Native Whey Induces Similar Post Exercise Muscle Anabolic Responses as Regular Whey, Despite Greater Leucinemia, in Elderly Individuals.

OBJECTIVE: Elderly muscle seems less sensitive to the anabolic stimulus of a meal. Changes in blood concentrations of leucine are suggested as one important trigger of the anabolic response in muscle. The aim of this study was to investigate whether native whey protein, containing high amounts of leucine, may be a more potent stimulator of muscle protein synthesis (MPS) in elderly than regular whey protein (WPC-80) or milk. DESIGN: Randomized controlled partial crossover. SETTING: Norwegian School of Sport Sciences. PARTICIPANTS: 21 healthy elderly men and women (≥70 years). INTERVENTION: Participants received either 20 g of WPC-80 and native whey (n = 11) on separate days in a crossover design, or milk (n = 10). Supplements were ingested immediately and two hours after a bout of lower body heavy-load resistance exercise. MEASUREMENTS: Blood samples and muscle biopsies were collected to measure blood concentrations of amino acids by gas-chromatography mass spectrometry (GCMS), phosphorylation of p70S6K, 4E-BP1 and eEF-2 by immunoblotting and mixed muscle fractional synthetic rate (FSR) by use of [2H5]phenylalanine-infusion, GCMS and isotope-ratio mass spectrometry. RESULTS: Native whey increased blood leucine concentrations more than WPC-80 (P < 0.05), but not p70S6K phosphorylation or mixed muscle FSR. Both whey supplements increased blood leucine concentrations (P < 0.01) and P70S6K phosphorylation more than milk (P = 0.014). Native whey reached higher mixed muscle FSR values than milk (P = 0.026) 1-3h after exercise. CONCLUSIONS: Despite greater increases in blood leucine concentrations than WPC-80 and milk, native whey was only superior to milk concerning increases in MPS and phosphorylation of P70S6K during a 5-hour post-exercise period in elderly individuals.

Vitamin C and E supplementation alters protein signalling after a strength training session, but not muscle growth during 10 weeks of training.

This study investigated the effects of vitamin C and E supplementation on acute responses and adaptations to strength training. Thirty-two recreationally strength-trained men and women were randomly allocated to receive a vitamin C and E supplement (1000 mg day(-1) and 235 mg day(-1), respectively), or a placebo, for 10 weeks. During this period the participants' training involved heavy-load resistance exercise four times per week. Muscle biopsies from m. vastus lateralis were collected, and 1 repetition maximum (1RM) and maximal isometric voluntary contraction force, body composition (dual-energy X-ray absorptiometry), and muscle cross-sectional area (magnetic resonance imaging) were measured before and after the intervention. Furthermore, the cellular responses to a single exercise session were assessed midway in the training period by measurements of muscle protein fractional synthetic rate and phosphorylation of several hypertrophic signalling proteins. Muscle biopsies were obtained from m. vastus lateralis twice before, and 100 and 150 min after, the exercise session (4 × 8RM, leg press and knee-extension). The supplementation did not affect the increase in muscle mass or the acute change in protein synthesis, but it hampered certain strength increases (biceps curl). Moreover, increased phosphorylation of p38 mitogen-activated protein kinase, Extracellular signal-regulated protein kinases 1 and 2 and p70S6 kinase after the exercise session was blunted by vitamin C and E supplementation. The total ubiquitination levels after the exercise session, however, were lower with vitamin C and E than placebo. We concluded that vitamin C and E supplementation interfered with the acute cellular response to heavy-load resistance exercise and demonstrated tentative long-term negative effects on adaptation to strength training.

No difference in the lipolytic response to beta-adrenoceptor stimulation in situ but a delayed increase in adipose tissue blood flow in moderately obese compared with lean men in the postexercise period.

This study was undertaken to determine the effect of previous exercise on adipose tissue responsiveness to beta-adrenoceptor stimulation and on adipose tissue blood flow (ATBF). Eight lean and 8 obese men (body mass index [BMI], 23.6 +/- 2.1 [SD] v 29.0 +/- 1.9 kg x m(-2)) were investigated with abdominal subcutaneous microdialysis and 133Xe clearance. A stepwise isoprenaline infusion (10(-8), 10(-7), and 10(-6) mol x L(-1)) was administered in situ in the microdialysis catheter before and 2 hours after a submaximal exercise bout (90 minutes of cycling at 55% of maximal O2 uptake). No differences in the response (increase in interstitial glycerol v preinfusion level) to isoprenaline infusions were found between the 2 groups. In both groups, there was no difference in the response to postexercise versus preexercise infusion. When the vasodilating agent hydralazine (0.125 g x L(-1)) was infused into the microdialysis catheter to control for the vascular effects of isoprenaline, an interaction effect between exercise and isoprenaline dose was found. Analyses showed an attenuated response to the high isoprenaline dose after exercise (lean, 251 +/- 42 [SE] micromol x L(-1); obese, 288 +/- 77 micromol x L(-1)) versus before exercise (lean, 352 +/- 62 micromol x L(-1), P = .045 v after; obese, 380 +/- 94 micromol x L(-1), P = .021 v after), indicating a desensitization of lipolysis to beta-adrenoceptor stimulation. ATBF and arterial plasma glycerol increased after exercise in both groups, but the increase was delayed in obese subjects. Arterial plasma insulin was higher in the obese versus lean subjects at all times, and decreased during recovery in both groups. In conclusion, abdominal subcutaneous adipose tissue responsiveness to beta-stimulation is not enhanced postexercise in lean and obese men, whereas previous exercise increases ATBF. Furthermore, the data suggest slower lipid mobilization postexercise and resistance to the antilipolytic effect of insulin in the obese.

Short-term effects of exercise on plasma very low density lipoproteins (VLDL) and fatty acids.

PURPOSE: In the fasted state the lipid fuels for muscle metabolism are free fatty acids (FFA) released either from intramuscular triglycerides (TG), plasma albumin, or TG in circulating very low density lipoproteins (VLDL). The purposes of this study were to determine the influence of acute exercise of moderate intensity on 1) plasma total concentration of TG and VLDL components, 2) the plasma concentration and distribution of individual albumin-bound long-chain FFA, and 3) lipid peroxidation as measured by thiobarbituric acid reactive substances (TBARS). METHODS: Eight healthy male subjects each participated in one exercise (EX) and one rest (RE) experiment. In EX the subjects exercised for 90 min at 58+/-5% (mean +/- SD) of maximal O2 uptake on a cycle ergometer followed by 4.5 h bedrest. RE followed the same protocol, but without exercise. RESULTS: In EX there was no immediate change in VLDL concentration during the exercise. After exercise there was a decrease in VLDL, VLDL-TG, -cholesterol, -protein and -phospholipids compared with those after RE. There was no change in percentage composition of VLDL as result of exercise. Total plasma FFA concentration increased appreciably during exercise and remained elevated for several hours postexercise. There was no correlation between the change in FFA concentration and VLDL-TG. There was a significant positive correlation between the exercise-related increments in the various long-chain FFA, but the effect varied so that the relative abundance of oleic acid increased and that of stearic and arachidonic acid decreased during exercise. Plasma TBARS concentration increased during the day in both experiments. CONCLUSION: The results indicate that there is a delay in the effect of an exercise bout on plasma VLDL and confirm that exercise affects various FFA in plasma differentially.

Effect of beta-adrenoceptor stimulation on oxygen consumption and triglyceride/fatty acid cycling after exercise.

The purpose of this study was to characterize the effects of prolonged beta-adrenoceptor stimulation on O2 uptake and triglyceride/fatty acid (TG/FA) cycling during rest with and without previous exercise. Eight men performed two exercise (90 min cycling at 56 +/- 3 (SD)% of maximal O2 uptake, followed by 4.5 h bed rest) and two rest-control experiments. In one rest and one exercise experiment a bolus dose (5 micrograms) of the beta-adrenoceptor agonist isoprenaline was given immediately after exercise, followed by a continuous infusion (20 ng kg-1 min-1), and at the corresponding time in the rest experiment. In the other experiments saline was given instead. The O2 uptake increased in the post-exercise period both with and without beta-stimulation. The total excess post-exercise oxygen consumption (EPOC) was not different between saline (8.1 +/- 1.8 (SE) L) and isoprenaline administration (10.8 +/- 1.8 L, P = 0.40). Also, the total accumulated increase in O2 uptake for the 4.5 h period after isoprenaline infusion was not different between the rest (12.5 +/- 2.0 L) and the exercise experiments (15.2 +/- 1.7 L, P = 0.40). The rate of TG/FA cycling increased after both exercise and isoprenaline treatment, but no interaction effect was found. In conclusion, the increases observed in O2 uptake and the rate of TG/FA cycling during beta-adrenoceptor stimulation were not increased by a previous exercise bout.

Adrenergic control of post-exercise metabolism.

After strenuous exercise there is a sustained increase in resting O2 consumption. The magnitude and duration of the excess post-exercise O2 consumption (EPOC) is a function of exercise intensity and exercise duration. Some of the mechanisms underlying the rapid EPOC component (<1 h) are well defined, while the mechanisms causing the prolonged EPOC component (>1 h) are not fully understood. It has been suggested that beta-adrenergic stimulation is of importance for the prolonged component. There is an increased level of plasma adrenaline and noradrenaline during exercise, and it is shown that catecholamines stimulate energy expenditure through beta-adrenoceptors. After exercise an increased fat oxidation and an increased rate of triglyceride fatty acid (TG-FA) cycling may account for a significant part of the prolonged EPOC component. These processes may be stimulated by catecholamines. However, the return of plasma concentration of catecholamines to resting levels after exercise is more rapid than the return of O2 uptake. But plasma concentration of catecholamines may be an insensitive indicator of sympathetic activity, since the clearance rate of catecholamines is high. Also, the sensitivity to catecholamines may be increased after exercise. A decreased post-exercise O2 uptake has been shown when beta-blockade is administered in dogs before the exercise bout. In a pilot study in humans, administration of beta-antagonist after exercise did not seem to change EPOC.

Effect of beta-adrenoceptor blockade on postexercise oxygen consumption and triglyceride/fatty acid cycling.

In the recovery period after strenuous exercise, there is increased O2 uptake, termed the excess postexercise O2 consumption (EPOC). One of the mechanisms suggested to explain EPOC is activation of the triglyceride/fatty acid (TG/FA) cycle by catecholamines. The purpose of this study was to determine the effect of selective beta1- and nonselective beta-adrenoceptor blockade on EPOC and the TG/FA cycle. Seven healthy young men each participated in three control and three exercise experiments in a randomized and balanced sequence. In the exercise experiments, subjects exercised for 90 minutes at 58% +/- 2% (mean +/- SD) of maximal O2 uptake on a cycle ergometer, followed by a 4.5-hour bedrest. The control experiments followed the same protocol, but without exercise. In one control and one exercise experiment, the selective beta1-adrenoceptor antagonist atenolol (0.062 mg.kg(-1) body weight) was administered intravenously immediately after the exercise (EXAT) and at the corresponding time in the rest-control experiment (REAT). In a second set of control and exercise experiments, the nonselective beta-adrenoceptor antagonist propranolol (0.15 mg.kg(-1) body weight) was administered (REPRO and EXPRO). In a third set of rest and exercise experiments, an injection of saline was given instead of beta-antagonist (RE and EX). TG/FA cycling was calculated by combining results obtained with a two-stage glycerol infusion and indirect calorimetry. O2 uptake was significantly increased above control levels throughout the recovery period after exercise with the nonselective beta-adrenoceptor antagonist, beta1-adrenoceptor antagonist, and saline. However, there was no difference between the time course or magnitude of EPOC in the three situations. After 4.5 hours of bedrest, the mean increase in O2 uptake was 8% to 9% in all three conditions. TG/FA cycling was increased after exercise, but no effects of beta-antagonists were observed. We conclude that EPOC and the rate of TG/FA cycling are not attenuated by selective beta1- or nonselective beta-adrenoceptor blockade after an acute prolonged exercise protocol.

Experiences of the 14C-ethanol technique for blood flow measurements in human subcutaneous adipose tissue.

We compared the 14C-ethanol technique and 133Xe-clearance for adipose tissue blood flow measurements in young healthy subjects before and after exercise on an ergometer bicycle. The results showed a decrease in outflow/inflow ratio of 14C-ethanol during the basal situation before the exercise, indicating an increased blood flow. However, there was a great range of values, and no correlation between the 14C-ethanol technique and 133Xe-clearance was found. Our data indicate that the 14C-ethanol technique can not be recommended in its current form.

Effect of beta-adrenoceptor blockade on post-exercise oxygen consumption.

In the recovery period after strenuous exercise, there is an increase in O2 uptake termed the excess post-exercise O2 consumption (EPOC), consisting of a rapid and a prolonged component. Mechanisms regulating the prolonged component of EPOC are not completely understood, but an effect of catecholamines has been suggested. The purpose of this study was to investigate the effect of beta-adrenoceptor blockade on EPOC. Six healthy young men were randomized to one control experiment and two exercise experiments, one with and one without nonselective beta-adrenoceptor blockade. In the exercise experiments, they exercised for 60 minutes at 78% +/- 3% (mean +/- SD) of maximal O2 uptake (VO2max) on a cycle ergometer followed by 6.5 hours' bedrest. In the beta-adrenoceptor blockade experiment, propranolol (0.1 mg.kg-1 body weight [BW]) was administered intravenously immediately after the exercise bout and again 3.5 hours after exercise. The control experiment was performed without exercise or beta-adrenoceptor blockade. EPOC was calculated as the difference in O2 uptake between the exercise and control experiments. A supplementary study on 15 subjects showed resting O2 uptake to be unaffected by propranolol. O2 uptake was significantly increased during the recovery period after exercise when no beta-adrenoceptor blocker was administered. After 6.5 hours of bedrest, the mean increase (+/- SE) in O2 uptake was 19 +/- 4 mL.min-1. In contrast, when propranolol was administered during recovery from exercise, O2 uptake was significantly increased for only the first 2 hours. Propranolol decreased total EPOC (+/- SE) by about one third, from 14.4 +/- 1.9 to 9.5 +/- 2.5 L.(ABSTRACT TRUNCATED AT 250 WORDS)