Biofeedback and progressive relaxation treatment of sleep-onset insomnia

Previous research suggests that self-defined insomniacs are distinguished from normals by high levels of anxiety and physiological arousal, which might be mitigated by muscle relaxation. This study assessed the relative effects of frontal EMG biofeedback, progressive relaxation, and a placebo set of “relaxation” exercises on the sleep of 18 onset insomniacs. Each subject was trained in one of these three methods for six half-hour sessions and slept in the laboratory for two consecutive nights before and after training. The experimental groups demonstrated significant decreases in physiological activity during training while changes in the control group were minimal. Reductions in sleep-onset time were: biofeedback group, 29.66 minutes; progressive relaxation group, 22.92 minutes; control group, 2.79 minutes. The experimental groups improved significantly ( p<.05 ) more than the control group, but did not differ from each other. No significant relationships between physiological levels and sleep-onset time were found, which suggests that muscle relaxation alone was not responsible for subjects' improvements. Since 20 minutes of daily practice were required to achieve an approximate 30-minute decrease in sleep-onset time, the practical utility of the methods is questioned.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/44085/1/10484_2005_Article_BF01001167.pd

Acute RyR1 Ca²⁺ leak enhances NADH-linked mitochondrial respiratory capacity.

Sustained ryanodine receptor (RyR) Ca &lt;sup&gt;2+&lt;/sup&gt; leak is associated with pathological conditions such as heart failure or skeletal muscle weakness. We report that a single session of sprint interval training (SIT), but not of moderate intensity continuous training (MICT), triggers RyR1 protein oxidation and nitrosylation leading to calstabin1 dissociation in healthy human muscle and in in vitro SIT models (simulated SIT or S-SIT). This is accompanied by decreased sarcoplasmic reticulum Ca &lt;sup&gt;2+&lt;/sup&gt; content, increased levels of mitochondrial oxidative phosphorylation proteins, supercomplex formation and enhanced NADH-linked mitochondrial respiratory capacity. Mechanistically, (S-)SIT increases mitochondrial Ca &lt;sup&gt;2+&lt;/sup&gt; uptake in mouse myotubes and muscle fibres, and decreases pyruvate dehydrogenase phosphorylation in human muscle and mouse myotubes. Countering Ca &lt;sup&gt;2+&lt;/sup&gt; leak or preventing mitochondrial Ca &lt;sup&gt;2+&lt;/sup&gt; uptake blunts S-SIT-induced adaptations, a result supported by proteomic analyses. Here we show that triggering acute transient Ca &lt;sup&gt;2+&lt;/sup&gt; leak through RyR1 in healthy muscle may contribute to the multiple health promoting benefits of exercise

Parental age effects, but no evidence for an intrauterine effect in the transmission of myotonic dystrophy type 1

Myotonic dystrophy type 1 (DM1) is caused by the expansion of an unstable CTG repeat (g.17294_17296(45_1000)) with more repeats associated with increased disease severity and reduced age at onset. Expanded disease-associated alleles are highly unstable in both the germline and soma. Germline instability is expansion biased, providing a molecular explanation for anticipation. Somatic instability is expansion biased, size- and age-dependent, features that have compromised genotype–phenotype correlations and intergenerational studies. We corrected these confounding factors by estimating the progenitor allele length in 54 father–offspring and 52 mother–offspring pairs in Costa Rican DM1 families. Not surprisingly, we found major parental allele length effects on the size of the allele transmitted, the magnitude of the intergenerational length change, the age at onset in the next generation and the degree of anticipation in both male and female transmissions. We also detected, for the first time, an age-of-parent effect for both male and female transmission. Interestingly, we found no evidence for an intrauterine effect in the transmission of congenital DM1, suggesting previous reports may have been an artefact of age-dependent somatic instability and sampling bias. These data provide new insights into the germline dynamics of the CTG repeat and opportunities for providing additional advice and more accurate risk assessments to prospective parents in DM1 families