Download Evidence that Contracting Rat Muscle Produces a Hormone

Biochemistty of Erercise
73
liquid nitrogen and analyzed for glycogen. Glycogen
breakdown was calculated as the difference between
the control and the stimulated strip. Adrenaline
caused a 10% reduction in glycogen content
(pcO.04; n=18) from 120.3 & 4.7 mmol x kg-' d.w.
in the control strips to 108.1 & 4.9 mmol x kg-' d.w.
in the muscles exposed to adrenaline (mean &
SEM). Electrical stimulation caused a 26%
reduction in glycogen level (p < 0.001; n=18); the
glycogen content was 152.4 4.9 and 112.3 2 5.5
mmol x kg-' d.w. in the control and stimulated strips,
respectively. Electrical stimulation in the presence of
adrenaline caused a marked reduction in glycogen
level of 46 %; from 129.9 +2 4.1 to 69.5
3.6
mmol x kg-' d.w. (p < 0.001; n=19). These results
show that adrenaline causes a small reduction in
glycogen content in the resting slow-twitch soleus
muscle in vifro. The electrical stimulation used in
this study caused glycogen breakdown, and
glycogenolysis was enhanced in the presence of
adrenaline (p<O.Ol). In conclusion, both adrenaline
and electrically induced contraction are able to
stimulate glycogenolysis in the slow-twitch soleus
muscle in vifro, and in combination they have a
synergistic effect.
was higher than simultaneous hepatic lactic acid
uptake @<0.05), and glucose output decreased to
basal levels, while lactate uptake rose to a plateau.
Furthermore, in separate experiments an increase in
lactate supply to isolated perfused livers increased
lactate uptake but not glucose output.
4. Soleus muscles were incubated and
electrically stimulated for 3-12 h. Intraarterial
injection of incubation medium in anaesthetizedrats
did not change plasma glucose concentrations.
5. Extracts were made from mixed muscle,
liver and fat tissue. In response to intraarterial
injection of either muscle or liver extracts a
prolonged increase (pcO.05) in plasma glucose
concentration was seen (for muscle extract from
5.220.08 mM to 8.3k1.5 mM).
6. In isolated perfused livers muscle extract
increased glucose output dose dependently, whereas
the effect of liver extract did not increase with dose.
Furthermore, only muscle extract increased hepatic
oxygen uptake.
7. Although not unambiguous the results
indicate that contracting skeletal muscle may
produce a hormone enhancing hepaticglycogenolysis
according to energy needs.
113
EFFECTS O F PHYSIOLOGICAL
CITRATE CONCENTRATIONS AND
ENHANCED ENZYME AGGREGATION
ON IN VITRO SKELETAL MUSCLE
PHOSPHOFRUCTOKINASE ACTIVITY
SJ Peters and LL Spriet, School of Human Biology,
University of Guelph, Ontario, Canada, N1G 2W1.
EVIDENCE THAT CONTRACTING RAT
MUSCLE PRODUCES A HORMONE
E N H A N C I N G H E P A T I C
GLYCOGENOLYSIS
XX Han, KJ Mikines, T Ploug and H Galbo.
Department of Medical Physiology, The Panum
Institute, University of Copenhagen, Blegdamsvej3,
DK-2200 Copenhagen N, Denmark.
1. Establishedneuroendocrine signalsdo not
sufficiently account for the exerciseinduced increase
in glucose production. An attractivepossibilitywould
be that contracting muscle produces a factor that
directly stimulates hepatic glycogenolysis.
2. Isolated rat hindquarterswere perfused in
series with isolated livers. Stimulation of the
ischiadic nerve of one or both legs resulted in an
increase in force which rapidly waned. In response
to one legged contractions hepatic glucose
production increased initially (from -0.93k0.48 (SE)
to 3.320.7 pmol/min, ~ ~ 0 . 0 5The
) . peak did not
differ significantly from that seen after 20 nM of
epinephrine (5.121.2 pmoVmin, p>0.05). In
response to two-legged contractions the increase in
hepatic glucose production (to 5.42 1.3 pmoVmin)
was higher (p<0.05) and lasted longer than during
one-legged contractions.
3. During contractions peak glucose output
114
Classic in vitro studies identified citrate as
a potent inhibitor of phosphofructokinase (PFK)
activity. These experiments were generally
performed with dilute enzyme and unphysiological
citrate and effector concentrations. Recent work,
using a crowding agent to mimic the physiological
enzyme milieu, demonstrated that dilution affects
PFK regulation and homologous protein-protein
interactions are involved in the relief of ATP
inhibition and increased substrate affinity. However,
these studies have not examined the effects of a
physiological range of citrate and effector
concentrations on PFK activity.
Therefore, the present study was designed to
examine the effect of physiological concentrations of
citrate (0-0.5 mM) on rabbit skeletal muscle PFK
activity. In vitro activity was determined with and
without the crowding agent polyethylene glycol
(PEG), which enhances the aggregation state of the
enzyme. Effector concentrations were chosen to