Journal of Applied Physiology, Vol 74, Issue 6 2860-2867, Copyright © 1993 by American Physiological Society
High lactate and NH3 release during arm vs. leg exercise is not due to beta-adrenoceptor stimulation
M. Jensen-Urstad, G. Ahlborg and K. Sahlin
Department of Clinical Physiology, Sodersjukhuset, Stockholm, Sweden.
To investigate the differences in metabolic response between arm exercise
(AE) and leg exercise (LE) and to elucidate the underlying mechanisms,
seven men were studied during 20 min of AE or LE both with (beta) and
without (control, C) nonselective beta-blockade (beta B) (propranolol). The
work loads corresponded to 59 and 60% of peak pulmonary O2 uptake (VO2)
during LE and AE, respectively. Pulmonary VO2 increased more slowly at the
onset of exercise during AEC (half time = 61 +/- 9 s) than during LEC (half
time = 35 +/- 3 s) and was not affected by beta B. At the onset of exercise
the arteriovenous O2 difference across the exercising limb increased above
that of steady state during AEC but not during LEC. This demonstrates that
the adjustment of O2 delivery is slower than that of arm VO2 during AE.
Despite the smaller exercising muscle mass, the release of lactate and NH3
was about twofold higher during AEC than during LEC. The difference in
metabolic response between AE and LE was not altered by beta B. Lactate
release was not reduced by beta B but, if anything, tended to increase
during both AE and LE (beta vs. C). beta B increased NH3 release during LE
(beta vs. C) but not during AE (beta vs. C). We conclude that AE compared
with LE at the same relative work load is associated with a greater release
of lactate and NH3, indicating a more severe metabolic stress during AE.
Furthermore, the present data suggest that the increase in blood lactate at
these submaximal exercise intensities is caused by factors other than
beta-adrenoceptor stimulation.
