Distinguishing capacity from power.
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Biomedical subjects
Publications and source records attributed to Roy J Shephard.
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The circulating blood normally contains no more than 1-2% of the body's population of leucocytes. The numbers and phenotypes of circulating leucocyte subsets can change dramatically during and immediately following exercise. The surface expression of adhesion molecules makes an important contribution to such responses by changing patterns of cell trafficking. Alterations in the surface expression of adhesion molecules could reflect a shedding of molecules, selective apoptosis or differential trafficking of cells with a particular phenotype, effects from mechanical deformation of the cytoplasm, active biochemical processes involving cytokines, catecholamines, glucocorticoids or other hormones, or changes in the induction of adhesion molecules. The expression of adhesion molecules changes with maturation and activation of leucocytes. Typically, mature cells express lower densities of L-selectin (CD62L), the homing receptor for secondary lymphoid organs, and higher densities of LFA-1 (CD11a), the molecule associated with trafficking to non-lymphoid reservoir sites. The neutrophils and natural killer cells that are mobilised during exercise also express high levels of Mac-1 (CD11b), a marker associated with cellular activation. Possibly, exercise demarginates older cells that are awaiting destruction in the spleen. Plasma concentrations of catecholamines rise dramatically with exercise, and there is growing evidence that catecholamines, acting through a cyclic adenosine monophosphate second messenger system, play an important role in modifying the surface expression of adhesion molecules. Analogous changes can be induced by other forms of stress that release catecholamines or by catecholamine infusion, and responses are blocked by beta(2)-blocking agents. Catecholamines also modify adherence and expression of adhesion molecules in vitro. Cell trafficking is modified by genetic deficiencies in the expression of adhesion molecules, but leucocyte responses to exercise and catecholamines are generally unaffected by splenectomy. A number of clinical conditions including atherogenesis and metaplasia are marked by an altered expression of adhesion molecules. The effects of exercise on these molecules could thus have important health implications.
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.
Physical stress is associated with circulating cytokinemia. However the mechanisms of cytokine regulation during such stress are not clearly defined. Non-steroidal anti-inflammatory drugs (NSAIDs), including indomethacin, are widely used in countering the effects of excessive exercise, but their impact on circulating pro- and anti-inflammatory cytokine production in healthy humans also remains unclear. This study investigated the effect of five days of oral indomethacin treatment (75 mg per day) on the serum concentrations of IL-6, IL-10, IL-12, and TNF-alpha induced by exercising healthy volunteers. The results demonstrate that indomethacin does not alter resting serum cytokine concentrations. Increased circulating levels were noted, however, for all four cytokines with exercise, but with a different time-course. During and after strenuous physical exercise, indomethacin treatment blunted serum IL-6, and augmented TNF-alpha and IL-10. These findings may have important implications for both host defense and the injuries associated with excessively vigorous exercise.
BACKGROUND: Predicting the risk of cardiac and all-cause death in patients with established coronary heart disease is important in counseling the individual and designing risk-stratified rehabilitation and secondary prevention programs. Cox proportional hazards and Kaplan-Meier survival curves were thus completed on initial assessment data obtained from patients referred to an outpatient cardiac rehabilitation center. METHODS AND RESULTS: A single-center prospective observational design took peak cardiorespiratory exercise test data for 12 169 male rehabilitation candidates aged 55.0+/-9.6 years (7096 myocardial infarctions [MIs], 3077 coronary artery bypass grafts [CABGs], and 1996 documented cases of ischemic heart disease [IHD]). A follow-up of 4 to 29 years (median, 7.9) yielded 107 698 man-years of experience. Entry data were tested for associations with time to cardiac and all-cause death. We recorded 1336 cardiac deaths (953 MI, 225 CABG, and 158 IHD) and 2352 all-cause deaths. A powerful predictor of cardiac and all-cause mortality was measured peak oxygen intake (VO2peak). For the overall sample, values of <15, 15 to 22, and >22 mL/kg per minute yielded respective multivariate adjusted hazard ratios of 1.00, 0.62, and 0.39 for cardiac and 1.00, 0.66, and 0.45 for all-cause deaths. For the separate diagnostic categories, apart from VO2peak, the only other significant predictors of cardiac death common to all 3 were smoking and digoxin, and for all-cause death, age, smoking, digoxin, and diabetes. CONCLUSIONS: Exercise capacity, as determined by direct measurement of VO2peak, exerts a major long-term influence on prognosis in men after MI, CABG, or IHD and can play a valuable role in risk stratification and counseling.
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Human Rights Tribunals require application of non-discriminatory fitness standards in the hiring, promotion, and retention of employees. This issue has become controversial for public safety officers such as police, where differences in average levels of absolute fitness between men and women cause a high proportion of female applicants to fail many entrance tests. The present review summarizes the impact on physical working capacity of commonly encountered gender differences in size, body composition, haemoglobin levels, and muscular strength. The principles applied in designing content- and construct-validity occupational fitness tests are described, and Human Rights policies are reviewed in the light of the Meiorin judgment. Criteria are indicated for establishing a bona-fide occupational fitness requirement, and description is given of the approach used in developing standards that satisfy these criteria. Requirements are based on the task to be accomplished. The potential training response of female applicants is likely at least to match that of their male peers, and the needs of female police recruits are thus best accommodated by providing every opportunity to augment fitness to the required minimum level. The main weakness of any current requirement is that most police forces do not yet apply an equivalent criterion to older incumbent officers, where similar issues may arise.
Ethical evaluation is a vital but sometimes neglected component of research policy in the exercise sciences. This article reviews some issues in human research, with particular reference to studies undertaken by the exercise scientist. The typical composition and functions of the research review committee are examined in the context of individual and institutional ethical norms. In multicentre trials, there are often problems in coordinating ethical approval between institutions. On-going monitoring of research may have value in the detection of fraud. A reduction in the secrecy of committee proceedings would allow a closer auditing of the research review process. Authors need to give more thought to developing appropriate research questions. Scarce resources may be wasted because of inappropriate study design or an inadequate statistical analysis of the results. The costs of any proposed investigation must be weighed carefully against possible benefits. Confidentiality is particularly important when collecting data at the worksite or over the internet. Informed consent should be based on a full disclosure of risks; the participant should be competent to understand the nature and magnitude of these risks, and undue pressure to participate in an experiment must be avoided. The opposition to placebo trials expressed in the Declaration of Helsinki requires careful consideration of the use of control groups, since regular exercise is known to benefit health. If research is conducted in under-developed societies, the standards of treatment of the participants should match those expected in developed societies. The publication of findings must be fair and well balanced; examples of fraud and misconduct continue to be reported. Some journals apparently still publish papers, even if they have not received an initial institutional review. Editors should restore meaning to the word 'author', avoid the bias to a publication of 'positive' results, limit the impact of commercial sponsorship on reporting and curtail the current trend to redundant presentations and publications. Development of academic courses in research ethics may help to avoid some of these abuses.
Several issues arise on reading the paper by Netz and Raviv. Their role in interpretation of the data and stimulating questions for further study is mentioned.
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.
This study evaluated intraindividual child-adult and interindividual child-parent relationships of body mass index (BMI) using data from the Trois-Rivières semilongitudinal study of growth and development. Intraindividual correlations between age 12 and 35 years were substantial (r(2) = 36% of variance in women, 30% of variance in men). Interindividual child-parent correlations for mothers and fathers age 36.6 +/- 0.4 and 39.5 +/- 0.4 years, respectively, were very low to low for daughters age 12 years (r = 0.09, NS and 0.34, P < 0.001 vs. father and mother, respectively) but all very low for sons age 12 years (r = 0.07, NS and 0.16, NS vs. father and mother, respectively). A multiple regression analysis predicted adult BMI from the individual's BMI at 10, 11, 12 years plus the maternal and paternal BMIs as calculated from self-reported heights and weights. The BMI at age 12 years was a better predictor of adult BMI than the parental BMI in both men and women (P < 0.001) and multivariate analysis revealed that this index at age 12 years was the sole significant predictor of adult BMI for both men and women. The results from our study do not support the hypothesis that parental BMI is a stronger predictor of adult BMI than childhood BMI. However, useful information for the prediction and prevention of adult overweight can be obtained from the BMI at age 12 years. Our results suggest that environmental influences may be the major factor in the present obesity epidemic.
Physical activity is an important part of the World Health Organization's integrated approach to the prevention and control of noncommunicable disease and the promotion of health, and, in particular, to the evolving World Health Organization Global Strategy on Diet and Physical Activity. To assist in these efforts, a joint World Health Organization/Centers for Disease Control and Prevention Consultation on Physical Activity Policy Development took place in Atlanta, Georgia, from September 29 through October 2, 2002. This article summarizes the context and outcomes of the consultation. It also includes elaboration of a Comprehensive Physical Activity Policy Framework developed as a product of the meeting.
Prescribing exercise for cardiac patients is comparable in many ways to prescribing medications; that is, one recommends an optimal dosage according to individual needs and clinical status. Recent research has shown that it is more accurate to prescribe exercise as a percentage of the oxygen uptake reserve (VO2R), which is the difference between resting and maximal or peak oxygen consumption, rather than as a percentage of the VO2 max. Moreover, it appears that a minimum of 1600 kcal/week of leisure-time physical activity may halt the progression of coronary artery disease, whereas regression may be achieved with a gross energy expenditure of 2200 kcal/week. Upper body and resistance training have also been shown to be safe and effective for clinically stable patients. Aerobic capacity serves as an independent predictor of all cause and cardiovascular mortality in patients referred to an outpatient cardiac rehabilitation program, with each 1 metabolic equivalent increase in aerobic fitness conferring an approximate 10% reduction in mortality. The goal of preventing recurrent cardiac events is, to a large extent, based on sustained compliance to multifactorial interventions, which can be influenced by numerous socioeconomic and clinical variables, and enhanced by home-based or group cardiac rehabilitation programs that are designed to circumvent or attenuate barriers to participation and adherence, so that many more individuals may realize the benefits that secondary prevention can provide.
PURPOSE: Cardiac rehabilitation is an integral component of comprehensive care for patients with coronary heart disease. Although the typical programmatic delivery of outpatient cardiac rehabilitation services often involves 36 sessions over 12 weeks, that format is based more on historical practice than on outcome data. This study aimed to determine the point at which during 52 weeks of outpatient cardiac rehabilitation, patients achieved peak values for selected outcomes, and whether the number of supervised exercise sessions had any effect on these outcomes. METHODS: In this study, 623 male patients with coronary heart disease admitted to an outpatient cardiac rehabilitation program were randomized to one of two 52-week program formats. One format (CR1) used one supervised exercise session per week over 52 weeks, and the second format (CR2) used weekly supervised sessions for 26 weeks followed by one supervised session per month for the remaining 26 weeks. Both formats used four unsupervised, documented exercise sessions per week. Selected clinical, physiologic, and psychological variables were measured at baseline, then at 4, 12, 26, 38, and 52 weeks. The program costs for both the CR1 and CR2 formats were calculated from known expenses. RESULTS: Because there were no significant intercohort differences between CR1 and CR2 and no significant interaction (time x group), data from the two cohorts were pooled for statistical analysis. Peak oxygen intake (VO(2peak)) significantly increased by 4.4 mL/kg per minute at 38 weeks, and the greatest percentage of patients (30.1%) also achieved their highest VO(2peak) at this time. The largest gain in Medical Outcomes Survey Short Form 36 role physical scores was from baseline to 38 weeks (52.4 versus 85.2), and the highest percentage of patients (72%) with role physical scores in the excellent category occurred at 38 weeks. Clinical depression at baseline (Beck Depression Inventory score > 10) had no significant effect on the dropout rate or the gain in VO(2peak) with exercise training. Program costs for these alternative formats of service were similar to the cost for a standard program format of 36 sessions. CONCLUSIONS: Patients achieved their highest functional capacity after 38 weeks of outpatient cardiac rehabilitation using a program format of only 29 to 38 supervised exercise sessions. The results of this study show that an outpatient cardiac rehabilitation program combining supervised with unsupervised exercise sessions and continuing for 38 weeks results in the greatest improvement in these selected outcomes.