Effect of High-Intensity Intermittent Swimming Training on Fatty Acid Oxidation Enzyme Activity in Rat Skeletal Muscle

Abstract

Repeated exercise sessions, defined as physical exercise training, increase mitochondrial enzyme activities in skeletal muscle recruited during exercise [1][2][3][4][5][6]. Among previous studies, the types of exercise included running and cycle ergometer exercises at ϳ50-70% of maximal oxygen uptake (VO 2 max ) for more than 30 min, which is regarded as low to moderate intensity [4,[7][8][9].With respect to high-intensity exercise training, Tabata et al. [10] demonstrated that exhaustive intermittent training, which consisted of seven to eight sets of 20 s exercise at an intensity of about 170% of VO 2 max with a 10 s rest between sessions, improved VO 2 max . Furthermore, we recently found that 8 d of high-intensity intermittent swimming training (fourteen 20 s exercise sessions [total exercise time 4 min and, 40 s]) bearing a weight equivalent to 14-16% of body weight increased the GLUT-4 isoform of the glucose transporter and citrate synthase (CS) activity, a marker of oxidative enzyme, in rat forelimb muscle to a level comparable to that observed after low-intensity prolonged exercise training (total exercise time Japanese Journal of Physiology, 54, [47][48][49][50][51][52] 2004 Key words: triceps muscle, 3-␤ hydroxyacyl-CoA dehydrogenase, hexokinase, citrate synthase Abstract:We previously reported that high-intensity exercise training significantly increased citrate synthase (CS) activity, a marker of oxidative enzyme, in rat skeletal muscle to a level equaling that attained after low-intensity prolonged exercise training (Terada et al., J Appl Physiol 90: 2019-2024). Since mitochondrial oxidative enzymes and fatty acid oxidation (FAO) enzymes are often increased simultaneously, we assessed the effect of high-intensity intermittent swimming training on FAO enzyme activity in rat skeletal muscle. Male Sprague-Dawley rats (3 to 4 weeks old) were assigned to a 10-day period of high-intensity intermittent exercise training (HIT), low-intensity prolonged exercise training (LIT), or sedentary control conditions. In the HIT group, the rats repeated fourteen 20 s swimming sessions with a weight equivalent to 14-16% of their body weight. Between the exercise sessions, a 10 s pause was allowed. Rats in the LIT group swam 6 h/day in two 3 h sessions separated by 45 min of rest. CS activity in the triceps muscle of rats in the HIT and LIT groups was significantly higher than that in the control rats by 36 and 39%, respectively. Furthermore, 3-␤ hydroxyacyl-CoA dehydrogenase (HAD) activity, an important enzyme in the FAO pathway in skeletal muscle, was higher in the two training groups than in the control rats (HIT: 100%, LIT: 88%). No significant difference in HAD activity was observed between the two training groups.In conclusion, the present investigation demonstrated that high-intensity intermittent swimming training elevated FAO enzyme activity in rat skeletal muscle to a level similar to that attained after 6 h of low-intensity prolonged swimming exercise training.

Review of High-intensity Interval Training in Cardiac Rehabilitation

“…First, it has been shown that increased peroxisome proliferator activated receptor-γcoactivator-1α (PGC-1α), regarded as the master regulator of mitochondrial biogenesis in muscle, is related to the enzyme activity of 5'-AMP-activated protein kinase (AMPK), which is activated proportionally to the exercise intensity (10,52). The reason for the improvement in the aerobic capacity in HIIT can be explained by the following intracellular signaling sequence (53): muscular stimulus by HIIT increase in AMPK activity in muscle cells increase in PGC-1α mRNA and protein increase in the mRNA of the mitochondrial oxygenation enzyme increase in mitochondrial oxygenation protein improvement in physical fitness (aerobic capacity) (54). Second, it is reasonable to speculate that higher shear stress in HIIT patients during exercise bouts may trigger greater responses at the cellular and molecular levels, leading to a partial recovery from endothelial dysfunction.…”

Extremely low-volume, high-intensity interval training improves exercise capacity and increases mitochondrial protein content in human skeletal muscle

“…While adapting the Tabata protocol to swimming in rats does improve markers of oxidative capacity [4,8] whether the Tabata protocol improves mitochondrial protein content in human skeletal muscle, an adaptation that could contribute to increased aerobic capacity, is not known. The impact of the Tabata protocol on postulated regulators of skeletal muscle transcriptional (peroxisome proliferator-activated receptor γ coactivator-1 alpha [PGC-1α], sirtuin 1 [SIRT1]), and translational (mammalian target of rapamycin [mTOR] and ribosomal protein S6 kinase [S6K1]) control of mitochondrial biogenesis has also not been examined in human skeletal muscle.…”

High Intensity Training (HIT) für die Verbesserung der Ausdauerleistungsfähigkeit von Normalpersonen und im Präventions- & Rehabilitationsbereich

“…Anpassungen des Energiestoffwechsels Im Gegensatz zu der bisher weit verbreiteten Meinung, dass nur niedrigintensives umfangsorientiertes Training Anpassungen des oxidativen Stoffwechsels hervorruft, kommt es offensichtlich auch durch hochintensives Training zu Anpassungen des oxidativen Stoffwechsels [20,21]. So werden nach HIT intrazelluläre Signalwege aktiviert, die u. a. für die mitochondriale Biogenese verantwortlich sind [22].…”

“…Zentrale Enzyme des oxidativen und glykolytischen Stoffwechsels (Hexokinase, Phosphofruktokinase, Citrat-Synthase, Succinat-Dehydrogenase, Malat-Dehydrogenase, Pyruvat-Dehydrogenase) sind sowohl in ihrer Dichte als auch in ihrer Aktivität nach HIT gesteigert [6,[23][24][25][26]. Des weiteren sind eine verminderte Kohlenhydratoxidation unter gleichzeitiger Erhöhung der Fettoxidation beschrieben [20,25,27,28]. Auch die muskulären Laktatkonzentrationen sind nach HIT vermindert [28].…”