Cycling exercise-induced myofiber transitions in skeletal muscle depend on basal fiber type distribution

The link between specific changes in myofiber type proportions and modulation of training in human skeletal muscle has yet to be unraveled. We investigated whether a defined increase in training volume induces a corresponding change of myofiber shifting in human skeletal muscle with distinct basal myofiber distribution. Twenty-one male cyclists (Age 26 ± 4 years) with different performance levels were exposed to increased cycling training volume with reduced power output for 3 months. Biopsies were taken from vastus lateralis muscle PRE-POST and the proportions of type I, IIa, IIx and IIc myofibers were determined. Total training time did not correlate to the degree of fiber type shifting of any type. In the entire sample of subjects, the proportion of type I myofibers tended to increase (P = 0.14) while IIa fibers decreased significantly (P < 0.05). Subgroups of subjects possessing higher (HPS) and lower proportions (LPS) of type I myofibers at baseline showed a distinct pattern in changing myofiber distribution. Subjects in HPS offered no change in myofiber proportions of any type. In contrast, subjects in LPS showed marked increases in type I (P = 0.06) and a significant reduction in IIa myofibers (P = 0.01). An inverse correlation between baseline proportion of type I and IIa myofibers and its change was observed. We conclude that individual myofiber composition constitutes a modulating factor for exercise-induced changes in its distribution. This might be influenced by altered demands of myofiber recruitment in relation to the intensity of muscle contraction but also by its relative abundance in contracting muscle.     

Impact of physical inactivity on adipose tissue low-grade inflammation in first-degree relatives of type 2 diabetic patients

OBJECTIVE

First-degree relatives (FDRs) of patients with type 2 diabetes may exhibit a disproportionately elevated risk of developing insulin resistance, obesity, and type 2 diabetes when exposed to physical inactivity, which to some unknown extent may involve low-grade inflammation. We investigated whether subjects who are nonobese FDRs show signs of low-grade inflammation before or after exposure to short-term physical inactivity.

RESEARCH DESIGN AND METHODS

We studied 13 healthy FDR subjects and 20 control (CON) subjects matched for age, sex, and BMI before and after 10 days of bed rest (BR). Insulin sensitivity was measured by the hyperinsulinemic euglycemic clamp. Key low-grade inflammation mediators were measured in arterial blood and microdialysate from subcutaneous abdominal (SCAAT) and femoral adipose tissue. Adipokine mRNA expression was determined in SCAAT.

RESULTS

Before BR, FDR subjects displayed insulin resistance, elevated plasma C-reactive protein, leptin, and monocyte chemoattractant protein (MCP)-1, high interleukin (IL)-6, and MCP-1 expressions, as well as low adiponectin and leptin expressions. FDR subjects responded to BR by decreasing plasma adiponectin and IL-10 expression and increasing plasma expression of IL-10 and tumor necrosis factor-α. In contrast, CON subjects responded to BR by increasing plasma adiponectin and adiponectin expression and by decreasing SCAAT microdialysate leptin.

CONCLUSIONS

Young and nonobese FDR of patients with type 2 diabetes exhibit low-grade inflammation, which is further and disproportionately aggravated when exposed to physical inactivity. The study provides support for the notion that people at increased risk of type 2 diabetes should avoid even short periods of physical inactivity.Human adipose tissue produces a variety of inflammatory mediators that act locally in the adipose tissue and systemically, leading to obesity-associated low-grade inflammation. Many of the inflammatory mediators can regulate insulin action in skeletal muscle and adipose tissue (1,2) and form putative links between adipose tissue and systemic metabolism (3). Chronic low-grade inflammation is pathophysiologically related to the development of type 2 diabetes and atherosclerosis.Physical inactivity contributes to a positive energy balance and the induction of obesity, but the relation between physical inactivity and low-grade inflammation may be independent of obesity. In a cross-sectional design, a low level of physical activity was associated with elevated plasma levels of interleukin (IL)-6 and C-reactive protein (CRP) independently of obesity (4). A review by Hamer (5) found an inverse association between the level of physical activity and one or more inflammatory markers in 27 of 40 observational studies after adjusting for measures of fatness. Furthermore, physically active individuals consistently demonstrated low concentrations of CRP. Recent intervention studies found that exercise training downregulated markers of chronic inflammation such as IL-6 and alanine aminotransferase (6,7). However, it is not known if physical inactivity per se in a longitudinal design upregulates inflammatory markers and changes molecular mechanisms relevant to the development of type 2 diabetes.First-degree relatives (FDRs) of type 2 diabetic patients bear a high lifetime risk of developing insulin resistance and represent a genetic model for studies into the cause of type 2 diabetes. Individuals who progress to type 2 diabetes display features of low-grade inflammation years before onset of the disease, suggesting that low-grade inflammation is involved in the pathogenetic processes (6,8). The objective of the current study was to investigate adipose tissue and systemic markers of low-grade inflammation in healthy, nonobese FDR and control (CON) subjects and in a longitudinal design to explore the effect of physical inactivity on these markers.     

Excess of neurons in the human newborn mediodorsal thalamus compared with that of the adult

The aim of this study was to quantify the total number of neurons and glial cells in the mediodorsal nucleus of the thalamus (MD) of 8 newborn human brains, in comparison to 8 adult human brains. The estimates of the cell numbers were obtained using the stereological principles of the optical fractionator. In the case of the adults, the total number of neurons in the entire MD was an average of 41% lower than in the newborn, which was statistically highly significant (P < 0.001). The estimated average total number of neurons in MD thalamus of the newborns was 11.2 million (coefficient of variation [CV] = standard deviation/mean = 0.16), compared with the adults' 6.43 million (CV = 0.15). The glial cell numbers were substantially higher in the adult brains, with an increase of almost 4 times from 10.6 million at birth to 36.3 million in the fully developed adult brain. This is the first demonstration of a higher number of human neurons in the brain of newborns compared with the adult.     

Prognostic importance of quantitative echocardiographic evaluation in patients suspected of first non-massive pulmonary embolism

Aims: Patients suspected of acute pulmonary embolism (PE) frequentlyundergo echocardiography as a part of the initial work-up. Prognosticimplication of routine echocardiography in patients suspectedof PE remain to be established. Methods and results: Transthoracic echocardiography, including tissue Doppler imaging,was performed in 283 consecutive patients referred for ventilation/perfusionscintigraphy (V/Q scan) on suspicion of first non-massive PE.The prognostic information of quantitative measures of rightventricular (RV) size, function, and pressure was assessed.Patients with PE had a follow-up echocardiography after 1 yearand changes in the parameters were assessed. Patients with PE and normal V/Q scans had similar age-adjusted1 year mortality [10 and 12%, NS (not significant)], althoughpatients with indeterminate scans carried a poorer prognosis(16% survival, P = 0.0004). Among all patients left ventricular(LV) ejection fraction as well as shortening of the pulmonaryartery (PA) acceleration time (a measure of RV after-load) wasassociated with increased mortality [hazard ratio (HR) = 0.84per 10 ms increase, P < 0.0001]. In patients with confirmed PE, the PA acceleration time is predictiveof event-free survival (all-cause mortality and heart failurehospitalizations) adjusted for LV ejection fraction, age, andsex (HR = 0.78 per 10 ms increase, P = 0.04). Measures of regional myocardial function were not related tooutcome in this study, regardless of presence of PE. Conclusion: PA acceleration time and LV systolic function are independentpredictors of mortality in patients suspected of PE, and areindependent predictors of event-free survival in patients withconfirmed PE.     

Relationships between the fibromyalgia impact questionnaire,tender point count,and muscle strength in female patients with fibromyalgia: A cohort study

Objective

To test the hypothesis that fibromyalgia (FM) patients with reduced lower extremity strength are more symptomatic and tender than FM patients with normal muscle strength.

Methods

A total of 840 FM patients and 122 healthy subjects were evaluated between 1998 and 2005. All of the patients completed version 1 of the Fibromyalgia Impact Questionnaire (FIQ) and were assessed for tender points and knee muscle strength. All subjects underwent bilateral isokinetic knee muscle strength testing in flexion and extension. Normative knee muscle strength values were calculated from the healthy subjects, and the FM cohort was divided in 2 groups: 1) patients with normal muscle strength and 2) patients with low muscle strength (2 SDs below normal). The clinical characteristics of these 2 groups were compared.

Results

Significantly reduced knee muscle strength was found in 52% of the patients. There were no clinically significant differences between patients with low versus normal muscle strength. There were no clinically significant correlations between total FIQ score, tender point count, and muscle strength. Only 4.6% of the FIQ scores and 5.1% of the tender point counts were explained by muscle strength.

Conclusion

Significantly reduced knee muscle strength was found in more than half of the patients. Patients with subnormal muscle strength were not more symptomatic or tender than patients with normal muscle strength. There were no clinically significant correlations between FIQ, tender point count, and muscle strength; therefore, reduced knee muscle strength appears to be a common objective abnormality in FM that is independent of measurements of disease activity. The implication of this finding in regard to the clinical assessment of FM needs further study.