Power Is More Relevant Than Ascensional Speed to Determine Metabolic Demand at Different Gradient Slopes During Running.

ABSTRACT: Hingrand, C, Olivier, N, Combes, A, Bensaid, S, and Daussin, FN. Power is more relevant than ascensional speed to determine metabolic demand at different gradient slopes during running. J Strength Cond Res 37(11): 2298-2301, 2023-Trail running is characterized by successive uphill and downhill running sessions. To prescribe training intensity, an assessment of maximal running capacity is required. This study compared 2 uphill incremental tests using the same ascensional speed increment to identify the influence of the slope gradient on performance. Ten subjects (8 men and 2 women) performed 3 incremental exercises on various slope (1%: IT01, 10%: IT10, and 25%: IT25), and the ascensional speed increment was similar between IT10 and IT25 (100 m·h-1 every minute). Gas exchanges, heart rate, and power were monitored continuously during the tests. Similar V̇o2max levels were observed in the 3 conditions: 68.7 ± 6.2 for IT01, 70.1 ± 7.3 for IT10, and 67.6 ± 7.0 for IT25. A greater maximal ascensional speed was reached in the IT25 (1760 ± 190 vs. 1,330 ± 106 for IT25 and IT10, respectively, p < 0.01). A significant relationship was observed between relative V̇o2 levels and relative power without any effect of slope. Power should be the parameter used for prescribing training intensity compared with ascensional speed in trail.

Evolution of the physical characteristics of the French women's rugby players: A 10-year longitudinal analysis by position and team.

Introduction: The study aimed to interpret the evolution of the physical performance of rugby sevens and rugby union French international players from 2009 to 2020. Methods: 631 players from the French national teams were divided into three groups: forwards, backs and sevens. The performances evaluated were anthropometric characteristics, strength tests (1 RM bench press and 1 RM pull-up), aerobic capacity (YoYo IR1 test) and speed tests (10 m, 20 m and 50 m). The best performance of each player over a two-year period was kept for the analysis. Fluctuations were observed across the decade. Results: The anthropometric characteristics of female rugby sevens players tend to be taller and lighter than rugby union players. In rugby sevens, a moderate increase in maximal aerobic capacity was observed while sprint performances remained similar. Improvements in height and weight were observed over the last 10 years in rugby union players with a difference between the position. A moderate increase in sprinting performances and strength were observed both in backs and forwards. Discussion: The overall improvement of strength and conditioning performances and anthropometrical evolution reflects the rugby environment characterized by the arrival of professional contracts and the structuration process of the clubs which allows a better quality of training and easier access to the infrastructures of the very high level.

Sepsis-like Energy Deficit Is Not Sufficient to Induce Early Muscle Fiber Atrophy and Mitochondrial Dysfunction in a Murine Sepsis Model.

Sepsis-induced myopathy is characterized by muscle fiber atrophy, mitochondrial dysfunction, and worsened outcomes. Whether whole-body energy deficit participates in the early alteration of skeletal muscle metabolism has never been investigated. Three groups were studied: "Sepsis" mice, fed ad libitum with a spontaneous decrease in caloric intake (n = 17), and "Sham" mice fed ad libitum (Sham fed (SF), n = 13) or subjected to pair-feeding (Sham pair fed (SPF), n = 12). Sepsis was induced by the intraperitoneal injection of cecal slurry in resuscitated C57BL6/J mice. The feeding of the SPF mice was restricted according to the food intake of the Sepsis mice. Energy balance was evaluated by indirect calorimetry over 24 h. The tibialis anterior cross-sectional area (TA CSA), mitochondrial function (high-resolution respirometry), and mitochondrial quality control pathways (RTqPCR and Western blot) were assessed 24 h after sepsis induction. The energy balance was positive in the SF group and negative in both the SPF and Sepsis groups. The TA CSA did not differ between the SF and SPF groups, but was reduced by 17% in the Sepsis group compared with the SPF group (p < 0.05). The complex-I-linked respiration in permeabilized soleus fibers was higher in the SPF group than the SF group (p < 0.05) and lower in the Sepsis group than the SPF group (p < 0.01). Pgc1α protein expression increased 3.9-fold in the SPF mice compared with the SF mice (p < 0.05) and remained unchanged in the Sepsis mice compared with the SPF mice; the Pgc1α mRNA expression decreased in the Sepsis compared with the SPF mice (p < 0.05). Thus, the sepsis-like energy deficit did not explain the early sepsis-induced muscle fiber atrophy and mitochondrial dysfunction, but led to specific metabolic adaptations not observed in sepsis.

Effect of Waters Enriched in O2 by Injection or Electrolysis on Performance and the Cardiopulmonary and Acid-Base Response to High Intensity Exercise.

Several brands of water enriched with O2 (O2-waters) are commercially available and are advertised as wellness and fitness waters with claims of physiological and psychological benefits, including improvement in exercise performance. However, these claims are based, at best, on anecdotal evidence or on a limited number of unreliable studies. The purpose of this double-blind randomized study was to compare the effect of two O2-waters (~110 mg O2·L-1) and a placebo (10 mg O2·L-1, i.e., close to the value at sea level, 9-12 mg O2·L-1) on the cardiopulmonary responses and on performance during high-intensity exercise. One of the two O2-waters and the placebo were prepared by injection of O2. The other O2-water was enriched by an electrolytic process. Twenty male subjects were randomly allocated to drink one of the three waters in a crossover study (2 L·day-1 × 2 days and 15 mL·kg-1 90 min before exercise). During each exercise trial, the subjects exercised at 95.9 ± 4.7% of maximal workload to volitional fatigue. Exercise time to exhaustion and the cardiopulmonary responses, arterial lactate concentration and pH were measured. Oxidative damage to proteins, lipids and DNA in blood was assessed at rest before exercise. Time to exhaustion (one-way ANOVA) and the responses to exercise (two-way ANOVA [Time; Waters] with repeated measurements) were not significantly different among the three waters. There was only a trend (p = 0.060) for a reduction in the time constant of the rapid component of VO2 kinetics with the water enriched in O2 by electrolysis. No difference in oxidative damage in blood was observed between the three waters. These results suggest that O2-water does not speed up cardiopulmonary response to exercise, does not increase performance and does not trigger oxidative stress measured at rest.

From mitochondria to sarcopenia: Role of inflammaging and RAGE-ligand axis implication.

Sarcopenia is characterized by a loss of muscle mass and function that reduces mobility, diminishes quality of life, and can lead to fall-related injuries. At the intracellular level, mitochondrial population alterations are considered as key contributors to the complex etiology of sarcopenia. Mitochondrial dysfunctions lead to reactive oxygen species production, altered cellular proteostasis, and promotes inflammation. Interestingly, the receptor for advanced glycation end-products (RAGE) is a pro-inflammatory receptor involved in inflammaging. In this review, after a brief description of sarcopenia, we will describe how mitochondria and the pathways controlling mitochondrial population quality could participate to age-induced muscle mass and force loss. Finally, we will discuss the RAGE-ligand axis during aging and its possible connection with mitochondria to control inflammaging and sarcopenia.

Effects of (-)-epicatechin on mitochondria.

Mitochondrial dysfunction is observed in a broad range of human diseases, including rare genetic disorders and complex acquired pathologies. For this reason, there is increasing interest in identifying safe and effective strategies to mitigate mitochondrial impairments. Natural compounds are widely used for multiple indications, and their broad healing properties suggest that several may improve mitochondrial function. This review focuses on (-)-epicatechin, a monomeric flavanol, and its effects on mitochondria. The review summarizes the available data on the effects of acute and chronic (-)-epicatechin supplementation on mitochondrial function, outlines the potential mechanisms involved in mitochondrial biogenesis induced by (-)-epicatechin supplementation and discusses some future therapeutic applications.

Relationships Between Isokinetic Shoulder Evaluation and Fitness Characteristics of Elite French Female Water-Polo Players.

Swimming and throwing are involved in water-polo player performance. These movements have a common biomechanical basis in the use of the internal shoulder rotation and adductor muscles. The aim of the study was to evaluate the relationship between shoulder isokinetic evaluation and throwing velocity as well as swimming performance in female water-polo players. Fifteen high level water-polo players completed two isokinetic shoulder evaluations to determine peak torque of shoulder rotators of the dominant shoulder (concentric and eccentric movements at an angular velocity of 60°·s-1 and concentric movements at an angular velocity of 240°·s-1) and shoulder extensors of both arms (concentric movements at an angular velocity of 60°·s-1 and 240°·s-1). Throwing velocity was measured using a radar gun placed 5 m behind the goal post. Front crawl swimming velocity was determined at 25 m, 100 m and 400 m distances. Concentric peak torque at 60°·s-1 and 240°·s-1 of internal rotators and eccentric peak torque at 60°·s-1 of external rotators were predictors of throwing velocity. The best model to explain the relationship between isokinetic evaluations and throwing velocity was obtained with concentric IR peak torque at 60°·s-1 and eccentric ER peak torque at 60°·s-1 (r2 = 0.52, p = 0.012). Relative total work done and peak torque of shoulder extensors were predictors of 25 m swimming velocity. Shoulder isokinetic evaluations correlate significantly with swimming performance and throwing velocity of female water-polo players. The results may help coaches to develop new strategies such as eccentric dry land training programs to increase both shoulder external rotators strength and throwing velocity.

Physiological comparison of intensity-controlled, isocaloric intermittent and continuous exercise.

VO2 fluctuations are argued to be an important mechanism underpinning chronic adaptations following interval training. We compared the effect of exercise modality, continuous vs. intermittent realized at a same intensity, on electrical muscular activity, muscular oxygenation and on whole body oxygen uptake. Twelve participants (24 ± 5 years; VO2peak: 43 ± 6 mL·â€…min-1·kg-1) performed (i) an incremental test to exhaustion to determine peak work rate (WRpeak); two randomized isocaloric exercises at 70%WRpeak; (ii) 1 bout of 30 min; (iii) 30 bouts of 1 min work intercepted with 1 min passive recovery. For electromyography, only the CON exercise showed change for the vastus lateralis root-mean-square (+6.4 ± 5.1%, P < .01, 95%CI 3.2, 8.3) and mean power frequency (-5.2 ± 4.8, P < .01, 95%CI -8.2, -3.5). Metabolic fluctuations (i.e. Oxygen Fluctuation Index and HHb Fluctuation Index) were higher in the intermittent modality, while post-exercise blood lactate concentrations (4.80 ± 1.50 vs. 2.32 ± 1.21 mM, respectively, for the CON and INT, P < .01, 95%CI 1.72, 3.12) and the time spent over 90% of VO2 target (1644 ± 152 vs. 356 ± 301 sec, respectively, for the CON and INT, P < .01, 95%CI 1130, 1446) were higher in the continuous modality. In conclusion, despite a similar energy expenditure and intensity, intermittent and continuous exercises showed two very different physiological responses. The intermittent modality would lead to a larger recruitment of fast twitch fibres that are less mitochondria-equipped and therefore may be more likely respondent to mitochondrial adaptations. In addition, this modality induces greater metabolic variations, a stimulus who could lead to mitochondrial development.

Effect of work:rest cycle duration on [Formula: see text] fluctuations during intermittent exercise.

The succession of on-transient phases that induce a repetition of metabolic changes is a possible mechanism responsible for the greater response to intermittent training (IT). The objective of this study was to quantify [Formula: see text] fluctuations during intermittent exercise characterised by the same work:rest ratio, but different durations and identify which duration leads to the greatest fluctuations. Ten participants (24 ± 5 years; [Formula: see text]: 42 ± 7 mL·min-1·kg-1) performed (1) an incremental test to exhaustion to determine peak work rate (WRpeak) and oxygen uptake ([Formula: see text]), (2), and three 1 h intermittent exercises alternating work period at 70% WRpeak with passive recovery period of different 1:1 work:recovery duty cycles (30 s:30 s, 60 s:60 s, 120 s:120 s). [Formula: see text] response analysis revealed differences in the fluctuations across the intermittent conditions despite an identical total energy expenditure. The sum of the cycle's nadir-to-peak [Formula: see text] differences (ΣΔ[Formula: see text]) and the oxygen fluctuation index (OFI) were both greater in the 60 s:60 s condition (ΣΔ[Formula: see text]: +38% ± 13% and +19% ± 18% vs. 120 s:120 s and 30 s:30 s, P < 0.05; OFI: +41% ± 29% and +67% ± 62% vs. 120 s:120 s and 30:30 s, P < 0.05). [Formula: see text] fluctuation analysis was successful in identifying the intermittent condition associated with the greatest disturbances: the 60 s:60 s duty cycle induces more [Formula: see text] fluctuations. The present findings also demonstrate that the selection of the duty cycle duration for submaximal intermittent exercise (70% of WRpeak) prescription is of interest to produce high [Formula: see text] fluctuations.

Exercise-induced metabolic fluctuations influence AMPK, p38-MAPK and CaMKII phosphorylation in human skeletal muscle.

During transition from rest to exercise, metabolic reaction rates increase substantially to sustain intracellular ATP use. These metabolic demands activate several kinases that initiate signal transduction pathways which modulate transcriptional regulation of mitochondrial biogenesis. The purpose of this study was to determine whether metabolic fluctuations per se affect the signaling cascades known to regulate peroxisome proliferator-activated receptor γ coactivator-1α (PGC-1α). On two separate occasions, nine men performed a continuous (30-min) and an intermittent exercise (30 × 1-min intervals separated by 1-min of recovery) at 70% of V˙O2peak. Skeletal muscle biopsies from the vastus lateralis were taken at rest and at +0 h and +3 h after each exercise. Metabolic fluctuations that correspond to exercise-induced variation in metabolic rates were determined by analysis of VO2 responses. During intermittent exercise metabolic fluctuations were 2.8-fold higher despite identical total work done to continuous exercise (317 ± 41 vs. 312 ± 56 kJ after intermittent and continuous exercise, respectively). Increased phosphorylation of AMP-activated protein kinase (AMPK) (~2.9-fold, P < 0.01), calcium/calmodulin-dependent protein kinase II (CaMKII) (~2.7-fold, P < 0.01) and p38-mitogen-activated protein kinase (MAPK) (~4.2-fold, P < 0.01) occurred immediately in both exercises and to a greater extent after the intermittent exercise (condition x time interaction, P < 0.05). A single bout of intermittent exercise induces a greater activation of these signaling pathways regulating PGC-1α when compared to a single bout of continuous exercise of matched work and intensity. Chronic adaptations to exercise on mitochondria biogenesis are yet to be investigated.

Different timing of changes in mitochondrial functions following endurance training.

PURPOSE: The objective of this study was to investigate the time course of the endurance training-induced adaptations in two major mitochondrial functions. METHODS: Forty rats were divided into four groups: a control group and three training groups--a 1-d training group, a 5-d training group, and a 10-d training group. The training protocol consisted of 30 min of running on a motorized treadmill (26 m·min(-1), 15% grade). Nuclear respiratory factor-1; transcription factor A, mitochondrial; superoxide dismutase-2; glutathione peroxidase-4; and citrate synthase (CS) messenger RNA levels were measured by qPCR. Mitochondrial respiration and H2O2 release were assessed using permeabilized fibers of white gastrocnemius in situ. Calculation of free radical leak was performed in two conditions where substrates were identical in both measurements. CS activity was assessed spectrophotometrically. RESULTS: An early time-dependent modulation in messenger RNA levels was observed with training: nuclear respiratory factor-1 and superoxide dismutase-2 levels increased after acute exercise, transcription factor A, mitochondrial and CS levels improved after 5 d, and glutathione peroxidase-4 levels increased after 10 d. CS activity improved by 29% ± 8% (P < 0.01) after 5 d together with a 50% ± 7% reduction in the free radical leak (P < 0.05). Finally, 10 d of endurance training did not significantly alter mitochondrial H2O2 release but increased mitochondrial respiration rates in situ (P < 0.05). CONCLUSIONS: Our results demonstrate that mitochondrial adaptations follow a sequential program in which mitochondrial respiration and free radical leak adaptations occur according to a different timing. Collectively, these results suggest early mitochondrial qualitative adaptations in response to endurance training.

Cyclophilin-D is dispensable for atrophy and mitochondrial apoptotic signalling in denervated muscle.

In the present study, we specifically determined whether the regulatory protein cyclophilin-D (CypD), and by extension opening of the permeability transition pore (PTP), is involved in the activation of mitochondria-derived apoptotic signalling previously described in skeletal muscle following loss of innervation. For this purpose, CypD-defficient (CypD-KO) mice and their littermate controls were submitted to unilateral sciatic nerve transection, and mitochondrial resistance to Ca2+-induced opening of the PTP, and muscle apoptotic signalling were investigated 14 days post-surgery. Denervation caused atrophy, facilitated Ca2+-induced opening of the PTP in vitro in permeabilized muscle fibres, and activation of the apoptotic proteolytic cascade in the whole muscle of both mouse strains. In CypD-KO mice, mitochondrial resistance to Ca2+-induced PTP opening was greater than in WT mice, in both the normal and the denervated state, indicating that lack of CypD desensitized to PTP opening. However, denervation in CypD-KO mice still resulted in a facilitation of PTP opening compared to normally innervated contralateral muscle, indicating that in vitro additional factors could poise mitochondria from denervated muscle toward PTP opening. At the whole muscle level, lack of CypD, despite conferring greater resistance to PTP opening, did not protect against atrophy, release of mitochondrial pro-apoptotic factors and activation of caspases following denervation. Altogether, these results provide direct evidence that CypD-dependent PTP opening is dispensable for atrophy and apoptotic signalling in skeletal muscle following denervation.

Effect of interval versus continuous training on cardiorespiratory and mitochondrial functions: relationship to aerobic performance improvements in sedentary subjects.

The goal of the study was to determine the effects of continuous (CT) vs. intermittent (IT) training yielding identical mechanical work and training duration on skeletal muscle and cardiorespiratory adaptations in sedentary subjects. Eleven subjects (6 men and 5 women, 45 +/- 3 years) were randomly assigned to either of the two 8-wk training programs in a cross-over design, separated by 12 wk of detraining. Maximal oxygen uptake (Vo2max) increased after both trainings (9% with CT vs. 15% with IT), whereas only IT was associated with faster Vo2 kinetics (tau: 68.0 +/- 1.6 vs. 54.9 +/- 0.7 s, P < 0.05) measured during a test to exhaustion (TTE) and with improvements in maximal cardiac output (Qmax, from 18.1 +/- 1.1 to 20.1 +/- 1.2 l/min; P < 0.01). Skeletal muscle mitochondrial oxidative capacities (Vmax) were only increased after IT (3.3 +/- 0.4 before and 4.5 +/- 0.6 micromol O2 x min(-1) x g dw(-1) after training; P < 0.05), whereas capillary density increased after both trainings, with a two-fold higher enhancement after CT (+21 +/- 1% for IT and +40 +/- 3% after CT, P < 0.05). The gain of Vmax was correlated with the gain of TTE and the gain of Vo2max with IT. The gain of Qmax was also correlated with the gain of VO2max. These results suggest that fluctuations of workload and oxygen uptake during training sessions, rather than exercise duration or global energy expenditure, are key factors in improving muscle oxidative capacities. In an integrative view, IT seems optimal in maximizing both peripheral muscle and central cardiorespiratory adaptations, permitting significant functional improvement. These data support the symmorphosis concept in sedentary subjects.

Training at high exercise intensity promotes qualitative adaptations of mitochondrial function in human skeletal muscle.

This study explored mitochondrial capacities to oxidize carbohydrate and fatty acids and functional optimization of mitochondrial respiratory chain complexes in athletes who regularly train at high exercise intensity (ATH, n = 7) compared with sedentary (SED, n = 7). Peak O(2) uptake (Vo(2max)) was measured, and muscle biopsies of vastus lateralis were collected. Maximal O(2) uptake of saponin-skinned myofibers was evaluated with several metabolic substrates [glutamate-malate (V(GM)), pyruvate (V(Pyr)), palmitoyl carnitine (V(PC))], and the activity of the mitochondrial respiratory complexes II and IV were assessed using succinate (V(s)) and N,N,N',N'-tetramethyl-p-phenylenediamine dihydrochloride (V(TMPD)), respectively. Vo(2max) was higher in ATH than in SED (57.8 +/- 2.2 vs. 31.4 +/- 1.3 ml.min(-1).kg(-1), P < 0.001). V(GM) was higher in ATH than in SED (8.6 +/- 0.5 vs. 3.3 +/- 0.3 micromol O(2).min(-1).g dry wt(-1), P < 0.001). V(Pyr) was higher in ATH than in SED (8.7 +/- 1.0 vs. 5.5 +/- 0.2 micromol O(2).min(-1).g dry wt(-1), P < 0.05), whereas V(PC) was not significantly different (5.3 +/- 0.9 vs. 4.4 +/- 0.5 micromol O(2).min(-1).g dry wt(-1)). V(S) was higher in ATH than in SED (11.0 +/- 0.6 vs. 6.0 +/- 0.3 micromol O(2).min(-1).g dry wt(-1), P < 0.001), as well as V(TMPD) (20.1 +/- 1.0 vs. 16.2 +/- 3.4 micromol O(2).min(-1).g dry wt(-1), P < 0.05). The ratios V(S)/V(GM) (1.3 +/- 0.1 vs. 2.0 +/- 0.1, P < 0.001) and V(TMPD)/V(GM) (2.4 +/- 1.0 vs. 5.2 +/- 1.8, P < 0.01) were lower in ATH than in SED. In conclusion, comparison of ATH vs. SED subjects suggests that regular endurance training at high intensity promotes the enhancement of maximal mitochondrial capacities to oxidize carbohydrate rather than fatty acid and induce specific adaptations of the mitochondrial respiratory chain at the level of complex I.

Improvement of VO2max by cardiac output and oxygen extraction adaptation during intermittent versus continuous endurance training.

Improvement of exercise capacity by continuous (CT) versus interval training (IT) remains debated. We tested the hypothesis that CT and IT might improve peripheral and/or central adaptations, respectively, by randomly assigning 10 healthy subjects to two periods of 24 trainings sessions over 8 weeks in a cross-over design, separated by 12 weeks of detraining. Maximal oxygen uptake (VO2max), cardiac output (Qmax) and maximal arteriovenous oxygen difference (Da-vO2max) were obtained during an exhaustive incremental test before and after each training period. VO2max and Qmax increased only after IT (from 26.3 +/- 1.6 to 35.2 +/- 3.8 ml min(-1) kg(-1) and from 17.5 +/- 1.3 to 19.5 +/- 1.8 l min(-1), respectively; P < 0.01). Da-vO2max increased after both protocols (from 11.0 +/- 0.8 to 12.7 +/- 1.0; P < 0.01 and from 11.0 +/- 0.8 to 12.1 +/- 1.0 ml 100 ml(-1), P < 0.05 in CT and IT, respectively). At submaximal intensity a significant rightward shift of the Q/Da-vO2 relationship appeared only after CT. These results suggest that in isoenergetic training, central and peripheral adaptations in oxygen transport and utilization are training-modality dependant. IT improves both central and peripheral components of Da-vO2max whereas CT is mainly associated with greater oxygen extraction.