Performance and perceived fatigability across the intensity spectrum: role of muscle mass during cycling.

The role of muscle mass in modulating performance and perceived fatigability across the entire intensity spectrum during cycling remains unexplored. We hypothesized that at task failure (Tlim), muscle contractile function would decline more following single- (SL) versus double-leg (DL) cycling within severe and extreme intensities, but not moderate and heavy intensities. After DL and SL ramp-incremental tests, on separate days, 11 recreationally active males (V̇o2max: 49.5 ± 7.7 mL·kg-1·min-1) completed SL and DL cycling until Tlim within each intensity domain. Power output for SL trials was set at 60% of the corresponding DL trial. Before and immediately after Tlim, participants performed an isometric maximal voluntary contraction (MVC) coupled with one superimposed and three resting femoral nerve stimulations [100 Hz; 10 Hz; single twitch (Qtw)] to measure performance fatigability. Perceived fatigue, leg pain, dyspnea, and effort were collected during trials. Tlim within each intensity domain was not different between SL and DL (all P > 0.05). MVC declined more for SL versus DL following heavy- (-42 ± 16% vs. -30 ± 18%; P = 0.011) and severe-intensity cycling (-41 ± 12% vs. -31 ± 15%; P = 0.036). Similarly, peak Qtw force declined more for SL following heavy- (-31 ± 12% vs. -22 ± 10%; P = 0.007) and severe-intensity cycling (-49 ± 13% vs. -40 ± 7%; P = 0.048). Except for heavy intensity, voluntary activation reductions were similar between modes. Similarly, except for dyspnea, which was lower for SL versus DL across all domains, ratings of fatigue, pain, and effort were similar at Tlim between exercise modes. Thus, the amount of muscle mass modulates the extent of contractile function impairment in an intensity-dependent manner.NEW & NOTEWORTHY We investigated the modulatory role of muscle mass on performance and perceived fatigability across the entire intensity spectrum. Despite similar time-to-task failure, single-leg cycling resulted in greater impairments in muscle contractile function within the heavy- and severe-intensity domains, but not the moderate- and extreme-intensity domains. Perceived fatigue, pain, and effort were similar between cycling modes. This indicates that the modulatory role of muscle mass on the extent of performance fatigability is intensity domain-dependent.

Effects of carbohydrate availability on cycling endurance at the maximal lactate steady state.

The impacts of carbohydrate (CHO) availability on time to task failure (TTF) and physiological responses to exercise at the maximal lactate steady state (MLSS) have not been studied. Ten participants (3 females, 7 males) completed this double-blinded, placebo-controlled study that involved a ramp incremental test, MLSS determination, and four TTF trials at MLSS, all performed on a cycle ergometer. With the use of a combination of nutritional (CHO, 7 g/kg, and placebo, PLA, 0 g/kg drinks) and exercise interventions [no exercise (REST) and glycogen-reducing exercise (EX)], the four conditions were expected to differ in preexercise CHO availability (RESTCHO > RESTPLA > EXCHO > EXPLA). TTF at MLSS was not improved by CHO loading, as RESTCHO (57.1 [16.6] min) and RESTPLA (57.1 [15.6] min) were not different (P = 1.00); however, TTF was ∼50% shorter in EX conditions compared with REST conditions on average (P < 0.05), with EXCHO (39.1 [9.2] min) ∼90% longer than EXPLA (20.6 [6.9] min; P < 0.001). There were effects of condition for all perceptual and cardiometabolic variables when compared at isotime (P < 0.05) and task failure (TF; P < 0.05), except for ventilation, perceptual responses, and neuromuscular function measures, which were not different at TF (P > 0.05). Blood lactate concentration was stable in all conditions for participants who completed 30 min of exercise. These findings indicate that TTF at MLSS is not enhanced by preexercise CHO supplementation, but recent intense exercise decreases TTF at MLSS even with CHO supplementation. Extreme fluctuations in diet and strenuous exercise that reduce CHO availability should be avoided before MLSS determination.NEW & NOTEWORTHY Carbohydrate (CHO) loading did not increase participants' ability to cycle at their maximal lactate steady state (MLSS); however, performing a glycogen depletion task the evening before cycling at MLSS reduced the time to task failure, even when paired with a high dose of CHO. These diet and exercise interventions influenced blood lactate concentration ([BLa]) but not the stability of [BLa]. Activities that reduce CHO availability should be avoided before MLSS determination.

Effects of acute simulated altitude on the maximal lactate steady state in humans.

We sought to determine the effects of acute simulated altitude on the maximal lactate steady state (MLSS) and physiological responses to cycling at and 10 W above the MLSS-associated power output (PO) (MLSSp and MLSSp+10, respectively). Eleven (4 female) participants (mean [SD]; 28 [4] years; V̇O2max: 54.3 [6.9] mL×kg-1×min-1) acclimatized to ~1100 m performed 30-min constant PO trials in simulated altitudes of 0 m (SL), 1111 m (MILD), and 2222 m (MOD). MLSSp, defined as the highest PO with stable (<1mM change) blood lactate concentration ([BLa]) between 10 and 30 min, was significantly lower in MOD (209 [54] W) compared to SL (230 [56] W; p<0.001) and MILD (225 [58] W; p=0.001), but MILD and SL were not different (p=0.12). V̇O2 and V̇CO2 decreased at higher simulated altitudes due to lower POs (p<0.05), but other end-exercise physiological responses (e.g., [BLa], ventilation (V̇E), heart rate (HR)) were not different between conditions at MLSSp or MLSSp+10 (p>0.05). At the same absolute intensity (MLSSp for MILD), [BLa], HR, and V̇E and all perceptual variables were exacerbated in MOD compared to SL and MILD (p<0.05). Maximum voluntary contraction, voluntary activation, and potentiated twitch forces were exacerbated at MLSSp+10 relative to MLSSp within conditions (p<0.05); however, condition did not affect performance fatiguability at the same relative or absolute intensity (p>0.05). As MLSSp decreased in hypoxia, adjustments in PO are needed to ensure the same relative intensity across altitudes, but common indices of exercise intensity may facilitate exercise prescription and monitoring in hypoxia.

Identifying physiological determinants of 800 m running performance using post-exercise blood lactate kinetics.

PURPOSE: The aims of the present study were to investigate blood lactate kinetics following high intensity exercise and identify the physiological determinants of 800 m running performance. METHODS: Fourteen competitive 800 m runners performed two running tests. First, participants performed a multistage graded exercise test to determine physiological indicators related to endurance performance. Second, participants performed four to six 30-s high intensity running bouts to determine post-exercise blood lactate kinetics. Using a biexponential time function, lactate exchange ability (γ1), lactate removal ability (γ2), and the quantity of lactate accumulated (QLaA) were calculated from individual blood lactate recovery data. RESULTS: 800 m running performance was significantly correlated with peak oxygen consumption (r = -0.794), γ1 and γ2 at 800 m race pace (r = -0.604 and -0.845, respectively), and QLaA at maximal running speed (r = -0.657). V ˙ O2peak and γ2 at 800 m race pace explained 83% of the variance in 800 m running performance. CONCLUSION: Our results indicate that (1) a high capacity to exchange and remove lactate, (2) a high capacity for short-term lactate accumulation and, (3) peak oxygen consumption, are critical elements of 800 m running performance. Accordingly, while lactate has primarily been utilized as a performance indicator for long-distance running, post-exercise lactate kinetics may also prove valuable as a performance determinant in middle-distance running.

The influence of skeletal muscle mitochondria and sex on critical torque and performance fatiguability in humans.

Critical torque (CT) represents the highest oxidative steady state for intermittent knee extensor exercise, but the extent to which it is influenced by skeletal muscle mitochondria and sex is unclear. Vastus lateralis muscle biopsy samples were collected from 12 females and 12 males -matched for relative maximal oxygen uptake normalized to fat-free mass (FFM) (F: 57.3 (7.5) ml (kg FFM)-1  min-1 ; M: 56.8 (7.6) ml (kg FFM)-1  min-1 ; P = 0.856) - prior to CT determination and performance fatiguability trials. Males had a lower proportion of myosin heavy chain (MHC) I isoform (40.6 (18.4)%) compared to females (59.5 (18.9)%; P = 0.021), but MHC IIa and IIx isoform distributions and protein markers of mitochondrial content were not different between sexes (P > 0.05). When normalized to maximum voluntary contraction (MVC), the relative CT (F: 42.9 (8.3)%; M: 37.9 (9.0)%; P = 0.172) and curvature constant, W' (F: 26.6 (11.0) N m s (N m)-1 ; M: 26.4 (6.5) N m s (N m)-1 ; P = 0.962) were not significantly different between sexes. All protein biomarkers of skeletal muscle mitochondrial content, as well as the proportion of MHC I isoform, positively correlated with relative CT (0.48 < r < 0.70; P < 0.05), and the proportion of MHC IIx isoform correlated positively with relative W' (r = 0.57; P = 0.007). Indices of performance fatiguability were not different between males and females for MVC- and CT-controlled trials (P > 0.05). Greater mitochondrial protein abundance was associated with attenuated declines in potentiated twitch torque for exercise at 60% MVC (P < 0.05); however, the influence of mitochondrial protein abundance on performance fatiguability was reduced when exercise was prescribed relative to CT. Whether these findings translate to whole-body exercise requires additional research. KEY POINTS: The quadriceps critical torque represents the highest intensity of intermittent knee extensor exercise for which an oxidative steady state is attainable, but its relationship with skeletal muscle mitochondrial protein abundance is unknown. Matching males and females for maximal oxygen uptake relative to fat-free mass facilitates investigations of sex differences in exercise physiology, but studies that have compared critical torque and performance fatiguability during intermittent knee extensor exercise have not ensured equal aerobic fitness between sexes. Skeletal muscle mitochondrial protein abundance was correlated with critical torque and fatigue resistance for exercise prescribed relative to maximum voluntary contraction but not for exercise performed relative to the critical torque. Differences between sexes in critical torque, skeletal muscle mitochondrial protein abundance and performance fatiguability were not statistically significant. Our results suggest that skeletal muscle mitochondrial protein abundance may contribute to fatigue resistance by influencing the critical intensity of exercise.

Human skeletal muscle mitochondrial responses to single-leg intermittent or continuous cycle exercise training matched for absolute intensity and total work.

There is renewed interest in the potential for interval (INT) training to increase skeletal muscle mitochondrial content including whether the response differs from continuous (CONT) training. Comparisons of INT and CONT exercise are impacted by the manner in which protocols are "matched", particularly with respect to exercise intensity, as well as inter-individual differences in training responses. We employed single-leg cycling to facilitate a within-participant design and test the hypothesis that short-term INT training would elicit a greater increase in mitochondrial content than work- and intensity-matched CONT training. Ten young healthy adults (five males and five females) completed 12 training sessions over 4 weeks with each leg. Legs were randomly assigned to complete either 30 min of CONT exercise at a challenging sustainable workload (~50% single-leg peak power output; Wpeak) or INT exercise that involved 10 × 3-min bouts at the same absolute workload. INT bouts were interspersed with 1 min of recovery at 10% Wpeak and each CONT session ended with 10 min at 10% Wpeak. Absolute and mean intensity, total training time, and volume were thus matched between legs but the pattern of exercise differed. Contrary to our hypothesis, biomarkers of mitochondrial content including citrate synthase maximal activity, mitochondrial protein content and subsarcolemmal mitochondrial volume increased after CONT (p < 0.05) but not INT training. Both training modes increased single-leg Wpeak (p < 0.01) and time to exhaustion at 70% of single-leg Wpeak (p < 0.01). In a work- and intensity-matched comparison, short-term CONT training increased skeletal muscle mitochondrial content whereas INT training did not.

Is Running Power a Useful Metric? Quantifying Training Intensity and Aerobic Fitness Using Stryd Running Power Near the Maximal Lactate Steady State.

We sought to determine the utility of Stryd, a commercially available inertial measurement unit, to quantify running intensity and aerobic fitness. Fifteen (eight male, seven female) runners (age = 30.2 [4.3] years; V·O2max = 54.5 [6.5] ml·kg-1·min-1) performed moderate- and heavy-intensity step transitions, an incremental exercise test, and constant-speed running trials to establish the maximal lactate steady state (MLSS). Stryd running power stability, sensitivity, and reliability were evaluated near the MLSS. Stryd running power was also compared to running speed, V·O2, and metabolic power measures to estimate running mechanical efficiency (EFF) and to determine the efficacy of using Stryd to delineate exercise intensities, quantify aerobic fitness, and estimate running economy (RE). Stryd running power was strongly associated with V·O2 (R2 = 0.84; p < 0.001) and running speed at the MLSS (R2 = 0.91; p < 0.001). Stryd running power measures were strongly correlated with RE at the MLSS when combined with metabolic data (R2 = 0.79; p < 0.001) but not in isolation from the metabolic data (R2 = 0.08; p = 0.313). Measures of running EFF near the MLSS were not different across intensities (~21%; p > 0.05). In conclusion, although Stryd could not quantify RE in isolation, it provided a stable, sensitive, and reliable metric that can estimate aerobic fitness, delineate exercise intensities, and approximate the metabolic requirements of running near the MLSS.

Physiological basis of brief, intense interval training to enhance maximal oxygen uptake: a mini-review.

Brief, intense interval training describes a style of exercise characterized by short bouts of strenuous effort interspersed with recovery periods. The method increases whole body maximal oxygen uptake (V̇o2max), but the underlying physiological basis is unclear. V̇o2max represents the functional limit of the integrative oxygen cascade, which refers to the physiological steps involved in oxygen transport and utilization from atmospheric air to mitochondrial metabolism. There is insufficient evidence to definitively state which steps in the oxygen cascade are responsible for the improvement in V̇o2max after brief, intense interval training. Studies typically focus on specific physiological variables that are often characterized as "central" or "peripheral" based in part on their location in the body. Recent work suggests that training for ≥6 wk improves V̇o2max in part by increasing maximal cardiac output and expanding blood volume, responses that are expected to augment central oxygen delivery. Other responses to brief, intense interval training, including increased capillary and mitochondrial density, may contribute to increases in V̇o2max via enhanced skeletal muscle oxygen extraction and/or increased muscle diffusing capacity. This is especially evident after relatively short-term training and despite no change in central oxygen delivery factors. Mechanistic investigations, particularly employing contemporary technologies, are needed to advance our understanding of the early time course of the V̇o2max response to brief, intense interval training and the extent to which changes in specific oxygen cascade processes compare with traditional endurance training.

Time course and fibre type-dependent nature of calcium-handling protein responses to sprint interval exercise in human skeletal muscle.

Sprint interval training (SIT) causes fragmentation of the skeletal muscle sarcoplasmic reticulum Ca2+ release channel, ryanodine receptor 1 (RyR1), 24 h post-exercise, potentially signalling mitochondrial biogenesis by increasing cytosolic [Ca2+ ]. Yet, the time course and skeletal muscle fibre type-specific patterns of RyR1 fragmentation following a session of SIT remain unknown. Ten participants (n = 4 females; n = 6 males) performed a session of SIT (6 × 30 s 'all-out' with 4.5 min rest after each sprint) with vastus lateralis muscle biopsy samples collected before and 3, 6 and 24 h after exercise. In whole muscle, full-length RyR1 protein content was significantly reduced 6 h (mean (SD); -38 (38)%; P < 0.05) and 24 h post-SIT (-30 (48)%; P < 0.05) compared to pre-exercise. Examining each participant's largest response in pooled samples, full-length RyR1 protein content was reduced in type II (-26 (30)%; P < 0.05) but not type I fibres (-11 (40)%; P > 0.05). Three hours post-SIT, there was also a decrease in sarco(endo)plasmic reticulum Ca2+ ATPase 1 in type II fibres (-23 (17)%; P < 0.05) and sarco(endo)plasmic reticulum Ca2+ ATPase 2a in type I fibres (-19 (21)%; P < 0.05), despite no time effect for either protein in whole muscle samples (P > 0.05). PGC1A mRNA content was elevated 3 and 6 h post-SIT (5.3- and 3.7-fold change from pre, respectively; P < 0.05 for both), but peak PGC1A mRNA expression was not significantly correlated with peak RyR1 fragmentation (r2  = 0.10; P > 0.05). In summary, altered Ca2+ -handling protein expression, which occurs primarily in type II muscle fibres, may influence signals for mitochondrial biogenesis as early as 3-6 h post-SIT in humans. KEY POINTS: Sprint interval training (SIT) has been shown to cause fragmentation of the sarcoplasmic reticulum calcium-release channel, ryanodine receptor 1 (RyR1), 24 h post-exercise, which may act as a signal for mitochondrial biogenesis. In this study, the time course was examined of RyR1 fragmentation in human whole muscle and pooled type I and type II skeletal muscle fibres following a single session of SIT. Full-length RyR1 protein content was significantly lower than pre-exercise by 6 h post-SIT in whole muscle, and fragmentation was detectable in type II but not type I fibres, though to a lesser extent than in whole muscle. The peak in PGC1A mRNA expression occurred earlier than RyR1 fragmentation. The increased temporal resolution and fibre type-specific responses for RyR1 fragmentation provide insights into its importance to mitochondrial biogenesis in humans.

Impairment in maximal lactate steady state after carbon monoxide inhalation is related to training status.

NEW FINDINGS: What is the central question of this study? What is the effect of an elevated carboxyhaemoglobin (COHb) concentration following carbon monoxide inhalation on the maximal lactate steady state (MLSS) in humans and is this effect dependent on aerobic fitness? What is the main finding and its importance? An elevated COHb concentration intensified physiological responses to exercise at the MLSS - including heart rate, ventilation and peripheral fatigue - in general and reduced the MLSS (i.e., destabilized the blood lactate concentration) in trained but not untrained males and females. ABSTRACT: This study investigated whether a lower effective [Hb], induced by carbon monoxide (CO) inhalation, reduces the peak oxygen uptake ( V ̇ O 2 peak ${\dot{V}}_{{{\rm{O}}}_{\rm{2}}{\rm{peak}}}$ ) and the maximal lactate steady state (MLSS) and whether training status explains individual variation in these impairments. Healthy young participants completed two ramp incremental tests (n = 20, 10 female) and two trials at MLSS (n = 16, eight female) following CO rebreathe tests and sham procedures (SHAM) in random orders. All fitness variables were normalized to fat-free mass (FFM) to account for sex-related differences in body composition, and males and females were matched for aerobic fitness. The V ̇ O 2 peak ${\dot{V}}_{{{\rm{O}}}_{\rm{2}}{\rm{peak}}}$ (mean (SD): -4.2 (3.7)%), peak power output (PPO) (-3.3 (2.2)%) and respiratory compensation point (RCP) (-6.3 (4.5)%) were reduced in CO compared with SHAM (P < 0.001 for all), but the gas exchange threshold (-3.3 (7.1)%) was not (P = 0.077). Decreases in V ̇ O 2 peak ${\dot{V}}_{{{\rm{O}}}_{\rm{2}}{\rm{peak}}}$ (r = -0.45; P = 0.047) and PPO (r = -0.49; P = 0.029) in CO were correlated with baseline aerobic fitness. Compared to SHAM, physiological and perceptual indicators of exercise-related stress were exacerbated by CO while cycling at MLSS. Notably, the mean blood lactate concentration ([La]) increased (i.e., Δ[La] >1.0 mM) between 10 min (5.5 (1.4) mM) and 30 min (6.8 (1.3) mM; P = 0.026) in CO, with 9/16 participants classified as unstable. These unstable participants had a higher V ̇ O 2 peak ${\dot{V}}_{{{\rm{O}}}_{\rm{2}}{\rm{peak}}}$ (66.2 (8.5) vs. 56.4 (8.8) ml kg FFM-1  min-1 , P = 0.042) and V ̇ O 2 ${\dot{V}}_{{{\rm{O}}}_{\rm{2}}}$ at MLSS (55.8 (7.0) vs. 44.3 (7.0) ml kg FFM-1  min-1 , P = 0.006) compared to the stable group. In conclusion, a reduced O2 -carrying capacity decreased maximal and submaximal exercise performance, with higher aerobic fitness associated with greater impairments in both.

Between-Day Reliability of Commonly Used IMU Features during a Fatiguing Run and the Effect of Speed.

The purpose of this study was to determine if fatigue-related changes in biomechanics derived from an inertial measurement unit (IMU) placed at the center of mass (CoM) are reliable day-to-day. Sixteen runners performed two runs at maximal lactate steady state (MLSS) on a treadmill, one run 5% above MLSS speed, and one run 5% below MLSS speed while wearing a CoM-mounted IMU. Trials were performed to volitional exhaustion or a specified termination time. IMU features were derived from each axis and the resultant. Feature means were calculated for each subject during non-fatigued and fatigued states. Comparisons were performed between the two trials at MLSS and between all four trials. The only significant fatigue state × trial interaction was the 25th percentile of the results when comparing all trials. There were no main effects for trial for either comparison method. There were main effects for fatigue state for most features in both comparison methods. Reliability, measured by an intraclass coefficient (ICC), was good-to-excellent for most features. These results suggest that fatigue-related changes in biomechanics derived from a CoM-mounted IMU are reliable day-to-day when participants ran at or around MLSS and are not significantly affected by slight deviations in speed.

Exercising muscle mass influences neuromuscular, cardiorespiratory, and perceptual responses during and following ramp-incremental cycling to task failure.

Neuromuscular (NM), cardiorespiratory, and perceptual responses to maximal-graded exercise using different amounts of active muscle mass remain unclear. We hypothesized that during dynamic exercise, peripheral NM fatigue (declined twitch force) and muscle pain would be greater using smaller muscle mass, whereas central fatigue (declined voluntary activation) and ventilatory variables would be greater using larger muscle mass. Twelve males (29.8 ± 4.7 years) performed two ramp-incremental cycling tests until task failure: 1) single-leg (SL) with 10 W·min-1 ramp and 2) double-leg (DL) with 20 W·min-1 ramp. NM fatigue was assessed at baseline, task failure (post), and after 1, 4, and 8 min of recovery. Cardiorespiratory and perceptual variables [i.e., ratings of perceived exertion (RPE), pain, and dyspnea] were measured throughout cycling. Exercise duration was similar between sessions (SL: 857.7 ± 263.6 s; DL: 855.0 ± 218.8 s; P = 0.923), and higher absolute peak power output was attained in DL (SL: 163.2 ± 43.8 W; DL: 307.0 ± 72.0 W; P < 0.001). Although central fatigue did not differ between conditions (SL: -6.6 ± 6.5%; DL: -3.5 ± 4.8%; P = 0.091), maximal voluntary contraction (SL: -41.6 ± 10.9%; DL: -33.7 ± 8.5%; P = 0.032) and single twitch forces (SL: -59.4 ± 18.8%; DL: -46.2 ± 16.2%; P = 0.003) declined more following SL. DL elicited higher peak oxygen uptake (SL: 42.1 ± 10.0 mL·kg-1·min-1; DL: 50.3 ± 9.3 mL·kg-1·min-1; P < 0.001), ventilation (SL: 137.1 ± 38.1 L·min-1; DL: 171.5 ± 33.2 L·min-1; P < 0.001), and heart rate (SL: 167 ± 21 bpm; DL: 187 ± 8 bpm; P = 0.005). Dyspnea (P = 0.025) was higher in DL; however, RPE (P = 0.005) and pain (P < 0.001) were higher in SL. These results suggest that interplay between NM, cardiorespiratory, and perceptual determinants of exercise performance during ramp-incremental cycling to task failure is muscle mass dependent.

Twelve weeks of sprint interval training increases peak cardiac output in previously untrained individuals.

INTRODUCTION: Sprint interval training (SIT), characterized by brief bouts of 'supramaximal' exercise interspersed with recovery periods, increases peak oxygen uptake ([Formula: see text]) despite a low total exercise volume. Per the Fick principle, increased [Formula: see text] is attributable to increased peak cardiac output ([Formula: see text]) and/or peak arterio-venous oxygen difference (a-vO2diff). There are limited and equivocal data regarding the physiological basis for SIT-induced increases in [Formula: see text], with most studies lasting ≤ 6 weeks. PURPOSE: To determine the effect of 12 weeks of SIT on [Formula: see text], measured using inert gas rebreathing, and the relationship between changes in [Formula: see text] and [Formula: see text]. METHODS: 15 healthy untrained adults [6 males, 9 females; 21 ± 2 y (mean ± SD)] performed 28 ± 3 training sessions. Each session involved a 2-min warm-up at 50 W, 3 × 20-s 'all-out' cycling bouts (581 ± 221 W) interspersed with 2-min of recovery, and a 3-min cool-down at 50 W. RESULTS: Measurements performed before and after training showed that 12 weeks of SIT increased [Formula: see text] (17.0 ± 3.7 vs 18.1 ± 4.6 L/min, p = 0.01, partial η2 = 0.28) and [Formula: see text] (2.63 ± 0.78 vs 3.18 ± 1.1 L/min, p < 0.01, partial η2 = 0.58). The changes in these two variables were correlated (r2 = 0.46, p < 0.01). Calculated peak a-vO2diff also increased after training (154 ± 22 vs 174 ± 23 ml O2/L; p < 0.01) and was correlated with the change in [Formula: see text] (r2 = 0.33, p = 0.03). Exploratory analyses revealed an interaction (p < 0.01) such that [Formula: see text] increased in male (+ 10%, p < 0.01) but not female participants (+ 0.6%, p = 0.96), suggesting potential sex-specific differences. CONCLUSION: Twelve weeks of SIT increased [Formula: see text] by 6% in previously untrained participants and the change was correlated with the larger 21% increase in [Formula: see text].

Effects of the menstrual and oral contraceptive cycle phases on microvascular reperfusion.

NEW FINDINGS: What is the central question of this study? What are the effects of the menstrual (early follicular and mid-luteal) or monophasic oral contraceptive (inactive- and active-pill) cycle phases on vascular reperfusion of lower limb microvasculature in healthy, active women using the near-infrared spectroscopy (NIRS) vascular occlusion test (VOT) technique? What is the main finding and its importance? We demonstrated that vascular responsiveness in the lower limb microvasculature remained unchanged between the early follicular and mid-luteal phases of the menstrual cycle and inactive- and active-pill phases of the oral contraceptive cycle. These data support that controlling for the cycle phases, within the specific times evaluated in this study, might not be necessary when assessing NIRS-VOT reperfusion rates. ABSTRACT: The objective was to examine whether the menstrual or monophasic oral contraceptive cycle phases affect microvascular responsiveness of the lower limb in healthy, active women. During the follicular or inactive-pill phase and the luteal or active-pill phase of the menstrual or oral contraceptive cycle, respectively, 15 non-oral contraceptive users (mean ± SD; 27 ± 6 years of age) and 15 monophasic oral contraceptive users (24 ± 4 years of age) underwent a lower-limb vascular occlusion test (5 min baseline, 5 min occlusion and 8 min post cuff release). Menstrual cycle phases were verified using an ovulation test. Vascular responsiveness was assessed by calculating the near-infrared spectroscopy-derived muscle oxygen saturation (StO2 ) reperfusion slope (slope 2 StO2 ) and the post occlusion StO2 area under the curve (StO2AUC ) of the tibialis anterior muscle. There were no differences in the reperfusion slope (as a percentage per second; follicular, 1.18 ± 0.48; luteal, 1.05 ± 0.48, inactive-pill, 0.95 ± 0.23; and active-pill, 0.87 ± 0.36; P = 0.09) and area under the curve (as a product of the percentage and seconds; follicular, 1067 ± 562; luteal, 918 ± 414, inactive-pill, 945 ± 702; and active-pill, 750 ± 519; P = 0.09) between the phases of the menstrual or oral contraceptive cycle, regardless of pill generation. The duration of oral contraceptive use was not associated with changes in slope 2 StO2 (r = 0.02, P = 0.94) or StO2AUC (r = -0.34, P = 0.22) between cycle phases. In conclusion, vascular responsiveness remained unchanged between the early follicular and mid-luteal phases of the menstrual cycle and the inactive-pill and active-pill phases of the oral contraceptive cycle.

Menstrual and oral contraceptive cycle phases do not affect submaximal and maximal exercise responses.

To examine whether the menstrual or monophasic oral contraceptive cycle phases affect submaximal (oxygen uptake ( V ˙ O2 ) kinetics, maximal lactate steady-state (MLSS)) and maximal ( V ˙ O2max , time-to-exhaustion (TTE)) responses to exercise in healthy, active women. During the mid-follicular or inactive-pill phase and the mid-luteal or active-pill phase of the respective menstrual or oral contraceptive cycle, 15 non-oral contraceptive users (mean and standard deviation (SD) (±): 27 ± 6 years; 171 ± 5 cm; 65 ± 7 kg) and 15 monophasic oral contraceptive users (24 ± 4 years; 169 ± 10 cm; 68 ± 10 kg) performed: one V ˙ O2 kinetics test; one ramp-incremental test; two to three 30-minute constant-load cycling trials to determine the power output corresponding to MLSS (MLSSp ), followed by a TTE trial. The phase of the menstrual or oral contraceptive cycle did not affect the time constant of the V ˙ O2 kinetics response (τ V ˙ O2 ) (mid-follicular, 20 ± 5 seconds and mid-luteal, 18 ± 3 seconds; inactive-pill, 22 ± 8 seconds and active-pill, 23 ± 6 seconds), V ˙ O2max (mid-follicular, 3.06 ± 0.32 L min-1 and mid-luteal, 3.00 ± 0.33 L min-1 ; inactive-pill, 2.87 ± 0.39 L min-1 and active-pill, 2.87 ± 0.45 L min-1 ), MLSSp (mid-follicular, 181 ± 30 W and mid-luteal, 182 ± 29 W; inactive-pill, 155 ± 26 W and active-pill, 155 ± 27 W), and TTE (mid-follicular, 147 ± 42 seconds and mid-luteal, 128 ± 54 seconds; inactive-pill, 146 ± 70 seconds and active-pill, 139 ± 77 seconds) (P > .05). The rate of perceived exertion (RPE) at minute 30 of the MLSSp trials was greater in the mid-follicular phase (6.2 ± 1.5) compared with the mid-luteal phase (5.3 ± 1.4) for non-oral contraceptive users (P = .022). The hormonal fluctuations between the menstrual and oral contraceptive cycle phases had no detectable effects on submaximal and maximal exercise performance, even when RPE differed.

Presleep α-Lactalbumin Consumption Does Not Improve Sleep Quality or Time-Trial Performance in Cyclists.

We tested the hypothesis that presleep consumption of α-lactalbumin (LA), a fraction of whey with a high abundance of tryptophan, would improve indices of sleep quality and time-trial (TT) performance in cyclists relative to an isonitrogenous collagen peptide (CP) supplement lacking tryptophan. Using randomized, double-blind, crossover designs, cyclists consumed either 40 g of LA or CP 2 hr prior to sleep. In Study 1, six elite male endurance track cyclists (age 23 ± 6 years, V˙O2peak 70.2 ± 4.4 ml·kg-1·min-1) consumed a supplement for three consecutive evenings before each 4-km TT on a velodrome track, whereas in Study 2, six well-trained cyclists (one female; age 24 ± 5 years, V˙O2peak 66.9 ± 8.3 ml·kg-1·min-1) consumed a supplement the evening before each 4-km TT on a stationary cycle ergometer. Indices of sleep quality were assessed with wrist-based actigraphy. There were no differences between the CP and LA supplements in terms of total time in bed, total sleep time, or sleep efficiency in Study 1 (LA: 568 ± 71 min, 503 ± 67 min, 88.3% ± 3.4%; CP: 546 ± 30 min, 479 ± 35 min, 87.8% ± 3.1%; p = .41, p = .32, p = .74, respectively) or Study 2 (LA: 519 ± 90 min, 450 ± 78 min, 87.2% ± 7.6%; CP: 536 ± 62 min, 467 ± 57 min, 87.3% ± 6.4%; p = .43, p = .44, p = .97, respectively). Similarly, time to complete the 4-km TT was unaffected by supplementation in Study 1 (LA: 274.9 ± 7.6 s; CP: 275.5 ± 7.2 s; p = .62) and Study 2 (LA: 344.3 ± 22.3 s; CP: 343.3 ± 23.0 s; p = .50). Thus, relative to CP, consuming LA 2 hr prior to sleep over 1-3 days did not improve actigraphy-based indices of sleep quality or 4-km TT performance in cyclists.

Cardiopulmonary Demand of 16-kg Kettlebell Snatches in Simulated Girevoy Sport.

Chan, M, MacInnis, MJ, Koch, S, MacLeod, KE, Lohse, KR, Gallo, ME, Sheel, AW, and Koehle, MS. Cardiopulmonary demand of 16-kg kettlebell snatches in simulated Girevoy Sport. J Strength Cond Res 34(6): 1625-1633, 2020-Kettlebell lifting has become popular both as a strength and conditioning training tool and as a sport in and of itself: Girevoy Sport (GS). Although several kettlebell multimovement protocols have been analyzed, little research has attempted to quantify the aerobic stimulus of the individual events in GS, which could better inform kettlebell-related exercise prescription. The purpose of this study was to quantify the cardiopulmonary demand, assessed primarily by oxygen consumption (V[Combining Dot Above]O2) and heart rate (HR), of continuous high-intensity kettlebell snatches-under conditions relevant to GS-and to compare this demand with a more traditional graded rowing ergometer maximal exercise test. Ten male participants (age = 28.4 ± 4.6 years, height = 185 ± 7 cm, body mass = 95.1 ± 14.9 kg) completed (a) a graded-exercise test on a rowing ergometer to determine maximal oxygen consumption (V[Combining Dot Above]O2max) and maximal heart rate (HRmax) and (b) a graded-exercise test consisting of continuous 16-kg kettlebell snatches to determine peak oxygen consumption (V[Combining Dot Above]O2peak) and peak heart rate (HRpeak) during a simulated GS snatch event. Subjects achieved a V[Combining Dot Above]O2max of 45.7 ± 6.7 ml·kg·min and HRmax of 177 ± 8.3 b·min on the rowing ergometer. The kettlebell snatch test produced a V[Combining Dot Above]O2peak of 37.6 ± 4.4 ml·kg·min (82.7 ± 6.5% V[Combining Dot Above]O2max) and a HRpeak of 174 ± 10 b·min (98.0 ± 3.4% HRmax). These findings suggest that GS kettlebell snatches with 16-kg can provide an adequate aerobic stimulus to improve cardiorespiratory fitness in those with a V[Combining Dot Above]O2max of ≤51 ml·kg·min, according to aerobic training recommendations from the American College of Sports Medicine.

Interlimb differences in parameters of aerobic function and local profiles of deoxygenation during double-leg and counterweighted single-leg cycling.

It is typically assumed that in the context of double-leg cycling, dominant (DOMLEG) and nondominant legs (NDOMLEG) have similar aerobic capacity and both contribute equally to the whole body physiological responses. However, there is a paucity of studies that have systematically investigated maximal and submaximal aerobic performance and characterized the profiles of local muscle deoxygenation in relation to leg dominance. Using counterweighted single-leg cycling, this study explored whether peak O2 consumption (V̇o2peak), maximal lactate steady-state (MLSSp), and profiles of local deoxygenation [HHb] would be different in the DOMLEG compared with the NDOMLEG. Twelve participants performed a series of double-leg and counterweighted single-leg DOMLEG and NDOMLEG ramp-exercise tests and 30-min constant-load trials. V̇o2peak was greater in the DOMLEG than in the NDOMLEG (2.87 ± 0.42 vs. 2.70 ± 0.39 L/min, P < 0.05). The difference in V̇o2peak persisted even after accounting for lean mass (P < 0.05). Similarly, MLSSp was greater in the DOMLEG than in the NDOMLEG (118 ± 31 vs. 109 ± 31 W; P < 0.05). Furthermore, the amplitude of the [HHb] signal during ramp exercise was larger in the DOMLEG than in the NDOMLEG during both double-leg (26.0 ± 8.4 vs. 20.2 ± 8.8 µM, P < 0.05) and counterweighted single-leg cycling (18.5 ± 7.9 vs. 14.9 ± 7.5 µM, P < 0.05). Additionally, the amplitudes of the [HHb] signal were highly to moderately correlated with the mode-specific V̇o2peak values (ranging from 0.91 to 0.54). These findings showed in a group of young men that maximal and submaximal aerobic capacities were greater in the DOMLEG than in the NDOMLEG and that superior peripheral adaptations of the DOMLEG may underpin these differences.NEW & NOTEWORTHY It is typically assumed that the dominant and nondominant legs contribute equally to the whole physiological responses. In this study, we found that the dominant leg achieved greater peak O2 uptake values, sustained greater power output while preserving whole body metabolic stability, and showed larger amplitudes of deoxygenation responses. These findings highlight heterogeneous aerobic capacities of the lower limbs, which have important implications when whole body physiological responses are examined.

Physiological adaptations to interval training and the role of exercise intensity.

Interval exercise typically involves repeated bouts of relatively intense exercise interspersed by short periods of recovery. A common classification scheme subdivides this method into high-intensity interval training (HIIT; 'near maximal' efforts) and sprint interval training (SIT; 'supramaximal' efforts). Both forms of interval training induce the classic physiological adaptations characteristic of moderate-intensity continuous training (MICT) such as increased aerobic capacity (V̇O2 max ) and mitochondrial content. This brief review considers the role of exercise intensity in mediating physiological adaptations to training, with a focus on the capacity for aerobic energy metabolism. With respect to skeletal muscle adaptations, cellular stress and the resultant metabolic signals for mitochondrial biogenesis depend largely on exercise intensity, with limited work suggesting that increases in mitochondrial content are superior after HIIT compared to MICT, at least when matched-work comparisons are made within the same individual. It is well established that SIT increases mitochondrial content to a similar extent to MICT despite a reduced exercise volume. At the whole-body level, V̇O2 max is generally increased more by HIIT than MICT for a given training volume, whereas SIT and MICT similarly improve V̇O2 max despite differences in training volume. There is less evidence available regarding the role of exercise intensity in mediating changes in skeletal muscle capillary density, maximum stroke volume and cardiac output, and blood volume. Furthermore, the interactions between intensity and duration and frequency have not been thoroughly explored. While interval training is clearly a potent stimulus for physiological remodelling in humans, the integrative response to this type of exercise warrants further attention, especially in comparison to traditional endurance training.

Superior mitochondrial adaptations in human skeletal muscle after interval compared to continuous single-leg cycling matched for total work.

KEY POINTS: A classic unresolved issue in human integrative physiology involves the role of exercise intensity, duration and volume in regulating skeletal muscle adaptations to training. We employed counterweighted single-leg cycling as a unique within-subject model to investigate the role of exercise intensity in promoting training-induced increases in skeletal muscle mitochondrial content. Six sessions of high-intensity interval training performed over 2 weeks elicited greater increases in citrate synthase maximal activity and mitochondrial respiration compared to moderate-intensity continuous training matched for total work and session duration. These data suggest that exercise intensity, and/or the pattern of contraction, is an important determinant of exercise-induced skeletal muscle remodelling in humans. ABSTRACT: We employed counterweighted single-leg cycling as a unique model to investigate the role of exercise intensity in human skeletal muscle remodelling. Ten young active men performed unilateral graded-exercise tests to measure single-leg V̇O2, peak and peak power (Wpeak ). Each leg was randomly assigned to complete six sessions of high-intensity interval training (HIIT) [4 × (5 min at 65% Wpeak and 2.5 min at 20% Wpeak )] or moderate-intensity continuous training (MICT) (30 min at 50% Wpeak ), which were performed 10 min apart on each day, in an alternating order. The work performed per session was matched for MICT (143 ± 8.4 kJ) and HIIT (144 ± 8.5 kJ, P > 0.05). Post-training, citrate synthase (CS) maximal activity (10.2 ± 0.8 vs. 8.4 ± 0.9 mmol kg protein-1  min-1 ) and mass-specific [pmol O2 •(s•mg wet weight)-1 ] oxidative phosphorylation capacities (complex I: 23.4 ± 3.2 vs. 17.1 ± 2.8; complexes I and II: 58.2 ± 7.5 vs. 42.2 ± 5.3) were greater in HIIT relative to MICT (interaction effects, P < 0.05); however, mitochondrial function [i.e. pmol O2 •(s•CS maximal activity)-1 ] measured under various conditions was unaffected by training (P > 0.05). In whole muscle, the protein content of COXIV (24%), NDUFA9 (11%) and mitofusin 2 (MFN2) (16%) increased similarly across groups (training effects, P < 0.05). Cytochrome c oxidase subunit IV (COXIV) and NADH:ubiquinone oxidoreductase subunit A9 (NDUFA9) were more abundant in type I than type II fibres (P < 0.05) but training did not increase the content of COXIV, NDUFA9 or MFN2 in either fibre type (P > 0.05). Single-leg V̇O2, peak was also unaffected by training (P > 0.05). In summary, single-leg cycling performed in an interval compared to a continuous manner elicited superior mitochondrial adaptations in human skeletal muscle despite equal total work.