). For 6 days, subjects consumed a random order of a high-fat (69% fat; FAT-adapt) or a high-CHO (70% CHO; HCHO) diet, each followed by 1 day of a high-CHO diet. Treatments were separated by an 18-day wash out. Substrate oxidation was determined during submaximal cycling (20 min at 65% VO(2peak)) prior to and following the 6 day dietary interventions. Fat oxidation at baseline was not different between treatments (17.4 +/- 2.1 vs. 16.1 +/- 1.3 g x 20 min(-1) for FAT-adapt and HCHO, respectively) but increased 34% after 6 days of FAT-adapt (to 23.3 +/- 0.9 g x 20 min(-1), p < .05) and decreased 30% after HCHO (to 11.3 +/- 1.4 g x 20 min(-1), p < .05). Glucose tolerance, determined by the area under the plasma [glucose] versus time curve during an oral glucose tolerance (OGTT) test, was similar at baseline (545 +/- 21 vs. 520 +/- 28 mmol x L(-1) x 90 min(-1)), after 5-d of dietary intervention (563 +/- 26 vs. 520 +/-18 mmol x L(-1) x 90 min(-1)) and after 1 d of high-CHO (491 +/- 28 vs. 489 +/- 22 mmol x L(-1) x 90 min(-1) for FAT- adapt and HCHO, respectively). An index of whole-body insulin sensitivity ( S(I), 10000/divided by fasting [glucose] x fasting [insulin] x mean [glucose] during OGTT x mean [insulin] during OGTT) was similar at baseline (15 +/- 2 vs. 17 +/- 5 arbitrary units), after 5-d of dietary intervention (15 +/- 2 vs. 15 +/- 2) and after 24 h of CHO loading (17 +/- 3 vs. 18 +/- 2 for FAT- adapt and HCHO, respectively). We conclude that despite marked changes in the pattern of substrate oxidation during submaximal exercise, short-term adaptation to a high-fat diet does not alter whole-body glucose tolerance or an index of insulin sensitivity in highly-trained individuals.

Adult↗