Knee strength deficits after hamstring tendon and patellar tendon anterior cruciate ligament reconstruction.

PURPOSE: The purpose of this study was to examine the strength of the knee flexors and knee extensors after two surgical techniques of ACL reconstruction and compare them to an age and activity level matched control group. METHODS: Twenty-four subjects who had undergone ACL reconstruction greater than 1 yr previously were placed into one of two groups according to autograft donor site: patellar tendon (BPB; N = 8) and hamstring (H; N = 16), and compared with an active, control group (N = 30). Knee flexor and extensor strength was evaluated using isovelocity dynamometry (5 speeds, eccentric and concentric, 5-95 degrees ROM). Strength maps were used to graphically analyze strength over a broad operational domain of the neuromuscular system. Average strength maps were determined for each autograft group and compared with controls. A difference map (control minus graft group) and confidence (t-test) maps were used to quantitatively identify strength deficits. RESULTS: The combined ACL group (N = 24) revealed a global 25.5% extensor strength deficit, with eccentric regional (angle and velocity matched) deficits up to 50% of control. Strength deficits covered over 86% of the sampled strength map area (P < 0.01). These knee extensor strength deficits are greater than previously reported. In addition, the BPB group demonstrated a concentric, low velocity, knee extensor strength deficit at 60-95 degrees that was not observed in the H group. Significant graft site dependent, regional knee flexor deficits of up to 50% of control were observed for the H group. CONCLUSIONS: Strength deficits localized to specific contraction types and ranges of motion were demonstrated between the ACL and control groups that were dependent upon autograft donor site. Postoperative rehabilitation protocols specific to these deficits should be devised.

A new formula for population-based estimation of whole body muscle mass in males.

A new equation to estimate muscle mass in males was developed using parameters common to the 1981 Canada Fitness Survey and the male cadaver data of Martin et al. (1990b). The cadavers (N = 12) were randomly divided into two groups. The equation was developed on cadaver Group A and then validated on Group B. Once the equation with the most suitable variables was validated on Group B, it was redeveloped on combined data from Groups A and B. The final equation is as follows: muscle mass (gm) = Ht (0.031MUThG2 + 0.064CCG2 + 0.089CAG2) - 3,006; adjusted R2 = .96, SEE = 1,488 gm, F = 87.5, p = .0001. Variables (in cm) were Ht, height; MUThG, modified upper thigh girth; CCG, corrected calf girth; and CAG, corrected arm girth. The predictive ability of this equation was comparable to the original equation of Martin et al. (1990b) and can be a valuable tool for muscle mass estimation of male subjects in the 1981 Canada Fitness Survey.

Field potential mapping of neurons in the lumbar spinal cord activated following stimulation of the mesencephalic locomotor region.

The spinal neurons involved in the control of locomotion in mammals have not been identified, and a major step that is necessary for this purpose is to determine where these cells are likely to be located. The principal objective of this study was to localize lumbar spinal interneurons activated by stimulation of the mesencephalic locomotor region (MLR) of the cat. For this purpose, extracellular recordings of MLR-evoked cord dorsum and intraspinal field potentials were obtained from the lumbosacral enlargement during fictive locomotion in the precollicular-postmammillary decerebrate cat preparation. Potentials recorded from the dorsal surface of the cord between the third lumbar (L3) and first sacral (S1) segments typically showed four short-latency positive waves (P1-P4). These P-waves were largest between the L4-L6 segments. The amplitude of the P2-4 waves increased with the appearance of locomotion and displayed rhythmic modulation during the locomotor step cycle. Microelectrode recordings from the L4-L7 spinal segments during fictive locomotion revealed the presence of both positive and negative short-latency MLR-evoked intraspinal field potentials, and were used to construct isopotential maps of the evoked potentials. Positive field potentials were observed throughout the dorsal horn of the L4-L7 spinal segments with the largest amplitude potentials occurring in laminae III-VI. Negative field potentials were found in laminae VI-X of the lumbar cord. The shortest latency negative field potentials were observed in lamina VII and at the border between laminae VI and VII and were considered to be evoked monosynaptically from the arrival of the descending volley. Short-latency mono- and disynaptic negative field potentials were also observed in lamina VIII. Longer latency, tri- and polysynaptic field potentials were observed in laminae VII and VIII. Many of the longer latency negative waves observed in laminae VII and VIII followed shorter latency negative potentials recorded from the same location. Laminae VII and VIII negative field potentials were largest in the L5-6 and L4-5 spinal segments, respectively. Negative field potentials were also evoked in the motor nuclei of the L4-7 spinal segments. The segmental latencies for these potentials indicate that they were evoked di- and trisynaptically.(ABSTRACT TRUNCATED AT 400 WORDS)

Mechanical entrainment of fictive locomotion in the decerebrate cat.

1. We examined the ability of muscular and joint afferents from the hip region to entrain fictive locomotion evoked by stimulation of the mesencephalic locomotor region in the decerebrate cat by mechanically imposed, sinusoidal hip flexion and extension movements. 2. A method is presented for qualitative and quantitative analysis of entrainment. 3. Hip joint capsular afferents were shown by denervation experiments to be unnecessary for mediating locomotor entrainment. 4. As the population of muscular afferents was progressively decreased by selective denervation, the strength of entrainment concomitantly decreased, even though a few as two small intrinsic hip muscles were still effective in producing entrainment. The ability to entrain locomotion was abolished with complete ipsilateral denervation. 5. Entrainment was observed with low amplitude hip angular displacement of 5-20 degrees, which would be expected to activate low-threshold, stretch-sensitive muscle afferents. 6. The extensor burst activity occurred during the period of imposed hip flexion, which corresponded to passive stretching and loading of the extensor muscles, while the flexor burst activity occurred during the latter portion of the imposed hip extension, which corresponded to passive stretching of the flexor muscles (when attached) and release of the extensors. During harmonic entrainment, the match of hip cycle duration and step cycle duration was accomplished by a variation in extensor electroneurogram (ENG) burst duration. These results are consistent with a positive feedback mechanism where low-threshold afferent activity from the extensor musculature is used by the rhythm generator to prolong the extension phase of locomotion. 7. A hip cycle frequency-dependent phase shift of ENG activity was observed. This may indicate that the locomotor rhythm generator is dependent on more than just static positional or threshold load information for modulation of the step cycle frequency and switching between flexion and extension phases. 8. Subharmonic forms of entrainment were observed when the number of innervated muscles was markedly reduced. The occurrence of subharmonic entrainment characterizes the locomotor rhythm generator as a nonlinear oscillator. 9. To modulate the stepping frequency, the afferent pathways responsible for entrainment must be directly connected to the neural circuitry responsible for rhythm generation. The rhythm generating interneurons must receive a high degree of convergence from afferents arising from a variety of muscles spanning the hip joint.

On the regulation of repetitive firing in lumbar motoneurones during fictive locomotion in the cat.

Repetitive firing of motoneurones was examined in decerebrate, unanaesthetised, paralysed cats in which fictive locomotion was induced by stimulation of the mesencephalic locomotor region. Repetitive firing produced by sustained intracellular current injection was compared with repetitive firing observed during fictive locomotion in 17 motoneurones. During similar interspike intervals, the afterhyperpolarisations (AHPs) during fictive locomotion were decreased in amplitude compared to the AHPs following action potentials produced by sustained depolarising current injections. Action potentials were evoked in 10 motoneurones by the injection of short duration pulses of depolarising current throughout the step cycles. When compared to the AHPs evoked at rest, the AHPs during fictive locomotion were reduced in amplitude at similar membrane potentials. The post-spike trajectories were also compared in different phases of the step cycle. The AHPs following these spikes were reduced in amplitude particularly in the depolarised phases of the step cycles. The frequency-current (f-I) relations of 7 motoneurones were examined in the presence and absence of fictive locomotion. Primary ranges of firing were observed in all cells in the absence of fictive locomotion. In most cells (6/7), however, there was no relation between the amount of current injected and the frequency of repetitive firing during fictive locomotion. In one cell, there was a large increase in the slope of the f-I relation. It is suggested that this increase in slope resulted from a reduction in the AHP conductance; furthermore, the usual elimination of the relation is consistent with the suggestions that the repetitive firing in motoneurones during fictive locomotion is not produced by somatic depolarisation alone, and that motoneurones do not behave as simple input-output devices during this behaviour. The correlation of firing level with increasing firing frequency which has previously been demonstrated during repetitive firing produced by afferent stimulation or by somatic current injection is not present during fictive locomotion. This lends further support to the suggestion that motoneurone repetitive firing during fictive locomotion is not produced or regulated by somatic depolarisation. It is suggested that although motoneurones possess the intrinsic ability to fire repetitively in response to somatic depolarisation, the nervous system need not rely on this ability in order to produce repetitive firing during motor acts. This capability to modify or bypass specific motoneuronal properties may lend the nervous system a high degree of control over its motor output.

The effect of selective brainstem or spinal cord lesions on treadmill locomotion evoked by stimulation of the mesencephalic or pontomedullary locomotor regions.

The descending pathways from the brainstem locomotor areas were investigated by utilizing reversible cooling (to block synaptic or fiber transmission) and irreversible subtotal lesions of the brainstem or spinal cord (C2-C3 level). Experiments were conducted on decerebrate cats induced to walk on a treadmill by electrical stimulation of the brainstem. Locomotion produced by stimulation of the mesencephalic locomotor region (MLR) was not abolished by caudal brainstem lesions that isolated the lateral tegmentum or by extended rostral/caudal dorsal hemisections of the spinal cord. These results demonstrate that the MLR does not require a pathway projecting through the lateral tegmentum of the brainstem or the dorsal half of the spinal cord, as previously suggested (Mori et al., 1977, 1978b; Shik and Yagodnitsyn, 1978; Shik, 1983). Rather, the results indicate that the descending pathway originating from the MLR projects through the medial reticular formation (MedRF) and the ventral half of the spinal cord. Locomotion produced by stimulation of the pontomedullary locomotor region (PLR) was blocked by reversible cooling of either the MedRF or the ventrolateral funiculus of the spinal cord. In some cases, locomotion could be produced by stimulation of the PLR following extended dorsal hemisections of the spinal cord. These results demonstrate that the PLR can also produce locomotion by activation of cells in the MedRF that project caudally through the ventral half of the spinal cord. Stimulation of the PLR could also elicit locomotion following its surgical isolation from the MedRF of the brainstem. Furthermore, lesions of the dorsal spinal cord resulted in the loss of PLR-evoked locomotion in some, but not all, cases. Thus, an alternative projection of the PLR through the dorsal half of the spinal cord (Kazennikov et al., 1980, 1983a,b; Shik, 1983) cannot be ruled out. Overall, these results demonstrate that the PLR is not an essential component of the motor pathway originating from the MLR. The organizational scheme of "brainstem locomotor regions" is discussed in the context of recent information demonstrating a link between the sensory component of the trigeminal system and locomotor pathways (Noga et al., 1988).

Oxygen consumption during exercise in a heated pool.

The heated hydrotherapy pool is a common exercise site for patients with painful musculoskeletal conditions. Oxygen consumption of swimming is 87 to 89% of maximum in postmyocardial infarction patients according to one recent investigation. We studied 13 able-bodied subjects to test the hypothesis that enough energy could be expended during various forms of hydrotherapy to produce both an aerobic training effect and a risk to patients with coronary artery disease. Oxygen consumption (VO2) was measured in six settings: resting supine; resting seated shoulder deep in the pool (36C); walking at comfortable speed in chest-deep water; running at the fastest speed possible in chest-deep water; using hand paddles; and running in place at shoulder depth. The mean VO2 expressed in ml/kg/min (and metabolic equivalents) were 4.91 (1.00), 4.93 (1.02), 9.34 (2.01), 27.79 (6.23), 18.25 (4.30) and 29.11 (7.09) respectively, suggesting that the more vigorous exercises stress aerobic capacity heavily but not excessively.