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Numerous interventions have been designed to modify children's physical activity and eating behaviors. While early research centered on the individual as the target of intervention, more recent work targets change in the environment. These studies have consistently supported the importance of environmental contributors to both physical activity and eating behavior, but little research has considered those who are responsible for implementing environmental change. For example, if we expect school environments to support activity and healthy eating, we must consider the motivation of school administrators to affect change. This review will present examples of an ecological approach to behavior change along with recent data to support this approach.

People with newly acquired and existing disability have one of the highest rates of physical inactivity compared with any other subgroup in the United States. For more than 50 million Americans with disabilities, lack of regular exercise increases their risk for developing the health problems associated with a sedentary lifestyle. Professionals in rehabilitation and exercise science must join forces in promoting higher levels of physical activity among people with newly acquired or existing disability after they are discharged from rehabilitation. Establishing a strong and cohesive relationship between rehabilitation providers and exercise professionals at the ‘infection point’ when rehabilitation ends and sustainable exercise must begin will capture individual awareness and knowledge of how and why extending the recovery process into community-based exercise facilities has substantial potential for improving their health and quality of life.

The concept that participation in exercise/physical activity reduces the risk for a host of chronic diseases is undisputed. Along with adaptations to habitual activity, each bout of exercise induces beneficial changes that last for a finite period of time, requiring subsequent exercise bouts to sustain the benefits. In this respect, exercise/physical activity is similar to other “medications” and the idea of “Exercise as Medicine” is becoming embedded in the popular lexicon. Like other medications, exercise has an optimal dose and frequency of application specific to each health outcome, as well as interactions with food and other medications. Using the prevention of type-2 diabetes as an exemplar, the application of exercise/physical activity as a medication for metabolic “rehabilitation” is considered in these terms. Some recommendations that are specific to diabetes prevention emerge, showing the process by which exercise can be prescribed to achieve health goals tailored to individual disease prevention outcomes.

In this paper, I argue that physical activity in the form of exercise provides wonderful health benefits for individuals with chronic stroke but fails to also reduce the wider effects of disability for these individuals. The argument proceeds first with a definition of terms, including the classification framework of health and disability according to the World Health Organization. Next follows a section on stroke, its prevalence, and major motor symptoms, including health status. The subsequent two sections include evidence for the health benefits of exercise and lack of evidence for the reduction of disability. The penultimate section expands upon the direction of research that should move us toward reducing disability. The final section concludes on how kinesiology fits into a model for improving both health and reducing disability for chronic stroke survivors.

Exercise immunology is a relatively new discipline in the exercise sciences that seeks to understand how exercise affects the immune system and susceptibility to infectious and chronic diseases. This brief review will focus on three major observations that have driven the field to date including: (1) acute exercise-induced leukocytosis, (2) the observation that intense, prolonged exercise results in upper respiratory tract symptoms, and (3) the paradoxical effect of acute and chronic exercise on inflammation. This framework will be used to examine the mechanisms and implications behind these seminal observations. Data generally support the conclusion that moderate intensity exercise enhances immune function, whereas prolonged, intense exercise diminishes immune function.

Alzheimer's disease is a chronic illness characterized by clinical cognitive impairment. A behavioral strategy that is being explored in the prevention of Alzheimer's disease is physical activity. Evidence from randomized controlled trials (RCTs) testing the effects of physical activity for cognitively normal older adults supports that physical activity benefits cognitive performance. Evidence from prospective studies supports a protective effect of physical activity with reductions in the risk of cognitive decline ranging from 28% to 45%. RCTs with cognitively impaired older adults also generally support positive effects with greater benefits evident for aerobic interventions. Research examining the potential moderating role of apolipoprotein E (APOE) has yielded mixed results, but the majority of the studies support that physical activity most benefits those who are at greatest genetic risk of Alzheimer's disease. Future directions for research are considered with an emphasis on the need for additional funding to support this promising area of research.

Physical activity has long been touted as a means of reducing susceptibility to age-related disease and multiple studies have shown reduced mortality rates in individuals with a lifestyle including regular exercise. A variety of mechanisms for how physical activity reduces age-related diseases have been explored and multiple, redundant explanatory mechanisms are likely to emerge. Evidence has emerged that physical activity may impact directly on telomere biology, one of the primary theories of cellular aging. Telomeres are located at the ends of chromosomes and as cells divide, incomplete DNA replication results in telomere shortening; once shortening reaches a critical threshold, cell senescence results. Investigators hypothesize that part of the favorable influence of physical activity on mortality rates and age-related disease occurs through a direct impact on telomere biology, including delaying rates of telomere shortening. The present review examines key recent findings in this area and explores some of the unanswered questions and future directions for the field.

A traditional focus of exercise scientists studying the interaction of drugs and exercise has been on the effects of drugs on exercise performance or functional capacity. In contrast, there is limited information available about the effects of exercise on the efficacy of drugs that have been prescribed and ingested for therapeutic reasons. Those requesting the approval for the manufacture, distribution, and sale of new drugs to the public are required to submit evidence of drug effectiveness and safety to drug regulatory bodies. But, there is no associated requirement to include among that evidence the interactions of exercise with drugs. However, the physiological adaptations to acute and chronic exercise are such that there is good reason to suspect that exercise has the potential to significantly influence drug absorption and bioavailability, drug distribution within the body, and drug elimination from the body. This paper reviews the potential for interaction between exercise and pharmacokinetics.