To study the effect of temperature on muscle metabolism during submaximal e
xercise, six endurance-trained men had one thigh warmed and the other coole
d for 40 min prior to exercise using water-perfused cuffs. One cuff was per
fused with water at 50-55 degrees C (HL) with the other being perfused with
water at 0 degrees C (CL). With the cuffs still in position, subjects perf
ormed cycling exercise for 20 min at a work load corresponding to 70% (V)ov
er dot (O2,peak) (where (V)over dot (O2,peak) is peak pulmonary oxygen upta
ke) in comfortable ambient conditions (20-22 degrees C). Muscle biopsies we
re obtained prior to and following exercise and forearm venous blood was co
llected prior to and throughout the exercise period. Muscle temperature (T-
mus) was not different prior to treatment, but treatment resulted in a larg
e difference in pre-exercise T-mus (difference = 6.9 +/- 0.9 degrees C; P <
0.01). Although this difference was reduced following exercise, it was non
etheless significant (difference = 0.4 +/- 0.1 degrees C; P < 0.05). Intram
uscular [ATP] was not affected by either exercise or muscle temperature. [P
hosphocreatine] decreased (P < 0.01) and [creatine] increased (P < 0.01) wi
th exercise but were not different when comparing HL with CL. Muscle lactat
e concentration was not different prior to treatment nor following exercise
when comparing HL with CL. Muscle glycogen concentration was not different
when comparing the trials before treatment, but the post exercise value wa
s lower (P < 0.05) in HL compared with CL. Thus, net muscle glycogen use wa
s greater during exercise with heating (208 +/- 23 vs. 118 +/- 22 mmol kg(-
1) for HL and CL, respectively; P < 0.05). These data demonstrate that musc
le glycogen use is augmented by increases in intramuscular temperature desp
ite no differences in high energy phosphagen metabolism being observed when
comparing treatments. This suggests that the increase in carbohydrate util
ization occurred as a direct effect of an elevated muscle temperature and w
as not secondary to allosteric activation of enzymes mediated by a reduced
ATP content.