When skeletal muscles are activated, muscle fibres attempt to shorten, but whether the fibres shorten, stay at the same length, or are lengthened, depends on the interaction between the force developed by the fibres and the external load on the muscle. With maximum activation, the force developed is greatest during lengthening, intermediate during isometric, and least during a shortening contraction. Of the three types of contractions, only lengthening contractions have the potential to cause injury to sarcomeres within fibres. In contrast, muscles fatigue most readily during shortening contractions when forces are low, but the energy cost is high. Both contraction-induced injury and fatigue cause a loss of function, but contraction-induced injury is due to mechanical factors, whereas muscle fatigue is due to metabolic factors. During bodily movements of humans, muscles undergo each of the three types of contractions for different durations and with varying intensities to perform a wide range of different movements (Faulkner et al., 2007). With aging, the skeletal muscles of old animals become smaller, weaker, slower, more fatigable, and more susceptible to contraction-induced injury. The skeletal muscles of humans consist of two different types of fibres, slow type 1 and fast type 2. The life-span of the two fibre-types differ enormously. The half-life for sarcomeric proteins is about 23 days, but the life-span of individual type 1 muscle fibres, as an entity, is equivalent to the life span of the organism. In contrast, the total number of type 2 fibres in the vastus lateralis muscles of males begins to decline linearly with time after 50 years of age (Lexell et al., 1988), simultaneous with a linear loss of motor units (Campbell et al, 1973). As a consequence, between 50 and 80 years of age, more than half the type 2 motor units are lost. The loss in type 2 fibres is slightly less than the loss in motor units, due to the capture of some of the denervated type 2 fibres by reinnervation due to axonal sprouting from fibres in the surviving type 1 motor units (Brown et al., 1981). The loss of muscle fibres with age results in a loss of muscle mass of 30% to 50% (Akima et al., 2001). The loss of fibres appears to involve most, if not all, of the ~365 muscles in the mammalian organism (Faulkner et al., 2007). Almost concurrent with the onset of the losses in fibre number beginning at age 50, are progressive losses in strength and power. The major factor in the loss of endurance with age is the simultaneous loss in maximum oxygen uptake, which involves both the loss of the powerful type 2 fibres and a loss of oxidative capacity of the remaining fibres of both types (Conley et al., 2000). In addition to the losses and impairments in structure and function observed for whole muscles, significant age-related changes are observed in permeabilized single fibres obtained from biopsies of vastus lateralis muscles from untrained humans. The significant changes with aging in single type 1 and type 2 fibres include: cross-sectional area (CSA) of type 1 increase of 17% and type 2 decrease of 28%; maximum force of type 1 increase of 15% and type 2 decrease of 29%; specific forces do not change significantly; and peak power does not change for type 1 fibres, but decreases 36% for type 2 fibres. When activated fibres are stretched, type 2 fibres are much more susceptible to contraction-induced injury than type 1 fibres, and for both types, fibres from old compared with young animals have greater force deficits and recover from the injury less well. During forced lengthening of a maximally activated permeabilized single muscle fibre, the applied strain is not distributed uniformly along the length of the fibre; regions having the longest sarcomere lengths prior to the stretch are strained the most during the stretch and are most likely to be injured. Following severe stretches of single fibres, or whole muscles, the fibres, or muscles from old animals experience a greater force deficit than those from young animals. The greater susceptibility of fibres in whole skeletal muscles of old animals to contraction-induced injury is due in part to an impaired capacity of skeletal muscles of old animals to transmit force laterally. The process of the lateral transmission of force is critical for the stability of weaker or damaged sarcomeres. Furthermore, if muscles of young and old animals are injured severely, but to the same degree, the muscles from young animals recover completely, whereas those of old animals display a permanent force deficit. Despite the disparities in the performance of muscles from young and old humans, carefully constructed and administered training programs, that include graded exposure to lengthening contractions, increase the strength and power and even prevent subsequent injury to muscles of the elderly (Faulkner et al., 2008).