A 30-Year Follow-Up of the Dallas Bed Rest and Training Study

Abstract

Background-Aerobic power declines with age. The degree to which this decline is reversible remains unclear. In a 30-year longitudinal follow-up study, the cardiovascular adaptations to exercise training in 5 middle-aged men previously trained in 1966 were evaluated to assess the degree to which the age-associated decline in aerobic power is attributable to deconditioning and to gain insight into the specific mechanisms involved. Methods and Results-The cardiovascular response to acute submaximal and maximal exercise were assessed before and after a 6-month endurance training program. On average, V O 2max increased 14% (2.9 versus 3.3 L/min), achieving the level observed at the baseline evaluations 30 years before. Likewise, V O 2max increased 16% when indexed to total body mass (31 versus 36 mL/kg per minute) or fat-free mass (44 versus 51 mL/kg fat-free mass per minute). Maximal heart rate declined (181 versus 171 beats/min) and maximal stroke volume increased (121 versus 129 mL) after training, with no change in maximal cardiac output (21.4 versus 21.7 L/min); submaximal heart rates also declined to a similar degree. Maximal AVDO 2 increased by 10% (13.8 versus 15.2 vol%) and accounted for the entire improvement of aerobic power associated with training. Conclusions-One hundred percent of the age-related decline in aerobic power among these 5 middle-aged men occurring over 30 years was reversed by a 6-month endurance training program. However, no subject achieved the same maximal V O 2 attained after training 30 years earlier, despite a similar relative training load. The improved aerobic power after training was primarily the result of peripheral adaptation, with no effective improvement in maximal oxygen delivery.

Exercise-training-induced changes in metabolic capacity with age: the role of central cardiovascular plasticity

“…Specifically, the typically lower initial baseline VO 2max in the old subjects mathematically biases this assessment of improvement in favor of the older subjects. Therefore, previous studies have indeed revealed robust improvements in VO 2max , presented as a percentage change, of 10-30 % in older subjects after training interventions lasting between 8 weeks and 1 year (Coggan et al 1992;Fujimoto et al 2010;Kohrt et al 1991;Makrides et al 1990;McGuire et al 2001b;Murias et al 2010;Osteras et al 2005). These percentage improvements in VO 2max are comparable, if not even higher than the improvements sometimes documented in young subjects Makrides et al 1990;Murias et al 2010).…”

“…Typically, maximal oxygen consumption (VO 2max ) falls steadily from 35 to 40 years of age at a rate of ∼10 % per decade (Fleg et al 2005;Hawkins and Wiswell 2003;McGuire et al 2001a;Ogawa et al 1992;Tanaka and Seals 2008). Although this decline in aerobic capacity with increasing age is often considered to be inevitable, it seems that this fall can be decelerated, maintained, or even reversed in the elderly by maintaining a high level of physical activity (Faulkner et al 2008;Fujimoto et al 2010;Grimsmo et al 2010;Heath et al 1981;McGuire et al 2001b;Murias et al 2010;Osteras et al 2005;Posner et al 1986;Rogers et al 1990;Trappe et al 2013;Trappe et al 1996).…”

“…Although this decline in aerobic capacity with increasing age is often considered to be inevitable, it seems that this fall can be decelerated, maintained, or even reversed in the elderly by maintaining a high level of physical activity (Faulkner et al 2008;Fujimoto et al 2010;Grimsmo et al 2010;Heath et al 1981;McGuire et al 2001b;Murias et al 2010;Osteras et al 2005;Posner et al 1986;Rogers et al 1990;Trappe et al 2013;Trappe et al 1996). Indeed, marathon running times of approximately 2.5 h or less, documented in males older than 60 years of age, reveal that a VO 2max of ∼70 mL min kg −1 (Helgerud 1994;Tokmakidis et al 1987), a high value exhibited by young endurance athletes at the peak of their careers, is still feasible with increasing age.…”

Optimal health and function among the elderly: lessening severity of ADL disability

“…As a consequence, mitochondrial partial dysfunction occurs due to unmatched or perhaps intrinsic mitochondrial function and regulation (abnormal mitochondrial function) and hence the inability of skeletal muscles to fully extract oxygen from the arterial blood due to considerably reduced normal oxygen conductance from the muscle capillary to the mitochondria [44]. The latter is most likely associated with a poor muscle microcirculatory network and capillarymyofiber dissociation [43]. The molecular defect in subjects with mitochondrial myopathies commonly involves the mitochondrial genome, with the detection of either single large-scale deletions or point mutations [46].…”

Muscular strength after total hip arthroplasty

“…Inactivity reduces muscular strength and physical function (McGuire et al 2001, Suesada et al 2007, Kortebein et al 2008), and muscular strength decreases substantially in the first week after total hip arthroplasty (THA) (Holm et al 2013). Early recovery and rehabilitation of the weakened musculature is therefore of importance (Sicard-Rosenbaum et al 2002).…”