5. Análisis y discusión de resultados de la práctica educativa
5.3 Categoría Educación inclusiva
5.3.2 Enfoques de la educación inclusiva
The ageing process, which is characterised by functional decline, affects all major/vital biological systems in the human body and could be defined as a progressive loss of physiological capacity that culminates in profound impairments o f function.
Thus ageing is associated with “a marked decline in muscle strength” [Cappola et al,
2001] and in “the magnitude o f reflex responses, a slowing o f rapid reactions, an increased postural instability coupled with increased hesitancy with goal-directed movements, reduced steadiness in performing submaximal contractions, and reduced manipulative capabilities” [Enoka, 1997]. At the physiological level, the changes associated with ageing are manifested in four ways.
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I. A loss of motor units [Doherty et al, 1993; Navarro e t al, 2001] and loss of muscle fibres (sarcopenia) [Evans, 1995; Jette e t al, 1997]. This decrease in muscle mass area [Essen-Gustavsson & Borges, 1986] has been suggested to be due to a preferential loss o f type II fibres [Grimby, 1995], and a decrease in type II fibre area [Aniansson e t al, 1981] which is greater that the decrease in type I fibre area [Fiatarone Singh e t a l, 1999]. Muscle fibre loss is also often linked to the replacement of muscle fibres by fat and connective tissue [Lexell, 1995; Kent-Braun e t a l, 2000]
II. A prolongation of the contraction time o f the remaining motor units [McDonagh e t a l., 1984; Nelson e t a l , 1984; Newton & Yemm, 1986; Newton e t a l , 1988; Soderberg e t a l , 1991].
III. A significant decrease in the firing rate o f the motor unit [Larsson & Ansved, 1995; Jakobi & Rice, 2001], perhaps parallel to increased contraction time
IV. Specific weakness, which is the characteristic o f a muscle producing less force than would be predicted by its mass [Bruce e t a l 1989a; Kallman e t a l , 1990; Phillips e t a l , 1992; Rook e t a l , 1992; Lexell, 1995; Jubrias et al,
1997].
Experimental evidence suggests that loss o f muscle fibres is largely o f neurogenic origin. Loss of motor units leaves fibres denervated. Motor unit rem o d ellin g can explain much of the age-associated muscle atrophy. Indeed remodelling appears to occur by selective den erva tio n (death/loss of neurones). Denervation is followed by incomplete rein n ervation o f “abandoned” muscle fibres, by axonal sprouting from adjacent innervated unit [Brooks & Faulkner, 1993], which means that many fibres atrophy due to not being innervated. R einnervation of only some of the denervated fibres may explain the clustering o f fibre types in muscles, since observations are that the motor units that are loss are predominantly o f type II [Fiatarone Singh e t al, 1999]. This also explains the increase in the relative size of slow motor units area, i.e. type I (possibly due to increased innervation ratio) [Aniansson e t al, 1981, Lexell, 1995].
However in addition to neurogenic factors, there may be muscle-based loss of fibres. In other words, non-neurogenic factors may cause further fibre loss, which is aggravated in
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old age by increased susceptibility of muscles to contraction-induced injury [Jozsi et al,
2000] and the impaired capacity for regeneration [Jozsi et al, 2000].
Cross sectional and longitudinal studies have revealed that strength increases into the thirties and declines at an accelerating rate after the fifth decade [Hurley, 1995; Bruce, 1989b]. A similar pattern is seen in the decline in muscle mass with age [Young et al,
1984; Davies et al, 1986; Bruce et al, 1989b; Lexell, 1995; Jubrias et al, 1997; Michael, 2000; Hughes et al, 2001]. However multiple regression analysis of grip strength shows that it is more strongly correlated with age (r^=0.38) than muscle mass (r^=0.16) [Kallman et al, 1990; Pearson et al, 1985], perhaps because an additional age related process influences strength.
Specific force (the force per cross sectional area (MVF/CSA)) of men and women after the age of 75 years is approximately 30% lower than young men and women [Weber, 1846; Bruce et al, 1989b; Rook et al, 1992; Lexell, 1995; Jubrias et al, 1997]. Specific muscle weakness is the characteristic o f a muscle (fibre, motor unit, whole muscle, or group of muscles) that produces less specific force than expected. Studies report declines in both total muscle strength (MVP) [Sunnerhagen et al, 2000], and specific muscle strength (MVF/CSA) with ageing [Bruce et al, 1989b; Jubrias et al, 1997], but the decline in MVF is not consistent with the decline in CSA (see table 2 below).
Table 2. Inconsistencies in the rates of muscle strength and size decline per year.
Study m uscle CSA m easuring a p p a ra tu s # Females
mm
MalesB m
Unexplained yearly strength decline R eferenceultrasound -0.62 -0.58 -0.71 -0.44 6 - 38% Young Young et al,et al, 1984; 1985
Q uadriceps Rutherford & Jones,
CAT scan -0.79 -0.49 -0.89 -0.53 38-41% 1992; Klitgaard et al,
1990 Triceps
surae
ultrasound -0.76 -0.48 -0.65 -0.33 37 - 49% Vandervoort &
McComas, 1986 anthropometry -0.58 -0.03 -0.75 -0.29 61 - 95% Davies et al, 1986 Adductor
anthropometry -0.58 -0.15 -0.55 0.16 72 - 75% Phillips et al, 1992 & a
pollicis -0.67 -0.27 - - 60% Phillips et al, 1998
Average -0.67 -0.33 -0.71 0.35 -5 2 %
Data is expressed as % decline per year. Pa = per annum. The unexplained yearly strength decline here relates to the yearly amount by which MVF loss is bigger than CSA loss
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There must therefore be other factors besides loss o f muscle mass contributing to loss of strength [Davies et al, 1986; Vandervoort & McComas, 1986; Bruce et al, 1989b; Kallman et al., 1990; Phillips et al, 1992a]. In other situations, it has been found that muscles may be relatively small/atrophied and still have a normal maximum specific force. A case in point is the example o f chronically undernourished and (90%) underweight patients with Crohn’s disease, who exhibited a normalised muscle force no different to that o f the healthy, normally nourished subjects [Bruce et al, 1989a].
The question is why should weakness in the elderly matter so much? It is intuitive that independent living involves the ability to carry out daily tasks such as rising from a chair, walking, cooking, and opening doors and cans with relative ease.
Muscle strength has been shown to correlate in varying degrees, with several measures o f functional status [Bassey et al, 1988; Buchner & De Lateur, 1991; Grimby et al,
1992a; Jette & Jette, 1997]. For instance, it was found that not only does isometric force and leg extensor power decline with age at a rate o f 1-2% per annum and 3.5% per annum, respectively, but these strength measures were also found to correlate with measures o f functional ability [Skelton et al, 1994].
Similarly, in a representative sample o f a general population of 405 individuals aged 75, isometric muscle strength was found to correlate strongly with functional ability in daily activities [Avlund et al, 1994]. A decrease in strength manifests itself most powerfully in the elderly as decreased domestic activities such as rising from a sitting position, walking up stairs, or carrying groceries home [Hyatt et al., 1990].
Low muscle strength, bone mineral density and high body sway are independent predictors o f falls and subsequent fracture incidence in the elderly [Simpson 1993]. For example a postmenopausal woman with high body sway and bone mineral density (BMD) in the lowest quartile, and low muscle strength, has a 13.1% risk o f fracture per annum [Nguyen, er «/, 1993].
Research on the association between one risk factor (muscle strength, i.e. the ability to perform a maximal contraction) and falling (with subsequent risk o f limb breaking) indicate that muscle weakness is an important risk factor for fall. Generally speaking,
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these studies found that muscle strength is lower among fallers than non-fallers [Studentski et al, 1991 ; Bruce et al, 1992; Simpson, 1993; Nguyen et al, 1993].
7,5.2. Mechanisms o f oestrogen skeletal muscle action
Hormone action is dependent on receptor presence. Evidence o f oestrogen receptors in human skeletal muscle is not yet conclusive. Although some studies do not always find evidence o f oestrogen receptors in skeletal muscle, others show oestrogen receptors presence and oestrogens affinity for skeletal muscle [Gustafsson et al, 1984].
That oestrogens can act (either directly or indirectly) on skeletal muscle has been shown (section 1.1.2.3. p20-27). Now we propose that there are four pathways by which these hormones can potentially influence muscle force:
I. Anabolic action, where they will influence size, fibre angles and fibre types II. Metabolic action, where Pi, pH status are changed, due to availability of energy
sources
III. Chronotropic action, where Ca^^ levels, fusion frequency o f actin-myosin complexes are affected
IV. Inotropic action, whereby neurotransmission, cross-bridge force or number of cross-bridges are changed
i) Oestrogens anabolic effects
Alteration in muscle size, architecture, or in muscle fibre type for that matter, would change the force that a muscle can exert. Indeed the muscle force is dependent on the number o f fibres normal to the axis o f force application. Similarly, fibre types have different contractile properties. Type II fibres exert more specific force (i.e. the force per unit cross-sectional area) than type I fibres [Botinelli et al, 1996].
A recent study on women with AIDS shows a high degree of positive correlation between muscle mass, bone density and oestrogen [Huang et al, 2001], hence suggesting anabolic oestrogen effects. At the middle o f the menstrual cycle increased levels o f oestrogens, androstenedione and testosterone (i.e. androgens) coincide. Because testosterone has been shown to have receptors in skeletal muscle and to have
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anabolic actions (possibly via IGF-1), this could be the reason for the presumed anabolic actions o f oestrogens. However, since total levels o f testosterone are similar pre and postmenopausal, this hormone cannot be the only anabolic factor in women [Ala-Fossi et al^ 1999].
The rapid response to decreased oestrogen at ovulation [Phillips et al, 1995] and changes at the menopause reversed by HRT are two separate evidences against an anabolic property. In other words, force change seen with oestrogen increase are not due to an anabolic effects (although it is possible that increased myofibrils might not be seen as a general increase in total muscle bulk, in a situation where this event would be concurrent with decreased fatty infiltration). It is observed that in fact fat infiltration increases with age but not enough to account for the decrease in specific force that is observed.
Furthermore, GH and IGF-1 are linked to skeletal mass and growth [Rutherford et al,
1995] and it is suggested that oestrogens might affect their axis (circulating levels). The literature suggests that oestrogen appears to positively affect GH axis premenopause, so that plasma GH levels are significantly lower during the luteal compared to the follicular phase [Orio et al, 2001]. Discrepancies occur in terms of postmenopausal oestrogen (replacement) and GH/IGF-1 axis. Whilst studies report no correlation between replacement oestrogens and GH levels [Cano et al, 1999], others show lowered postmenopausal levels of oestrogen correlating with decreased GH axis. Postmenopausal oestrogen replacement (and it would appear, as long as it is not combined with progesterone), has been shown to reverse the postmenopausal GH decrease seen [Moe et al, 1998; Fonseca et al, 1999]. Weissberger et al, (1991) however suggest that it is the route of oestrogen replacement that is the main determinant of it effects on GH and/or IGF-1. While oral replacement oestrogen route was found to increase GH levels and to suppress IGF-1 levels, transdermal replacement oestrogen was found to increase IGF-1 levels, but had no effect on levels o f circulating GH.
ii) Oestrogens metabolic effects
Despite the widespread use of oestrogenic agents to enhance meat production in farm animals, their effects do not appear to result from a straightforward interaction with the
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muscle cells. There are suggestions that the effects might be attributable, amongst other effects to increased glucose metabolism. Indeed in general, IGF-1 (and insulin) stimulates amino acid and glucose uptake into tissues, whereas growth hormone (GH (and glucocorticoids)) has anti-insulin actions, which result in fuel mobilisation. Studies show that oestrogen positively influences glycogen (one of the energy substrates in muscles) formation. Hence, thyroid hormones, glucocorticoids and oestrogen are said to have a wealth o f metabolically regulating activities in various tissues, including skeletal muscle.
Moreover, it is known that during sustained contractile efforts, the energy supply to the muscle is affected, resulting in changes in intracellular levels of inorganic phosphate (Pi) and in acidity (pH). The muscle becomes fatigued and its force producing ability is therefore reduced (De Ruiter & De Haan (2001) have shown that with fatigue and at all temperatures, muscles show more decline in isometric and concentric force than in eccentric force, resulting in an elevated stretch/isometric ratio). It is suggested that there are two possible ways in which oestrogen might affect this pathway: first, it might alter the supply of energy to the muscle, or second it might affect the sensitivity o f the muscle to Pi and/or pH levels. A metabolic action for oestrogen is also ruled out by the observation that there are no changes either in intracellular P, level [Phillips et al., 1993 and 1993d] or in pH [Phillips et ah, 1993d].
Hi) Oestrogens chronotropic effects
Other factors affecting skeletal muscle force development are the rate of calcium release from the sarcoplasmic reticulum and the rate o f actin-myosin coupling. Similarly, relaxation rate depends on rate of calcium re-uptake (into the sarcoplasmic reticulum via the enzymatic actions of the calcium ATPase) and actin-myosin uncoupling.
Diet (ergocalciferol /VitDi) and ultra-violet light (cholecalciferol/VitDg) are both natural sources o f Vitamin D, which have been proved to be involved in skeletal muscle strength development [Bischoff et al, 1999 & 2000]. Calcifediol (a derivative of VitDg) which helps maintain plasma levels o f calcium, has been shown to rise after oestrogen administration [Van Hoof et al, 1999]. Like all steroids, oestrogens, particularly (17b- oestradiol) have been shown to increase the lipid mobility o f cell membranes, and to
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increase the activity o f calcium ATPase o f the sarcoplasmic reticulum membrane, hence increasing fusion frequency. Also, studies show that thyroid hormones increase the activity o f the sarcoplasmic reticulum calcium pump. Since these hormones are found to be influenced by sex hormones, this could be another path for the oestrogen effects on skeletal muscle force development.
iv) Oestrogens inotropic effects
Last but not least, a factor in skeletal muscle force development is not only the number of cross-bridges that are attached (see chronotropic effects), but also the force that each cross-bridge is able to produce.
The changes during the menstrual cycle, and pre- vs. post-menopause, are seen in isometric but not in eccentric forces [Phillips et al, 1993b & c]. Similarly, it has been established that specific isometric force is significantly reduced in post-menopausal women compared to controls [Phillips et al 1992]. In contrast, specific active stretch force is not dependent on age, which results in an increased stretch/isometric force ratio in the oestrogen deficient muscle [Phillips efa/1991].
Because o f these reasons, it is suggested that the end target for oestrogen activities be at the level o f the cross-bridge. This suggests that the weakness o f female ageing is through the equilibrium between the high and low force-states of the active cross bridge. In other words, weakness is not due to a reduction in the number o f attached cross-bridges, but rather, it is due (at least in part) to a decrease in the amount o f force per cross-bridge.
A study reports investigating the dependence of muscle strength with the phases o f the oestrus cycle, with relation to the period of incubation o f the test tissue [McGoldrick et al, 1998]. In the fresh tissue, maximum muscle force decrement was observed when oestrogen was low (mouse dioestrus phase). They also found that this force dependence of muscle strength with oestrous cycle disappeared if test had been carried out on the muscle late (1.5-2 hours) after excision. The investigators hence suggested that an antagonistic substance, the level of which depends on the phase o f the oestrus cycle, was present in the fresh muscle. It can therefore be inferred from this that that rather
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than having direct inotropic effects, oestrogen possibly acts by preventing the inhibitory effects o f another agent. Just which, is not quite clear at present.
As mentioned earlier, one o f the strategies for increasing force lies with increasing the number o f action potentials to the target muscle. Studies show that not only do oestrogens (and oestrogen receptors) play an important role in the development and survival o f dorsal root ganglion neurones [Patrone et al, 1999], but they also increase neuromuscular transmission [Jing et al, 1997]. Recent findings support the model in which local non-genomic and genomic actions o f oestrogen participate in the regulation of synapse formation [McEwen et al, 2001].
Furthermore, activation o f the sympathetic nervous system is involved in the control of the cardiovascular system in as much as it causes increased heart rate, increased blood pressure (vasoconstriction), and increased contractions o f the myocardium [Rowell & O’Leary, 1990]. These responses are seen with static effort attempts such as maximal handgrip strength [Wallin et al, 1989]. Studies show that during static handgrip exercise, muscle sympathetic nerve activity is increased during the menstrual (low oestrogen) compared with the follicular (high oestrogen) phase [Ettinger et al, 1998]. This change may therefore explain the reported increases in handgrip strength seen at