The present study was designed to address whether exercise influences
the experimental metastasis of a mouse mammary tumour; a related issue
was the impact of timing of exercise onset relative to tumour exposur
e on NK and LAK mediated cytotoxicity. After 8 weeks of forced treadmi
ll exercise or voluntary wheel running or remaining sedentary, female
BALB/c mice received an intravenous (i. v.) injection of MMT line 66 t
umour cells. Mice were then randomized into continuation of activity (
TT, WW), cessation of activity (TS, WS), initiation of activity (ST, S
W) and maintenance of sedentary condition (SS) for three weeks. Tumour
control (TC) mice, who were matched to the SS mice for age, received
an i.v. injection of heat-killed MMT 66 tumour cells. In total there w
ere 8 groups including the tumour control. The average number of lung
tumours did not differ by activity condition; however, the mice in the
continuous treadmill group (TT) tended to have a higher tumour multip
licity (162 +/- 22) and those in the treadmill x sedentary condition (
TS) tended to have lower tumour multiplicity (109 +/- 16) compared wit
h the other groups except the SW group (95 +/- 15). The lymphokine act
ivated killer activity in the spleen was significantly elevated in the
TS (49 +/- 3%) and WS (44 +/- 3%) mice compared with the sedentary an
imals'(30 +/- 3%) (p<0.003 and 0.05, respectively). NK activity was lo
wer in the mice that had stopped exercising (TS and WS) after injectio
n of tumour compared with sedentary animals. These data suggest that a
lthough exercise training influences natural immune cytotoxic mechanis
ms in vitro, this may not translate into clinically significant change
s in tumour burden. The dissociation between natural immunity and tumo
ur outcome may reflect the relative resistance of the tumour line to l
ysis by natural killer cells. It remains to be tested if infusion of I
L-2 (to induce LAK activity), in exercise trained animals results in f
ewer tumour metastases.