Tracking of physical activity from childhood to adulthood

PURPOSE: To examine 1) relationships between adult PA at 35 yr and PA as a child, and 2) the influence of enhanced primary school physical education (physed+) and of parental PA upon the long-term tracking of PA in the offspring. METHODS: PA data from the 1970-1977 Trois-Rivieres Growth and Development Study, completed when the children were aged 10-12 yr, were compared with PA data collected on 166 of the same subjects in 1996-1998, when aged 34.9 +/- 1.1 yr. The weekly duration of total PA, intense PA, light PA, organized PA, and total sedentary behaviors other than sleep as a child were each correlated with a questionnaire assessment of total weekly PA as an adult. RESULTS: Considering males and females jointly, adult PA showed a significant but weak association with childhood PA, correlations for total PA, intense PA, light organized PA, and nonorganized PA amounting to r = 0.20, 0.18, 0.12, and 0.19, respectively. In males (N = 79), the total time spent during childhood in organized PA was associated with adult PA (r = 0.26, P < 0.05), due to students who received physed+ (r = 0.34). In females, also, a higher PA frequency as an adult was significantly associated with physed+. There was no association of PA patterns between children and their parents. CONCLUSION: Our results suggest a positive impact of early required physical education upon adult PA but provide little evidence of an overall association between time spent in other categories of PA during childhood and PA as an adult.     

Test–retest errors and the apparent heterogeneity of training response

Published reports have shown large apparent inter-individual differences of gains in maximal oxygen intake (O_2max) in response to a standard 20-week programme of aerobic conditioning that progressed to 75% of the individuals initial O_2max. The observed gains of O_2max ranged from 0 to 1,000 ml min^–1, with a coefficient of variation (CV) of 8.4%. The present analysis evaluates the potential contribution of test–retest errors to these apparent large inter-individual differences in training response. The 2-day test–retest CV for O_2max readings in 742 healthy adults was initially 5.0%, dropping to 4.1% after training. Published training responses were estimated from the mean of paired measurements obtained before and after training if readings agreed by <5%, but from the highest of paired values if these differed by >5%. Taking account of the relative proportions of single and paired observations, the weighted O_2max data for the entire sample had an effective 2-day CV of 4.3% before and 3.4% after training. Assumption 1: if the 20-week test–retest error remained similar to the 2-day figure, measurement error would contribute a CV of 5.5% to apparent training responses, or (for the stated initial mean O_2max of 2,409 ml min^–1) an SD of 132 ml min^–1. Assumption 2: if the 20-week CV was similar to that in other long-term studies (~5%), measurement error would contribute a CV of 6.1%, or a SD of 146 ml min^–1. The published data show a total SD of 202 ml min^–1 for apparent inter-individual differences in training response, with age, gender, race and baseline O_2max accounting for only 11% of this variance. After estimating the likely effect of test–retest measurement errors, the SD due to inter-individual differences would decrease to 138 ml minO_2max (assumption 1) or 123 ml min^–1 (assumption 2). We conclude that when estimating the extent of inter-individual differences in training response, allowance must be made not only for the minor effects of recognized covariates (age, gender, race and initial fitness), but also for the larger influence of test-retest measurement errors. Nevertheless, substantial inter-individual differences persist after making such adjustments. The most likely explanation of these differences is a familial aggregation of training responses.     

Fumonisin B1-induced hepatocellular and cholangiocellular tumors in male Fischer 344 rats: potentiating effects of 2-acetylaminofluorene on oval cell proliferation and neoplastic development in a discontinued feeding study

Fumonisin B1 (FB1) is a naturally occurring mycotoxin produced by Fusarium verticillioides. Dietary exposure to FB1 has been linked to human cancer in certain parts of the world, and treatment with FB1 causes oval cell proliferation and liver tumors in rats. To study the potential role of oval (liver progenitor) cells in the cellular pathogenesis of FB1-induced liver tumors, we gave male F344 rats prolonged treatment with FB1 for 25 weeks, followed by return to control diet until 50 weeks ('stop study'). The time course of FB1-induced liver lesions was followed by examination of serial liver biopsies at set time intervals and post-mortem liver tissue at the end of the study. The effects of different FB1 treatment regimens (5 versus 25 weeks), as well as the modulating effect of 2-acetylaminofluorene (2-AAF), on the kinetics of oval cell proliferation and development of liver tumors were compared. Prolonged treatment with FB1 in normal diet caused persistent oval cell proliferation and generation of both hepatic adenomas and cholangiofibromas (CFs). These liver lesions occurred in the setting of chronic toxic hepatitis and liver fibrosis/cirrhosis, similar to that seen in human hepatocarcinogenesis. Some adenomas and CFs were dysplastic, and one post-mortem liver contained a hepatocellular carcinoma. OV-6+ oval cells were noted in close relation to proliferative neoplastic liver lesions, and some of these lesions expressed OV-6, suggesting that all these cell types were derived from a common progenitor cell. 2-AAF enhanced the size of FB1-induced glutathione S-transferase pi+ hepatocellular lesions and the incidence of CFs in post-mortem liver specimens, but this was not statistically significant. In conclusion, this study supports the involvement of dietary FB1 in liver carcinogenesis in male F344 rats. Oval cells may be the source of both the hepatocellular and cholangiocellular tumors induced by prolonged treatment with FB1. 2-AAF appears to have an enhancing effect on FB1-induced liver tumors, presumably due to its potent inhibitory effects on hepatocyte regeneration.     

Cytokine responses to physical activity,with particular reference to IL-6: sources,actions, and clinical implications

The present review examines the cytokine response to acute exercise stress, with particular emphasis on the balance between proinflammatory and anti-inflammatory mechanisms, and the release of IL-6. Prolonged endurance exercise induces a sequenced release of pro- and anti-inflammatory cytokines, and IL-6 plays a dominant role. The magnitude of this response bears a general relationship to the intensity of effort, but the duration of activity and many environmental factors also modulate cytokine release. Although many types of cells are capable of producing cytokines, the main source of the exercise-induced IL-6 production appears to be the exercising muscle. The primary function of the additional IL-6 may be to regulate the supply of carbohydrate as muscle reserves of glycogen become depleted. There is also a delayed release of cytokines following eccentric exercise that is related to the repair of muscle injury. Since the production of cytokines is greater with endurance than with resistance exercise, it seems unlikely that they play an important role in the hypertrophy of muscle and bone. More research is needed on a number of important clinical issues where the exercise-induced release of cytokines may have relevance. Exercise-induced cytokine secretion has the potential to provide a simple model of sepsis. Preliminary observations suggest it may also modulate the risk of type 2 diabetes mellitus. Cytokine concentrations are increased in chronic fatigue syndrome, although it is less dear that the cytokine secretion is responsible for fatigue in humans. Exercise-induced modulations in cytokine secretion may contribute to allergies, bronchospasm, and upper respiratory infections in the endurance athlete. Further, the cytokine cascade is involved in the process of atherogenesis, and exercise-induced changes in cytokine production may expose latent HIV to chemotherapeutic agents.     

Evidence-based medicine in primary care: qualitative study of family physicians

Background

The objectives of this study were: a) to examine physician attitudes to and experience of the practice of evidence-based medicine (EBM) in primary care; b) to investigate the influence of patient preferences on clinical decision-making; and c) to explore the role of intuition in family practice.

Method

Qualitative analysis of semi-structured interviews of 15 family physicians purposively selected from respondents to a national survey on EBM mailed to a random sample of Canadian family physicians.

Results

Participants mainly welcomed the promotion of EBM in the primary care setting. A significant number of barriers and limitations to the implementation of EBM were identified. EBM is perceived by some physicians as a devaluation of the 'art of medicine' and a threat to their professional/clinical autonomy. Issues regarding the trustworthiness and credibility of evidence were of great concern, especially with respect to the influence of the pharmaceutical industry. Attempts to become more evidence-based often result in the experience of conflicts. Patient factors exert a powerful influence on clinical decision-making and can serve as trumps to research evidence. A widespread belief that intuition plays a vital role in primary care reinforced views that research evidence must be considered alongside other factors such as patient preferences and the clinical judgement and experience of the physician.

Discussion

Primary care physicians are increasingly keen to consider research evidence in clinical decision-making, but there are significant concerns about the current model of EBM. Our findings support the proposed revisions to EBM wherein greater emphasis is placed on clinical expertise and patient preferences, both of which remain powerful influences on physician behaviour.

     

Regression to the mean. A threat to exercise science?

Regression to the mean (RTM) can bias any investigation where the response to treatment is classified relative to initial values for a given variable without the use of an appropriate control group. The phenomenon and resulting errors of interpretation have been recognised by clinicians in a number of disciplines. The causes of RTM include both intra-individual variance and measurement error. The magnitude of RTM can be estimated quite simply, given a knowledge of intra- and inter-individual variance. RTM can be avoided by using a fully controlled experimental design. Difficulties can also be minimised by making duplicate measurements prior to the experimental manipulation, the first measurement serving for classification, and the second (with randomly distributed variance) allowing an assessment of the response to treatment. Less satisfactorily, surrogate measurements (for example, plasma volume for maximal oxygen intake [VO2(max)]) can assess the bias introduced by an initial non-random sorting of study participants. The impact of RTM on the design and interpretation of investigations has as yet received little consideration by exercise scientists and sports physicians. The response to training is often related to initial measurements of a dependent variable such as heart size, ST segmental depression, fitness or level of physical activity. In particular, analyses of this type have been adduced to support the belief that the response to aerobic training is inversely related to an individual's VO2(max). In fact, RTM may account for a major part of this apparent relationship.