Novel whole blood transcriptome signatures of changes in maximal aerobic capacity in response to endurance exercise training in healthy women.

Maximal aerobic exercise capacity [maximal oxygen consumption (V̇o2max)] is one of the strongest predictors of morbidity and mortality. Aerobic exercise training can increase V̇o2max, but inter-individual variability is marked and unexplained physiologically. The mechanisms underlying this variability have major clinical implications for extending human healthspan. Here, we report a novel transcriptome signature related to ΔV̇o2max with exercise training detected in whole blood RNA. We used RNA-Seq to characterize transcriptomic signatures of ΔV̇o2max in healthy women who completed a 16-wk randomized controlled trial comparing supervised, higher versus lower aerobic exercise training volume and intensity (4 training groups, fully crossed). We found significant baseline gene expression differences in subjects who responded to aerobic exercise training with robust versus little/no ΔV̇o2max, and differentially expressed genes/transcripts were mostly related to inflammatory signaling and mitochondrial function/protein translation. Baseline gene expression signatures associated with robust versus little/no ΔV̇o2max were also modulated by exercise training in a dose-dependent manner, and they predicted ΔV̇o2max in this and a separate dataset. Collectively, our data demonstrate the potential utility of using whole blood transcriptomics to study the biology of inter-individual variability in responsiveness to the same exercise training stimulus.

Lipid oxidation during thermogenesis in high-altitude deer mice (Peromyscus maniculatus).

When at their maximum thermogenic capacity (cold-induced V̇o2max), small endotherms reach levels of aerobic metabolism as high, or even higher, than running V̇o2max. How these high rates of thermogenesis are supported by substrate oxidation is currently unclear. The appropriate utilization of metabolic fuels that could sustain thermogenesis over extended periods may be important for survival in cold environments, like high altitude. Previous studies show that high capacities for lipid use in high-altitude deer mice may have evolved in concert with greater thermogenic capacities. The purpose of this study was to determine how lipid utilization at both moderate and maximal thermogenic intensities may differ in high- and low-altitude deer mice, and strictly low-altitude white-footed mice. We also examined the phenotypic plasticity of lipid use after acclimation to cold hypoxia (CH), conditions simulating high altitude. We found that lipids were the primary fuel supporting both moderate and maximal rates of thermogenesis in both species of mice. Lipid oxidation increased threefold in mice from 30°C to 0°C, consistent with increases in oxidation of [13C]palmitic acid. CH acclimation led to an increase in [13C]palmitic acid oxidation at 30°C but did not affect total lipid oxidation. Lipid oxidation rates at cold-induced V̇o2max were two- to fourfold those at 0°C and increased further after CH acclimation, especially in high-altitude deer mice. These are the highest mass-specific lipid oxidation rates observed in any land mammal. Uncovering the mechanisms that allow for these high rates of oxidation will aid our understanding of the regulation of lipid metabolism.

Deletion of CD73 increases exercise power in mice.

Ecto-5'-nucleotidase or CD73 is the main source of extracellular adenosine involved in the activation of adenosine A2A receptors, responsible for the ergogenic effects of caffeine. We now investigated the role of CD73 in exercise by comparing female wild-type (WT) and CD73 knockout (KO) mice in a treadmill-graded test to evaluate running power, oxygen uptake (V̇O2), and respiratory exchange ratio (RER) - the gold standards characterizing physical performance. Spontaneous locomotion in the open field and submaximal running power and V̇O2 in the treadmill were similar between CD73-KO and WT mice; V̇O2max also demonstrated equivalent aerobic power, but CD73-KO mice displayed a 43.7 ± 4.2% larger critical power (large effect size, P < 0.05) and 3.8 ± 0.4% increase of maximum RER (small effect size, P < 0.05). Thus, KO of CD73 was ergogenic; i.e., it increased physical performance.

Cardiopulmonary function during supramaximal exercise in hypoxia, normoxia and hyperoxia in Thoroughbred horses.

Supramaximal exercise while inspiring different O2 gases may induce different responses in cardiopulmonary function at the same relative and/or absolute exercise intensity. The purpose of this study was to compare the effects of supramaximal exercise in hypoxia, normoxia and hyperoxia on cardiopulmonary function in Thoroughbred horses. Using a crossover design, five well-trained horses were made to run up a 6% grade on a treadmill at supramaximal speeds sustainable for approximately 110 sec (approximately 115% V̇O2max) while breathing normoxic gas (NO, 21% O2) or hypoxic gas (LO, 15.3% O2) in random order. Horses also ran at the same speed, incline and run time as in NO while breathing hyperoxic gas (HONO, 28.8% O2) and as in LO while breathing normoxic gas (NOLO). Runs were on different days, and cardiopulmonary variables were analyzed with repeated-measures ANOVA and the Holm-Sidák method for pairwise comparisons. Supramaximal speeds differed significantly between NO and LO (14.0 ± 0.5 [SD] m/sec vs. 12.6 ± 0.5 m/sec), but run times to exhaustion did not (112 ± 17 sec vs. 103 ± 14 sec). The V̇O2max in NO was higher than that in LO (165 ± 11 vs. 120 ± 15 ml (min× kg)), as was the arterial oxygen tension (66 ± 5 vs. 45 ± 2 Torr). Oxygen consumption was increased in HONO and NOLO compared with the values in NO and LO, respectively. Supramaximal exercise in hypoxia induces more severe hypoxemia and decreases V̇O2max compared with normoxia at the same relative intensity. Conversely, supramaximal exercise in hyperoxia alleviates hypoxemia and increases V̇O2 compared with normoxia at the same absolute intensity.

Progressive exercise training improves maximal aerobic capacity in individuals with well-healed burn injuries.

Long-term rehabilitative strategies are important for individuals with well-healed burn injuries. Such information is particularly critical because patients are routinely surviving severe burn injuries given medical advances in the acute care setting. The purpose of this study was to test the hypothesis that a 6-mo community-based exercise training program will increase maximal aerobic capacity (V̇o2max) in subjects with prior burn injuries, with the extent of that increase influenced by the severity of the burn injury (i.e., percent body surface area burned). Maximal aerobic capacity (indirect calorimetry) and skeletal muscle oxidative enzyme activity (biopsy of the vastus lateralis muscle) were measured pre- and postexercise training in noninjured control subjects (n = 11) and in individuals with well-healed burn injuries (n = 13, moderate body surface area burned; n = 20, high body surface area burned). Exercise training increased V̇o2max in all groups (control: 15 ± 5%; moderate body surface area: 11 ± 3%; high body surface area: 11 ± 2%; P < 0.05), though the magnitude of this improvement did not differ between groups (P = 0.7). Exercise training also increased the activity of the skeletal muscle oxidative enzymes citrate synthase (P < 0.05) and cytochrome c oxidase (P < 0.05), an effect that did not differ between groups (P = 0.2). These data suggest that 6 mo of progressive exercise training improves V̇o2max in individuals with burn injuries and that the magnitude of body surface area burned does not lessen this adaptive response.

Chronic ß2 -adrenoceptor agonist treatment alters muscle proteome and functional adaptations induced by high intensity training in young men.

KEY POINTS: While several studies have investigated the effects of exercise training in human skeletal muscle and the chronic effect of ß2 -agonist treatment in rodent muscle, their effects on muscle proteome signature with related functional measures in humans are still incompletely understood. Herein we show that daily ß2 -agonist treatment attenuates training-induced enhancements in exercise performance and maximal oxygen consumption, and alters muscle proteome signature and phenotype in trained young men. Daily ß2 -agonist treatment abolished several of the training-induced enhancements in muscle oxidative capacity and caused a repression of muscle metabolic pathways; furthermore, ß2 -agonist treatment induced a slow-to-fast twitch muscle phenotype transition. The present study indicates that chronic ß2 -agonist treatment confounds the positive effect of high intensity training on exercise performance and oxidative capacity, which is of interest for the large proportion of persons using inhaled ß2 -agonists on a daily basis, including athletes. ABSTRACT: Although the effects of training have been studied for decades, data on muscle proteome signature remodelling induced by high intensity training in relation to functional changes in humans remains incomplete. Likewise, ß2 -agonists are frequently used to counteract exercise-induced bronchoconstriction, but the effects ß2 -agonist treatment on muscle remodelling and adaptations to training are unknown. In a placebo-controlled parallel study, we randomly assigned 21 trained men to 4 weeks of high intensity training with (HIT+ß2 A) or without (HIT) daily inhalation of ß2 -agonist (terbutaline, 4 mg dose-1 ). Of 486 proteins identified by mass-spectrometry proteomics of muscle biopsies sampled before and after the intervention, 32 and 85 were changing (false discovery rate (FDR) ≤5%) with the intervention in HIT and HIT+ß2 A, respectively. Proteome signature changes were different in HIT and HIT+ß2 A (P = 0.005), wherein ß2 -agonist caused a repression of 25 proteins in HIT+ß2 A compared to HIT, and an upregulation of 7 proteins compared to HIT. ß2 -Agonist repressed or even downregulated training-induced enrichment of pathways related to oxidative phosphorylation and glycogen metabolism, but upregulated pathways related to histone trimethylation and the nucleosome. Muscle contractile phenotype changed differently in HIT and HIT+ß2 A (P ≤ 0.001), with a fast-to-slow twitch transition in HIT and a slow-to-fast twitch transition in HIT+ß2 A. ß2 -Agonist attenuated training-induced enhancements in maximal oxygen consumption (P ≤ 0.01) and exercise performance (6.1 vs. 11.6%, P ≤ 0.05) in HIT+ß2 A compared to HIT. These findings indicate that daily ß2 -agonist treatment attenuates the beneficial effects of high intensity training on exercise performance and oxidative capacity, and causes remodelling of muscle proteome signature towards a fast-twitch phenotype.

Individualised training at different intensities, in untrained participants, results in similar physiological and performance benefits.

This study compared effects of training at moderate, high, or a combination of the two intensities (mixed) on performance and physiological adaptations, when training durations were individualised. Untrained participants (n = 34) were assigned to a moderate, high, or mixed group. Maximal oxygen uptake (V̇O2max), power output at V̇O2max (MAP), time-to-exhaustion and gross efficiency were recorded before and after four weeks of cycling training (four times per week). The moderate group cycled at 60% MAP in blocks of 5 min with 1 min recovery, and training duration was individualised to 100% of pre-training time-to-exhaustion. The high group cycled at 100% MAP for 2 min with 3 min recovery, and training duration was set as the maximum number of repetitions completed in the first training session. The mixed group completed two moderate- and two high-intensity sessions each week, on alternate days. V̇O2max, MAP, and time-to-exhaustion increased after training (P < 0.05), but were not different between groups (P > 0.05). The mixed group improved their gross efficiency at 50% MAP more than the other two groups (P = 0.044) after training. When training is individualised for untrained participants, similar improvements in performance and physiological measures are found, despite marked differences in exercise intensity and total training duration.

Hypoxic training increases maximal oxygen consumption in Thoroughbred horses well-trained in normoxia.

Hypoxic training is effective for improving athletic performance in humans. It increases maximal oxygen consumption (V̇O2max) more than normoxic training in untrained horses. However, the effects of hypoxic training on well-trained horses are unclear. We measured the effects of hypoxic training on V̇O2max of 5 well-trained horses in which V̇O2max had not increased over 3 consecutive weeks of supramaximal treadmill training in normoxia which was performed twice a week. The horses trained with hypoxia (15% inspired O2) twice a week. Cardiorespiratory valuables were analyzed with analysis of variance between before and after 3 weeks of hypoxic training. Mass-specific V̇O2max increased after 3 weeks of hypoxic training (178 ± 10 vs. 194 ± 12.3 ml O2 (STPD)/(kg × min), P<0.05) even though all-out training in normoxia had not increased V̇O2max. Absolute V̇O2max also increased after hypoxic training (86.6 ± 6.2 vs. 93.6 ± 6.6 l O2 (STPD)/min, P<0.05). Total running distance after hypoxic training increased 12% compared to that before hypoxic training; however, the difference was not significant. There were no significant differences between pre- and post-hypoxic training for end-run plasma lactate concentrations or packed cell volumes. Hypoxic training may increase V̇O2max even though it is not increased by normoxic training in well-trained horses, at least for the durations of time evaluated in this study. Training while breathing hypoxic gas may have the potential to enhance normoxic performance of Thoroughbred horses.

The Effects of Non-Contingent Feedback on the Incidence of Plateau at V̇O2max.

The purpose of this study was to examine the effects of non-contingent feedback in the form of heart rate (HR) on the incidence of plateau at V̇O2max. Ten physically active males (age 24.8 yrs ± 4.2; mass 81.4 ± 9.0 kg; stature 1.80 ± 0.11 m, V̇O2max 53.2 ± 5.8 ml·kg-1.min-1) who were V̇O2max testing naïve but were cognisant as to the heart rate responses to exercise completed four incremental tests to volitional exhaustion, separated by ~72 h for the determination of V̇O2max and gas exchange threshold. The first trial served as a familiarisation with the remaining three being experimental conditions where HR was presented in a screen projection as either the actual response (HR-A) or 10 b·min-1 higher than recorded (HR-H) or 10 b·min-1 lower (HR-L). Throughout all trials V̇O2 was recorded on a breath-by-breath basis with plateau criteria of ≤ 50 ml·min-1. RESULTS: A significant difference was observed for Δ V̇O2 over the final two consecutive 30s sampling periods between HR-A, both HR-L and HR-H (p = 0.049) and for the incidence of plateau response between condition (p = 0.021). An additional significant difference was observed for sub-maximal Δ V̇O2 responses between HR-A and HR-H (p = 0.049) and HR-A and HR-L (p = 0.006). Non-significant differences were observed for all other criteria. These data indicate that when presented with non-contingent feedback in the form of HR, that the perceptually orientated pacing schema becomes disrupted promoting a sparing of the finite anaerobic capacity to compensate for the imbalance between the afferent signal and perception of effort.

Twin-sibling study and meta-analysis on the heritability of maximal oxygen consumption.

Large individual differences exist in aerobic fitness in childhood and adolescence, but the relative contribution of genetic factors to this variation remains to be established. In a sample of adolescent twins and siblings (n = 479), heart rate (HR) and maximal oxygen uptake (V̇o2max) were recorded during the climax of a graded maximal exercise test. In addition, V̇o2max was predicted in two graded submaximal exercise tests on the cycle ergometer and the treadmill, using extrapolation of the HR/V̇o2 curve to the predicted HRmax. Heritability estimates for measured V̇o2max were 60% in ml/min and 55% for V̇o2max in ml·min(-1)·kg(-1). Phenotypic correlations between measured V̇o2max and predicted V̇o2max from either submaximal treadmill or cycle ergometer tests were modest (0.57 < r < 0.70), in part because of the poor agreement between predicted and actual HRmax. The majority of this correlation was explained by genetic factors; therefore, the submaximal exercise tests still led to very comparable estimates of heritability of V̇o2max. To arrive at a robust estimate for the heritability of V̇o2max in children to young adults, a sample size weighted meta-analysis was performed on all extant twin and sibling studies in this age range. Eight studies, including the current study, were meta-analyzed and resulted in a weighted heritability estimate of 59% (ml/min) and 72% (ml·min(-1)·kg(-1)) for V̇o2max. Taken together, the twin-sibling study and meta-analyses showed that from childhood to early adulthood genetic factors determine more than half of the individual differences in V̇o2max.

The HO-1/CO system regulates mitochondrial-capillary density relationships in human skeletal muscle.

The heme oxygenase-1 (HO-1)/carbon monoxide (CO) system induces mitochondrial biogenesis, but its biological impact in human skeletal muscle is uncertain. The enzyme system generates CO, which stimulates mitochondrial proliferation in normal muscle. Here we examined whether CO breathing can be used to produce a coordinated metabolic and vascular response in human skeletal muscle. In 19 healthy subjects, we performed vastus lateralis muscle biopsies and tested one-legged maximal O2 uptake (V̇o2max) before and after breathing air or CO (200 ppm) for 1 h daily for 5 days. In response to CO, there was robust HO-1 induction along with increased mRNA levels for nuclear-encoded mitochondrial transcription factor A (Tfam), cytochrome c, cytochrome oxidase subunit IV (COX IV), and mitochondrial-encoded COX I and NADH dehydrogenase subunit 1 (NDI). CO breathing did not increase V̇o2max (1.96 ± 0.51 pre-CO, 1.87 ± 0.50 post-CO l/min; P = not significant) but did increase muscle citrate synthase, mitochondrial density (139.0 ± 34.9 pre-CO, 219.0 ± 36.2 post-CO; no. of mitochondrial profiles/field), myoglobin content and glucose transporter (GLUT4) protein level and led to GLUT4 localization to the myocyte membrane, all consistent with expansion of the tissue O2 transport system. These responses were attended by increased cluster of differentiation 31 (CD31)-positive muscle capillaries (1.78 ± 0.16 pre-CO, 2.37 ± 0.59 post-CO; capillaries/muscle fiber), implying the enrichment of microvascular O2 reserve. The findings support that induction of the HO-1/CO system by CO not only improves muscle mitochondrial density, but regulates myoglobin content, GLUT4 localization, and capillarity in accordance with current concepts of skeletal muscle plasticity.

Carbohydrate mouth rinse failed to reduce central fatigue, lower perceived exertion, and improve performance during incremental exercise.

We examined if carbohydrate (CHO) mouth rinse may reduce central fatigue and perceived exertion, thus improving maximal incremental test (MIT) performance. Nine recreational cyclists warmed up for 6 min before rinsing a carbohydrate (CHO) or placebo (PLA) solution in their mouth for 10 s in a double-blind, counterbalanced manner. Thereafter, they performed the MIT (25 W·min-1 increases until exhaustion) while cardiopulmonary and ratings of perceived exertion (RPE) responses were obtained. Pre- to post-MIT alterations in voluntary activation (VA) and peak twitch torque (Tw) were determined. Time-to-exhaustion (p = 0.24), peak power output (PPO; p = 0.45), and V̇O2MAX (p = 0.60) were comparable between conditions. Neither treatment main effect nor time-treatment interaction effect were observed in the first and second ventilatory threshold when expressed as absolute or relative V̇O2 (p = 0.78 and p = 0.96, respectively) and power output (p = 0.28 and p = 0.45, respectively) values, although with moderate-to-large effect sizes. RPE increased similarly throughout the tests and was comparable at the ventilatory thresholds (p = 0.56). Despite the time main effect revealing an MIT-induced central and peripheral fatigue as indicated by the reduced VA and Tw, CHO mouth rinse was ineffective in attenuating both fatigues. Hence, rinsing the mouth with CHO was ineffective in reducing central fatigue, lowering RPE, and improving MIT performance expressed as PPO and time-to-exhaustion. However, moderate-to-large effect sizes in power output values at VT1 and VT2 may suggest some beneficial CHO mouth rinse effects on these MIT outcomes.

"Impact of aging on maximal oxygen uptake adjusted for lower limb lean mass, total body mass, and absolute values in runners".

Performance in endurance sports decreases with aging, which has been primarily attributed to cardiovascular and musculoskeletal aging; however, there is still no clear information on the factors that are most affected by aging. The aim of this study was to compare two groups of runners (< 50 and > 50 years of age) according to their absolute, weight-adjusted maximal oxygen uptake (V̇O2max), lower limb lean mass-adjusted V̇O2max, ventilatory threshold, and respiratory compensation point (RCP). A total of 78 male recreational long-distance runners were divided into Group 1 (38.12 ± 6.87 years) and Group 2 (57.55 ± 6.14 years). Participants were evaluated for body composition, V̇O2max, VT, and RCP. Group 1 showed higher absolute and body mass-adjusted V̇O2max (4.60 ± 0.57 l·min-1 and 61.95 ± 8.25 ml·kg-1·min-1, respectively) than Group 2 (3.77 ± 0.56 l·min-1 and 51.50 ± 10.22 ml·kg-1·min-1, respectively), indicating a significant difference (p < 0.001, d = - 1.46 and p < 0.001, d = - 1.16). Correspondingly, Group 1 showed a significantly higher lower limb lean mass-adjusted V̇O2max (251.72 ± 29.60 ml·kgLM-1·min-1) than Group 2 (226.36 ± 43.94 ml·kgLM-1·min-1) (p = 0.008, d = - 0.71). VT (%V̇O2max) (p = 0.19, d = 0.19) and RCP (%V̇O2max) (p = 0.24, d = 0.22) did not differ between the groups. These findings suggest that both variables that are limited by central or peripheral conditions are negatively affected by aging, but the magnitude of the effect is higher in variables limited by central conditions. These results contribute to our understanding of how aging affects master runners.

Attenuated peripheral oxygen extraction and greater cardiac output in women with posttraumatic stress disorder during exercise.

Posttraumatic stress disorder (PTSD) is associated with an increased risk of developing cardiovascular disease, especially in women. Evidence indicates that men with PTSD exhibit lower maximal oxygen uptake (V̇o2max) relative to controls; however, whether V̇o2max is blunted in women with PTSD remains unknown. Furthermore, it is unclear what determinants (i.e., central and/or peripheral) of V̇o2max are impacted by PTSD. Therefore, we evaluated the central (i.e., cardiac output; Q̇c) and peripheral (i.e., arteriovenous oxygen difference) determinants of V̇o2max in women with PTSD; hypothesizing that V̇o2max would be lower in women with PTSD compared with women without PTSD (controls), primarily due to smaller increases in stroke volume (SV), and therefore Q̇c. Oxygen uptake (V̇o2), heart rate (HR), Q̇c, SV, and arteriovenous oxygen difference were measured in women with PTSD (n = 14; mean [SD]: 43 [11] yr,) and controls (n = 17; 45 [11] yr) at rest, and during an incremental maximal treadmill exercise test, and the Q̇c/V̇o2 slope was calculated. V̇o2max was not different between women with and without PTSD (24.3 [5.6] vs. 26.4 [5.0] mL/kg/min; P = 0.265). However, women with PTSD had higher Q̇c [P = 0.002; primarily due to greater SV (P = 0.069), not HR (P = 0.285)], and lower arteriovenous oxygen difference (P = 0.002) throughout exercise compared with controls. Furthermore, the Q̇c/V̇o2 slope was steeper in women with PTSD relative to controls (6.6 [1.4] vs. 5.7 [1.0] AU; P = 0.033). Following maximal exercise, women with PTSD exhibited slower HR recovery than controls (P = 0.046). Thus, despite attenuated peripheral oxygen extraction, V̇o2max is not reduced in women with PTSD, likely due to larger increases in Q̇c.NEW & NOTEWORTHY The current study indicates that V̇o2max is not different between women with and without PTSD; however, women with PTSD exhibit blunted peripheral extraction of oxygen, thus requiring an increase in Q̇c to meet metabolic demand during exercise. Furthermore, following exercise, women with PTSD demonstrate impaired autonomic cardiovascular control relative to sedentary controls. We interpret these data to indicate that women with PTSD demonstrate aberrant cardiovascular responses during and immediately following fatiguing exercise.

Accuracy of a non-exercise method using seismocardiography for the estimation of V̇O2peak in sub-elite football players.

A non-exercise method equation using seismocardiography for estimating V̇O2peak (SCG V̇O2peak) has previously been validated in healthy subjects. However, the performance of the SCG V̇O2peak within a trained population is unknown, and the ability of the model to detect changes over time is not well elucidated. Forty-seven sub-elite football players were tested at the start of pre-season (SPS) and 36 players completed a test after eight weeks at the end of the pre-season (EPS). Testing included an SCG V̇O2peak estimation at rest and a graded cardiopulmonary exercise test (CPET) on a treadmill for determination of V̇O2peak. Agreement between SCG V̇O2peak and CPET V̇O2peak showed a large underestimation at SPS (bias ± 95% CI: -9.9 ± 1.8, 95% Limits of Agreement: 2.2 to -22.0 mL·min-1 kg-1). At EPS no interaction (p = 0.3590) but a main effect of time (p < 0.0001) and methods (p < 0.0001) was observed between SCG and CPET V̇O2peak. No correlation in V̇O2peak changes was observed between SCG and CPET (r = -20.0, p = 0.2484) but a fair agreement in classifying the correct directional change in V̇O2peak with the SCG method was found (Cohen's κ coefficient = 0.28 ± 0.25). Overall, the SCG V̇O2peak method lacks accuracy and despite being able to estimate group changes, it was incapable of detecting individual changes in V̇O2peak following a pre-season period in sub-elite football players. The SCG algorithm needs to be further adjusted and the accuracy and precision improved for the method to be applicable for use within a trained population.

Agreement of Air Bike and Treadmill Protocols to Assess Maximal Oxygen Uptake: An Exploratory Study.

Maximal oxygen consumption (V̇O2max) is an important measure of aerobic fitness, with applications in evaluating fitness, designing training programs, and assessing overall health. While treadmill assessments are considered the gold standard, airbikes (ABs) are increasingly popular exercise machines. However, limited research exists on AB-based V̇O2max assessments, particularly regarding agreement with treadmill graded exercise tests. To address this gap, a randomized crossover study was conducted, involving 15 healthy adults (9M, 6F, 7 familiar with AB) aged 30.1 ± 8.6 years. Paired t-tests, intraclass correlation coefficients (ICC), Bland-Altman and Principal component (PC) analyses were used to assess agreement between protocols. The results demonstrated good to excellent agreement in V̇O2max, maximum heart rate (HR), and rating of perceived exertion (ICC range: 0.89-0.92). However, significant differences were observed in several measures, including V̇O2max and maximum HR (p < 0.01). Overall a systematic bias 3.31 mL/kg/min (treadmill > AB, 95%CI[1.67,4.94]) was observed, no proportional bias was present; however, regular AB users (systematic bias: 1.27 (95%CI[0.20,2.34]) mL/kg/min) exhibited higher agreement in V̇O2max measures compared to non-regular users (systematic bias: 5.09 (95%CI[3.69,6.49]) mL/kg/min). There were no significant differences in cardiorespiratory coordination, between the AB and the treadmill. These findings suggest that for individuals familiar with the AB, it can be a suitable alternative for assessing V̇O2max compared to the treadmill. Future research with larger samples should focus on developing prediction equations for field AB tests to predict V̇O2max. Practitioners should consider using the AB to assess V̇O2max in individuals who prefer it over running.

Relationship between maximal oxygen uptake, within-set fatigue and between-set recovery during resistance exercise in resistance-trained men and women.

BACKGROUND: The primary aim of this study was to examine the relationship between maximal oxygen update (V̇O2max) and within-set fatigue and between-set recovery during resistance exercise in men and women. METHODS: We examined the relationship between V̇O2max and various indices of fatigue and recovery during parallel squats (3 sets, 90 s rest, 70% of 1RM to failure) and isokinetic knee extensions (3 × 10 maximal repetitions at 60 deg/s, 45 s rest) in 28 (age 27.0 ± 3.6 years) resistance-trained subjects (14 men and 14 women). We also examined whether there were sex differences in within-set fatigue and between-set recovery. RESULTS: V̇O2max was weakly related to recovery and fatigue in both men and women (range of P-values for V̇O2max as a covariate; 0.312-0.998, range of R-values, 0.005-0.604). There were no differences between the sexes in fatigue within a set for the squat, but men showed less within-set fatigue than women in the first set of the isokinetic knee extension exercise (~ 8% torque loss difference, main effect of sex P = 0.034). Regarding recovery between sets, men showed greater relative peak power (P = 0.016) and peak torque (P = 0.034) loss between sets in both exercises, respectively, compared to women. Women also tended to complete more repetitions than men (main effect of sex, P = 0.057). Loss of peak torque between sets in knee extension was evident in both absolute and relative (%) values in men but not in women. CONCLUSIONS: Our study suggests that aerobic capacity is weakly associated with within-set fatigue and between-set recovery in resistance training in both men and women. Women and men show comparable levels of within-set fatigue in the multi-joint squat, but women show more within-set fatigue during the single-joint isokinetic knee extension compared with men. In contrast, women recover better than men between sets in both exercises.

The exercise power-duration relationship is equally reproducible in eumenorrheic female and male humans.

This study aims to investigate the effect of the menstrual cycle (MC) on exercise performance across the power-duration relationship (PDR). We hypothesized females would exhibit greater variability in the PDR across the MC than males across a similar timespan, with critical power (CP) and work-prime (W') being lower during the early follicular phase than the late follicular and midluteal phases. Seven eumenorrheic, endurance-trained female adults performed multiple constant-load-to-task-failure and maximum-power tests at three timepoints across the MC (early follicular, late follicular, and midluteal phases). Ten endurance-trained male adults performed the same tests approximately 10 days apart. No differences across the PDR were observed between MC phases (CP: 186.74 ± 31.00 W, P = 0.955, CV = 0.81 ± 0.65%) (W': 7,961.81 ± 2,537.68 J, P = 0.476, CV = 10.48 ± 3.06%). CP was similar for male and female subjects (11.82 ± 1.42 W·kg-1 vs. 11.56 ± 1.51 W·kg-1, respectively) when controlling for leg lean mass. However, W' was larger (P = 0.047) for male subjects (617.28 ± 130.10 J·kg-1) than female subjects (490.03 ± 136.70 J·kg-1) when controlling for leg lean mass. MC phase does not need to be controlled when conducting aerobic endurance performance research on eumenorrheic female subjects without menstrual dysfunction. Nevertheless, several sex differences in the power-duration relationship exist, even after normalizing for body composition. Therefore, previous studies describing the physiology of exercise performance in male subjects may not perfectly describe that of female subjects.NEW & NOTEWORTHY Females are often excluded from exercise performance research due to experimental challenges in controlling for the menstrual cycle (MC), causing uncertainty regarding how the MC impacts female performance. The present study examined the influences that biological sex and the MC have on the power-duration relationship (PDR) by comparing critical power (CP), Work-prime (W'), and maximum power output (PMAX) in males and females. Our data provide evidence that the MC does not influence the PDR and that females exhibit similar reproducibility as males. Thus, when conducting aerobic endurance exercise research on eumenorrheic females without menstrual dysfunction, the phase of the MC does not need to be controlled. Although differences in body composition account for some differences between the sexes, sex differences in W' and PMAX persisted even after normalizing for different metrics of body composition. These data highlight the necessity and feasibility of examining sex differences in performance, as previously generated male-only data within the literature may not apply to female subjects.

Aging increases metabolic capacity and reduces work efficiency during handgrip exercise in males.

Maximal oxygen uptake and exercise performance typically decline with age. However, there are indications of preserved vascular function and blood flow regulation during arm exercise. Yet, it is unknown if this potential physiological preservation with age is mirrored in peripheral metabolic capacity and V̇o2/W ratio. Thus, to investigate the effects of aging in the arms, we measured metabolic and vascular responses to 6-min bouts of dynamic handgrip exercise at 40% and 80% of maximal work rate (WRmax) in 11 young (26 ± 2 yr) and 12 old (80 ± 6 yr) males, applying Doppler-ultrasound combined with blood samples from a deep forearm vein. At baseline, the old had a larger arterial diameter compared with young (P < 0.001). During exercise, the two groups reached the same WRmax. V̇o2, blood flow, and oxygen supply were higher (40%WRmax; 80%WRmax, all P < 0.01), and arteriovenous oxygen difference was lower (80%WRmax, P < 0.02), in old compared with young. Old also had a higher oxygen excess at 80%WRmax (P < 0.01) than young, whereas no difference in muscle diffusion or oxygen extraction was detected. Only young exhibited an increase in intensity-induced arterial dilation (P < 0.05), and they had a lower mean arterial pressure than old at 80%WRmax (P < 0.001). V̇o2/W (40%WRmax; 80%WRmax) was reduced in old compared with young (both P < 0.05). In conclusion, in old and young males with a similar handgrip WRmax, old had a higher V̇o2 during 80%WRmax intensity, achieved by an increased blood flow. This may be a result of the available cardiac output reserve, compensating for reduced work efficiency and attenuated vascular response observed in old.NEW & NOTEWORTHY Contrasting the typically observed decline in V̇o2max with age, the current study reveals an age-related increase in forearm metabolic capacity during handgrip exercise in old, mediated by an increased forearm blood flow. Exercise with a small muscle mass in arms, where central components of the oxygen transport are not limiting, allows old to attain a similar maximal work rate as young despite their increased V̇o2/W ratio.

Running vs. resistance exercise to counteract deconditioning induced by 90-day head-down bedrest.

Spaceflight is associated with enhanced inactivity, resulting in muscular and cardiovascular deconditioning. Although physical exercise is commonly used as a countermeasure, separate applications of running and resistive exercise modalities have never been directly compared during long-term bedrest. This study aimed to compare the effectiveness of two exercise countermeasure programs, running and resistance training, applied separately, for counteracting cardiovascular deconditioning induced by 90-day head-down bedrest (HDBR). Maximal oxygen uptake ( V ˙ O2max), orthostatic tolerance, continuous ECG and blood pressure (BP), body composition, and leg circumferences were measured in the control group (CON: n = 8), running exercise group (RUN: n = 7), and resistive exercise group (RES: n = 7). After HDBR, the decrease in V ˙ O2max was prevented by RUN countermeasure and limited by RES countermeasure (-26% in CON p < 0.05, -15% in RES p < 0.05, and -4% in RUN ns). Subjects demonstrated surprisingly modest orthostatic tolerance decrease for different groups, including controls. Lean mass loss was limited by RES and RUN protocols (-10% in CON vs. -5% to 6% in RES and RUN). Both countermeasures prevented the loss in thigh circumference (-7% in CON p < 0.05, -2% in RES ns, and -0.6% in RUN ns) and limited loss in calf circumference (-10% in CON vs. -7% in RES vs. -5% in RUN). Day-night variations in systolic BP were preserved during HDBR. Decrease in V ˙ O2max positively correlated with decrease in thigh (r = 0.54 and p = 0.009) and calf (r = 0.52 and p = 0.012) circumferences. During this 90-day strict HDBR, running exercise successfully preserved V ˙ O2max, and resistance exercise limited its decline. Both countermeasures limited loss in global lean mass and leg circumferences. The V ˙ O2max reduction seems to be conditioned more by muscular than by cardiovascular parameters.