Low-intensity Swimming Exercise Research Articles

Change in PGC-1α Expression in Rat Skeletal Muscle after Low-intensity Prolonged Swimming Exercise

After 6-h low-intensity swimming exercise (LIE), peroxisome proliferator-activated receptor γ coactivator -1α (PGC-1α) in whole and nuclear fractions in rat skeletal muscle was higher than the control rats' muscles up to 18 h after LIE. However, no study has reported change in PGC-1α content after that. Therefore, we measured PGC-1α in whole and nuclear fractions in rat skeletal muscle up to 24 h after LIE. Furthermore, we evaluated change in the mRNA of δ-aminolevulinate synthase (ALAS), a mitochondrial protein, to clarify in which fraction of PGC-1α has a physiological role as a transcriptional coactivator for enhancing the mitochondrial oxidative enzymes after exercise. We measured PGC-1α protein content in whole and nuclear fractions in the epitrochlearis (EPI) muscle of male Sprague-Dawley rats (age: 6 w; body weight: 180-200 g) after LIE by Western-blot analysis. The ALAS mRNA content was quantified by RT-PCR. The PGC-1α contents in whole fractions in the rat EPI muscle were 73% and 75% higher than that of the control rats' muscle, 18 h and 24 h after LIE, respectively. The PGC-1α content in nuclear fractions in the muscle and ALAS mRNA was higher than that of the control rats' muscle by 58% and 25%, respectively, while they returned to the control level 24 h after LIE. The present investigation demonstrated that the time-course of PGC-1α content in nuclear fractions in the EPI muscle was the same as the ALAS mRNA, suggesting that PGC-1α in the nucleus may have a physiological function as a transcriptional coactivator for enhancing mitochondrial protein expression after exercise.

EFFECTS OF SHORT-LASTING HIGH-INTENSITY SWIMMING ON PGC-1 PROTEIN EXPRESSION IN RAT EPITROCHLEARIS MUSCLE

PURPOSE We reported that the peroxisome proliferator-activated receptor γ coactivator-1 (PGC-1) mRNA in rat epitrochlearis (EPI) muscle was significantly increased after 18-h incubation with AICAR (a AMPK activator)(BBRC,2002). Since AMPK was shown to be activated in an exercise-intensity dependent manner, in the present investigation, we assessed the effects of short-lasting high-intensity swimming exercise, which is postulated to substantially increase AMPK activity, on PGC-1 protein content in rat EPI muscle, and to compare its effects on PGC-1 protein with that observed after low-intensity prolonged swimming exercise, which is known to increase PGC-1 mRNA. METHOD Male SD rats (5–6 week-old) were randomly assigned to high-intensity swimming exercise (HIS), or low intensity swimming exercise (LIS). Age-matched sedentary rats were used as a control (CON). During HIS, the rats repeated fourteen 20-s swimming with a weight equivalent to 14% of body weight. Between exercise sessions, a 10-s pause was allowed. Rats in the LIS group swam without a load for 6-h in two 3-h sessions, separated by 45-min rest. RESULT PGC-1 protein in rat EPI muscle was significantly increased by 126, 140, and 126% at 2-h, 6-h, and 18-h, respectively, after HIS, compared with that of the CON muscle (p < 0.001). Immediately, 6-h, and 18-h after the LIS, the PGC-1 protein content in the muscle was significantly elevated by 84, 95, and 67%, respectively (p < 0.001). The increment in PGC-1 protein at 6-h after the HIS did not differ from that observed after the LIS at the same time point. Both HIS and LIS induced significant increases (7- and 3-fold higher than that of CON muscle, respectively) in AMPK activity. CONCLUSION The present investigation demonstrated that the PGC-1 protein in rat EPI muscle rapidly increased in response to an acute bouts of swimming exercise. Further, the results showed that extremely high-intensity intermittent swimming exercise lasting only 280 s elevated the PGC-1 protein in rat EPI muscle to a level comparable to that attained after the 6-h low-intensity swimming exercise.