We hypothesized that the elevated primary O2 uptake (V˙o 2) amplitude during the second of two bouts of heavy cycle exercise would be accompanied by an increase in the integrated electromyogram (iEMG) measured from three leg muscles (gluteus maximus, vastus lateralis, and vastus medialis). Eight healthy men performed two 6-min bouts of heavy leg cycling (at 70% of the difference between the lactate threshold and peakV˙o 2) separated by 12 min of recovery. The iEMG was measured throughout each exercise bout. The amplitude of the primary V˙o 2 response was increased after prior heavy leg exercise (from mean ± SE 2.11 ± 0.12 to 2.44 ± 0.10 l/min, P < 0.05) with no change in the time constant of the primary response (from 21.7 ± 2.3 to 25.2 ± 3.3 s), and the amplitude of theV˙o 2 slow component was reduced (from 0.79 ± 0.08 to 0.40 ± 0.08 l/min, P < 0.05). The elevated primary V˙o 2 amplitude after leg cycling was accompanied by a 19% increase in the averaged iEMG of the three muscles in the first 2 min of exercise (491 ± 108 vs. 604 ± 151% increase above baseline values, P < 0.05), whereas mean power frequency was unchanged (80.1 ± 0.9 vs. 80.6 ± 1.0 Hz). The results of the present study indicate that the increased primaryV˙o 2 amplitude observed during the second of two bouts of heavy exercise is related to a greater recruitment of motor units at the onset of exercise.

In this study, we estimated the specific tensions of soleus (Sol) and tibialis anterior (TA) muscles in six men. Joint moments were measured during maximum voluntary contraction (MVC) and during electrical stimulation. Moment arm lengths and muscle volumes were measured using magnetic resonance imaging, and pennation angles and fascicular lengths were measured using ultrasonography. Tendon and muscle forces were modeled. Two approaches were followed to estimate specific tension. First, muscle moments during electrical stimulation and moment arm lengths, fascicular lengths, and pennation angles during MVC were used (data set A). Then, MVC moments, moment arm lengths at rest, and cadaveric fascicular lengths and pennation angles were used (data set B). The use of data set B yielded the unrealistic specific tension estimates of 104 kN/m(2) in Sol and 658 kN/m(2) in TA. The use of data set A, however, yielded values of 150 and 155 kN/m(2) in Sol and TA, respectively, which agree with in vitro results from fiber type I-predominant muscles. In fact, both Sol and TA are such muscles. Our study demonstrates the feasibility of accurate in vivo estimates of human muscle intrinsic strength.

In conclusion, exercise appeared to be beneficial in renal rehabilitation by correcting the fibre atrophy, increasing the cross-section fibre area and improving the capillarization in the skeletal muscle of renal failure patients.

Since a non-locomotor muscle was examined, the effects of disuse as a cause of atrophy have been minimized. It is likely, therefore, that the decreased muscle fibre CSA and capillary density of RFPs compared to controls were due predominantly to uraemia itself.