Читать книгу Pathy's Principles and Practice of Geriatric Medicine - Группа авторов - Страница 175

There is a great similarity between the physiological changes attributable to disuse and those typically observed in ageing populations, leading to the speculation that the way we age may be modulated with attention to activity levels.⁴⁶ As previously stated,¹⁹ the detrimental effects of exercise removal (such as enforced bed rest) on these physiological systems can be compared to the symptomatology presented by patients with diagnosed frailty. As the benefits of exercise affect a broad range of physiology, exercise deficiency will affect systems traditionally thought of as being exercise‐dependent and also more remote systems, mimicking the mosaic of presenting symptoms in frailty. With continued lack of physical activity, additional systems failures are inevitable as the toxic mix of inactivity and factors such as poor diet, pain, depressive symptoms, cognitive dysfunction, and fatigue negatively impact and distort the trajectory of the inherent ageing process. The parallels that exist between frailty and exercise deficiency can be seen in the unpredictable presentations and variation of symptomology that can occur. Because of the tenuous links between the value of a physiological function and a specific age, it can be predicted that the degree of exercise deficiency in each individual, rather than their chronological age, will be better correlated to clinical outcomes. Similarly, because of the inherent heterogeneity, the length of time an individual has been sedentary may not correlate with severity of symptoms.¹⁹ The most important physiological changes associated with ageing or disuse that impact exercise capacity are presented in Tables 7.1–7.4. In most physiological systems, the normal ageing processes do not result in significant impairment or dysfunction in the absence of other pathology and under resting conditions. However, in response to a stressor or prolonged and profound disuse, the age‐related reduction in physiological reserves (homeostenosis) may result in difficulty completing a task requiring near‐maximum effort. This could be as ‘simple’ a task as rising from a chair, which may exceed the hip and knee extensor strength of a frail octogenarian, for example.

Table 7.1 Changes in exercise capacity due to ageing or disuse, potentially modifiable by physical activity.

Component of exercise capacity	Effect of ageing or disuse
Maximal/peak aerobic capacity	Decrease
Tissue elasticity	Decrease
Muscle strength, power, endurance, coordination	Decrease
Oxidative and glycolytic enzyme capacity, mitochondrial volume density	Decrease
Gait speed, step length, cadence, gait stability	Decrease
Static and dynamic balance	Decrease

Table 7.2 Changes in cardiorespiratory function due to ageing or disuse, potentially modifiable by physical activity.

Cardiorespiratory function	Effect of ageing or disuse
Heart rate and blood pressure response to submaximal exercise	Increase
Maximal heart rate	Decrease
Resting heart rate	No change
Maximal cardiac output, stroke volume	Decrease
Endothelial cell reactivity	Decrease
Heart rate variability	Decrease
Maximal skeletal muscle blood flow	Decrease
Capillary density	Decrease
Arterial distensibility	Decrease
Vascular insulin sensitivity	Decrease
Plasma volume, haematocrit	No change, decrease
Postural hypotension in response to stressors	Increase
Total lung capacity, vital capacity	Decrease
Maximal pulmonary flow rates	Decrease

Table 7.3 Changes in metabolism and body composition due to ageing or disuse, potentially modifiable by physical activity.

Metabolic/body composition change	Effect of ageing or disuse
Resting metabolic rate	Decrease
Total energy expenditure	Decrease
Thermic effect of meals	Decrease, no change
Total body water	Decrease
Total body potassium, nitrogen, calcium	Decrease
Muscle mass	Decrease
Fat mass, visceral fat, intramuscular fat/connective tissue	Increase
Bone mass, density, tensile strength	Decrease
Protein synthesis rate, amino acid uptake into skeletal muscle, nitrogen retention, protein turnover	Decrease
Gastrointestinal transit time	Increase
Appetite, energy intake	Decrease, no change
Glycogen storage capacity, glycogen synthase, GLUT‐4 transporter protein content and translocation to membrane, oxidative and glycolytic enzyme capacity	Decrease
Lipoprotein lipase activity	Decrease
Total cholesterol, LDL cholesterol	Increase
HDL cholesterol	Decrease, no change
Hormonal and sympathetic nervous system response to stress	Increase
Growth hormone, IGF‐1a	Decrease
Heat and cold tolerance, temperature regulatory ability	Decrease

LDL, low‐density lipoprotein; HDL, high‐density lipoprotein.

^a Most training studies show no change in growth hormone or circulating IGF‐1, although tissue levels of IGF‐1 may increase.

Table 7.4 Changes in the central and peripheral nervous system due to ageing or disuse potentially modifiable by physical activity.

Function	Effect of ageing or disuse
REM and slow‐wave 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.