Arabidopsis SMO2 modulates ribosome biogenesis by maintaining the RID2 abundance during organ growth.

Ribosome biogenesis is a process of making ribosomes that is tightly linked with plant growth and development. Here, through a suppressor screen for the smo2 mutant, we found that lack of a ribosomal stress response mediator, ANAC082 partially restored growth defects of the smo2 mutant, indicating SMO2 is required for the repression of nucleolar stress. Consistently, the smo2 knock-out mutant exhibited typical phenotypes characteristic of ribosome biogenesis mutants, such as pointed leaves, aberrant leaf venation, disrupted nucleolar structure, abnormal distribution of rRNA precursors, and enhanced tolerance to aminoglycoside antibiotics that target ribosomes. SMO2 interacted with ROOT INITIATION DEFECTIVE 2 (RID2), a methyltransferase-like protein required for pre-rRNA processing. SMO2 enhanced RID2 solubility in Escherichia coli and the loss of function of SMO2 in plant cells reduced RID2 abundance, which may result in abnormal accumulation of FIBRILLARIN 1 (FIB1) and NOP56, two key nucleolar proteins, in high-molecular-weight protein complex. Taken together, our results characterized a novel plant ribosome biogenesis factor, SMO2 that maintains the abundance of RID2, thereby sustaining ribosome biogenesis during plant organ growth.

Muscle oxygen saturation rates coincide with lactate-based exercise thresholds.

INTRODUCTION: Monitoring muscle metabolic activity via blood lactate is a useful tool for understanding the physiological response to a given exercise intensity. Recent indications suggest that skeletal muscle oxygen saturation (SmO2), an index of the balance between local O2 supply and demand, may describe and predict endurance performance outcomes. PURPOSE: We tested the hypothesis that SmO2 rate is tightly related to blood lactate concentration across exercise intensities, and that deflections in SmO2 rate would coincide with established blood lactate thresholds (i.e., lactate thresholds 1 and 2). METHODS: Ten elite male soccer players completed an incremental running protocol to exhaustion using 3-min work to 30 s rest intervals. Blood lactate samples were collected during rest and SmO2 was collected continuously via near-infrared spectroscopy from the right and left vastus lateralis, left biceps femoris and the left gastrocnemius. RESULTS: Muscle O2 saturation rate (%/min) was quantified after the initial 60 s of each 3-min segment. The SmO2 rate was significantly correlated with blood lactate concentrations for all muscle sites; RVL, r = - 0.974; LVL, r = - 0.969; LG, r = - 0.942; LHAM, r = - 0.907. Breakpoints in SmO2 rate were not significantly different from LT1 or LT2 at any muscle sites (P > 0.05). Bland-Altman analysis showed speed threshold estimates via SmO2 rate and lactate are similar at LT2, but slightly greater for SmO2 rate at LT1. CONCLUSIONS: Muscle O2 saturation rate appears to provide actionable information about maximal metabolic steady state and is consistent with bioenergetic reliance on oxygen and its involvement in the attainment of metabolic steady state.

Acute responses of muscle oxygen saturation during different cluster training configurations in resistance-trained individuals.

This study compared the perceptual responses, physiological indicators and technical parameters between different training protocols focused on upper body exercises. A randomized crossover design was performed, and 12 trained individuals (age: 27.1 ± 5.7 years; height: 173.7 ± 10.7 cm; BMI: 23.9 ± 2.3) completed three resistance training sessions under different protocols separated by at least 72 h: traditional training (TT) (4 x 6 repetitions at 85% of 1RM with 120 s of rest between sets), cluster 1 (CL1) (4 x 2+2+2 repetitions at 85% of 1RM with 15 s of intra-rep rest and 80 s between sets), and cluster 2 (CL2) (24 repetitions at 85% of 1RM with 15 s of inter-set recovery). Before training, arterial blood pressure (BP) and repetitions to failure of pull-up and push-up (FT) were collected. Muscle oxygen saturation (SmO2) in the chest and movement velocity were evaluated in barbell bench press during the training session. After finishing, lactate, BP, rate of perceived exertion and FT were assessed. The percentage of velocity loss (TT: 19.24%; CL1: 5.02% and CL2: 7.30%) in the bench press and lactate concentration (TT: 8.90 mmol·l-1; CL1: 6.13 mmol·l-1 and CL2: 5.48 mmol·l-1) were significantly higher (p < 0.05) for TT compared to both CLs. RPE values were higher (p < 0.05) in TT compared to CL1 (7.95 a.u. vs. 6.91 a.u., respectively). No differences (p > 0.05) were found between protocols for SmO2, BP, FT, pain or heart rate between set configurations. Cluster configurations allow one to maintain higher movement velocity and lower lactate and RPE values compared to a traditional configuration, but with similar concentrations of SmO2.

Repeated short cold-water immersions are sufficient to habituate to the cold, but do not lead to adaptations during exercise in normobaric hypoxia.

We sought to assess the effects of repeated cold-water immersions (CWI) on respiratory, metabolic, and sympathoadrenal responses to graded exercise in hypoxia. Sixteen (2 female) participants (age: 21.2 ± 1.3 years; body fat: 12.3 ± 7.7%; body surface area 1.87 ± 0.16 m2, VO2peak: 48.7 ± 7.9 mL/kg/min) underwent 6 CWI in 12.0 ± 1.2 °C. Each CWI was 5 min, twice daily, separated by ≥4 h, for three consecutive days, during which metabolic data were collected. The day before and after the repeated CWI intervention, participants ran in normobaric hypoxia (FIO2 = 0.135) for 4 min at 25%, 40%, 60%, and 75% of their sea level peak oxygen consumption (VO2peak). CWI had no effect on VO2 (p > 0.05), but reduced the VE (CWI #1: 27.1 ± 17.8 versus CWI #6: 19.9 ± 12.1 L/min) (p < 0.01), VT (CWI #1: 1.3 ± 0.4 vs CWI #6: 1.1 ± 0.4 L) (p < 0.01), and VE:VO2 (CWI #1: 53.5 ± 24.1 vs CWI #6: 41.6 ± 20.5) (p < 0.01) during subsequent CWI. Further, post exercise plasma epinephrine was lower after CWI compared to before (103.3 ± 43.1; 73.4 ± 34.6 pg/mL) (p = 0.03), with no change in pre-exercising values (75.4 ± 30.7; 72.5 ± 25.9 pg/mL). While these changes were noteworthy, it is important to acknowledge there were no changes in pulmonary (VE, VT, and VE:VO2) or metabolic (VO2, SmO2, and SpO2) variables across multiple hypoxic exercise workloads following repeated CWI. CWI habituated participants to cold water, but this did not lead to adaptations during exercise in normobaric hypoxia.

Agreement between Ventilatory Thresholds and Bilaterally Measured Vastus Lateralis Muscle Oxygen Saturation Breakpoints in Trained Cyclists: Effects of Age and Performance.

This study focused on comparing metabolic thresholds derived from local muscle oxygen saturation (SmO2) signals, obtained using near-infrared spectroscopy (NIRS), with global pulmonary ventilation rates measured at the mouth. It was conducted among various Age Groups within a well-trained cyclist population. Additionally, the study examined how cycling performance characteristics impact the discrepancies between ventilatory thresholds (VTs) and SmO2 breakpoints (BPs). METHODS: Junior (n = 18) and Senior (n = 15) cyclists underwent incremental cycling tests to assess their aerobic performance and to determine aerobic (AeT) and anaerobic (AnT) threshold characteristics through pulmonary gas exchange and changes in linearity of the vastus lateralis (VL) muscle SmO2 signals. We compared the relative power (Pkg) at ventilatory thresholds (VTs) and breakpoints (BPs) for the nondominant (ND), dominant (DO), and bilaterally averaged (Avr) SmO2 during the agreement analysis. Additionally, a 30 s sprint test was performed to estimate anaerobic performance capabilities and to assess the cyclists' phenotype, defined as the ratio of P@VT2 to the highest 5 s sprint power. RESULTS: The Pkg@BP for Avr SmO2 had higher agreement with VT values than ND and DO. Avr SmO2 Pkg@BP1 was lower (p < 0.05) than Pkg@VT1 (mean bias: 0.12 ± 0.29 W/kg; Limits of Agreement (LOA): -0.45 to 0.68 W/kg; R2 = 0.72) and mainly among Seniors (0.21 ± 0.22 W/kg; LOA: -0.22 to 0.63 W/kg); there was no difference (p > 0.05) between Avr Pkg@BP2 and Pkg@VT2 (0.03 ± 0.22 W/kg; LOA: -0.40 to 0.45 W/kg; R2 = 0.86). The bias between two methods correlated significantly with the phenotype (r = -0.385 and r = -0.515 for AeT and AnT, respectively). CONCLUSIONS: Two breakpoints can be defined in the NIRS-captured SmO2 signal of VL, but the agreement between the two methods at the individual level was too low for interchangeable usage of those methods in the practical training process. Older cyclists generally exhibited earlier thresholds in muscle oxygenation signals compared to systemic responses, unlike younger cyclists who showed greater variability and no significant differences in this regard in bias values between the two threshold evaluation methods with no significant difference between methods. More sprinter-type cyclists tended to have systemic VT thresholds earlier than local NIRS-derived thresholds than athletes with relatively higher aerobic abilities.

Age-Related Changes in Skeletal Muscle Oxygen Utilization.

The cardiovascular and skeletal muscle systems are intrinsically interconnected, sharing the goal of delivering oxygen to metabolically active tissue. Deficiencies within those systems that affect oxygen delivery to working tissues are a hallmark of advancing age. Oxygen delivery and utilization are reflected as muscle oxygen saturation (SmO2) and are assessed using near-infrared resonance spectroscopy (NIRS). SmO2 has been observed to be reduced by ~38% at rest, ~24% during submaximal exercise, and ~59% during maximal exercise with aging (>65 y). Furthermore, aging prolongs restoration of SmO2 back to baseline by >50% after intense exercise. Regulatory factors that contribute to reduced SmO2 with age include blood flow, capillarization, endothelial cells, nitric oxide, and mitochondrial function. These mechanisms are governed by reactive oxygen species (ROS) at the cellular level. However, mishandling of ROS with age ultimately leads to alterations in structure and function of the regulatory factors tasked with maintaining SmO2. The purpose of this review is to provide an update on the current state of the literature regarding age-related effects in SmO2. Furthermore, we attempt to bridge the gap between SmO2 and associated underlying mechanisms affected by aging.

Muscle Oxygen Demands of the Vastus Lateralis in Back and Front Squats.

In resistance training squats are often used to strengthen the muscles of the lower extremities and core muscles. There are two common forms of squats that use a barbell for loading, the back squat and the front squat. The technique and loading of each squat differ markedly. However, the energetic demands on the muscle between the two forms are not well understood. The purpose of this study was to investigate the difference in energy demands between front and back squats by measuring the change in skeletal muscle oxygen saturation (SmO2) through the use of near infrared spectroscopy (NIRS). METHODS: Eleven resistance trained individuals, (5 female, 6 male) with an average age of 23.7 ± 1.4, completed 3 sets of 15 repetitions at 70% of their 1-RM weight for both back and front squats. Skeletal muscle oxygen saturation (SmO2) of the vastus lateralis was measured using a wireless NIRS device. RESULTS: The ΔSmO2 was not significantly different between back and front squats but was different between sets 1-3 (44.76 ± 3.24% vs. 55.19 ± 2.75% vs. 56.30 ± 2.63%), main effect p ≤ 0.0001. The recovery of SmO2 was significantly different between back (42.5 ± 3.4 sec) and front squats (30.9 ± 2.8 sec), main effect p ≤ 0.05. CONCLUSIONS: The findings of this study suggest that the energetic demands placed on the vastus lateralis during both front and back squats are similar with a slower recovery of energetics in the back squat.

Comparison of the toxicity of sulfur mustard and its oxidation products in vitro.

The molecular toxicology of the chemical warfare agent sulfur mustard (SM) is still not completely understood. It has been suggested that in addition to SM itself also biotransformation products thereof mediate cytotoxicity. In the current study, we assessed this aspect by exposing a human hepatocyte cell line (HepG2) to SM or to its oxidation products sulfur mustard sulfoxide (SMO), sulfur mustard sulfone (SMO2), and divinyl sulfone (DVS). Cytotoxicity, determined with the XTT assay, revealed a significant higher toxicity of SMO2 and DVS compared to SM while SMO had no effect at any concentration. The exact biotransformation of SM leading to SMO, SMO2 and finally DVS is unknown so far. Involvement of the CYP450 system is discussed and was also investigated in the presented study. Modulation of CYP1A2 activity, taken as a model enzyme for CYP450, affected cytotoxicity of SM, SMO2 or DVS significantly. Induction of CYP1A2 with omeprazole led to decreased cytotoxicity for all compounds whereas inhibition with cimetidine resulted in an increased cytotoxicity for SM, but not for SMO2 and DVS. Our results indicate a distinctive role of the CYP450 system in SM poisoning. Future studies should address the metabolic conversion of SM in more detail. Our data may suggest the well-tolerated drug omeprazole as a potential co-treatment after contact to SM.

Effects of Cycling on Subsequent Running Performance, Stride Length, and Muscle Oxygen Saturation in Triathletes.

Running performance is a determinant factor for victory in Sprint and Olympic distance triathlon. Previous cycling may impair running performance in triathlons, so brick training becomes an important part of training. Wearable technology that is used by triathletes can offer several metrics for optimising training in real-time. The aim of this study was to analyse the effect of previous cycling on subsequent running performance in a field test, while using kinematics metrics and SmO2 provided by wearable devices that are potentially used by triathletes. Ten trained triathletes participated in a randomised crossover study, performing two trial sessions that were separated by seven days: the isolated run trial (IRT) and the bike-run trial (BRT). Running kinematics, physiological outcomes, and perceptual parameters were assessed before and after each running test. The running distance was significantly lower in the BRT when compared to the IRT, with a decrease in stride length of 0.1 m (p = 0.00) and higher %SmO2 (p = 0.00) in spite of the maximal intensity of exercise. No effects were reported in vertical oscillation, ground contact time, running cadence, and average heart rate. These findings may only be relevant to 'moderate level' triathletes, but not to 'elite' ones. Triathletes might monitor their %SmO2 and stride length during brick training and then compare it with isolated running to evaluate performance changes. Using wearable technology (near-infrared spectroscopy, accelerometry) for specific brick training may be a good option for triathletes.

Role of Arabidopsis sterol 4α-methyl oxidase2 family in embryo and postembryonic development.

Sterols play important roles in plant growth, including embryogenesis, cell expansion, vascular differentiation, male fertility, and endocytosis. Sterols become functional only after removal of the 2 methyl groups at C-4. There are 2 distinct sterol C-4-methyl oxidase (SMO) families in higher plants, SMO1 and SMO2, which contain 3 and 2 isoforms, respectively, involving in the removal of the first and second C4 methyl groups during sterols biosynthesis. In a recent study we showed that single smo2-1 and smo2-2 mutants displayed no significant phenotype, while smo2-1 smo2-2 double mutant was embryonic lethal. smo2-1/+ smo2-2 and smo2-1 smo2-2/+ mutants showed defect in abnormal embryo patterning and smo2-1 smo2-2/+ mutant displayed dwarf phenotype. In this mini-review, we summarize the functions and regulatory mechanisms of SMO2-1 and SMO2-2 in embryo and postembryonic development.