Carl J. Hulston

Training with low muscle glycogen enhances fat metabolism in well-trained cyclists.

PURPOSE To determine the effects of training with low muscle glycogen on exercise performance, substrate metabolism, and skeletal muscle adaptation. METHODS Fourteen well-trained cyclists were pair-matched and randomly assigned to HIGH- or LOW-glycogen training groups. Subjects performed nine aerobic training (AT; 90 min at 70% VO2max) and nine high-intensity interval training sessions (HIT; 8 × 5-min efforts, 1-min recovery) during a 3-wk period. HIGH trained once daily, alternating between AT on day 1 and HIT the following day, whereas LOW trained twice every second day, first performing AT and then, 1 h later, performing HIT. Pretraining and posttraining measures were a resting muscle biopsy, metabolic measures during steady-state cycling, and a time trial. RESULTS Power output during HIT was 297 ± 8 W in LOW compared with 323 ± 9 W in HIGH (P < 0.05); however, time trial performance improved by ∼10% in both groups (P < 0.05). Fat oxidation during steady-state cycling increased after training in LOW (from 26 ± 2 to 34 ± 2 μmol·kg−¹·min−¹, P < 0.01). Plasma free fatty acid oxidation was similar before and after training in both groups, but muscle-derived triacylglycerol oxidation increased after training in LOW (from 16 ± 1 to 23 ± 1 μmol·kg−¹·min−¹, P < 0.05). Training with low muscle glycogen also increased β-hydroxyacyl-CoA-dehydrogenase protein content (P < 0.01). CONCLUSIONS Training with low muscle glycogen reduced training intensity and, in performance, was no more effective than training with high muscle glycogen. However, fat oxidation was increased after training with low muscle glycogen, which may have been due to the enhanced metabolic adaptations in skeletal muscle.

Acceleration versus heart rate for estimating energy expenditure and speed during locomotion in animals: Tests with an easy model species, Homo sapiens

An important element in the measurement of energy budgets of free-living animals is the estimation of energy costs during locomotion. Using humans as a particularly tractable model species, we conducted treadmill experiments to test the validity of tri-axial accelerometry loggers, designed for use with animals in the field, to estimate rate of oxygen consumption (VO2: an indirect measure of metabolic rate) and speed during locomotion. The predictive power of overall dynamic body acceleration (ODBA) obtained from loggers attached to different parts of the body was compared to that of heart rate (fH). When subject identity was included in the statistical analysis, ODBA was a good, though slightly poorer, predictor of VO2 and speed during locomotion on the flat (mean of two-part regressions: R2=0.91 and 0.91, from a logger placed on the neck) and VO2 during gradient walking (single regression: R2=0.77 from a logger placed on the upper back) than was fH (R2=0.96, 0.94, 0.86, respectively). For locomotion on the flat, ODBA was still a good predictor when subject identity was replaced by subject mass and height (morphometrics typically obtainable from animals in the field; R2=0.92 and 0.89) and a slightly better overall predictor than fH (R2=0.92 and 0.85). For gradient walking, ODBA predicted VO2 more accurately than before (R2=0.83) and considerably better than did fH (R2=0.77). ODBA and fH combined were the most powerful predictor of VO2 and speed during locomotion. However, ODBA alone appears to be a good predictor and suitable for use in the field in particular, given that accelerometry traces also provide information on the timing, frequency and duration of locomotion events, and also the gait being used.

Substrate metabolism and exercise performance with caffeine and carbohydrate intake.

PURPOSE 1) To investigate the effect of caffeine on exogenous carbohydrate (CHO) oxidation and glucose kinetics during exercise; and 2) to determine whether combined ingestion of caffeine and CHO enhanced cycling performance compared with CHO alone. METHODS Ten endurance-trained cyclists performed three experimental trials consisting of 105 min steady-state (SS) cycling at 62% VO2max followed by a time trial (TT) lasting approximately 45 min. During exercise, subjects ingested either of the following: a 6.4% glucose solution (GLU), a 6.4% glucose plus caffeine solution providing 5.3 mg kg(-1) of caffeine (GLU + CAF), or a placebo (PLA). Glucose solutions contained a trace amount of [U-C]glucose, and eight subjects received a primed continuous [6,6-H2]glucose infusion. RESULTS Peak exogenous CHO oxidation rates were not significantly different between GLU and GLU + CAF trials (52.6 +/- 2.7 and 49.1 +/- 2.1 micromol kg.min(-1), respectively). Rates of appearance (Ra) and disappearance (Rd) of glucose were significantly higher with CHO ingestion than PLA (P < 0.01) but were not significantly different between GLU and GLU + CAF trials. Performance times were 43.45 +/- 0.86, 45.45 +/- 1.07, and 47.40 +/- 1.30 min for GLU + CAF, GLU, and PLA, respectively. Therefore, GLU + CAF ingestion enhanced TT performance by 4.6% (P < 0.05) compared with GLU and 9% (P < 0.05) compared with PLA. CONCLUSION The coingestion of caffeine (5.3 mg kg(-1)) with CHO during exercise enhanced TT performance by 4.6% compared with CHO and 9.0% compared with water placebo. However, caffeine did not influence exogenous CHO oxidation or glucose kinetics during SS exercise.

Exogenous CHO oxidation with glucose plus fructose intake during exercise.

PURPOSE The purpose of the present study was to determine whether combined ingestion of moderate amounts of glucose plus fructose would result in higher rates of exogenous CHO oxidation compared with an isocaloric amount of glucose alone. METHODS Seven endurance-trained male cyclists performed three experimental trials consisting of 150 min of cycling at 65% VO(2max). Subjects ingested a CHO solution providing glucose (GLU) at an average rate of 0.8 g min(-1), glucose (0.54 g min(-1)) plus fructose (0.26 g min(-1)) (GLU + FRU), or plain water (WAT) during exercise. To quantify exogenous CHO oxidation, we prepared CHO solutions using corn-derived GLU and FRU, with a high natural abundance of 13C. RESULTS Peak exogenous CHO oxidation rates were not significantly different between GLU and GLU + FRU (0.60 +/- 0.06 and 0.57 +/- 0.06 g min(-1), respectively). Furthermore, average exogenous CHO oxidation rates during the final 90 min of exercise were not significantly different between GLU and GLU + FRU (0.58 +/- 0.05 and 0.56 +/- 0.06 g min(-1), respectively). CONCLUSION The present study demonstrates that ingesting moderate amounts of glucose plus fructose does not increase exogenous CHO oxidation above that of an isocaloric amount of glucose alone.

Probiotic supplementation prevents high-fat, overfeeding-induced insulin resistance in human subjects

The purpose of the present study was to determine whether probiotic supplementation (Lactobacillus casei Shirota (LcS)) prevents diet-induced insulin resistance in human subjects. A total of seventeen healthy subjects were randomised to either a probiotic (n 8) or a control (n 9) group. The probiotic group consumed a LcS-fermented milk drink twice daily for 4 weeks, whereas the control group received no supplementation. Subjects maintained their normal diet for the first 3 weeks of the study, after which they consumed a high-fat (65 % of energy), high-energy (50 % increase in energy intake) diet for 7 d. Whole-body insulin sensitivity was assessed by an oral glucose tolerance test conducted before and after overfeeding. Body mass increased by 0·6 (SE 0·2) kg in the control group (P< 0·05) and by 0·3 (SE 0·2) kg in the probiotic group (P>0·05). Fasting plasma glucose concentrations increased following 7 d of overeating (control group: 5·3 (SE 0·1) v. 5·6 (SE 0·2) mmol/l before and after overfeeding, respectively, P< 0·05), whereas fasting serum insulin concentrations were maintained in both groups. Glucose AUC values increased by 10 % (from 817 (SE 45) to 899 (SE 39) mmol/l per 120 min, P< 0·05) and whole-body insulin sensitivity decreased by 27 % (from 5·3 (SE 1·4) to 3·9 (SE 0·9), P< 0·05) in the control group, whereas normal insulin sensitivity was maintained in the probiotic group (4·4 (SE 0·8) and 4·5 (SE 0·9) before and after overeating, respectively (P>0·05). These results suggest that probiotic supplementation may be useful in the prevention of diet-induced metabolic diseases such as type 2 diabetes.

Postexercise Muscle Glycogen Synthesis with Combined Glucose and Fructose Ingestion

PURPOSE To evaluate the efficacy of using combined glucose and fructose (GF) ingestion as a means to stimulate short-term (4 h) postexercise muscle glycogen synthesis compared to glucose only (G). METHODS On two separate occasions, six endurance-trained men performed an exhaustive glycogen-depleting exercise bout followed by a 4-h recovery period. Muscle biopsy samples were obtained from the vastus lateralis muscle at 0, 1, and 4 h after exercise. Subjects ingested carbohydrate solutions containing G (90 g x h(-1)) or GF (G = 60 g x h(-1); F = 30 g x h(-1)) commencing immediately after exercise and every 30 min thereafter. RESULTS Immediate postexercise muscle glycogen concentrations were similar in both trials (G = 128 +/- 25 mmol x kg(-1) dry muscle (dm) vs GF = 112 +/- 16 mmol x kg(-1) dm; P > 0.05). Total glycogen storage during the 4-h recovery period was 176 +/- 33 and 155 +/- 31 mmol x kg(-1) dm for G and GF, respectively (G vs GF, P > 0.05). Hence, mean muscle glycogen synthesis rates during the 4-h recovery period did not differ between the two conditions (G = 44 +/- 8 mmol x kg(-1) dm x h(-1) vs GF = 39 +/- 8 mmol x kg(-1) dm x h(-1), P > 0.05). Plasma glucose and serum insulin responses during the recovery period were similar in both conditions, although plasma lactate concentrations were significantly elevated during GF compared to G (by approximately 0.8 mmol x L(-1), P < 0.05). CONCLUSIONS Glucose and glucose/fructose (2:1 ratio) solutions, ingested at a rate of 90 g x h(-1), are equally effective at restoring muscle glycogen in exercised muscles during the recovery from exhaustive exercise.

Erythropoietin down‐regulates proximal renal tubular reabsorption and causes a fall in glomerular filtration rate in humans

Non‐technical summary  Recombinant human erythropoietin (rHuEPO) decreases circulating levels of renin and aldosterone, two hormones regulating water and salt homeostasis, but the effect of rHuEPO on renal function is unknown. This study demonstrates that rHuEPO reduces the reabsorption of water and sodium in the proximal renal tubules and, probably by activation of the tubuloglomerular feedback mechanism, also causes a fall in glomerular filtration rate. Thus, the decrease in plasma concentrations of renin and aldosterone may be secondary to increased end‐proximal tubular delivery of water and sodium. In conclusion, the fall in proximal reabsorption together with a reduced filtered load and a decrease in angiotensin II and aldosterone‐dependent tubular reabsorption are expected to increase the oxygen tension in the renal tissue. This may serve to down‐regulate the endogenous renal synthesis of EPO in the presence of high levels of circulating rHuEPO.

Protein intake does not increase vastus lateralis muscle protein synthesis during cycling.

PURPOSE This study aimed to investigate the effect of protein ingestion on leg protein turnover and vastus lateralis muscle protein synthesis during bicycle exercise and recovery. METHODS Eight healthy males participated in two experiments in which they ingested either a carbohydrate solution (CHO) providing 0.49 g·kg(-1)·h(-1), or a carbohydrate and protein solution (CHO + P) providing 0.49 and 0.16 g·kg(-1)·h(-1), during 3 h of bicycle exercise and 3 h of recovery. Leg protein turnover was determined from stable isotope infusion (l-[ring-C6]phenylalanine), femoral-arterial venous blood sampling, and blood flow measurements. Muscle protein synthesis was calculated from the incorporation of l-[ring-C6]phenylalanine into protein. RESULTS Consuming protein during exercise increased leg protein synthesis and decreased net leg protein breakdown; however, protein ingestion did not increase protein synthesis within the highly active vastus lateralis muscle (0.029%·h(-1), ± 0.004%·h(-1), and 0.030%·h(-1), ± 0.003%·h(-1), in CHO and CHO + P, respectively; P = 0.88). In contrast, consuming protein, during exercise and recovery, increased postexercise vastus lateralis muscle protein synthesis by 51% ± 22% (0.070%·h(-1), ± 0.003%·h(-1), and 0.105%·h(-1), ± 0.013%·h(-1), in CHO and CHO+P, respectively; P < 0.01). Furthermore, leg protein net balance was negative during recovery with CHO intake, whereas positive leg protein net balance was achieved with CHO+P intake. CONCLUSIONS We conclude that consuming protein during prolonged bicycle exercise does not increase protein synthesis within highly active leg muscles. However, protein intake may have stimulated protein synthesis within less active leg muscles and/or other nonmuscle leg tissue. Finally, protein supplementation, during exercise and recovery, enhanced postexercise muscle protein synthesis and resulted in positive leg protein net balance.

Short-term, high-fat overfeeding impairs glycaemic control but does not alter gut hormone responses to a mixed meal tolerance test in healthy, normal-weight individuals

Obesity is undoubtedly caused by a chronic positive energy balance. However, the early metabolic and hormonal responses to overeating are poorly described. This study determined glycaemic control and selected gut hormone responses to nutrient intake before and after 7 d of high-fat overfeeding. Nine healthy individuals (five males, four females) performed a mixed meal tolerance test (MTT) before and after consuming a high-fat (65 %), high-energy (+50 %) diet for 7 d. Measurements of plasma glucose, NEFA, acylated ghrelin, glucagon-like peptide-1 (GLP-1), gastric inhibitory polypeptide (GIP) and serum insulin were taken before (fasting) and at 30-min intervals throughout the 180-min MTT (postprandial). Body mass increased by 0·79 (sem 0·14) kg after high-fat overfeeding (P<0·0001), and BMI increased by 0·27 (sem 0·05) kg/m2 (P=0·002). High-fat overfeeding also resulted in an 11·6 % increase in postprandial glucose AUC (P=0·007) and a 25·9 % increase in postprandial insulin AUC (P=0·005). Acylated ghrelin, GLP-1 and GIP responses to the MTT were all unaffected by the high-fat, high-energy diet. These findings demonstrate that even brief periods of overeating are sufficient to disrupt glycaemic control. However, as the postprandial orexigenic (ghrelin) and anorexigenic/insulintropic (GLP-1 and GIP) hormone responses were unaffected by the diet intervention, it appears that these hormones are resistant to short-term changes in energy balance, and that they do not play a role in the rapid reduction in glycaemic control.

A Single Day of Excessive Dietary Fat Intake Reduces Whole-Body Insulin Sensitivity: The Metabolic Consequence of Binge Eating

Consuming excessive amounts of energy as dietary fat for several days or weeks can impair glycemic control and reduce insulin sensitivity in healthy adults. However, individuals who demonstrate binge eating behavior overconsume for much shorter periods of time; the metabolic consequences of such behavior remain unknown. The aim of this study was to determine the effect of a single day of high-fat overfeeding on whole-body insulin sensitivity. Fifteen young, healthy adults underwent an oral glucose tolerance test before and after consuming a high-fat (68% of total energy), high-energy (78% greater than daily requirements) diet for one day. Fasting and postprandial plasma concentrations of glucose, insulin, non-esterified fatty acids, and triglyceride were measured and the Matsuda insulin sensitivity index was calculated. One day of high-fat overfeeding increased postprandial glucose area under the curve (AUC) by 17.1% (p < 0.0001) and insulin AUC by 16.4% (p = 0.007). Whole-body insulin sensitivity decreased by 28% (p = 0.001). In conclusion, a single day of high-fat, overfeeding impaired whole-body insulin sensitivity in young, healthy adults. This highlights the rapidity with which excessive consumption of calories through high-fat food can impair glucose metabolism, and suggests that acute binge eating may have immediate metabolic health consequences for the individual.