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.

We investigated the test-retest reliability of, and age-related differences in, markers of skeletal muscle metabolism and microvascular function derived from the near-infrared spectroscopy with vascular occlusion test (NIRS-VOT) in younger women (YW) and middle-aged and older women (MAOW). Seventeen YW (age 23 ± 4 years) and 17 MAOW (age 59 ± 8 years) completed this study. Participants completed identical experimental visits separated by ∼4 weeks during which the NIRS-VOT was used to quantify the occlusion slope, minimum and maximum tissue saturation, ischaemic index, reperfusion magnitude, the reperfusion and 10-s reperfusion slopes (slope 2 and slope 2 10-s ), time to max tissue saturation, and area under the reperfusion curve using the local tissue oxygen saturation signal. Except for slope 2 10-s (intraclass correlation coefficient (ICC) = 0.37; coefficient of variation (CV) = 31%), time to max tissue saturation (ICC = 0.21), and ischaemic index (ICC = 0.37) for MAOW, all of the NIRS variables demonstrated good to excellent relative reliability for the YW (ICCs = 0.74-0.86) and the MAOW (ICCs = 0.51-0.87), with CVs of 2-21% and 2-22%, respectively.The occlusion slope was significantly lower, indicating accelerated deoxygenation, while maximum tissue saturation, reperfusion magnitude, and ischaemic index were significantly higher in YW versus MAOW. No other group differences were found. In conclusion, our data support the use of the NIRS-VOT as a simple, reliable, non-invasive technique for the assessment of peripheral skeletal muscle metabolism and microvascular function in women, with the reliability being generally greater in YW versus MAOW. Further, our data suggest that ageing is associated with lower skeletal muscle metabolism and microvascular hyperaemic responsiveness in women.

No abstract

The reactive capacity of the muscle-tendon complex is commonly assessed using the reactive strength index (RSI). Conventionally, the RSI is a ratio of rebound jump height to ground contact time in depth jumping. Several assumptions regarding the linear mechanics acting through the whole-body center of gravity may threaten the internal validity of computation and interpretation of RSI scores. First, it is common for rebound jump height to be predicted from rebound jump flight time. This assumes that the angular positioning of body segments is equivalent at the time instances of rebound jump take-off and landing. Prior literature supports a mixed-methods approach for computing the RSI that is void of this assumption. The mixed-methods approach gives a more valid estimation of rebound jump height. In this approach, rebound jump height is estimated from rebound jump take-off velocity of the whole-body center of mass. This is accomplished by subtracting an estimate of impact velocity, acquired using videography, from change in whole-body center of mass velocity estimated from integrated vertical ground reaction force data. Second, it is often assumed that vertical displacement of the whole-body center of mass during the drop phase of the depth jump is predicted perfectly from the height of the platform used to perform the drop. This assumption may affect the internal validity of comparing RSI scores across individuals and within individuals performing depth jumps from varied heights. The purpose of the present study was to investigate the internal validity of RSI scores computed using the conventional approach and impact velocity variability, which may affect the interpretation of RSI scores. Seventy physically active young adults performed depth jumps from drop heights of 0.51, 0.66, and 0.81 m. RSI was computed using the conventional approach and a mixed-methods approach featuring the use of 2-dimensional videography, body segment parameters, and force platform dynamometry. The two computational methods were compared using linear regression performed on data from each drop height. In addition, a 2 (computational method) by 3 (drop height) Analysis of Variance (ANOVA) was performed to evaluate for main effects and interactions in RSI data. Multiple one sample t-tests were performed to compare estimated and theoretical impact velocities. The ANOVA revealed no main effect or interactions between computational approaches (p = 0.467–0.938). Linear regression revealed moderately strong associations between RSI scores computed using the conventional and mixed-methods approaches (R2 = 0.685–0.741). Moreover, linear regressions revealed that the conventional approach tends to overestimate the mixed methods approach for RSI scores below 1.0 and underestimate the mixed methods approach for RSI scores above 1.0. Lastly, estimated impact velocities were observed to be as much as 13% lower versus theoretical (p < 0.001). Researchers with access to motion capture and force platform technology may consider using a mixed-methods approach for computing the RSI, which likely maximizes the internal validity of scores. In addition, results suggest for practitioners to practice caution when comparing conventional RSI scores across individuals.

Sarcopenia, or the age‐related loss of skeletal muscle mass and function, is an increasingly prevalent condition that contributes to reduced quality of life, morbidity, and mortality in older adults. Older adults display blunted anabolic responses to otherwise anabolic stimuli—a phenomenon that has been termed anabolic resistance (AR)—which is likely a casual factor in sarcopenia development. AR is multifaceted, but historically much of the mechanistic focus has been on signalling impairments, and less focus has been placed on the role of the vasculature in postprandial protein kinetics. The vascular endothelium plays an indispensable role in regulating vascular tone and blood flow, and age‐related impairments in vascular health may impede nutrient‐stimulated vasodilation and subsequently the ability to deliver nutrients (e.g. amino acids) to skeletal muscle. Although the majority of data has been obtained studying younger adults, the relatively limited data on the effect of blood flow on protein kinetics in older adults suggest that vasodilatory function, especially of the microvasculature, strongly influences the muscle protein synthetic response to amino acid feedings. In this narrative review, we examine evidence of AR in older adults following amino acid and mixed meal consumption, examine the evidence linking vascular dysfunction and insulin resistance to age‐related AR, review the influence of nitric oxide and endothelin‐1 on age‐related vascular dysfunction as it relates to AR, briefly review the potential causal role of arterial stiffness in promoting skeletal muscle microvascular dysfunction and AR, and provide a brief overview and future considerations for research examining age‐related AR.