The effects of chronic concentric and eccentric training on position sense and joint reaction angle of the knee extensors.

The aim of the present study was to compare the effect of chronic concentric or eccentric training on position sense and joint reaction angle, in healthy, untrained young men. Twenty-four men were randomly assigned into a pure concentric (CT) or a pure eccentric (ET) group and performed for 8 weeks, one training session/week, 75 maximal knee extensors contractions. Before and 48 h after the first (W1) and the last (W8) training sessions, knee joint position sense and joint reaction angle were assessed at three different knee angles (i.e. 30°, 45° and 60°). At the same time points, indirect indices of exercise-induced muscle damage (EIMD) were evaluated (i.e. range of motion [ROM], optimal angle, maximum isometric, concentric and eccentric torques, delayed onset muscle soreness [DOMS] and blood creatine kinase concentrations [CK]). Forty-eight hours post W1, position sense, reaction angle and all EIMD indices were significantly changed for both groups (p < 0.05; η2: 0.125-0.618), however, greater alterations were observed after ET. Significant correlations were found, in both groups, between the training-induced changes of position sense, reaction angles and the changes of EIMD biomarkers (r: -0.855-0.825; p < 0.005). No significant changes were found 48 h post W8 for position sense, reaction angle and EIMD indices (p > 0.285) for both CT or ET groups. In conclusion, exercise-induced changes in position sense and reaction angle, were related to the magnitude of EIMD, and not by the type of muscle contraction per se.HighlightsExercise induced changes in position sense and reaction angle, were related to the magnitude of EIMD, and not by the type of muscle contraction per se.After the 1st training session eccentric exercise caused greater disturbances, compared to concentric exercise, in EIMD indices which caused concomitant disturbances to position sense and knee reaction angle.8 weeks of either eccentric or concentric training leads to preservation of position sense and knee reaction angle 48 h after maximal intensity exercise of either types of muscle contraction.

Redox basis of exercise physiology.

Redox reactions control fundamental processes of human biology. Therefore, it is safe to assume that the responses and adaptations to exercise are, at least in part, mediated by redox reactions. In this review, we are trying to show that redox reactions are the basis of exercise physiology by outlining the redox signaling pathways that regulate four characteristic acute exercise-induced responses (muscle contractile function, glucose uptake, blood flow and bioenergetics) and four chronic exercise-induced adaptations (mitochondrial biogenesis, muscle hypertrophy, angiogenesis and redox homeostasis). Based on our analysis, we argue that redox regulation should be acknowledged as central to exercise physiology.

Rapid decreases of key antioxidant molecules in critically ill patients: A personalized approach.

BACKGROUND & AIMS: Oxidative stress is regarded a key component of critical illness and has been associated with poor prognosis in Intensive Care Unit (ICU) patients. Diverse antioxidant treatments have been applied to combat oxidative stress in ICU, yet the results were typically disappointing. An explanation for this failure is that all studies utilized antioxidants indiscriminately and did not take into account the antioxidant profile of the patients. The aim of the present study was to investigate whether critically ill patients experience different insufficiencies in three major antioxidants with a "recycling" redox relationship (vitamin C, vitamin E and glutathione) and in the central reductant molecule of many enzymatic antioxidants (NADPH). METHODS: Sixty mechanically-ventilated adult medical critically ill patients (age: 63.5 ± 17.1; APACHE II score: 21.2 ± 7.4; Glasgow Coma Scale: 6.2 ± 1.9) were enrolled in the study, while 20 healthy age-matched volunteers served as control group. The antioxidant profile and the level of systemic oxidative stress (F2-isoprostanes) were measured at ICU admission and at days 1 and 7. RESULTS: The majority of the ICU patients developed rapid and severe antioxidant insufficiencies (by exhibiting less than 50% of the control values) in one (22/60), two (7/60) or three (2/60) of the antioxidants measured, despite the almost similar levels of oxidative stress. CONCLUSIONS: The wide heterogeneity in antioxidant decreases in response to ICU stay highlights the importance of patient stratification when planning to apply antioxidant treatments and indicates that the successful delivery of personalized clinical nutrition may depend on our ability to identify "responsive" phenotypes.

Acute nicotinamide riboside supplementation improves redox homeostasis and exercise performance in old individuals: a double-blind cross-over study.

PURPOSE: Older individuals suffer from low NADH levels. We have previously shown that nicotinamide riboside [NR; a NAD(P)(H) precursor] administration impaired exercise performance in young rats. It has been suggested that supplementation of redox agents exerts ergogenic effect only in deficient individuals. We hypothesized that old individuals would more likely benefit from NR supplementation. We investigated the effect of acute NR supplementation on redox homeostasis and physical performance in young and old individuals. METHODS: Twelve young and twelve old men received NR or placebo in a double-blind cross-over design. Before and 2 h after NR or placebo supplementation, blood and urine samples were collected, while physical performance (VO2max, muscle strength, and fatigue) was assessed after the second blood sample collection. RESULTS: At rest, old individuals exhibited lower erythrocyte NAD(P)H levels, higher urine F2-isoprostanes and lower erythrocyte glutathione levels compared to young (P < 0.05). NR supplementation increased NADH (51% young; 59% old) and NADPH (32% young; 38% old) levels in both groups (P < 0.05), decreased F2-isoprostanes by 18% (P < 0.05), and tended to increase glutathione (P = 0.078) only in the old. NR supplementation did not affect VO2max and concentric peak torque, but improved isometric peak torque by 8% (P = 0.048) and the fatigue index by 15% (P = 0.012) in the old. In contrast, NR supplementation did not exert any redox or physiological effect in the young. CONCLUSIONS: NR supplementation increased NAD(P)H levels, decreased oxidative stress, and improved physical performance only in old subjects, substantiating that redox supplementation may be beneficial only in individuals with antioxidant deficiencies.

Nicotinamide riboside supplementation dysregulates redox and energy metabolism in rats: Implications for exercise performance.

NEW FINDINGS: What is the central question of this study? The aim was to investigate the potential metabolic and redox mechanisms that impaired exercise performance after 21 days of supplementation with 300 mg (kg body weight)-1 of nicotinamide riboside in rats. What is the main finding and its importance? Nicotinamide riboside disturbed energy and redox metabolism and impaired exercise performance in heathy rats. Exogenously administered redox agents in heathy populations might lead to adverse effects. ABSTRACT: Nicotinamide riboside is a recently discovered form of vitamin B3 that can increase NAD(P) levels. NAD(P) plays key roles in energy metabolism, and its main function is the transfer of electrons in various cellular reactions. Research in aged or diseased mice reported that nicotinamide riboside increases NAD(H) levels, reduces morbidity and improves health and muscle function. We have recently shown that in healthy young rats, chronic administration of nicotinamide riboside marginally non-significantly decreased exercise performance by 35% (P = 0.071). As a follow-up to this finding, we analysed samples from these animals, in an attempt to reveal the potential mechanisms driving this adverse effect, focusing on redox homeostasis and bioenergetics. Thirty-eight Wistar rats were divided into four groups: control (n = 10), exercise (n = 9), nicotinamide riboside (n = 10) and exercise plus nicotinamide riboside (n = 9). Nicotinamide riboside was administered for 21 days [300 mg (kg body weight)-1 daily]. At the end of administration, the exercise and the exercise plus nicotinamide riboside groups performed an incremental swimming performance test until exhaustion. Nicotinamide riboside supplementation increased the levels of NADPH in the liver (P = 0.050), increased the levels of F2 -isoprostanes in plasma (P = 0.047), decreased the activity of glutathione peroxidase (P = 0.017), glutathione reductase (P < 0.001) and catalase (P = 0.024) in erythrocytes, increased the level of glycogen in the liver (P < 0.001) and decreased the concentration of glucose (P = 0.016) and maximal lactate accumulation in plasma (P = 0.084). These findings support the prevailing idea that exogenously administered redox agents in heathy populations might lead to adverse effects and not necessarily to beneficial or neutral effects.

Adaptations to endurance training depend on exercise-induced oxidative stress: exploiting redox interindividual variability.

AIM: The aim of this study was to reveal the role of reactive oxygen and nitrogen species (RONS) in exercise adaptations under physiological in vivo conditions and without the interference from other exogenous redox agents (e.g. a pro-oxidant or antioxidant). METHODS: We invented a novel methodological set-up that exploited the large redox interindividual variability in exercise responses. More specifically, we used exercise-induced oxidative stress as the 'classifier' measure (i.e. low, moderate and high) and investigated the physiological and redox adaptations after a 6-week endurance training protocol. RESULTS: We demonstrated that the group with the low exercise-induced oxidative stress exhibited the lowest improvements in a battery of classic adaptations to endurance training (VO2 max, time trial and Wingate test) as well as in a set of redox biomarkers (oxidative stress biomarkers and antioxidants), compared to the high and moderate oxidative stress groups. CONCLUSION: The findings of this study substantiate, for the first time in a human in vivo physiological context, and in the absence of any exogenous redox manipulation, the vital role of RONS produced during exercise in adaptations. The stratification approach, based on a redox phenotype, implemented in this study could be a useful experimental strategy to reveal the role of RONS and antioxidants in other biological manifestations as well.

Going retro: Oxidative stress biomarkers in modern redox biology.

The field of redox biology is inherently intertwined with oxidative stress biomarkers. Oxidative stress biomarkers have been utilized for many different objectives. Our analysis indicates that oxidative stress biomarkers have several salient applications: (1) diagnosing oxidative stress, (2) pinpointing likely redox components in a physiological or pathological process and (3) estimating the severity, progression and/or regression of a disease. On the contrary, oxidative stress biomarkers do not report on redox signaling. Alternative approaches to gain more mechanistic insights are: (1) measuring molecules that are integrated in pathways linking redox biochemistry with physiology, (2) using the exomarker approach and (3) exploiting -omics techniques. More sophisticated approaches and large trials are needed to establish oxidative stress biomarkers in the clinical setting.

Reductive stress after exercise: The issue of redox individuality.

Exercise has been consistently used as an oxidant stimulus in redox biology studies. However, previous studies have focused on group differences and did not examine individual differences. As a result, it remains untested whether all individuals experience oxidative stress after acute exercise. Therefore, the main aim of the present study was to investigate whether some individuals exhibit unexpected responses after an acute eccentric (i.e., muscle-damaging) exercise session. Ninety eight (N = 98) young men performed an isokinetic eccentric exercise bout with the knee extensors. Plasma, erythrocytes and urine samples were collected immediately before and 2 days post-exercise. Three commonly used redox biomarkers (F2-isoprostanes, protein carbonyls and glutathione) were assayed. As expected, the two oxidant biomarkers (F2-isoprostanes and protein carbonyls) significantly increased 2 days after exercise (46% and 61%, respectively); whereas a significant decrease in glutathione levels (by -21%) was observed after exercise. A considerable number of the participants exhibited changes in the levels of biomarkers in the opposite, unexpected direction than the group average. More specifically, 13% of the participants exhibited a decrease in F2-isoprostanes and protein carbonyls and 10% of the participants exhibited an increase in glutathione levels. Furthermore, more than 1 out of 3 individuals exhibited either unexpected or negligible (from 0% to ± 5%) responses to exercise in at least one redox biomarker. It was also observed that the initial values of redox biomarkers are important predictors of the responses to exercise. In conclusion, although exercise induces oxidative stress in the majority of individuals, it can induce reductive stress or negligible stress in a considerable number of people. The data presented herein emphasize that the mean response to a redox stimulus can be very misleading. We believe that the wide variability (including the cases of reductive stress) described is not limited to the oxidant stimulus used and the biomarkers selected.