Adaptations to Aerobic and Resistance Exercise in the Elderly

Maximal aerobic exercise capacity (VO2 max) is the product of maximal cardiac output (Q) and the maximal arteriovenous oxygen difference (A-VO2diff) (VO2 = Q X AVO2). Generally speaking, cardiac output represents oxygen delivery to the working muscle and A-VO2 difference is oxygen extraction at the muscle tissue level. Maximal Q is product of stroke volume (SV), the amount of blood pumped per heart beat, and heart rate (HR) or the number of times the heart beats/min (Q = SV X HR). VO2 max declines ∼1%/year after the age of 25 in non-training individuals [1–3]. Thus, the VO2 max of an untrained elderly individual is significantly lower than that of an untrained young individual. However, this decline in maximal oxygen consumption is ∼0.5%/year in master athletes who participate in aerobic activities [4]. Further, Pollock et al. [5] reported that there was a non-significant 1.7% decline in VO2 max over 10.1 years in master athletes who remained competitive and maintained their training intensity while in other master athletes who continued to train but reduced their training intensity there was a significant 12.6% decline in VO2 max over the 10.1 year period. The reason for the decline in maximal aerobic capacity in sedentary individuals is likely due to 3 major factors. A decline in maximal cardiac output [6], a decline in muscle oxidative capacity due to aging and/or inactivity [7], and a decline in metabolically active muscle mass with a concomitant increase in metabolically inactive fat mass [8]. To examine the effect of the reduction in muscle mass/and increase in fat mass in the elderly on VO2 max, Proctor et al. [8] expressed VO2 max relative to appendicular muscle mass. These investigators reported that ∼50% of the decline in VO2 max with aging was accounted for by the decline in muscle mass and increase in fat mass. Thus, the other ∼50% was related to a decline in oxygen delivery and/or oxygen extraction. Other investigators have reported that the decline in fat free mass accounts for ∼35% of the decline in VO2 max [9]. It is clear that the maximal cardiac output declines with aging but whether muscle oxidative capacity (which is a major determinant of A-VO2 difference) declines with aging is a question that is presently under scientific debate. The results of early studies of aerobic exercise training in the elderly suggested that there was little adaptation in aerobic capacity [10–13]. These early studies have been criticized as a result of the exercise intensity being inadequate to stimulate adaptation. Subsequent studies with relatively high exercise intensities suggested that the magnitude of the adaptation in fitness level of elderly individuals is similar to that of younger individuals [14–18]. In a seminal study, Kohrt et al. [17] had elderly individuals (age 60–71) exercise 4 days/wk, 45 min/day for 9–12 months with exercise intensity gradually increasing from 76% of heart rate maximum to ∼83% of heart rate maximum over the training period. These investigators reported a significant improvement of VO2 max of 24%. When subjects were grouped by age (60–62, 63–66, and 67–71 years) there were no differences between groups in the improvement of VO2 max. Similar increases in VO2 max have been observed by other investigators utilizing strenuous aerobic exercise training [14–16]. Elderly women appear to adapt to exercise training with similar increases in VO2 max as elderly men. Interestingly, however, the mechanism by which elderly men and women increase their VO2 max appears to be different. Using a similar exercise training paradigm as Kohrt et al. [17], Spina et al. [19] reported that ∼66% of the improvement in VO2 max in elderly men was due to an increase in cardiac output and more specifically stroke volume. However, in elderly women these investigators reported that the improvement in VO2 max was due to an enhanced A-VO2 difference with no change in cardiac output. Spina et al. [20,21] using echocardiography, the drug atropine (which releases vagal tone) and the β-adrenergic agonist isoproterenol reported that the endurance exercise training in women had no effect on left ventricular function or left