Inverse association between changes in energetic cost of walking and vertical accelerations in non-metastatic breast cancer survivors Abstract Purpose With accelerometry, the utility to detect changes in physical activity are predicated on the assumption that walking energetics and gait mechanics do not change. The present work examined associations between changes (∆) in walking energetics, exercise self-efficacy, and several accelerometer-derived metrics. Methods Secondary analyses were performed among a sub-sample (n = 29) of breast cancer survivors participating in a larger randomized trial. During 4 min of treadmill walking (0.89 m s−1, 0% grade), indirect calorimetry quantified steady-state energy expenditure (EE), wherein, participants were fitted with a heart rate monitor and hip-worn triaxial accelerometer. Exercise self-efficacy was measured using a 9-item questionnaire, while vector magnitude (VM) and individual planes (e.g., mediolateral, vertical, and anteroposterior) of the movement were extracted for data analyses. Evaluations were made at baseline and after 3 months. Results From baseline to 3 months, the energetic cost of walking (kcals min−1) significantly decreased by an average of  − 5.1% (p = 0.001; d = 0.46). Conversely, VM significantly increased (p = 0.007; d = 0.53), exclusively due to greater vertical accelerations (acc) (+ 5.7 ± 7.8 acc; p = 0.001; d = 0.69). Changes in vertical accelerations were inversely and positively associated with ∆walking EE (r = − 0.37; p = 0.047) and ∆exercise self-efficacy (r = 0.39; p = 0.034), respectively. Conclusion Hip-worn accelerometers do not appear well-suited to correctly detect changes in ease of walking as evidenced by reduced energetic cost. Further research should determine if a divergence between measured EE and vertical accelerations could contribute to erroneous inferences in free-living physical activity.

No ergogenic effects of a 10-day combined heat and hypoxic acclimation on aerobic performance in normoxic thermoneutral or hot conditions Abstract Purpose Hypoxic acclimation enhances convective oxygen delivery to the muscles. Heat acclimation-elicited thermoregulatory benefits have been suggested not to be negated by adding daily exposure to hypoxia. Whether concomitant acclimation to both heat and hypoxia offers a synergistic enhancement of aerobic performance in thermoneutral or hot conditions remains unresolved. Methods Eight young males (\(\dot{V}{\text{O}}_{2\max }\): 51.6 ± 4.6 mL min−1 kg−1) underwent a 10-day normobaric hypoxic confinement (FiO2 = 0.14) interspersed with daily 90-min normoxic controlled hyperthermia (target rectal temperature: 38.5 °C) exercise sessions. Prior to, and following the confinement, the participants conducted a 30-min steady-state exercise followed by incremental exercise to exhaustion on a cycle ergometer in thermoneutral normoxic (NOR), thermoneutral hypoxic (FiO2 = 0.14; HYP) and hot (35 °C, 50% relative humidity; HE) conditions in a randomized and counterbalanced order. The steady-state exercise was performed at 40% NOR peak power output (Wpeak) to evaluate thermoregulatory function. Blood samples were obtained from an antecubital vein before, on days 1 and 10, and the first day post-acclimation. Results \(\dot{V}{\text{O}}_{2\max }\) and ventilatory thresholds were not modified in any environment following acclimation. Wpeak increased by 6.3 ± 3.4% in NOR and 4.0 ± 4.9% in HE, respectively. The magnitude and gain of the forehead sweating response were augmented in HE post-acclimation. EPO increased from baseline (17.8 ± 7.0 mIU mL−1) by 10.7 ± 8.8 mIU mL−1 on day 1 but returned to baseline levels by day 10 (15.7 ± 5.9 mIU mL−1). Discussion A 10-day combined heat and hypoxic acclimation conferred only minor benefits in aerobic performance and thermoregulation in thermoneutral or hot conditions. Thus, adoption of such a protocol does not seem warranted.

Acute glutamine supplementation does not improve 20-km self-paced cycling performance in the heat Abstract Introduction The premise of this study was to investigate the effect of acute glutamine supplementation on 20 km time trial cycling performance in the heat, neuromuscular function, inflammation and endotoxemia. Methods Twelve cyclists completed two, 20-km time trials (20TT) in 35 °C (50% relative humidity). Participants ingested either glutamine (GLUT; 0.9 g kg−1 fat-free mass) or a placebo (CON) 60 min before each 20TT. Physiological and perceptual measures were recorded during each 20TT, and neuromuscular function assessed pre- and post-exercise. Venous blood was analysed for endotoxins, markers of gut damage (inflammatory fatty acid binding protein; I-FABP) and inflammatory cytokines (interleukin-6, IL-6; tumour necrosis factor-alpha, TNF-α). Data were analysed using linear mixed models in a Bayesian framework. Results 20TT in the heat increased I-FABP and elevated inflammatory cytokines (IL-6 and TNF-α) compared to pre-exercise values but did not result in endotoxemia. Completion time was not statistically different between conditions (mean difference [95% credible interval] = 11 s [− 23, 44]). Relative to CON, GLUT did not alter any physiological or perceptual measures during the 20TT. Conclusion Glutamine supplementation does not improve 20TT performance in the heat or preserve neuromuscular function when compared to a placebo. These findings suggest that glutamine is not an ergogenic aid or prophylactic intervention for heat-induced gut damage during short-duration self-paced exercise in hot environments.

Impact of stimulation frequency on neuromuscular fatigue Abstract Purpose The aim of the present study was to examine the frequency effects (20 Hz and 100 Hz) on neuromuscular fatigue using stimulation parameters favoring an indirect motor unit recruitment through the afferent pathway. Methods Nineteen subjects were divided into two groups: 20 Hz (n = 10) and 100 Hz (n = 9). The electrical stimulation session consisted of 25 stimulation trains (20 s ON/20 s OFF, pulse width: 1 ms) applied over the tibial nerve and delivered at an intensity evoking 10% maximal voluntary isometric contraction (MVIC). Before and after these protocols, MVIC was assessed, while neural changes were evaluated by the level of activation (VAL) and muscle changes were evaluated by the twitch associated with the maximal M-wave (Pt). For all stimulation trains, the real and the theoretical values of the torque-time integral (TTIr and TTIth, respectively) were calculated. The TTIr/TTIth ratio of the first train was calculated to evaluate the presence of extra torque. Results The main results showed a similar decrease in MVIC torque after both protocols accompanied by neural and muscle changes, as evidenced by the decrease in VAL and Pt. TTIr values across the 20-Hz trains remained constant, whereas they significantly decreased during the 100-Hz stimulation trains. The relative MVIC decrease was negatively correlated with TTIr/TTIth. Conclusion Results give evidence of an identical neuromuscular fatigue development between protocols, while lower stimulation frequency permitted preservation of a given torque level during the stimulation trains. The negative correlation between this fatigue development and TTIr/TTIth suggests that extra torque production induces greater voluntary torque losses.

Multilevel allometric modelling of maximal stroke volume and peak oxygen uptake in 11–13-year-olds Abstract Purpose To investigate (1) whether maximal stroke volume (SVmax) occurs at submaximal exercise intensities, (2) sex differences in SVmax once fat-free mass (FFM) has been controlled for, and, (3) the contribution of concurrent changes in FFM and SVmax to the sex-specific development of peak oxygen uptake \( \left( {{\dot{\text{V}}\text{O}}_{2} } \right) \). Methods The peak \( {\dot{\text{V}}\text{O}}_{2} \) s of 61 (34 boys) 11–12-year-olds were determined and their SV determined during treadmill running at 2.28 and 2.50 m s−1 using carbon dioxide rebreathing. The SVmax and peak \( {\dot{\text{V}}\text{O}}_{2} \) of 51 (32 boys) students who volunteered to be tested treadmill running at 2.50 m s−1 on three annual occasions were investigated using multilevel allometric modelling. The models were founded on 111 (71 from boys) determinations of SVmax, FFM, and peak \( {\dot{\text{V}}\text{O}}_{2} \). Results Progressive increases in treadmill running speed resulted in significant (p < 0.01) increases in \( {\dot{\text{V}}\text{O}}_{2} \), but SV levelled-off with nonsignificant (p > 0.05) changes within ~ 2–3%. In the multilevel models, SVmax increased proportionally to FFM0.72 and with FFM controlled for, there were no significant (p > 0.05) sex differences. Peak \( {\dot{\text{V}}\text{O}}_{2} \) increased with FFM but after adjusting for FFM0.98, a significant (p < 0.05) sex difference in peak \( {\dot{\text{V}}\text{O}}_{2} \) remained. Introducing SVmax to the multilevel model revealed a significant (p < 0.05), but small additional effect of SVmax on peak \( {\dot{\text{V}}\text{O}}_{2} \). Conclusions Fat-free mass explained sex differences in SVmax, but with FFM controlled for, there was still a ~ 5% sex difference in peak \( {\dot{\text{V}}\text{O}}_{2} \). SVmax made a modest additional contribution to explain the development of peak \( {\dot{\text{V}}\text{O}}_{2} , \) but there remained an unresolved sex difference of ~ 4%.

Steady-state cerebral blood flow regulation at altitude: interaction between oxygen and carbon dioxide Abstract High-altitude ascent imposes a unique cerebrovascular challenge due to two opposing blood gas chemostimuli. Specifically, hypoxia causes cerebral vasodilation, whereas respiratory-induced hypocapnia causes vasoconstriction. The conflicting nature of these two superimposed chemostimuli presents a challenge in quantifying cerebrovascular reactivity (CVR) in chronic hypoxia. During incremental ascent to 4240 m over 7 days in the Nepal Himalaya, we aimed to (a) characterize the relationship between arterial blood gas stimuli and anterior, posterior and global (g)CBF, (b) develop a novel index to quantify cerebral blood flow (CBF) in relation to conflicting steady-state chemostimuli, and (c) assess these relationships with cerebral oxygenation (rSO2). On rest days during ascent, participants underwent supine resting measures at 1045 m (baseline), 3440 m (day 3) and 4240 m (day 7). These measures included pressure of arterial (Pa)CO2, PaO2, arterial O2 saturation (SaO2; arterial blood draws), unilateral anterior, posterior and gCBF (duplex ultrasound; internal carotid artery [ICA] and vertebral artery [VA], gCBF [{ICA + VA} × 2], respectively) and rSO2 (near-infrared spectroscopy). We developed a novel stimulus index (SI), taking into account both chemostimuli (PaCO2/SaO2). Subsequently, CBF was indexed against the SI to assess steady-state cerebrovascular responsiveness (SS-CVR). When both competing chemostimuli are taken into account, (a) SS-CVR was significantly higher in ICA, VA and gCBF at 4240 m compared to lower altitudes, (b) delta SS-CVR with ascent (1045 m vs. 4240 m) was higher in ICA vs. VA, suggesting regional differences in CBF regulation, and (c) ICA SS-CVR was strongly and positively correlated (r = 0.79) with rSO2 at 4240 m.

Prediction of upper extremity peak oxygen consumption from heart rate during submaximal arm cycling in young and middle-aged adults Abstract Based on the strong linear relationship between heart rate (HR) and oxygen consumption, the Åstrand–Ryhming cycle ergometer test (Astrand and Ryhming in J Appl Physiol 7:218–221, 1954) is a widely used submaximal test to predict whole body maximal oxygen consumption (\(\dot{V}{\text{O}}_{2\!\max }\)). However, a similar test predicting peak oxygen consumption (\(\dot{V}{\text{O}}_{{2{\text{peak}}}}\)) in the upper extremities is not established, and may be very useful for individuals unable to use their lower extremities or/and if separation of upper extremity aerobic capacity is sought after. Thus, the aim of the current study was to develop a submaximal test predicting \(\dot{V}{\text{O}}_{{2{\text{peak}}}}\) in arm-cycling. Forty-nine healthy volunteers (25 women: 38 ± 13 years; 24 men: 39 ± 12 years) tested arm-cycle \(\dot{V}{\text{O}}_{{2{\text{peak}}}}\) on a protocol with 4-min, 21-W increments to exhaustion. The data were contrasted to treadmill \(\dot{V}{\text{O}}_{2\!\max }\) values. Arm-cycle \(\dot{V}{\text{O}}_{{2{\text{peak}}}}\) was 66 ± 8% of \(\dot{V}{\text{O}}_{2\!\max }\) (r = 0.92, p < 0.001; women: 1.9 ± 0.4 L min−1; men: 3.0 ± 0.7 L min−1). Arm-cycle HR and \(\% \dot{V}{\text{O}}_{2}\) exhibited correlations of r = 0.79 and r = 0.78 for women and men, respectively, while corresponding correlations between work rate and \(\dot{V}{\text{O}}_{2}\) were r = 0.95 (women) and r = 0.89 (men) (all p < 0.001). Arm-cycle \(\dot{V}{\text{O}}_{{2{\text{peak}}}}\) prediction revealed a standard error of estimate (SEE) of 11.2% (women) and 10.2% (men), and was primarily due to individual arm-cycle maximal HR (women: 173 ± 13 beats min−1; men: 174 ± 10 beats min−1; correction factor: 5–7%). In conclusion, from a single 4-min stage of submaximal arm cycling, \(\dot{V}{\text{O}}_{{2{\text{peak}}}}\) can be predicted with a SEE of 10–11%. The arm-cycle test may have important value for individuals who rely on arms in sports and occupations, and for patients with lower extremity disabilities.

Transcutaneous electrical nerve stimulation improves fatigue performance of the treated and contralateral knee extensors Abstract Purpose Transcutaneous electrical nerve stimulation (TENS) can reduce acute and chronic pain. Unilateral fatigue can produce discomfort in the affected limb and force and activation deficits in contralateral non-exercised muscles. TENS-induced local pain analgesia effects on non-local fatigue performance are unknown. Hence, the aim of the study was to determine if TENS-induced pain suppression would augment force output during a fatiguing protocol in the treated and contralateral muscles. Methods Three experiments were integrated for this article. Following pre-tests, each experiment involved 20 min of TENS, sham, or a control condition on the dominant quadriceps. Then either the TENS-treated quadriceps (TENS_Treated) or the contralateral quadriceps (TENS_Contra) was tested. In a third experiment, the TENS and sham conditions involved two\; 100-s isometric maximal voluntary contractions (MVC) (30-s recovery) followed by testing of the contralateral quadriceps (TENS_Contra-Fatigue). Testing involved single knee extensors (KE) MVCs (pre- and post-test) and a post-test 30% MVC to task failure. Results The TENS-treated study induced greater (p = 0.03; 11.0%) time to KE (treated leg) failure versus control. The TENS_Contra-Fatigue induced significant (p = 0.04; 11.7%) and near-significant (p = 0.1; 7.1%) greater time to contralateral KE failure versus sham and control, respectively. There was a 14.5% (p = 0.02) higher fatigue index with the TENS (36.2 ± 10.1%) versus sham (31.6 ± 10.6%) conditions in the second fatigue intervention set (treated leg). There was no significant post-fatigue KE fatigue interaction with the TENS_Contra. Conclusions Unilateral TENS application to the dominant KE prolonged time to failure in the treated and contralateral KE suggesting a global pain modulatory response.

Passive muscle stretching impairs rapid force production and neuromuscular function in human plantar flexors Abstract Purpose We examined the effect of muscle stretching on the ability to produce rapid torque and the mechanisms underpinning the changes. Methods Eighteen men performed three conditions: (1) continuous stretch (1 set of 5 min), (2) intermittent stretch (5 sets of 1 min with 15-s inter-stretch interval), and (3) control. Isometric plantar flexor rate of torque development was measured during explosive maximal voluntary contractions (MVC) in the intervals 0–100 ms (RTDV100) and 0–200 ms (RTDV200), and in electrically evoked 0.5-s tetanic contractions (20 Hz, 20 Hz preceded by a doublet and 80 Hz). The rate of EMG rise, electromechanical delay during MVC (EMDV) and during a single twitch contraction (EMDtwitch) were assessed. Results RTDV200 was decreased (P < 0.05) immediately after continuous (− 15%) and intermittent stretch (− 30%) with no differences between protocols. The rate of torque development during tetanic stimulations was reduced (P < 0.05) immediately after continuous (− 8%) and intermittent stretch (− 10%), when averaged across stimulation frequencies. Lateral gastrocnemius rate of EMG rise was reduced after intermittent stretch (− 27%), and changes in triceps surae rate of EMG rise were correlated with changes in RTDV200 after both continuous (r = 0.64) and intermittent stretch (r = 0.65). EMDV increased immediately (31%) and 15 min (17%) after intermittent stretch and was correlated with changes in RTDV200 (r = − 0.56). EMDtwitch increased immediately after continuous (4%), and immediately (5.4%), 15 min (6.3%), and 30 min after (6.4%) intermittent stretch (P < 0.05). Conclusions Reductions in the rate of torque development immediately after stretching were associated with both neural and mechanical mechanisms.

The time course and mechanisms of change in biomarkers of joint metabolism in response to acute exercise and chronic training in physiologic and pathological conditions Abstract Purpose The benefits of exercise across the lifespan and for a wide spectrum of health and diseases are well known. However, there remains less clarity as to the effects of both acute and chronic exercise on joint health. Serum biomarkers of joint metabolism are sensitive to change and have the potential to differentiate between normal and adverse adaptations to acute and chronic load. Therefore, the primary objective of this review is to evaluate how serum biomarkers can inform our understanding of how exercise affects joint metabolism. Methods A comprehensive literature search was completed to identify joint biomarkers previously used to investigate acute and chronic exercise training. Results Identified biomarkers included those related to joint cartilage, bone, synovium, synovial fluid, and inflammation. However, current research has largely focused on the response of serum cartilage oligomeric matrix protein (COMP) to acute loading in healthy young individuals. Studies demonstrate how acute loading transiently increases serum COMP (i.e., cartilage metabolism), which is mostly dependent on the duration of exercise. This response does not appear to be associated with any lasting deleterious changes, cartilage degradation, or osteoarthritis. Conclusion Several promising biomarkers for assessing joint metabolism exist and may in future enhance our understanding of the physiological response to acute and chronic exercise. Defining ‘normal’ and ‘abnormal’ biomarker responses to exercise and methodological standardisation would greatly improve the potential of research in this area to understand mechanisms and inform practice.