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Exercise is a potent stimulus for growth hormone (GH) release, although aging appears to attenuate this response. The aim of this study was to investigate GH responses to different exercise stimuli in young and early middle-aged men. Eight men aged 18–25 y and 8 men aged 40–50 y completed 3 trials, at least 7 days apart, in a random order: 30 s cycle-ergometer sprint (sprint), 30 min resistance exercise bout (resistance), 30 min cycle at 70% maximal oxygen consumption (endurance). Blood samples were taken pre-, during, and post-exercise, and area under the GH vs. time curve was calculated for a total of 120 min. Mean blood lactate concentrations and percentage heart rate maximum at which the participants were working were not different between groups in any of the trials. In both groups, blood lactate concentrations were significantly lower in the endurance trial than in the sprint and resistance trials. There were no significant differences in resting GH concentration between groups or trials. GH AUC was significantly greater in the young group than the early middle-aged group, in both sprint (531 (±347) vs. 81 (±54) µg·L–1 per 120 min, p = 0.003) and endurance trials (842 (±616) vs. 177 (±137) µg·L–1 per 120 min, p = 0.010). Endurance exercise elicits a greater GH response than sprint and resistance exercise; however, aging per se, factors associated with aging, or an inability to achieve a sufficient absolute exercise intensity results in a smaller GH response to an exercise stimulus in early middle-aged men.

Udgivelsesdato: 2009-Jun OBJECTIVE: We tested the hypothesis that lycopene supplementation reduces the expression of oxidant-responsive heme oxygenase-1 (HO-1) in basal conditions and in response to an oxidant challenge and determined whether this is temporally associated with increased cell viability. METHODS: We determined basal and stimulated ex vivo expression of HO-1 and cell viability in lymphocytes from volunteers after lycopene supplementation. Twenty-four healthy young men on a low lycopene diet consumed 1) 170 g of passata sauce with butter or 2) butter alone for 3 wk in a randomized crossover design. RESULTS: Plasma lycopene concentrations at the end of the tomato and control trials were 0.54 +/- 0.20 versus 0.20 +/- 0.15 micromol/L, respectively (P < 0.05). There was a significant increase in the proportion of live cells (91 +/- 5% versus 87 +/- 9%) and a corresponding reduction in apoptosis (6 +/- 4% versus 11 +/- 9%) in untreated lymphocytes after supplementation (P < 0.05), with no effect on cell viability in response to hydrogen peroxide treatment. HO-1 protein expression in basal conditions and induction of HO-1 after hydrogen peroxide treatment was not different between trials. CONCLUSION: Lycopene supplementation did not affect basal oxidative stress or susceptibility to oxidant-induced stress as indicated by the expression of the oxidant-responsive protein HO-1 and cell viability in response to hydrogen peroxide treatment. However, lycopene supplementation significantly reduced apoptosis in freshly harvested untreated lymphocytes. We conclude that this was not through an oxidant-mediated mechanism because of the lack of an effect on oxidant-responsive HO-1.

Strenuous exercise induces an initial pro- and subsequent anti-inflammatory response, and it has been suggested that this may be one of the ways that regular exercise reduces chronic inflammation and therefore the risk of cardiovascular disease. However, public health recommendations emphasize moderate-intensity physical activity, and it is important to understand whether moderate-intensity exercise has a similar anti-inflammatory effect. Twelve sedentary male volunteers (age 54 ± 4 yr) completed two main trials, moderate-intensity exercise and rest (30 min at 50% maximal oxygen uptake vs. sitting, respectively). There were no significant changes in circulating neutrophils, lymphocytes, monocytes, or serum interleukin-6, interleukin-10, and C-reactive protein concentration over the 7 days following exercise. Similarly, lymphocyte adhesion to cultured endothelial cells and heme oxygenase-1 (HO-1) expression in lymphocytes and monocytes were not affected by walking at any time point. These results suggest that the long-term anti-inflammatory and antiatherogenic effects of regular moderate-intensity physical activity must be explained by something other than a profound net anti-inflammatory response to each exercise bout since a single bout of walking did not lead to a change in various markers of inflammation or lymphocyte adherence to cultured endothelial cells.

Oxidative stress induces the expression of the cytoprotective and anti-inflammatory protein haem oxygenase-1 (HO-1). In the present investigation, we show that anticipation of subsequent exercise elevates the expression of HO-1 mRNA in lymphocytes. A between-groups comparison of HO-1 mRNA expression in subjects about to complete a half marathon race vs. subjects who were asked to sit quietly in the laboratory showed an elevated expression of HO-1 mRNA prior to exercise (2.6-fold higher in subjects prior to the half marathon, P0.01). This observation led us to examine whether anticipation of subsequent exercise leads to differences in lymphocyte HO-1 mRNA expression within the same subjects. In a second experiment, the same individuals completed two trials, one exercise and one rest, approximately 2 weeks apart in a randomised cross-over design. Lymphocyte HO-1 mRNA expression was greater prior to exercise (1.4 +/- 0.3-fold higher in the exercise trial, P0.05). These results suggest that knowledge of subsequent demanding exercise may lead to an anticipatory induction of HO-1 mRNA. We tentatively propose that this process has evolved to prepare lymphocytes for subsequent exercise-induced oxidative stress although the mechanism remains to be elucidated.

Aim To assess the error in predicting physical activity energy expenditure (PAEE), using a multisensor device in wheelchair users, and to examine the efficacy of using an individual heart rate calibration (IC) method. Methods 15 manual wheelchair users (36±10 years, 72±11 kg) completed 10 activities: resting, folding clothes, wheelchair propulsion on a 1% gradient (3456 and 7 km/h) and propulsion at 4 km/h (with an additional 8% of body mass, 2% and 3% gradient) on a motorised wheelchair treadmill. Criterion PAEE was measured using a computerised indirect calorimetry system. Participants wore a combined accelerometer and heart rate monitor (Actiheart). They also performed an incremental arm crank ergometry test to exhaustion which permitted retrospective individual calibration of the Actiheart for the activity protocol. Linear regression analysis was conducted between criterion (indirect calorimetry) and estimated PAEE from the Actiheart using the manufacturer's proprietary algorithms (group calibration, GC) or IC. Bland-Altman plots were used and mean absolute error was calculated to assess the agreement between criterion values and estimated PAEE. Results Predicted PAEE was significantly (p

The aim of the present investigation was to determine whether an acute bout of exercise increases heme oxygenase-1 (HO-1) mRNA accumulation in human lymphocytes. Eight male subjects performed separate exercise and rest trials in a randomised order at least 10 days apart. In the exercise trial subjects ran for 75-min at a speed corresponding to 70% maximal oxygen uptake, and in the resting trial subjects sat calmly in the laboratory for an equivalent period of time. Lymphocytes were harvested from blood samples taken before and after each trial. Total RNA was isolated and used to determine the fold-change in HO-1 mRNA accumulation relative to baseline values using real time reverse transcription-polymerase chain reaction. HO-1 protein was determined by Western blotting. Six of the eight subjects showed an increase in HO-1 mRNA greater than two-fold after exercise. The median peak fold-change was 2.7 fold with one subject showing a particularly pronounced response (20-fold) 24 h post-exercise. In the rest trial the level of HO-1 mRNA did not change over the period of investigation. There was also an increase in HO-1 protein 2 h after exercise. These results complement an earlier study showing that acute exercise of a different type (half marathon) leads to an increase in HO-1 expression in lymphocytes.

We have previously shown that vitamin C supplementation affects recovery from an unaccustomed bout of demanding exercise, with the most pronounced effect being that on plasma interleukin-6 concentration. However, because of the proposed role of interleukin-6 in the regulation of metabolism, it was unclear whether this represented a reduced response to muscle damage or some form of interaction with the metabolic demands of the activity. Therefore, the aim of the present study was to investigate the effect of the same form of supplementation on a bout of exercise that initiated similar muscle damage but had a low metabolic cost. Fourteen male subjects were allocated to either a placebo (P) or a vitamin C (VC) group. The VC group consumed 200 mg of ascorbic acid twice a day for 14 days prior to a bout of exercise and for the 3 days after exercise. The P group consumed identical capsules that contained 200 mg lactose. Subjects performed 30 min of downhill running at a gradient of -18% and recovery was monitored for up to 3 days after exercise. Plasma VC concentrations in the VC group increased following supplementation. Nevertheless, downhill running provoked a similar increase in circulating markers of muscle damage (creatine kinase activity and myoglobin concentration) and muscle soreness in P and VC groups. Similarly, although downhill running increased plasma interleukin-6, there was no effect from VC supplementation. These results suggest that vitamin C supplementation does not affect interleukin-6 concentrations following eccentric exercise that has a low metabolic component.

This study aimed to compare the performance of a new portable lactate analyser against other standard laboratory methods in three conditions, normal (20 +/- 1.3 degrees C; 40 +/- 5 % RH), hot (40 +/- 2.5 degrees C; 40 +/- 5 % RH), and humid (20 +/- 1.1 degrees C; 82 +/- 6 % RH) conditions. Seven healthy males, ([Mean +/- SE]: age, 26.3 +/- 1.3 yr; height, 177.7 +/- 1.6 cm; weight, 77.4 +/- 0.9 kg, .VO(2)max, 56.1 +/- 1.9 ml x kg x min(-1)) undertook a maximal cycle ergometry test to exhaustion in the three conditions. Blood was taken every 3 min at the end of each stage and was analysed using the Lactate Pro LT-1710, the Accusport, the Analox GM7 and the Kodak Ektachem systems. The MANOVA (Analyser Type x Condition x Workload) indicated no interaction effect (F(42,660), = 0.45, p > 0.99, Power = 0.53). The data across all workloads indicated that the machines measured significantly differently to each other (F(4,743) = 14.652, p < 0.0001, Power = 1.00). The data were moderately to highly correlated. We conclude that the Lactate Pro is a simple and effective measurement device for taking blood lactate in a field or laboratory setting. However, we would caution against using this machine to compare data from other machines.

The aim of this study was to examine the effects of a 7-day Zone diet compared with a normal diet on maximal oxygen uptake (V(O)2 max), running time to exhaustion during endurance performance, and body composition. Eight men, with the following physical characteristics (mean +/- SE), participated in this study: age, 26.1 +/- 1.9 years; height, 178 +/- 1.7 cm; mass, 70.7 +/- 2.1 kg; and V(O)2 max, 54.6 +/- 3.1 ml x kg(-1) x min(-1). All subjects undertook pretesting for V(O)2 max, time to exhaustion (80% V(O)2 max), and body composition (Biostat 1500) before following either the normal diet or the Zone diet for 7 days. These performance trials were performed before and after the dietary period. There was a significant (p < 0.05) decrease in total energy consumption from a mean of 2,314 +/- 334 kcal on a pretest diet to 1,994 +/- 438 kcal on the Zone diet. Subjects showed a significant reduction (p < 0.02) in body mass from 70.7 +/- 2.1 kg to 69.8 +/- 2.1 kg. In the 80% V(O)2 max time to exhaustion trial, there was a significant reduction (p < 0.05) in time to exhaustion from 37.68 +/- 8.6 minutes for the pretest diet to 34.11 +/- 7.01 minutes for the Zone diet. In conclusion, the claim of the authors of the Zone diet that performance time and V(O)2 max can be improved was not shown in this 1-week research trial. We would suggest that this is not a nutritional strategy that athletes should use until further work has been conducted.

Exercise-induced free-radical production may be partly responsible for muscle soreness and damage following demanding exercise. A number of studies have investigated the effect of antioxidant supplementation although there is a paucity of information regarding vitamin C. Therefore the aim of the present study was to investigate the effect of vitamin C supplementation on exercise-induced muscle soreness and damage. Nine habitually active males consumed a 1 g dose of vitamin C 2 h before exercise, and on another occasion consumed an identical placebo. The exercise comprised a 90 min intermittent shuttle-running test, which was designed to simulate the multiple-sprint sports. Vitamin C supplementation increased plasma concentrations of vitamin C before exercise, and plasma concentrations continued to increase during the shuttle-run to reach a peak of approximately 200 micromol x l(-1) immediately after exercise. However, muscle soreness, and markers of both muscle damage (creatine kinase and aspartate aminotransferase) and lipid peroxidation (malondialdehyde) were elevated to an equal extent after exercise in placebo and supplemented trials. Therefore acute supplementation with vitamin C had no beneficial effects although it is possible that such short-term vitamin C supplementation was ineffective because it occurred at an inappropriate time.

Harrison et al. (2009) and MacEneaney et al. (2009) recently reported an increase in circulating concentrations of interleukin-6 (IL-6) after the consumption of a meal. In the Wrst investigation, it was reported that exercise performed the day before a high-fat meal had no eVect on postprandial IL-6 concentration in active young men (Harrison et al. 2009). Six hours after the meal, IL-6 concentration had increased »3-fold. It was also reported that prior exercise did not aVect the primary outcome measure of the study (endothelial microparticle response). The authors concluded that prior exercise has no eVect on either endothelial activation (endothelial microparticle response) or postprandial IL-6, in spite of a powerful eVect on postprandial lipaemia (Harrison et al. 2009). In the second investigation, it was reported that exercise the day before a high-fat meal had no eVect on postprandial IL-6 in either lean or overweight adolescent boys (MacEneaney et al. 2009). Several markers of inXammation were included although IL-6 was the only one to increase (»2-fold) 6 h after the meal. The increase in IL-6 occurred in spite of a reduction in postprandial lipaemia. This led the authors to conclude that the inXammatory response in the postprandial state was not attenuated by acute exercise in spite of reductions in postprandial triacylglycerol concentrations (MacEneaney et al. 2009). Notably, both these studies used an indwelling catheter for blood sampling. Until recently, we would have drawn similar conclusions to the authors. However, our views have now changed since it appears that measures of IL-6 are very heavily inXuenced by blood sampling method. In a recent report, we undertook a similar experiment to those reported above (Dixon et al. 2009). In this study, we examined whether a diVerence in physical activity (and associated postprandial glycaemia/ lipaemia) was reXected in diVerences in postprandial inXammation. Using blood drawn from a catheter, IL-6 concentration progressively increased so that 8 h after a high-fat meal it was 3–4-fold greater than at baseline (irrespective of physical activity status). Based on this observation alone, we would have concluded that physical activity has no eVect on post-prandial inXammation as gauged by IL-6 concentration (in spite of a large eVect on postprandial glycaemia/lipaemia). However, because we were aware of one report that IL-6 concentration is inXuenced by blood-sampling method (Haack et al. 2002), we also decided to include single venepuncture samples before and 8 h after the meal in around half the participants. In contrast to a 4-fold increase in venous blood taken via the catheter, there was only a tiny increase in IL-6 taken by venepuncture from the contralateral arm (Dixon et al. 2009). We went on to show that even removing a large amount of blood from the catheter prior to measurement of IL-6 did not seem to overcome this eVect. Of course, based only on these observations, we do not know whether diVerent meals (e.g. with a diVerent composition) would increase postprandial IL-6. As we discuss in our paper, most studies that show an increase in IL-6 after a meal have used a catheter, but there has been at least one report of an increase in postprandial IL-6 in venous blood sampled by venepuncture (Nappo et al. 2002). Therefore, some of the various reports of changes in IL-6 after a meal could be real phenomena, and others could be a product of the blood sampling method that has been used. In the context of the recent reports in the European Journal of Applied Physiology (Harrison et al. 2009; D. Thompson (&) · N. Dixon University of Bath, Bath, UK e-mail: d.thompson@bath.ac.uk

The aim of this study was to examine the impact of prolonged intermittent high-intensity shuttle running on soreness and markers of muscle damage. Sixteen males took part in the study, half of whom were assigned to a running group and half to a resting control group. The exercise protocol involved 90 min of intermittent shuttle running and walking (Loughborough Intermittent Shuttle Test: LIST), reflecting the activity pattern found in multiple-sprint sports such as soccer. Immediately after exercise, there was a significant increase (P0.05) in serum activities of creatine kinase and aspartate aminotransferase, and values remained above baseline for 48 h (P0.05). Median peak activities of creatine kinase and aspartate aminotransferase occurred 24 h post-exercise and were 774 and 43 U x l(-1), respectively. The intensity of general muscle soreness, and in the specific muscles investigated, was greater than baseline for 72 h after the shuttle test (P0.05), peaking 24-48 h post-exercise (P0.05). Muscle soreness was not correlated with either creatine kinase or aspartate aminotransferase activity. Soreness was most frequently reported in the hamstrings. Neither soreness nor serum enzyme activity changed in the controls over the 4 day observation period. It appears that unaccustomed performance of prolonged intermittent shuttle running produces a significant increase in both soreness and markers of muscle damage.

Second-order ordinary differential equations of the Numerov type (no first derivative and the given function linear in the solution) are common in physics, but little discussion is devoted to the special first step that is needed before one can apply the general algorithm. We give an explicit algorithm to calculate the first point of the solution with an accuracy appropriate to that obtained with the general algorithm. © 1997 American Institute of Physics.

Skeletal muscle mass is in a constant state of turnover, and atrophy is the result of a shift in the balance of muscle protein synthesis and breakdown resulting in net muscle protein loss. Total disuse of skeletal muscle quickly leads to muscle atrophy and loss of strength, and this has been repeatedly demonstrated in studies employing bed rest and lower limb immobilisation methodologies in young healthy participants. Fewer studies have focused on older participants (>65 years of age), but those that have provide evidence that advancing age brings increased vulnerability to rapid and marked loss of muscle size and strength during period of total muscle unloading. Increased systemic inflammation and reduced protein synthetic responses to protein feeding and muscle contraction might influence the severity of muscle protein loss during periods of total unloading compared with younger individuals. Less extreme reductions in muscle loading (e.g., 2 weeks of reducing daily ambulation to

Purpose Most of what we know about adipose tissue is restricted to observations derived after an overnight fast. However, humans spend the majority of waking hours in a postprandial (fed) state, and it is unclear whether increasing adiposity impacts adipose tissue responses to feeding. The aim of this research was to investigate postprandial responses in adipose tissue across varying degrees of adiposity. Methods Thirty males aged 35–55 years with waist circumference 81–118 cm were divided equally into groups categorized as either lean, overweight or obese. Participants consumed a meal and insulinaemic, glycaemic and lipidaemic responses were monitored over 6 h. Subcutaneous adipose tissue samples were obtained at baseline and after 6 h to examine changes in gene expression and adipose tissue secretion of various adipokines. Results Following consumption of the meal, insulin and glucose responses were higher with increased adiposity (total AUC effects of group; p = 0.058 and p = 0.027, respectively). At 6 h, significant time effects reflected increases in IL-6 (F = 14.7, p = 0.001) and MCP-1 (F = 10.7, p = 0.003) and reduction in IRS2 adipose tissue gene expression (F = 24.6, p

Background/Objectives: \ud \ud Breakfast omission is positively associated with obesity and increased risk of disease. However, little is known about the acute effects of extended morning fasting upon subsequent energy intake and associated metabolic/regulatory factors in obese adults.\ud Subjects/Methods: \ud \ud In a randomised cross-over design, 24 obese men (n=8) and women (n=16) extended their overnight fast by omitting breakfast consumption or ingesting a typical carbohydrate-rich breakfast of 2183±393 kJ (521±94 kcal), before an ad libitum pasta lunch 3 h later. Blood samples were obtained throughout the day until 3 h post lunch and analysed for hormones implicated in appetite regulation, along with metabolic outcomes and subjective appetite measures.\ud Results: \ud \ud Lunch intake was unaffected by extended morning fasting (difference=218 kJ, 95% confidence interval −54 kJ, 490 kJ; P=0.1) resulting in lower total intake in the fasting trial (difference=−1964 kJ, 95% confidence interval −1645 kJ, −2281 kJ; P

Low-to-moderate intensity physical activity thermogenesis is a highly variable and quantitatively important component of total energy expenditure that is difficult to assess outside the laboratory. Greater precision and accuracy in the measurement of this key contributor to energy balance is a research priority. We developed a laboratory-based protocol that simulated a range of low-to-moderate intensity physical activities. We characterized the bias and random (individual) error in estimating energy expenditure using combined accelerometry and heart rate (AHR) with branched-equalion modeling and a simple motion sensor (pedometer) against an indirect calorimetry criterion. Twenty young adult subjects performed a 2-h laboratory-based protocol, simulating 6 low-to-moderate intensity physical activities interspersed with periods of rest. The physical activity level during the laboratory-based protocol reflected an energy expenditure toward the lower end of the active category. We found that AHR-derived energy expenditure showed no evidence of substantial fixed or proportional bias (mean bias 6%), whereas pedometer-derived energy expenditure showed both fixed and proportional bias (bias at minimum, mean, and maximum energy expenditure +11, -20, and -36%, respectively). It appears that AHR provides an accurate estimate of criterion energy expenditure whereas a simple motion sensor (pedometer) does not. It is noteworthy that AHR provides quantitative information about the nature and patterns of physical activity, such as the amount of time and/or energy spent engaged in physical activity above critical health-related thresholds.

The aim of this study was to investigate whether post-exercise vitamin C supplementation influences recovery from an unaccustomed bout of exercise. Sixteen male subjects were allocated to either a placebo (P; n=8) or vitamin C (VC) group ( n=8). Subjects performed a prolonged (90-min) intermittent shuttle-running test, and supplementation began after the cessation of exercise. Immediately after exercise the VC group consumed 200 mg of VC dissolved in a 500 ml drink, whereas the subjects in the P group consumed the drink alone. Later on the same day and then in the morning and evening of the following 2 days, subjects consumed additional identical drinks. Plasma VC concentrations in the VC group increased above those in the P group 1 h after exercise and remained above P values for the 3 days after exercise. Nevertheless, post-exercise VC supplementation was not associated with improved recovery. Post-exercise serum creatine kinase activities and myoglobin concentrations were unaffected by supplementation. Muscle soreness and the recovery of muscle function in the leg flexors and extensors were not different in VC and P groups. Furthermore, although plasma concentrations of interleukin-6 and malondialdehyde increased following exercise, there was no difference between VC and P groups. These results suggest that either free radicals are not involved in delaying the recovery process following a bout of unaccustomed exercise, or that the consumption of VC wholly after exercise is unable to deliver this antioxidant to the appropriate sites with sufficient expediency to improve recovery.

Background Exercise has a beta cell preserving effect in patients with type 2 diabetes. This benefit of exercise has not been examined in type 1 diabetes. Significant beta cell function is present at the time of diagnosis of type 1 diabetes and therefore studies of beta cell preservation are ideally conducted immediately after diagnosis. Many of the variables required to design and power such a study are currently unknown. The aim of EXTOD is to obtain the information required to design a formal study of exercise and beta cell preservation in newly diagnosed patients with type 1 diabetes. Methods Barriers to exercise will initially be assessed in a qualitative study of newly diagnosed patients. Then, sixty newly diagnosed adult type 1 diabetes patients will be randomized to either conventional treatment or exercise, stratified on beta cell function and fitness. The exercise group will be encouraged to increase their level of activity to a minimum of 150 minutes of moderate to vigorous intensity exercise per week, aiming for 240 minutes per week of exercise for 12 months. Beta cell function will be measured by meal-stimulated C peptide. Primary outcomes are recruitment, adherence to exercise, loss to follow-up, and exercise levels in the non-intervention arm (contamination). The secondary outcome of the study is rate of loss of beta cell function. Discussion The outcomes of the EXTOD study will help define the barriers, uptake and benefits of exercise in adults newly diagnosed with type 1 diabetes. This information will enable design of a formal study to assess the effect of exercise on beta cell preservation in newly diagnosed patients with type 1 diabetes. Trial registration Current controlled trials ISRCTN91388505