Wf. Brechue et al., METABOLIC AND WORK CAPACITY OF SKELETAL-MUSCLE OF PFK-DEFICIENT DOGS STUDIED IN-SITU, Journal of applied physiology, 77(5), 1994, pp. 2456-2467
Mechanical and metabolic relationships of muscle lacking phosphofructo
kinase (PFKD) activity were compared with muscle having normal phospho
fructokinase (NORM) activity by using the gastrocnemius-plantaris musc
le group with isolated circulation in situ. Muscle contractile propert
ies were similar in both groups. Initial power output (W) during repet
itive tetanic (200 ms, 50 impulses/s) isotonic contractions was simila
r in both groups; however, W declined significantly more (30-80%) in P
FKD than in NORM muscle over time, with a constant O-2 uptake (VO2)/W.
Despite similar O-2 and substrate delivery, PFKD muscle had a lower V
O2 (42-55%), less glucose uptake, similar free fatty acid uptake, and
lactic acid uptake, rather than output, during contractions. Muscle ve
nous H+ concentration, strong ion difference, and PCO2 increased durin
g contractions, the magnitude of change being smaller in PFKD muscle.
Elevating arterial lactate concentration before contractions in PFKD m
uscle resulted in significant improvements in W and VO2 without alteri
ng the acid-base exchange at the muscle. Increasing O-2 delivery by in
creasing arterial O-2 concentration in PFKD dogs did not improve W or
VO2., We conclude that, despite no inherent mechanical or contractile
differences, PFKD muscle has a severely limited oxidative capacity and
exaggerated fatigue and blood flow responses to contractions due to l
imited substrate metabolism resulting from the inability to utilize gl
ycogen and/or glucose.