Expressed in absolute terms, V O2 max achieved in exercise with the preferred legs was significantly larger than the non-preferred legs (2-84 cf. 2-74 l/min; P less than 0-01) and a similar but non-significant difference was found between the arms (1-10 cf. 1-05 l/min). If, however, V O2 max is standardized for the size of the active muscle mass (LV, muscle plus bone) these differences between the preferred and non-preferred limbs disappear. The implications of these observations are discussed.
At the start of rehabilitation, muscle volume was significantly smaller (860 ml, 16 per cent) in the injured than in the uninjured leg. By the end of rehabilitation (mean 50 days) the injured leg had siginficantly increased by 360 ml (8 per cent) over its initial volume, and the uninjured one had increased but not significantly (120 ml, 2 per cent), so that the injured leg was still approximately 11 per cent (620 ml) small than the uninjured. The initial degree of atrophy and the period of immobilization were not significantly correlated, although the latter showed a negative relationship (P greater than 0.05) with the rate of increase of muscle volume in the injured leg. No significant correlation was found between the ratio of injured/uninjured leg volumes and muscle width measurements at 1/3 subischial, at 12.7 cm above the knee joint space or at the maximum calf. In systematic studies involving atrophy muscle volume must therefore be estimated either by anthropometry or by X-ray measurements.
Prediction of VO2 max from leg muscle (plus bone) volume gave the same order of accuracy. However, it was shown that the VO2 max of the injured leg could be predicted with an accuracy of +/- 5%, if the observed VO2 max data of the uninjured leg and two legs were combined and utilized in the following formula: VO2 max (injured leg) = (A X 2) – VO2 max (uninjured leg), where A is the mean one-leg VO2 max predicted from the two-leg VO2 max observed. It was concluded that wherever possible the one-leg and two-leg VO2 max of patients undergoing rehabilitation therapy should be measured directly. If the patient is unable to pedal the bicycle ergometer with his injured leg alone then the VO2 max of this limb may be predicted from leg volume measurements or from the observed uninjured and two-leg VO2 max with an accuracy of approximately 8%.
In the transition from the 1st to the 10th contractions, the fascicular length at 80% of MVC decreased from 34 +/- 4 (means +/- SD) to 30 +/- 3 mm (P < 0.001), the pennation angle increased from 35 +/- 3 to 42 +/- 3 degrees (P < 0.001), the myotendinous junction displacement increased from 5 +/- 3 to 10 +/- 3 mm (P < 0.001), and the average fascicular curvature remained constant (P > 0.05) at approximately 4.3 m(-1). No changes (P > 0.05) were found in fascicular length, pennation angle, and myotendinous junction displacement after the fifth contraction. Electrogoniometry showed that the ankle rotated by approximately 6.5 degrees during contraction, but no differences (P > 0.05) were obtained between contractions. The present results show that repeated contractions induce tendon creep, which substantially affects the geometry of the in-series contracting muscles, thus altering their potential for force and joint moment generation.
In this research programme supervised by Professor Anthony J Sargeant we were able to document some of the effects of training on the muscles of spinal cord injured people.
Relatively high levels of MHC type I were found in three subjects and this corresponded with a high degree of fusion in 10-Hz force responses (r=0.88). Fatigability was related to the activity of succinate dehydrogenase (SDH) (r=0.79). Furthermore, some differentiation between fibre types in terms of metabolic properties were present, with type I fibres expressing the highest levels of SDH and lowest levels of alpha-glycerophosphate dehydrogenase. After training, SDH activity increased by 76+/-26% but fibre diameter and MHC expression remained unchanged. The results indicate that expression of contractile proteins and metabolic properties seem to underlie the relatively normal functional muscle characteristics observed in some paralysed muscles. Furthermore, training-induced changes in fatigue resistance seem to arise, in part, from an improved oxidative capacity
MVA was reduced in 18 polio subjects and normal in all controls. PPS subjects differed from non-PPS subjects only in that the MVA of the more-affected quadriceps was significantly lower. Both CSA and MVA were found to be associated with muscle strength. Quadriceps strength in polio subjects was dependent not only on muscle mass, but also on the ability to activate the muscles. Since impaired activation was more pronounced in PPS subjects, the new muscle weakness and functional decline in PPS may be due not only to a gradual loss of muscle fibers, but also to an increasing inability to activate the muscles.