LITMIR.BIZ

Скачать книгу

sleep duration, sleep efficiency Decrease Cognitive processing speed, accuracy Decrease, no change Attention span Decrease, no change Memory No change, decrease Executive function Decrease, no change Motor coordination, force control Decrease Neural reaction time, neural recruitment Decrease Autonomic nervous system function Decrease

      REM, rapid eye movement.

      Although changes in absolute work capacity (aerobic fitness or maximal oxygen consumption) are immediately noticeable and disastrous for an elite athlete, they may accrue insidiously in non‐athletic populations because most sedentary individuals rarely call upon themselves to exert maximum effort in daily life. Women are particularly susceptible here because their initial reserve of muscle mass is so much lower than that of men, owing to gender differences in the anabolic hormonal milieu and also lifestyle/occupational factors. Therefore, they cross the threshold where losses of musculoskeletal capacity (sarcopenia) impact frailty/functional status at least 10 years before men do on average.

Another important consequence of age‐related changes in physiological capacity is the increased perception of effort associated with submaximal work (a lowering of the anaerobic threshold or the approximate level at which significant dyspnoea occurs). This changing physical capacity has the unfortunate negative side effect of increasing the tendency to avoid stressful activity. Such behavioural change compounds the sedentariness caused by changing job requirements or retirement, societal roles and expectations, and other psychosocial influences. Thus, a vicious cycle is set up: ‘usual’ ageing leading to decreasing exercise capacity, resulting in an elevated perception of effort, subsequently causing avoidance of activity, and finally feeding back to exacerbation of the age‐related declines secondary to the superimposition of disuse on biological ageing.

      As noted above, ageing is associated with declines in muscle function and cardiorespiratory fitness, resulting in an impaired capacity to perform daily activities and maintain independent functioning.^47‐49 Insufficiently active individuals lose large amounts of muscle mass over the course of adult life (20–40%), and this process plays a significant role in the similarly large losses in muscle strength observed in both cross‐sectional and longitudinal studies,⁵⁰ with the combination of the two termed sarcopenia. However, unlike many other changes that impact exercise capacity, muscle mass cannot usually be maintained into old age even with regular aerobic activities in either general populations or master athletes. Only overloading muscle with weight‐lifting exercise (resistance training) has been shown largely to avert losses of muscle mass (and strength) in older individuals. For example, Klitgaard et al.⁵¹ found that elderly men who swam or ran had age‐related reductions in muscle size, strength, and metabolism similar to their sedentary peers, whereas the muscle of older men who had been weight‐lifting for 12–17 years was almost indistinguishable, and even superior in some aspects, to that of healthy men 40–50 years younger than them.

Skeletal muscle power decreases to an even greater extent than muscle strength with advancing age^48,52 and is more strongly associated with functional test performance than muscle strength in older populations,^52,53 as well as being important for balance⁵⁴ and fall risk. One of the major contributing factors to the loss of strength and power is a gradual of reduction in cycles of degeneration/regeneration of spinal motor neurons. Partial functional muscle denervation following by reinnervation of abandoned fibres is also believed to occur, resulting in an increased size of remaining motor units (type grouping) that results in impaired force steadiness and fine motor control with ageing.^53,55,56 Moreover, age‐related decline in strength may also be due to decreased maximal voluntary activation of the agonist muscles or changes in degree of agonist‐antagonist coactivation.⁵⁷

      This age‐related loss of spinal motor neurons leads to a decline in the size and/or number of individual muscle fibres, especially fast‐twitch fibres.^58,59 The consequences include impaired mechanical muscle performance (i.e., reduced maximal muscle strength, power) that can adversely affect an older person's ability to remain functionally independent to perform daily activity tasks⁶⁰ (e.g., walking, stair climbing, rising from a chair). Along with a decrease in muscle size, ageing is also associated with a decrease in muscle quality due to increased amount of intramyocellular adipose tissue and connective tissue.^61,62 Physical inactivity greatly exacerbates the catabolism and atrophy of skeletal muscle associated with normal ageing.

      Many studies suggest that habitual engagement in physical activity/exercise can markedly attenuate most decrements in exercise capacity that would otherwise occur with ageing (see Tables 7.1–7.4), with the notable exception of maximal heart rate (due to declining sensitivity to β‐adrenergic stimulation in the ageing heart).⁶³ Although the peak exercise workload achievable is therefore always lower in aged individuals, the cardiovascular and musculoskeletal adaptations to chronic aerobic exercise enable the trained individual to sustain higher submaximal workloads with less of a cardiorespiratory response (heart rate, blood pressure, and dyspnoea) and also less overall and musculoskeletal fatigue. However, exercise adaptation is specific to the modality chosen, with some overlap. Aerobic capacity is best addressed with moderate‐ to‐ vigorous‐ntensity aerobic exercise, with the greatest benefits seen when high‐intensity interval training (HIIT, 85–95% peak heart rate for 1–4 minutes intervals) is undertaken. However, HIIT has been primarily studied in healthy and cardiovascular cohorts, in whom its efficacy and safety have been well‐reported⁶⁴; its feasibility in frail older adults with multiple comorbidities remains to be established. High‐intensity resistance training is the optimal prescription to address sarcopenia and may also enhance balance.⁶⁵ Less well known is that resistance training improves aerobic capacity to a similar extent as moderate‐intensity aerobic training in older adults,⁶⁶ thus targeting the two major changes in exercise capacity of ageing with one efficient prescription. Importantly, aerobic exercise does not enhance strength or balance and is thus insufficient as an isolated prescription for most older adults. Systematic reviews clearly indicate that falls‐prevention programmes inclusive of walking are inferior to those focusing on strength and balance exercises and have also been associated with increases in osteoporotic fracture rates in those at risk.⁶⁷

      Similar to aerobic and resistance training, there is evidence that balance training and flexibility training⁶⁸ induce adaptations in associated fitness declines in these areas. Balance enhancement is clearly related to reduction in fall risk⁶⁷ and also functional mobility. Although stretching is generally included in most position stands,^7,79 there is limited evidence that improvements in flexibility by themselves are associated with important clinical outcomes. Therefore, it is best conceptualised as a component of cool‐down after the actual exercise session has been completed. Stretching prior to exercise has not been shown to reduce musculoskeletal injuries as once thought and in fact results in reduced post‐stretching muscle performance. The best warm‐up for cardiovascular and musculoskeletal systems is simply to do what is about to be done but at a lower intensity. This may mean, for example, walking at a slow pace or performing a set of weightlifting repetitions with a light load.

Optimisation of body composition with ageing

‘Usual ageing’ is associated with significant losses of bone and muscle (lean mass) and increases in adipose tissue, along with

Скачать книгу