David J. Stensel

Health-enhancing physical activity and sedentary behaviour in children and adolescents

We provide a wide-ranging review of health-related physical activity in children and adolescents using a behavioural epidemiology framework. In contrast to many other reviews, we highlight issues associated with true sedentary behaviours alongside physically active behaviours. Specifically, we review the evidence concerning the links between physical activity and cardiovascular disease, overweight and obesity, psychosocial measures, type II diabetes, and skeletal health. Although the evidence is unconvincing at times, several factors lead to the conclusion that promoting physical activity in youth is desirable. A review of the prevalence of physical activity and sedentary behaviours shows that many young people are active, but this declines with age. A substantial number are not adequately active for health benefits and current trends in juvenile obesity are a cause for concern. Prevalence data on sedentary behaviours are less extensive but suggest that total media use by young people has not changed greatly in recent years. Most children and adolescents do not exceed recommended daily hours of TV viewing. Physical activity is unrelated to TV viewing. We also identified the key determinants of physical activity in this age group, highlighting demographic, biological, psychological, behavioural, social and environmental determinants. Interventions were considered for school, family and community environments. Finally, policy recommendations are offered for the education, governmental, sport and recreation, health, and mass media sectors.

The anti-inflammatory effects of exercise: mechanisms and implications for the prevention and treatment of disease

Regular exercise reduces the risk of chronic metabolic and cardiorespiratory diseases, in part because exercise exerts anti-inflammatory effects. However, these effects are also likely to be responsible for the suppressed immunity that makes elite athletes more susceptible to infections. The anti-inflammatory effects of regular exercise may be mediated via both a reduction in visceral fat mass (with a subsequent decreased release of adipokines) and the induction of an anti-inflammatory environment with each bout of exercise. In this Review, we focus on the known mechanisms by which exercise — both acute and chronic — exerts its anti-inflammatory effects, and we discuss the implications of these effects for the prevention and treatment of disease.

Influence of resistance and aerobic exercise on hunger, circulating levels of acylated ghrelin, and peptide YY in healthy males

Resistance (muscle strengthening) exercise is a key component of exercise recommendations for weight control, yet very little is known about the effects of resistance exercise on appetite. We investigated the effects of resistance and aerobic exercise on hunger and circulating levels of the gut hormones acylated ghrelin and peptide YY (PYY). Eleven healthy male students: age 21.1 +/- 0.3 yr, body mass index 23.1 +/- 0.4 kg/m(2), maximum oxygen uptake 62.1 +/- 1.8 ml.kg(-1).min(-1) (means +/- SE) undertook three, 8-h trials, 1) resistance exercise: a 90-min free weight lifting session followed by a 6.5-h rest period, 2) aerobic exercise: a 60-min run followed by a 7-h rest period, 3) control: an 8-h rest, in a randomized crossover design. Meals were provided 2 and 5 h into each trial. Hunger ratings and plasma concentrations of acylated ghrelin and PYY were measured throughout. Two-way ANOVA revealed significant (P < 0.05) interaction effects for hunger, acylated ghrelin, and PYY, indicating suppressed hunger and acylated ghrelin during aerobic and resistance exercise and increased PYY during aerobic exercise. A significant trial effect was observed for PYY, indicating higher concentrations on the aerobic exercise trial than the other trials (8 h area under the curve: control 1,411 +/- 110, resistance 1,381 +/- 97, aerobic 1,750 +/- 170 pg/ml 8 h). These findings suggest ghrelin and PYY may regulate appetite during and after exercise, but further research is required to establish whether exercise-induced changes in ghrelin and PYY influence subsequent food intake.

Influence of prolonged treadmill running on appetite, energy intake and circulating concentrations of acylated ghrelin.

The effects of prolonged treadmill running on appetite, energy intake and acylated ghrelin (an appetite stimulating hormone) were examined in 9 healthy males over the course of 24h. Participants completed 2 experimental trials (exercise and control) in a randomised-crossover fashion. In the exercise trial participants ran for 90 min at 68.8 + or - 0.8% of maximum oxygen uptake followed by 8.5 h of rest. Participants returned to the laboratory on the following morning to provide a fasting blood sample and ratings of appetite (24 h measurement). No exercise was performed on the control trial. Appetite was measured within the laboratory using visual analogue scales and energy intake was assessed from ad libitum buffet meals. Acylated ghrelin was determined from plasma using an ELISA assay. Exercise transiently suppressed appetite and acylated ghrelin but each remained no different from control values in the hours afterwards. Furthermore, despite participants expending 5324 kJ during exercise there was no compensatory increase in energy intake (24 h energy intake; control 17,191 kJ, exercise 17,606 kJ). These findings suggest that large energy deficits induced by exercise do not lead to acute compensatory responses in appetite, energy intake or acylated ghrelin.

Breaking Up Prolonged Sitting With Standing or Walking Attenuates the Postprandial Metabolic Response in Postmenopausal Women: A Randomized Acute Study

OBJECTIVE To determine whether breaking up prolonged sitting with short bouts of standing or walking improves postprandial markers of cardiometabolic health in women at high risk of type 2 diabetes. RESEARCH DESIGN AND METHODS Twenty-two overweight/obese, dysglycemic, postmenopausal women (mean ± SD age 66.6 ± 4.7 years) each participated in two of the following treatments: prolonged, unbroken sitting (7.5 h) or prolonged sitting broken up with either standing or walking at a self-perceived light intensity (for 5 min every 30 min). Both allocation and treatment order were randomized. The incremental area under the curves (iAUCs) for glucose, insulin, nonesterified fatty acids (NEFA), and triglycerides were calculated for each treatment condition (mean ± SEM). The following day, all participants underwent the 7.5-h sitting protocol. RESULTS Compared with a prolonged bout of sitting (iAUC 5.3 ± 0.8 mmol/L ⋅ h), both standing (3.5 ± 0.8 mmol/L ⋅ h) and walking (3.8 ± 0.7 mmol/L ⋅ h) significantly reduced the glucose iAUC (both P < 0.05). When compared with prolonged sitting (548.2 ± 71.8 mU/L ⋅ h), insulin was also reduced for both activity conditions (standing, 437.2 ± 73.5 mU/L ⋅ h; walking, 347.9 ± 78.7 mU/L ⋅ h; both P < 0.05). Both standing (−1.0 ± 0.2 mmol/L ⋅ h) and walking (−0.8 ± 0.2 mmol/L ⋅ h) attenuated the suppression of NEFA compared with prolonged sitting (−1.5 ± 0.2 mmol/L ⋅ h) (both P < 0.05). There was no significant effect on triglyceride iAUC. The effects on glucose (standing and walking) and insulin (walking only) persisted into the following day. CONCLUSIONS Breaking up prolonged sitting with 5-min bouts of standing or walking at a self-perceived light intensity reduced postprandial glucose, insulin, and NEFA responses in women at high risk of type 2 diabetes. This simple, behavioral approach could inform future public health interventions aimed at improving the metabolic profile of postmenopausal, dysglycemic women.

Effect of a school-based intervention to promote healthy lifestyles in 7–11 year old children

BackgroundPhysical inactivity is recognised as a public health concern within children and interventions to increase physical activity are needed. The purpose of this research was to evaluate the effect of a school-based healthy lifestyles intervention on physical activity, fruit and vegetable consumption, body composition, knowledge, and psychological variables.MethodA non-randomised controlled study involving 8 primary schools (4 intervention, 4 control). Participants were 589 children aged 7–11 years. The intervention lasted 10 months and comprised a CD-rom learning and teaching resource for teachers; an interactive website for pupils, teachers and parents; two highlight physical activity events (1 mile school runs/walks); a local media campaign; and a summer activity wall planner and record. Primary outcome measures were objectively measured physical activity (pedometers and accelerometers) and fruit and vegetable consumption. Secondary outcomes included body mass index, waist circumference, estimated percent body fat, knowledge, psychological variables. Multi-level modelling was employed for the data analysis.ResultsRelative to children in control schools, those in intervention schools significantly increased their total time in moderate-to-vigorous physical activity (MVPA) (by 9 minutes/day vs a decrease of 10 minutes/day), their time in MVPA bouts lasting at least one minute (10 minutes/day increase vs no change) and increased daily steps (3059 steps per day increase vs 1527 steps per day increase). A similar pattern of results was seen in a subset of the least active participants at baseline. Older participants in intervention schools showed a significant slowing in the rate of increase in estimated percent body fat, BMI, and waist circumference. There were no differences between groups in fruit and vegetable intake. Extrinsic motivation decreased more in the intervention group.ConclusionThe intervention produced positive changes in physical activity levels and body composition. It appeared to have little or no effect on consumption of fruit and vegetables. Schools are a suitable setting for the promotion of healthy lifestyles although more work, particularly focussed on dietary change, is needed in a variety of schools and social settings.

Differential acylated ghrelin, peptide YY3-36, appetite, and food intake responses to equivalent energy deficits created by exercise and food restriction.

CONTEXT Acute energy deficits imposed by food restriction increase appetite and energy intake; however, these outcomes remain unchanged when energy deficits are imposed by exercise. OBJECTIVE Our objective was to determine the potential role of acylated ghrelin and peptide YY(3-36) (PYY(3-36)) in mediating appetite and energy intake responses to identical energy deficits imposed by food restriction and exercise. DESIGN Twelve healthy males completed three 9-h trials (exercise deficit, food deficit, and control) in a randomized counterbalanced design. Participants ran for 90 min (70% of VO(2) max) at the beginning of the exercise deficit trial and then rested for 7.5 h. Participants remained sedentary throughout the food deficit and control trials. Test meals were consumed by participants at 2 and 4.75 h in all trials. The amount provided in the food deficit trial was restricted so that an energy deficit (equivalent to that imposed by exercise) was induced relative to control. Participants were permitted access to a buffet meal at 8 h. RESULTS The energy deficits imposed by food restriction (4820 ± 151 kJ) and exercise (4715 ± 113 kJ) were similar. Appetite and ad libitum energy intake responded in a compensatory fashion to food restriction yet were not influenced by exercise. Plasma acylated ghrelin concentrations increased, whereas PYY(3-36) decreased, in response to food restriction (two-way ANOVA, trial × time interaction, P < 0.001 for each). Exercise did not induce such compensatory responses. CONCLUSIONS These findings suggest a mediating role of acylated ghrelin and PYY(3-36) in determining divergent feeding responses to energy deficits imposed by food restriction and exercise.

Exercise, Appetite and Appetite-Regulating Hormones: Implications for Food Intake and Weight Control

Knowledge about the relationship between exercise and appetite is important both for athletes wishing to optimise performance and for those interested in maintaining a healthy body weight. A variety of hormones are involved in appetite regulation including both episodic hormones, which are responsive to episodes of feeding, and tonic hormones, which are important regulators of energy storage over the longer term (e.g. insulin and leptin). Notable among the episodic appetite-regulating hormones is ghrelin, which plays a unique role in stimulating appetite and energy intake. Many studies have demonstrated that acute bouts of moderately vigorous exercise transiently suppress appetite and this has been termed ‘exercise-induced anorexia’. The mechanisms by which acute exercise suppresses appetite are not fully understood but may involve lowered concentrations of ghrelin and increased concentrations of satiety hormones, notably peptide YY and glucagon-like peptide 1. Evidence suggests that chronic exercise training typically causes a partial but incomplete compensation in energy intake perhaps due to beneficial changes in appetite-regulating hormones. The lack of a full compensatory response of appetite to exercise may facilitate the development of a negative energy balance and weight loss although there is individual variability in the response to exercise. From a practical standpoint athletes should not feel concerned that exercise will cause overeating as there is limited evidence to support this. For those desiring weight loss there may be some merit in performing exercise in the postprandial period as a means of enhancing the satiating effect of a meal but additional evidence is required to confirm the effectiveness of this strategy.

A single session of treadmill running has no effect on plasma total ghrelin concentrations

Abstract Ghrelin is a hormone that stimulates hunger. Intense exercise has been shown to temporarily suppress hunger after exercise. In the present study, we investigated whether post-exercise hunger suppression is mediated by reduced plasma total ghrelin concentrations. Nine men and nine women participated in the study. Their mean physical characteristics were as follows: age 24.8 (s x = 0.9) years, body mass index 22.9 (s x = 0.6) kg · m−2, maximal oxygen uptake ([Vdot]O2max) 57.7 (s x = 2.2) ml · kg−1 · min−1. The participants completed two 3-h trials (exercise and control) on separate days in a randomized balanced design after overnight fasts. The exercise trial involved a 1-h treadmill run at 73.5% of [Vdot]O2max followed by 2 h of rest. The control trial consisted of 3 h of rest. Blood samples were collected at 0, 0.5, 1, 1.5, 2, and 3 h. Total ghrelin concentrations were determined from plasma. Hunger was assessed following blood sampling using a 15-point scale. The data were analysed using repeated-measures analysis of variance. Hunger scores were lower in the exercise trial than in the control trial (trial, P = 0.009; time, P < 0.001; trial × time, P < 0.001). Plasma total ghrelin concentrations did not differ between trials. These findings indicate that treadmill running suppresses hunger but this effect is not mediated by changes in plasma total ghrelin concentration.

Influence of brisk walking on appetite, energy intake, and plasma acylated ghrelin

PURPOSE This study examined the effect of an acute bout of brisk walking on appetite, energy intake, and the appetite-stimulating hormone-acylated ghrelin. METHODS Fourteen healthy young males (age 21.9 +/- 0.5 yr, body mass index 23.4 +/- 0.6 kg x m(-2), (.)VO2max 55.9 +/- 1.8 mL x kg(-1) x min(-1); mean +/- SEM) completed two 8-h trials (brisk walking and control) in a randomized counterbalanced fashion. The brisk walking trial commenced with 60 min of subjectively paced brisk walking on a level-motorized treadmill after which participants rested for 7 h. Participants rested for the duration of the control trial. Ad libitum buffet meals were offered twice during main trials (1.5-2 and 5-5.5 h). Appetite (hunger, fullness, satisfaction, and prospective food consumption) was assessed at 30-min intervals throughout. Levels of acylated ghrelin, glucose, insulin, and triacylglycerol were determined from plasma. RESULTS Sixty minutes of brisk walking (7.0 +/- 0.1 km x h(-1) yielded a net (exercise minus resting) energy expenditure of 2008 +/- 134 kJ, yet it did not significantly influence appetite, energy/macronutrient intake, or the plasma concentration of acylated ghrelin either during or after exercise(P > 0.05). Participants did not compensate for energy expended during walking, therefore a deficit in energy was induced (1836 kJ, 439 kcal) relative to control. CONCLUSIONS This study demonstrates that, despite inducing a moderate energy deficit, an acute bout of subjectively paced brisk walking does not elicit compensatory responses in acylated ghrelin, appetite, or energy intake. This finding lends support for a role of brisk walking in weight management.