This paper is a theoretical study of electrokinetic flow in narrow cylindrical capillaries.It is concerned with the dependence of the usual electrokinetic phenomena on the electrokinetic radius. The results obtained for this dependence must, however, be treated with caution for the higher values of the interface potential due to the use of the Debye-Huckel approximation. Of interest is the prediction of a maximum in the electroviscous effect.

The rate of motor unit (MU) loss and its influence on the progression of sarcopenia is not well understood. Therefore, the main purpose of this study was to estimate and compare numbers of MUs in the tibialis anterior (TA) of young men ( approximately 25 years) and two groups of older men ( approximately 65 years and >/=80 years). Decomposition-enhanced spike-triggered averaging was used to collect surface and intramuscular electromyographic signals during isometric dorsiflexions at 25% of maximum voluntary contraction. The mean surface-MU potential size was divided into the maximum M wave to calculate the motor unit number estimate (MUNE). The MUNE was significantly reduced in the old (91) compared to young (150) men, and further reduced in the very old men (59). Despite the smaller MUNE at age 65, strength was not reduced until beyond 80 years. This suggests that age-related MU loss in the TA does not limit function until a critical threshold is reached.

The purpose of this study was to determine whether the loss of muscle strength in the elderly could be explained entirely by a decline in the physiological cross-sectional area (PCSA) of muscle. Isometric force, muscle activation (twitch interpolation), and coactivation (surface electromyograph) were measured during maximal voluntary contractions (MVCs) of the elbow flexors (EFs) and extensors (EEs) in 20 young (23 +/- 3 yr) and 13 older (81 +/- 6 yr) healthy men. PCSA was determined using magnetic resonance imaging, and normalized force (NF) was calculated as the MVC/PCSA ratio. The PCSA was smaller in the old compared with the young men, more so in the EEs (28%) compared with the EFs (19%) (P < 0.001); however, the decline in MVC (approximately 30%) with age was similar in the two muscle groups. Muscle activation was not different between the groups, but coactivation was greater (5%) (P < 0.001) in the old men for both muscles. NF was less (11%) in the EFs (P < 0.01) and tended to be unchanged in the EEs of the old compared with young subjects. The relative maintenance of NF in the EEs compared with the EFs may be related to age-associated changes in the architecture of the triceps brachii muscle. In conclusion, although the decline in PCSA explained the majority of strength loss in the old men, additional factors such as greater coactivation or reduced specific tension also may have contributed to the age-related loss of isometric strength.

Changes in the neuromuscular system affecting the ageing motor unit manifest structurally as a reduction in motor unit number secondary to motor neuron loss; fibre type grouping due to repeating cycles of denervation-reinnervation; and instability of the neuromuscular junction that may be due to either or both of a gradual perturbation in postsynaptic signalling mechanisms necessary for maintenance of the endplate acetylcholine receptor clusters or a sudden process involving motor neuron death or traumatic injury to the muscle fibre. Functionally, these changes manifest as a reduction in strength and coordination that precedes a loss in muscle mass and contributes to impairments in fatigue. Regular muscle activation in postural muscles or through habitual physical activity can attenuate some of these structural and functional changes up to a point along the ageing continuum. On the other hand, regular muscle activation in advanced age (>75 years) loses its efficacy, and at least in rodents may exacerbate age-related motor neuron death. Transgenic mouse studies aimed at identifying potential mechanisms of motor unit disruptions in ageing muscle are not conclusive due to many different mechanisms converging on similar motor unit alterations, many of which phenocopy ageing muscle. Longitudinal studies of ageing models and humans will help clarify the cause and effect relationships and thus, identify relevant therapeutic targets to better preserve muscle function across the lifespan. Abbreviations AChR, acetylcholine receptor; MHC, myosin heavy chain; MU, motor unit.

The effects of aging on motoneuron firing rates and muscle contractile properties were studied in tibialis anterior muscle by comparing results from six young (20.8 +/- 0.8 yr) and six old men (82.0 +/- 1.7 yr). For each subject, data were collected from repeated tests over a 2-wk period. Contractile tests included maximal voluntary contraction (MVC) with twitch interpolation and stimulated twitch contractions. The old men had 26% lower MVC torque (P < 0.01) than did the young men, but percent activation was not different (99.1 and 99.3%, respectively). Twitch contraction durations were 23% longer (P < 0.01) in the old compared with the young men. During a series of repeated brief steady-state contractions at 10, 25, 50, 75, and 100% MVC, motor unit firing rates were recorded. Results from approximately 950 motor unit trains in each subject group indicated that at all relative torque levels mean firing rates were 30-35% lower (P < 0.01) in the old subjects. Comparisons between young and old subjects' mean firing rates at each of 10%, 50%, and MVC torques and their corresponding mean twitch contraction duration yielded a range of moderate-to-high correlations (r = -0.67 to -0.84). That lower firing rates were matched to longer twitch contraction durations in the muscle of old men, and relatively higher firing rates were matched with shorter contraction times from the young men, indirectly supports the neuromuscular age-related remodeling principle.

Hemorrhage-induced hypotension in trauma patients is predictive of high mortality (54%) and morbidity. The requirement for large volumes of crystalloid was associated with increased mortality.

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These results demonstrate that lifelong high-intensity physical activity could potentially mitigate the loss of MU associated with aging well into the seventh decade of life.