Added sugars and risk factors for obesity, diabetes and heart disease.

The effects of added sugars on various chronic conditions are highly controversial. Some investigators have argued that added sugars increase the risk of obesity, diabetes and cardiovascular disease. However, few randomized controlled trials are available to support these assertions. The literature is further complicated by animal studies, as well as studies which compare pure fructose to pure glucose (neither of which is consumed to any appreciable degree in the human diet) and studies where large doses of added sugars beyond normal levels of human consumption have been administered. Various scientific and public health organizations have offered disparate recommendations for upper limits of added sugar. In this article, we will review recent randomized controlled trials and prospective cohort studies. We conclude that the normal added sugars in the human diet (for example, sucrose, high-fructose corn syrup and isoglucose) when consumed within the normal range of normal human consumption or substituted isoenergetically for other carbohydrates, do not appear to cause a unique risk of obesity, diabetes or cardiovascular disease.

Adiposity attenuates muscle quality and the adaptive response to resistance exercise in non-obese, healthy adults.

BACKGROUND: Emerging data have revealed a negative association between adiposity and muscle quality (MQ). There is a lack of research to examine this interaction among young, healthy individuals, and to evaluate the contribution of adiposity to adaptation after resistance exercise (RE). OBJECTIVE: The purpose of this investigation was to examine the influence of subcutaneous adipose tissue (SAT) on muscle function among non-obese individuals before and after RE. DESIGN: Analyses included 634 non-obese (body mass index <30 kg m(-2)) subjects (253 males, 381 females; age=23.3 ± 5.2 years). SAT and muscle mass (magnetic resonance imaging-derived SAT and biceps muscle volume), isometric and dynamic biceps strength, and MQ (strength/muscle volume), were analyzed at baseline and after 12 weeks of unilateral RE. RESULTS: At baseline, SAT was independently associated with lower MQ for males (ß=-0.55; P<0.01) and females (ß=-0.45; P<0.01), controlling for body mass and age. Adaptation to RE revealed a significant negative association between SAT and changes for strength capacity (ß=-0.13; p=0.03) and MQ (ß=-0.14; P<0.01) among males. No attenuation was identified among females. Post-intervention SAT remained a negative predictor of MQ for males and females (ß=-0.47; P<0.01). CONCLUSIONS: The findings reveal that SAT is a negative predictor of MQ among non-obese, healthy adults, and that after 12 weeks of progressive RE this association was not ameliorated. Data suggest that SAT exerts a weak, negative influence on the adaptive response to strength and MQ among males.

Leptin responses to long-term cardiorespiratory exercise training without concomitant weight loss: a prospective study.

AIM: The aims of the present study were to examine 1) whether changes in circulating leptin levels occur in response to six months of aerobic exercise training (ET) without concomitant weight loss; 2) whether there is a different response with respect to gender; and 3) the relationship between age and leptin and whether this relationship has any impact on the response to ET without weight-loss. METHODS: Thirty-eight healthy, sedentary men and women (age 38.43+/-2.24, range 18-59 years) participated in 6 months of supervised, moderate intensity (ET) performed 4 days per week. Maintenance of usual dietary practices were encouraged to minimize weight-loss. Participants were evaluated for circulating fasting leptin, body mass, body fat percentage and maximal aerobic power (VO2max) prior to and after ET. RESULTS: There was no decrease in body weight or leptin concentration (17.69+/-2.67 vs 16.85+/-3.12 ng dL(-1)). Gender did not affect the response to exercise training. The bivariate correlation between leptin and age was not significant, but the relationship reached significance after controlling for body fat percentage and VO2max (r = -0.358, P < 0.05). Age did not affect the response of leptin concentration to ET. CONCLUSION: It is probable that changes in leptin concentration reported previously with ET may be attributable to concomitant weight loss, but age does not play a role in how leptin responds to ET.

Mechanisms of impaired exercise capacity in short duration experimental hyperthyroidism.

To investigate the mechanism of reduced exercise tolerance in hyperthyroidism, we characterized cardiovascular function and determinants of skeletal muscle metabolism in 18 healthy subjects aged 26 +/- 1 yr (mean +/- SE) before and after 2 wk of daily ingestion of 100 micrograms of triiodothyronine (T3). Resting oxygen uptake, heart rate, and cardiac output increased and heart rate and cardiac output at the same submaximal exercise intensity were higher in the hyperthyroid state (P less than 0.05). However, maximal oxygen uptake decreased after T3 administration (3.08 +/- 0.17 vs. 2.94 +/- 0.19 l/min; P less than 0.001) despite increased heart rate and cardiac output at maximal exercise (P less than 0.05). Plasma lactic acid concentration at an equivalent submaximal exercise intensity was elevated 25% (P less than 0.01) and the arteriovenous oxygen difference at maximal effort was reduced (P less than 0.05) in the hyperthyroid state. These effects were associated with a 21-37% decline in activities of oxidative (P less than 0.001) and glycolytic (P less than 0.05) enzymes in skeletal muscle and a 15% decrease in type IIA muscle fiber cross-sectional area (P less than 0.05). Lean body mass was reduced (P less than 0.001) and the rates of whole body leucine oxidation and protein breakdown were enhanced (P less than 0.05). Thus, exercise tolerance is impaired in short duration hyperthyroidism because of decreased skeletal muscle mass and oxidative capacity related to accelerated protein catabolism but cardiac pump function is not reduced.

The reliability of isokinetic and isometric leg strength measures among individuals with symptoms of mild osteoarthritis.

AIM: The aim of the study is to evaluate the test-retest reliability of measures of isokinetic and isometric leg strength and joint function among individuals exhibiting symptoms of mild osteoarthritis. Reliable procedures are needed to assess the effectiveness of an intervention on osteoarthritic symptoms. METHODS: Test-retest reliability of two leg strength protocols was assessed using the intraclass correlation coefficient (R). Testing was completed on two occasions separated by 7 days. Eighteen subjects (9 male and 9 female; 54.1+/-11 years) completed an isokinetic testing trial, which consisted of a set of 5 maximal repetitions of the quadriceps and hamstrings at 60 deg/s followed by a set of 15 maximal contractions at 180 deg/s with a 2-min rest between sets and an isometric testing trial, which consist of 3 maximal contractions of the quadriceps for 6 s with a 30-s rest between contractions at 30, 45, and 80 degrees of knee flexion for a total of 9 isometric contractions. A 90-s rest occurred between angles. RESULTS: Most of the isokinetic variables showed moderate to high intraclass reliability (ICC). Two of the calculated isokinetic variables (work fatigue at 180 degrees /s for extension and for flexion) showed low intraclass reliability (ICC=0.78, resp. ICC=0.6). All calculated ICC values of the isometric variables were moderate to high. CONCLUSIONS: Test-retest reliability of isokinetic and isometric leg strength was high, allowing the intervention protocol to monitor changes in leg strength and joint function among those exhibiting symptoms of mild osteoarthritis.

Short-term growth hormone treatment does not increase muscle protein synthesis in experienced weight lifters.

The purpose of this study was to determine whether recombinant human growth hormone (GH) administration enhances muscle protein anabolism in experienced weight lifters. The fractional rate of skeletal muscle protein synthesis and the whole body rate of protein breakdown were determined during a constant intravenous infusion of [13C]leucine in 7 young (23 +/- 2 yr; 86.2 +/- 4.6 kg) healthy experienced male weight lifters before and at the end of 14 days of subcutaneous GH administration (40 microgram.kg-1 x day-1). GH administration increased fasting serum insulin-like growth factor-I (from 224 +/- 20 to 589 +/- 80 ng/ml, P = 0.002) but did not increase the fractional rate of muscle protein synthesis (from 0.034 +/- 0.004 to 0.034 +/- 0.002%/h) or reduce the rate of whole body protein breakdown (from 103 +/- 4 to 108 +/- 5 mumol.kg-1 x h-1). These findings suggest that short-term GH treatment does not increase the rate of muscle protein synthesis or reduce the rate of whole body protein breakdown, metabolic alterations that would promote muscle protein anabolism in experienced weight lifters attempting to further increase muscle mass.

Effect of a single exercise bout on serum triglycerides in untrained men.

Seven sedentary men (mean age, 22.5 yrs) were studied during and after treadmill exercise at 65% VO2max to determine the effect of a typical acute exercise bout on serum triglycerides. A venous blood sample was drawn immediately prior to a 30 minute treadmill exercise session, 5 min, 24 and 48 h after exercise. There were no significant differences in triglycerides and total cholesterol between the selected blood sampling points. Total HDL-C was higher (p < 0.05) at 5 min (44.0 SE +/- 3.0 mg.dl-1) than pre-exercise (41.5, SE +/- 3.0 mg.dl-1). Total HDL-C did not differ between pre-exercise and both 24 and 48 h. Unlike prolonged heavy exercise, a typical exercise session does not bring about alterations in serum triglycerides.

Leptin and leptin receptor genetic variants associate with habitual physical activity and the arm body composition response to resistance training.

PURPOSE: We investigated the influence of Leptin (LEP) and leptin receptor (LEPR) SNPs on habitual physical activity (PA) and body composition response to a unilateral, upper body resistance training (RT) program. METHODS: European-derived American volunteers (men=111, women=131, 23.4 ± 5.4 yr, 24.4 ± 4.6 kg·m(-2)) were genotyped for LEP 19 G>A (rs2167270), and LEPR 326 A>G (rs1137100), 668 A>G (rs1137101), 3057 G>A (rs1805096), and 1968 G>C (rs8179183). They completed the Paffenbarger PA Questionnaire. Arm muscle and subcutaneous fat volumes were measured before and after 12 wk of supervised RT with MRI. Multivariate and repeated measures ANCOVA tested differences among phenotypes by genotype and gender with age and body mass index as covariates. RESULTS: Adults with the LEP 19 GG genotype reported more kcal/wk in vigorous intensity PA (1273.3 ± 176.8, p=0.017) and sports/recreation (1922.8 ± 226.0, p<0.04) than A allele carriers (718.0 ± 147.2, 1328.6 ± 188.2, respectively). Those with the LEP 19 GG genotype spent more h/wk in light intensity PA (39.7 ± 1.6) than A allele carriers (35.0 ± 1.4, p=0.03). In response to RT, adults with the LEPR 668 G allele gained greater arm muscle volume (67,687.05 ± 3186.7 vs. 52,321.87 ± 5125.05 mm(3), p=0.01) and subcutaneous fat volume (10,599.89 ± 3683.57 vs. -5224.73 ± 5923.98 mm(3), p=0.02) than adults with the LEPR 668 AA genotype, respectively. CONCLUSION: LEP19 G>A and LEPR 668 A>G associated with habitual PA and the body composition response to RT. These LEP and LEPR SNPs are located in coding exons likely influencing LEP and LEPR function. Further investigation is needed to confirm our findings and establish mechanisms for LEP and LEPR genotype and PA and body composition associations we observed.

Beta-endorphin immunoreactivity during high-intensity exercise with and without opiate blockade.

Nine highly fit men [mean (SE) maximum oxygen uptake, VO2max: 63.9 (1.7) ml x kg(-1) x min(-1); age 27.6 (1.6) years] were studied during two treadmill exercise trials to determine plasma beta-endorphin immunoreactivity during intense exercise (80% VO2max). A double-blind experimental design was used, and subjects performed the two exercise trials in counterbalanced order. Exercise trials were 30 min in duration and were conducted 7 days apart. One exercise trial was undertaken following administration of naloxone (1.2 3 cm3) and the other after receiving a placebo (0.9% NaCl saline; 3 cm3). Prior to each experimental trial, a flexible catheter was placed into an antecubital vein and baseline blood samples were collected. Thereafter, each subject received either a naloxone or placebo bolus injection. Blood samples were also collected after 10, 20 and 30 min of continuous exercise. beta-Endorphin was higher (P < 0.05) during exercise when compared to pre-exercise in both trials. However, no statistically significant difference was found (P> 0.05) between exercise time points within either experimental trial. beta-endorphin immunoreactivity was greater (P < 0.05) in the naloxone than in the placebo trial during each exercise sampling time point [10 min: 63.7 (3.9) pg x ml(-1) vs 78.7 (3.8) pg x ml(-1); 20 min: 68.7 (4.1) pg x ml(-1) vs (4.3) pg x ml(-1); 30 min: 71.0 (4.3) pg x ml(-1) vs 82.5(3.2) pg x ml(-1)]. These data suggest that intense exer induces significant increases in beta-endorphin that are maintained over time during steady-rate exercise. Exercise and naloxone had an interactive effect on beta-endorphin release that warrants further investigation.

Exercise induces human lipoprotein lipase gene expression in skeletal muscle but not adipose tissue.

Lipoprotein lipase (LPL) is regulated by exercise in humans, but the effects of exercise on LPL expression in different tissues and the molecular mechanisms involved are unclear. We assessed the effects of 5-13 consecutive days of supervised exercise on tissue LPL expression as well as fasting plasma lipids and lipoproteins in 32 sedentary, weight-stable adult men. In skeletal muscle, exercise training increased the mean LPL mRNA level by 117% (P = 0.037), LPL protein mass by 53% (P = 0.038), and total LPL enzyme activity by 35% (P = 0.025). In adipose tissue, mean LPL mRNA, protein mass, and activity did not change. Exercise decreased triglycerides [from 172 +/- 4.3 to 127 +/- 3.2 (SE) mg/dl, P = 0.002], total cholesterol (from 188 +/- 1.2 to 181 +/- 1.0 mg/dl, P = 0.011), and very low-density lipoprotein-cholesterol (from 30.1 +/- 0.9 to 22.0 +/- 0.8, P = 0.004) and increased high-density lipoprotein cholesterol (HDL-C; from 43.4 +/- 0.35 to 45.0 +/- 0.37, P = 0.030) and HDL2-C (from 6.6 +/- 0.21 to 7.7 +/- 0.19, P = 0.021). Changes in muscle but not adipose tissue heparin-releasable LPL activity were inversely correlated (r = -0.435, P < 0.034) with changes in triglycerides. These data suggest the existence of an exercise stimulus intrinsic to skeletal muscle, which raises LPL activity in part by pretranslational mechanisms, a process that contributes to the improvement in circulating lipids seen with physical activity.

Effect of short-term recombinant growth hormone administration on plasma lipoproteins in elderly adults.

To characterize the effects of recombinant human growth hormone (rhGH) on plasma lipids and lipoproteins, rhGH was administered daily at a dose of 40 micrograms.kg-1 (Genentech) for 14 days in 7 healthy elderly male (67.4 +/- 1.9 years, 75.8 +/- 2.6 kg) adults. Six other healthy males (63.9 +/- 0.7 years, 77.8 +/- 3.8 kg) served as concurrent controls. Total plasma cholesterol (TC), triglycerides (TG), very-low-density lipoprotein-cholesterol, low-density lipoprotein-cholesterol, high-density lipoprotein-cholesterol, very-low-density lipoprotein-TG (VLDL-TG) and apolipoprotein AI and apolipoprotein B were determined after an overnight fast before and after the 14-day period of rhGH administration. Subcutaneous rhGH administration was physiologically effective, as shown by a threefold increase in insulin-like growth factor-I (from 110.8 +/- 8.2 to 355.5 +/- 41.6 ng.ml-1; p < 0.05). Plasma fasting insulin also increased from 38.0 +/- 6.5 to 129.9 +/- 43.8 mumol.l-1 (p < 0.05) at the end of the 14 days of rhGH treatment. With respect to plasma lipid/lipoprotein changes, rhGH administration increased plasma TG levels (from 1.5 +/- 0.3 to 2.2 +/- 0.4 mmol.l-1; p < 0.05) and VLDL-TG (from 1.1 +/- 0.3 to 1.8 +/- 0.4 mmol.l-1; p < 0.05), but did not change TC (from 5.0 +/- 0.4 to 5.2 +/- 0.3 mmol.l-1) or any other lipid/lipoprotein variables measured. No significant lipid changes were noted in the control group over the 14-day period. These data suggest that short-term rhGH treatment significantly alters plasma variables of TG profile, perhaps by altering metabolic parameters (i.e. synthesis and/or clearance rates) of VLDL metabolism.

Significant changes in VLDL-triacylglycerol and glucose tolerance in obese subjects following ten days of training.

We characterized the effect of ten days of training on lipid metabolism in 6 [age 37.2 (2.3) years] sedentary, obese [BMI 34.4 (3.0) kg x m(-2)] males with normal glucose tolerance. An oral glucose tolerance test was performed prior to and at the end of the 10 d of training period. The duration of each daily exercise session was 40 min at an intensity equivalent to approximately 75% of the age predicted maximum heart rate. Blood measurements were performed after an overnight fast, before and at the end of the 10 d period. Plasma triacylglycerol was significantly (p < 0.05) reduced following exercise training (2.15+/-0.29 vs. 1.55+/-0.28 mmol x l(-1)). Very low density lipoprotein-triacylglycerol was also significantly (p < 0.05) reduced (1.82+/-0.3 vs. 1.29+/-0.29 mmol x l(-1)). No significant changes in high density lipoprotein-cholesterol were observed as a result of training. Following training fasting plasma glucose and fasting plasma insulin were significantly reduced [Glucose: 5.9 (0.2) mmol x l(-1) vs. 5.3 (0.22) mmol x l(-1) (p < 0.05); Insulin 264.3 (53.8) rho x mol x l(-1) vs. 200.9 (30.1) rho x mol x l(-1), p=0.05]. The total area under the glucose curve during the OGTT decreased significantly (p < 0.05). These preliminary data suggest that short-term exercise, without concomitant loss of body mass, induces favorable changes in plasma triacylglycerol, and very low density lipoprotein-triacylglycerol and glucose tolerance but has no effect on high density lipoprotein-cholesterol.

Insulin and glucagon immunoreactivity during high-intensity exercise under opiate blockade.

Eight fit men [maximum oxygen consumption (VO2max) 64.6 (1.9) ml x kg(-1)xmin(-1), aged 28.3 (1.7) years (SE in parentheses) were studied during two treadmill exercise trials to determine the effect of endogenous opioids on insulin and glucagon immunoreactivity during intense exercise (80% VO2max). A double-blind experimental design was used with subjects undertaking the two exercise trials in counterbalanced order. Exercise trials were 20 min in duration and were conducted 7 days apart. One exercise trial was undertaken following administration of naloxone (N; 1.2 mg; 3 ml) and the other after receiving a placebo (P; 0.9% NaCl saline; 3 ml). Prior to each experimental trial a flexible catheter was placed into an antecubital vein and baseline blood samples were collected. Immediately after, each subject received either a N or P bolus injection. Blood samples were also collected after 20 min of continuous exercise (running). Glucagon was higher (P < 0.05), while insulin was lower (P < 0.05), during exercise compared with pre-exercise values in both trials. However, glucagon was higher (P < 0.05) in the P than in the N exercise trial [141.4 (8.3) ng x 1(-1) vs 127.2 (7.6) ng x 1(-1)]. There were no differences in insulin during exercise between the P and N trials [50.2 (4.3) pmol x 1(-1) vs 43.8 (5) pmol x 1(-1)]. These data suggest that endogenous opioids may augment the glucagon response during intense exercise.

Beta-endorphin infusion alters pancreatic hormone and glucose levels during exercise in rats.

beta-Endorphin (BE) infusion at rest can influence insulin and glucagon levels and thus may affect glucose availability during exercise. To clarify the effect of BE on levels of insulin, glucagon and glucose during exercise, 72 untrained male Sprague-Dawley rats were infused i.v. with either: (1) BE (bolus 0.05 mg.kg-1 + 0.05 mg.kg-1.h-1, n = 24); (2) naloxone (N, bolus 0.8 mg.kg-1 + 0.4 mg.kg-1, n = 24); or (3) volume-matched saline (S, n = 24). Six rats from each group were killed after 0, 60, 90 or 120 min of running at 22 m.min-1, at 0% gradient. BE infusion resulted in higher plasma glucose levels at 60 min [5.93 (0.32) mM] and 90 min [4,16 (0.29) mM] of exercise compared to S [4.62 (0.27) and 3.41 (0.26 mM] and N [4.97 (0.38) and 3.44 (0.25) mM]. Insulin levels decreased to a greater extent with BE [21.5 (0.9) and 18.3 (0.6) uIU.ml-1] at 60 and 90 min compared to S [24.5 (0.5) and 20.6 (0.6) uIU.ml-1] and N [24.5 (0.4) and 21.6 (0.7) uIU.ml-1] groups. Plasma C-peptide declined to a greater extent at 60 and 90 min of exercise with BE infusion compared to both S and N. BE infusion increased glucagon at all times during exercise compared to S and N. These data suggest that BE infusion during exercise influences plasma glucose by augmenting glucagon levels and attenuating insulin release.

Effect of repeated exercise bouts on high density lipoprotein-cholesterol and its subfractions HDL2-C and HDL3-C.

Nine sedentary men (mean age, 22.8 yrs) were studied during and after treadmill exercise at 65% VO2max to determine the number of repeated exercise bouts required to bring about a sustained elevation in HDL-cholesterol and its subfraction HDL2-C and HDL3-C. A Latin square counterbalanced design was used. Thirty minute exercise sessions were undertaken in the following patterns: (1) single bout, (2) two bouts on alternate days, and (3) three bouts on alternate days. The exercise bouts in patterns 2 and 3 were separated by 48 h. Patterns 1, 2 and 3 were conducted 7 days apart. Blood samples were obtained prior to each pattern and at 5 min, 24 and 48 h after the last session within each pattern. There were no significant differences in triglycerides and total cholesterol between the selected blood sampling points for all patterns. Total HDL-C remained higher (p < 0.05) than the pre-exercise level 5 min [pattern 1: 39.0 vs 41.2 mg.dl-1, pattern 2: 37.1 vs 39.2 mg.dl-1, pattern 3: 38.8 vs 42.7 mg.dl-1] and 24 h [pattern 1: 39.0 vs 39.4 mg.dl-1, pattern 2: 37.1 vs 39.1 mg.dl-1, pattern 3: 38.8 vs 42.6 mg.dl-1] post-exercise. Total HDL-C declined to pre-exercise values 48 h post-exercise in all patterns. HDL2-C was lower (p < 0.05) than pre-exercise 48 h for all exercise patterns. For all patterns, HDL3-C levels were higher (p < 0.05) at the 5 min and 48 h post-exercise time points than at the pre-exercise.(ABSTRACT TRUNCATED AT 250 WORDS)

Endogenous opioids may modulate catecholamine secretion during high intensity exercise.

To determine the effect of endogenous opioids on catecholamine response during intense exercise [80% maximal oxygen uptake (VO2max)], nine fit men [mean (SE) VO2max, 63.9 (1.7) ml.kg-1.min-1; age 27.6 (1.6) years] were studied during two treadmill exercise trials. A double-blind experimental design was used with subjects undertaking the two exercise trials in counterbalanced order. Exercise trials were 20 min in duration and were conducted 7 days apart. One exercise trial was undertaken following administration of naloxone (N; 1.2 mmol.l-1; 3 ml) and the other after receiving a placebo (P; 0.9% saline; 3 ml). Prior to each experimental trial a flexible catheter was placed into an antecubital vein and baseline blood samples were collected. Immediately afterwards, each subject received bolus injection of either N or P. Blood samples were also collected after 20 min of continuous exercise while running. Epinephrine and norepinephrine were higher (P < 0.05) in the N than P exercise trial with mean (SE) values of 1679 (196) versus 1196 (155) pmol.l-1 and 24 (2.2) versus 20 (1.7) nmol.l-1, respectively. Glucose and lactate were higher (P < 0.05) in the N than P exercise trial with values of 7 (0.37) versus 5.9 (0.31) mmol.l-1 and 6.9 (1.1) versus 5.3 (0.9) mmol.l-1 respectively. These data suggest an opioid inhibition in the release of catecholamines during intense exercise.