All previous analyses of axonal responses to traumatic axonal injury (TAI) have described the ultrastructure of changes in the cytoskeleton and axolemma within 6 h of injury. In the present study we tested the hypothesis that there are, in addition, ultrastructural pathological changes up to 1 week after injury. TAI was induced in the adult guinea pig optic nerve of nine animals. Three animals were killed at either 4 h, 24 h, or 7 days (d) after injury. Quantitative analysis of the number or proportion of axons within 0.5-micro m-wide bins showed an increase in the number of axons with a diameter of less than 0.5 micro m at 4 h, 24 h, and 7 d, the presence of lucent axons at 24 h and 7 d and that the highest number of injured axons occurred about half way along the length of the nerve. A spectrum of pathological changes occurred in injured fibers-pathology of mitochondria; dissociation of myelin lamellae but little damage to the axon; loss of linear register of the axonal cytoskeleton; differential responses between microtubules (MT) and neurofilaments (NF) in different sizes of axon; two different sites of compaction of NF; loss of both NF (with an increase in their spacing) and MT (with a reduction in their spacing); replacement of the axoplasm by a flocculent precipitate; and an increased length of the nodal gap. These provide the first ultrastructural evidence for Wallerian degeneration of nerve fibers in an animal model of TAI.

Different methods of ball carrying can be used when a player runs with the ball in rugby union. We examined how three methods of ball carrying influenced sprinting speed: using both hands, under the left arm and under the right arm. These methods were compared with running without the ball. Our aim was to determine which method of ball carrying optimizes sprinting speed. Altogether, 48 rugby union players (age 21 +/- 2 years, height 1.83 +/- 0.1 m, body mass 85.3 +/- 12 kg, body fat 14 +/- 5%; mean +/- s) were recruited. The players performed twelve 30-m sprints in total (each player performed three trials under each of three methods of carrying the ball and sprinting without the ball). The design of the study was a form of Latin rectangle, balanced across the trial order for each of the methods and for pairwise combinations of the methods in blocks of four per trial. Each sprint consisted of a 10-m rolling start, followed by a 20-m timed section using electronic timing gates. Compared with sprinting 20 m without the ball (2.58 +/- 0.16 s), using both hands (2.62 +/- 0.16 s) led to a significantly slower time (P < 0.05). Sprinting 20 m with the ball under the left arm (2.61 +/- 0.15 s) or under the right arm (2.60 +/- 0.17 s) was significantly quicker than when using 'both hands' (P < 0.05), and both these methods were significantly slower than when running without the ball (P < 0.05). Accordingly, running with the ball in both hands led to the greatest decrement in sprinting performance, although carrying the ball under one arm also reduced the players' sprinting ability. Our results indicate that to gain a speed advantage players should carry the ball under one arm.

Introduction:  Stretch‐injury to the optic nerve of the guinea‐pig results in cytoskeletal pathology. We tested the hypothesis that post‐traumatic changes may continue up to 1 week after injury. Material and methods:  Six animals were injured under controlled conditions. Under terminal anaesthesia, three controls and three animals were killed at 24 h or 1 week. Unbiased stereological analysis of the axonal cytoskeleton was undertaken. Results:  At 4 h, 20% of nerve fibres are injured (Jafari et al. J Neurotrauma 1998; 15: 955). In the present study, no evidence for a change in the proportion of injured nerve fibres at longer survivals was obtained. At 24 h, three types of injured fibre occur: (i) some are compacted as at 4 h; (ii) some, termed ‘degenerating’, show loss/increased spacing between neurofilaments and microtubules (P = 0.005); and (iii) in some, empty myelin figures occur. At 7 days, both degenerating fibres and empty myelin figures are increased (P = 0.032). Conclusions:  These results demonstrate that injured nerve fibres undergo secondary axotomy between 4 and 24 h and there are increased numbers of degenerating fibres at 7 days. However, not all injured fibres undergo axotomy between 4 and 24 h, because, at 7 days fibres undergoing axotomy are present.