Geschatte leestijd: 3 minuten“Training resistance.” Not resistance training, not the weight you train with, and not a personal aversion to training. We’re talking about a body that doesn’t respond to training as usual. Japanese research sheds light on one reason why some people don’t see the effects of training.
Training Resistance
Selenoprotein P, a type of hepatokine hormone secreted by the liver, is believed to cause the phenomenon of ‘training resistance.’ This means that the benefits of training are not achieved. This is revealed by Japanese research on mice and clinical studies[1].
In Japan, as in other parts of the world, ‘lifestyle diseases’ such as diabetes, metabolic syndrome, and high blood pressure are becoming more common due to decreasing levels of physical activity. Training is normally recommended as therapy for and prevention of these problems. However, there are significant differences in how different people respond to the same training. Some people seem to derive little benefit from it. Although the publication of the research consistently speaks of ‘training,’ it’s important to emphasize that this refers to cardiovascular training and not resistance or strength training.
Researchers at Kanazawa University refer to earlier research showing that selenoprotein P occurs in high concentrations in the blood of people with type 2 diabetes. Furthermore, previous research shows that selenoprotein P promotes insulin resistance, which means that insulin is less able to stabilize blood sugar levels, leading to higher blood sugar levels [2]. However, the influence on the effects of (cardiovascular) training was not previously known.
The study found that special mice that lack selenoprotein P had twice the training capacity of normal mice (think maximal oxygen uptake) after a month of treadmill training. Additionally, their blood sugar was better lowered when injected with insulin compared to normal mice.
Normal mice that were administered selenoprotein P had lower levels of AMPK phosphorylation*3 after a month of training. AMPK phosphorylation is considered to be associated with several different beneficial effects of training. Other mice used lacked LRP1, a receptor for selenoprotein P. This means that selenoprotein P cannot function in their bodies. In these mice, the administration of selenoprotein P did not result in lower levels of AMPK phosphorylation after training.
Thirty-one healthy but sedentary mice without overweight or type 2 diabetes underwent 8 weeks of cardio training. Afterward, their maximal oxygen uptake was measured. Overall, it was increased by training. However, some mice showed no or minimal increase in oxygen uptake. These were the mice that had high levels of selenoprotein P in their blood prior to training.
This demonstrates that both high levels of selenoprotein P and the receptor for this protein, LRP1, contribute to resistance to the effects of cardiovascular training.
Applications
The researchers hope that their research will lead to further studies on medication that can reduce selenoprotein P levels in the blood or ‘block’ LRP1 (by designing other substances that bind to LRP1, preventing selenoprotein P from binding and thus rendering it ineffective).
In addition, in overweight and diabetic individuals, selenoprotein P levels could be measured to assess how much benefit they would derive from training. If training is found to have little effect, the advice could be to pay more attention to dietary adjustments.
References
- Hirofumi Misu, Hiroaki Takayama, Yoshiro Saito, Yuichiro Mita, Akihiro Kikuchi, Kiyo-aki Ishii, Keita Chikamoto, Takehiro Kanamori, Natsumi Tajima, Fei Lan, Yumie Takeshita, Masao Honda, Mutsumi Tanaka, Seiji Kato, Naoto Matsuyama, Yuya Yoshioka, Kaito Iwayama, Kumpei Tokuyama, Nobuhiko Akazawa, Seiji Maeda, Kazuhiro Takekoshi, Seiichi Matsugo, Noriko Noguchi, Shuichi Kaneko, Toshinari Takamura. Deficiency of the hepatokine selenoprotein P increases responsiveness to exercise in mice through upregulation of reactive oxygen species and AMP-activated protein kinase in muscle. Nature Medicine, 2017; DOI: 10.1038/nm.4295
- Cell Metabolism 2010; 12(5), 483
