Because of the influence of cardiorespiratory fitness on functional independence, quality of life, and cardiovascular disease and all-cause mortality, tremendous interest has been directed towards describing the age-related change in maximal oxygen consumption (VO(2max)). Current evidence supports a 10% per decade decline in VO(2max) in men and women regardless of activity level. High-intensity exercise may reduce this loss by up to 50% in young and middle-aged men, but not older men, if maintained long term. Middle-aged and older women do not appear to be able to reduce loss rates in VO(2max) to less than 10% per decade, which may be related to estrogen status. However, maintaining high-intensity training seems limited to approximately one decade at best and to a select few individuals. While the factors limiting the ability to maintain high-intensity training are not completely known, aging most likely plays a role as studies have demonstrated that training maintenance becomes more difficult with advancing age. Age-related loss of VO(2max) seems to occur in a non-linear fashion in association with declines in physical activity. In sedentary individuals, this non-linear decline generally occurs during the twenties and thirties whereas athletic individuals demonstrate a non-linear decline upon decreasing or ceasing training. Non-linear loss rates are also demonstrated in individuals over the age of 70 years. The decline in VO(2max) seems to be due to both central and peripheral adaptations, primarily reductions in maximal heart rate (HR(max)) and lean body mass (LBM). Exercise training does not influence declines in HR(max), while LBM can be maintained to some degree by exercise. Recommendations for exercise training should include aerobic activities utilising guidelines established by the American College of Sports Medicine for improving CV fitness and health, as well as strength training activities for enhancing LBM.

In conclusion, these data suggest that VO2max declines in male and female master athletes at a rate similar to or greater than that expected in sedentary older adults. Additionally, these data suggest that maintenance of LBM and VO2max were associated in men, whereas in women, estrogen replacement and maintenance of training volume were associated with maintained VO2max.

Although limited by the lack of a sedentary comparison group, these data suggest that age-related losses in VO2max may not be different from data previously reported for older sedentary adults and that loss in muscle strength and performance with aging is not linear.

Exercise as a therapeutic or prophylactic measure is a topic of particular interest in sarcopenia research. Clearly, exercise can be effectively utilized in the treatment of sarcopenia to recover muscle mass and muscle function in older adults. However, perhaps a more important question is the role of exercise in the prevention of age-related decrements in physiological capacities and function. The master athlete has been proposed as an ideal model to determine successful aging due to his or her chronic participation in high-intensity exercise. While extensive research has been conducted describing the age-related decrements in maximal aerobic capacity, the influence of chronic exercise on muscle mass and muscle function has not been as extensively studied. This article reviews the existing evidence concerning the influence of chronic exercise on body composition and skeletal muscle mass, and proposes areas that remain unstudied.