The Senior Athlete

An age-associated decline in cardiac output may be attributed to reductions in maximal heart rate, myocardial contractility, and stroke volume; these changes can result in an age-related drop in myocardial oxygen consumption/utilization (mVO ₂ ).

Regular cardiovascular exercise and endurance training have been shown to increase mVO ₂ in individuals aged up to 70 years.

Fatty and fibrous tissue deposits may occur in the myocardium that can interrupt normal conduction pathways, contributing to the occurrence of arrhythmias.

Cardiac valves may thicken and lose compliance, contributing to the formation of valvular regurgitation, clinically manifesting as a murmur.

Vascular physiology is affected by age-related changes in vascular compliance, microcirculation, and baroreceptor function; these changes, combined with atherosclerosis, can produce an increased peripheral vascular resistance, resulting in increased cardiac effort to maintain cardiac output.

• Increased blood pressure and orthostatic hypotension are commonly observed as consequences of vascular changes.

• Decreased capillary density and impaired vascular proliferation have also been implicated in reducing the exercise capacity of aging individuals.

Reduction in pulmonary microvasculature and alveoli number results in limitations in oxygen exchange and an increased sense of respiratory effort exerted during exercise.

Decreased lung compliance results from weakness of respiratory and accessory muscles, decreased alveolar tissue elasticity, and stiffening of costovertebral and sternocostal cartilages.

Overall, these changes contribute to a decrease in total lung capacity; vital lung capacity; inspiratory and expiratory air flows; and an increase in residual volume, respiratory frequency, and work of breathing.

A progressive loss in the number of glomeruli, along with increased vascular rigidity and atherosclerosis, results in a decreased glomerular filtration rate with aging. Coexisting renal disease and nephrotoxic medications can exacerbate this age-related decline.

In addition, the ability of the kidneys to concentrate urine decreases with age, resulting in a greater relative water output; this can negatively affect a senior athlete’s ability to remain adequately hydrated.

Progressive central nervous system deterioration has been shown to result in impaired hearing, short-term memory, balance, fine motor skills, and cognition. In addition, extrapyramidal dysfunction can result in impaired coordination and rapidity of motions and with a resultant increase in motor response time.

Even in the absence of any known neurologic disease, peripheral nerve conduction velocities are known to decrease with age, affecting vibration and proprioception nerve fibers first.

Progressive vision impairment is common with age. Typical changes include decreased visual acuity, accommodation, contrast sensitivity, peripheral vision, and ability to adapt to low-light situations.

As part of a normal consequence of aging, hormone levels gradually decline. Effects of this decline are noted in multiple organ systems:

• With age, basal metabolic rate decreases, along with increased rates of metabolic syndrome, diabetes mellitus type 2, and obesity.

• Adrenal function is reduced, resulting in decreased aldosterone and reduced ability to regulate fluid/electrolyte balance, as well as decreased stress response by cortisol.

• Moreover, decreased rates of trophic hormones such as testosterone and insulin-like growth factor are associated with a decrease in skeletal muscle mass with age.

Senile sarcopenia is the age-related decrease in skeletal muscle mass. Between the ages of 50 and 80 years, an average person will lose one-third of their muscle mass. At the cellular level, decreased cell numbers and proliferative capacity of satellite cells leads to decreased muscle regeneration and response to injury. Extracellularly, dysfunction of actin-myosin cross-linking causes muscle units to become stiffer and more susceptible to injury, particularly muscular strains.

The structure of both ligaments and tendons changes with aging. Aging ligaments exhibit fewer fibroblasts and mechanoreceptors, which may contribute to decreased ultimate failure load and mechanical stiffness. On the other hand, aging tendons exhibit fewer fibroblasts and increased degenerative changes; this, along with a less robust blood supply (watershed areas), helps explain the epidemic of tendon injuries in senior athletes.

Articular cartilage is particularly susceptible to injury and degeneration with aging ( Fig. 13.1 ). Few, if any, chondrocytes are produced after skeletal maturity. Production of extracellular matrix proteoglycans is more variable with time, rendering them less effective. Response to mechanical loading is impaired by decreasing cartilage water content and more rigid collagen fibrils, secondary to increased cross-linking, which increases the risk of fissuring or shear injury.

With age, a progressive loss of bone mineral density results in compensatory widening of the diaphysis. Consequently, the susceptibility to fragility fractures and stress injuries increases.

Men exhibit a 0.5%–0.75% annual loss of bone mass after the age of 40 years. In women, bone mass decreases much more rapidly, at a pace of 1.5%–2.0% before menopause and accelerating further after menopause to up to 3% per year.