Introduction: The purpose of this investigation was to: (1) to determine the reliability of rectus femoris muscle cross-sectional area and echo intensity obtained using panoramic ultrasound imaging during seated and supine lying positions before and after a 5-minute rest period and (2) to determine the influence of body position and rest period on the magnitude of rectus femoris muscle cross-sectional area and echo intensity measurements. Methods: A total of 23 males and females (age ¼ 21.5 AE 1.9 years) visited the laboratory on two separate occasions. During each visit, panoramic ultrasound images of the rectus femoris were obtained in both a seated and a supine position before (T1) and after a 5-minute (T2) rest period to quantify any potential changes in either muscle cross-sectional area and/or echo intensity. Results: None of the muscle cross-sectional area or echo intensity measurements exhibited systematic variability, and the ICCs were 0.98-0.99 and 0.88-0.91, and the coefficients of variation were 3.9% and 8.2% for muscle cross-sectional area and echo intensity, respectively. Our results indicated that muscle cross-sectional area was greater in the seated than supine position, whereas echo intensity was greater in the supine position. Further, echo intensity increased in the seated position from T1 to T2. Conclusion: Both rectus femoris muscle cross-sectional area and echo intensity may be reliably measured in either a seated or supine lying position before or after a 5-minute rest period. Aside from echo intensity in the seated position, rest period had no influence on the magnitude of muscle cross-sectional area or echo intensity. Comparison of muscle cross-sectional area values that are obtained in different body positions is ill-advised.
The liver enzyme cytochrome P450 1A2 (CYP1A2) is responsible for 90% of caffeine metabolism, while caffeine exerts many of its effects via antagonist binding to adenosine A2a receptors (ADORA2A). This study aimed to examine whether functional single nucleotide polymorphisms (SNPs) in 1976T > C (ADORA2A; rs5751876) and −163C > A (CYP1A2; rs762551) influence the effect of caffeine on the postprandial glucose (GLU) response to a carbohydrate meal. We report that individuals with the 1976T > C CC, but not CT/TT genotypes display elevated GLU levels after consuming caffeine and carbohydrate (CHO + CAFF) versus carbohydrate only (CHO). The GLU area under the curve (AUC) was also greater during the CHO + CAFF condition compared to the CHO condition in CC, but not the CT/TT genotypes. The −163C > A AC/CC, but not AA, genotypes displayed greater GLU concentrations 60-min post meal during CHO + CAFF versus CHO. Our data suggest that caffeine-induced impairments in postprandial glycaemia are related to 1976T > C and −163C > A SNPs.
Previous investigations have reported a relationship between skeletal muscle phenotype and motor unit (MU) firing parameters during submaximal contractions. The purpose of the current investigation, however, was to examine the relationships between motor unit firing behavior during a maximal voluntary contraction, Myosin Heavy Chain (MHC) isoform content, and various molecular neuromuscular targets of the vastus lateralis (VL) muscle in resistance‐trained men. Ten resistance‐trained males completed a trapezoidal ramp contraction up to 100% of their maximal voluntary isometric strength (MVIC). Surface electromyography was recorded from the VL using a multichannel electrode array and decomposed to examine the firing characteristics of individual MUs. A skeletal muscle biopsy of the VL was also collected from each subject. Regression analyses were performed to identify relationships between type II fiber area and the slopes and/or intercepts of the mean firing rate (FRMEAN) versus recruitment threshold (RT), max firing rate (FRMAX) versus RT, and RT versus MU action potential amplitude (MUAPPP) relationships. There were significant inverse relationships between type II fiber area and the y‐intercept of the FR versus RT relationship (P < 0.05). Additionally, strong relationships (r > 0.5) were found between type II fiber area and FRMEAN versus RT slope and RT versus MUAPPP slope and intercept. These data further support the hypothesis that skeletal muscle phenotype is related to MU behavior during isometric contraction. However, our data, in concert with previous investigations, may suggest that these relationships are influenced by the intensity of the contraction.
Adverse childhood experiences (ACEs) are psychosocial stressors that occur during sensitive developmental windows and are associated with increased lifetime cardiovascular disease (CVD) risk in a dose-dependent manner. Vascular endothelial dysfunction is a pathophysiological mechanism that promotes hypertension and CVD, and may be a mechanism by which ACEs contribute to lifetime CVD risk. We examined whether exposure to ACEs is associated with reduced vascular endothelial function (VEF) in otherwise healthy, young adult women (20.7 ± 3 years) with (ACE+) versus without (ACE-) ACEs, explored whether differences in circulating SIRT1 or systemic oxidative stress could explain ACEs-related differences in VEF, and examined the ability of a pilot, 8-week exercise intervention to augment VEF and SIRT1, or reduce oxidized LDL cholesterol (oxLDL) in ACE+ young adult women. Forty-two otherwise healthy young adults completed this study. Prior to the intervention, VEF (P = 0.002) and SIRT1 (P = 0.004) were lower in the ACE+ than ACE- group, but oxLDL concentrations were not different (P = 0.77). There were also significant associations (P ≤ 0.04) among FMD, SIRT1, and oxLDL in the ACE+, but not ACE- group. Adjusting for circulating SIRT1 and oxLDL reduced the differences in FMD observed between groups (P = 0.10), but only SIRT1 was a significant adjuster of the means (P < 0.05). The exercise intervention employed was unable to enhance VEF or SIRT1 in the ACE+ exercise group. Our data suggest that ACEs likely increase susceptibility to hypertension and CVD via reduced vascular function, perhaps through a SIRT1 pathway-related mechanism.
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