One or the other: Why strength training might come at the expense of endurance muscles

July 25, 2019

Science Daily/University of Basel

The neurotransmitter brain-derived neurotrophic factor (BDNF) acts in the muscle, so that during strength training endurance muscle fiber number is decreased. Researchers at the University of Basel's Biozentrum have more closely investigated this factor, from the group of myokines, and demonstrated that it is produced by the muscle and acts on both muscles and synapses. The results published in PNAS also provide new insights into age-related muscle atrophy.

Fitness clubs are booming: New gyms are springing up like mushrooms. More and more people are striving to build up and strengthen their muscles. But what exactly happens in the muscle during training? In their recent work, Prof. Christoph Handschin's research group at the Biozentrum, University of Basel, has more closely studied strength muscles and the myokine brain-derived neurotrophic factor (BDNF), which plays an important role in the formation of strength muscle fibers.

Handschin's team has demonstrated that this factor is produced by the muscle itself and remodels the neuromuscular synapses, the neuronal junctions between the motor neurons and muscle. BDNF not only causes the strength muscles to develop, but at the same time leads to endurance muscle fiber number decline.

BDNF acts on muscles and synapses

Generally, it is differentiated between two types of muscle, depending on the type of fibers they are made of: There are the slow-twitch fibers for endurance muscles, which are formed mainly during endurance sports. Marathon runners primarily exercise this type of muscle. A great deal less well studied is the second form of muscle consisting of fast-twitch fibers. These strength muscles gain in volume during strength training and provide particularly great muscular power.

Christoph Handschin's team has now studied the hormone-like neurotransmitter from the myokine family in the mouse model. Myokines are released by the muscle during contraction. "It is interesting that BDNF is produced by the muscle itself and not only exerts an influence on the muscle. At the same time, it affects the neuromuscular synapses, which are the junctions between the motor neurons and muscle," explains Handschin.

BDNF converts endurance muscles into strength muscles

This remodeling of the neuromuscular synapses during strength training results in the body developing more strength muscle fibers. "However, strength muscle growth occurs at the expense of the endurance fibers. More precisely, through the release of BDNF, the endurance muscles are transformed into strength muscles," clarifies Handschin. This makes BDNF a factor proven to be produced by the muscle itself and to influence the type of muscle fibers formed.

Relevance to muscle training and age-related muscle atrophy

The new knowledge gained about the myokine BDNF also provides a possible explanation for the decrease in endurance musculature seen as a result of strength training. This correlation is already being taken into account in the training plan for high performance sports. Particularly in sporting disciplines such as rowing, which are geared towards strength and endurance, the muscle remodeling must be considered.

Moreover, in a follow-up study, the research group showed that in muscle lacking BDNF the age-related decline in muscle mass and function is reduced. "We didn't expect this result," says Handschin. "It also makes the findings interesting for treatment approaches for muscle atrophy in the elderly."

https://www.sciencedaily.com/releases/2019/07/190725112607.htm

Cannabis use in adolescence linked to schizophrenia

Psychoactive compound in cannabis may trigger the brain disorder, researchers say

April 26, 2017

Science Daily/American Friends of Tel Aviv University

Scientists believe that schizophrenia, a disorder caused by an imbalance in the brain's chemical reactions, is triggered by a genetic interaction with environmental factors. A new Tel Aviv University study published in Human Molecular Genetics now points to cannabis as a trigger for schizophrenia.

The research, conducted by Dr. Ran Barzilay and led by Prof. Dani Offen, both of TAU's Sackler School of Medicine, finds that smoking pot or using cannabis in other ways during adolescence may serve as a catalyst for schizophrenia in individuals already susceptible to the disorder.

"Our research demonstrates that cannabis has a differential risk on susceptible versus non-susceptible individuals," said Dr. Barzilay, principal investigator of the study. "In other words, young people with a genetic susceptibility to schizophrenia -- those who have psychiatric disorders in their families -- should bear in mind that they're playing with fire if they smoke pot during adolescence."

The research team included Prof. Inna Slutsky and Hadar Segal-Gavish, both of TAU's Sackler School of Medicine, and Prof. Abraham Weizman of Geha Medical Health Center and Prof. Akira Sawa of Johns Hopkins Medical Center.

Clinical picture of mouse models mimics human adolescence

Researchers exposed mouse models with a genetic susceptibility to schizophrenia -- the mutant DISC-1 gene -- to THC, the psychoactive compound in cannabis. During a time period similar to that of human adolescence, the susceptible mice were found to be at a far higher risk for lasting brain defects associated with the onset of schizophrenia.

Four categories of mice were used in the experiment: Genetically susceptible and exposed to cannabis; genetically susceptible and not exposed to cannabis; genetically intact and exposed to cannabis; and, finally, genetically intact and not exposed to cannabis. Only the genetically susceptible mice developed behavioral and biochemical brain pathologies related to schizophrenia after being exposed to cannabis, behavioral tests and neurological biochemical analyses revealed.

"The study was conducted on mice but it mimics a clinical picture of 'first episode' schizophrenia, which presents during adolescence in proximity to robust cannabis use," said Dr. Barzilay, a child and adolescent psychiatrist.

The researchers also discovered the mechanism through which the cannabis and the specific gene interact.

"A protective mechanism was observed in the non-susceptible mice," said Prof. Offen. "This mechanism involves the upregulation of a protective neurotrophic factor, BDNF, in the hippocampus. We showed in the study that if we artificially deliver BDNF to the genetically susceptible mice, they could be protected from the deleterious effect of THC during adolescence.

"This research clearly has implications in terms of public health," Prof. Offen concluded. "The novel protective mechanism identified in the study may serve as a basis for the future development of compounds capable of attenuating the deleterious effect of cannabis on brain development. However, until that time, it is important that young people at risk for psychiatric disorders (i.e., have psychiatric disorders in their family or have reacted strongly to drugs in the past) should be particularly cautious with cannabis use during adolescence."

https://www.sciencedaily.com/releases/2017/04/170426124305.htm