3+ 4/2002 - Společnost pro pojivové tkáně

sectional data suggest that in the knee
extensor muscles this decline may occur at
arate of ~1–2 % per year (relative to a 77year-old's
value) after 65 years of age. The
loss of muscle strength is most closely associated
with a reduction in muscle cross-sectional
area. However, this does not explain
all of the strength loss, i.e. there is a loss of
force per unit area of muscle. When measured
in vivo, this may result from an
underestimate of the increased proportions
of the aged muscle occupied by fat and
connective tissue and potentially from
poorer levels of neural drive. However, at
the intracellular level,there are a number of
reported changes, which may contribute to
this phenomenon, such as changes in the
kinetics of Ca 2+ release from the sarcoplasmic
reticulum. Recent studies using human
single muscle fibres which have been
chemically skinned,suggest that fibres from
older people may be intrinsically weaker
then those from a young muscle.The mechanisms
are unclear, but a reduction in the
number of cross-bridges, a lowering in the
force potential of individual cross-bridge or
achange in the density of myofilaments has
all been postulated as contributory factors.
Fundamental changes in the contractile
component of the older muscle are supported
by a slowing in the speed of movement
of actin filaments studied using the in
vitro motility assay and an increased stretch
force to isometric force ratio. There is also
some evidence to link the role of certain
hormones such as oestrogen and progesterone
to the loss of specific force. Muscle
power, the product of force and velocity of
contraction appears to be affected by the
ageing process to an even greater extent
than isometric strength. This may result, in
part, from a selective atrophy of the type II
fibres leading to a reduction in the overall
proportion of the muscles occupied by fast
MHC-IIA and MHC-IIX isoforms. This will
result in a slower velocity of shortening
adding to an already weaker muscle in
reducing power output. This phenomenon
may be further compounded by a reduction
in the maximum velocity of shortening of
fibres expressing the same myosin isoforms.
Whole body exercise capacity, as indicated
by maximal oxygen consumption.
(VO 2max ) is reduced in older people,
resulting in an increase in the percentage of
VO 2max needed to perform exercise at
agiven workload. The muscles of weaker
older people are thus performing at higher
relative intensities, than the young people
in order to perform similar absolute levels
of power output. Such an unfair comparison
suggests that old muscles are thus more
fatiguable. However, if muscle fatigue resistance
is studied under controlled conditions
such as those in which subject volition
is removed by electrically evoking
contractions and fatigue resistance is normalised
to allow for differences in muscle
mass,then an aged muscle appears to be no
more fatiguable than a young muscle. However,
increasing evidence suggests that ageing
is associated with increased mutations
in mitochondrial DNA.The functional implications
of such changes remain unclear,
because in contrast, analysis of key mitochondrial
enzymes involved in the oxidation
of glucose and fats suggest that their
activities, are similar to young subjects, particularly
if the level of physical activities of
the subjects from which the muscle samples
are taken is controlled. Furthermore,
the results of nuclear magnetic resonance
studies have similarly failed to show differences
in skeletal muscle energetic between
young and elderly subjects.
POHYBOVÉ ÚSTROJÍ, ročník 9, 2002, č. 3+4 99