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.

Acute Ketone Monoester Supplementation Impairs 20-min Time-Trial Performance in Trained Cyclists: A Randomized, Crossover Trial.

Acute ketone monoester (KE) supplementation can alter exercise responses, but the performance effect is unclear. The limited and equivocal data to date are likely related to factors including the KE dose, test conditions, and caliber of athletes studied. We tested the hypothesis that mean power output during a 20-min cycling time trial (TT) would be different after KE ingestion compared to a placebo (PL). A sample size of 22 was estimated to provide 80% power to detect an effect size dz of 0.63 at an alpha level of .05 with a two-tailed paired t test. This determination considered 2.0% as the minimal important difference in performance. Twenty-three trained cyclists (N = 23; peak oxygen uptake: 65 ± 12 ml·kg-1 min-1; M ± SD), who were regularly cycling >5 hr/week, completed a familiarization trial followed by two experimental trials. Participants self-selected and replicated their diet and exercise for ∼24 hr before each trial. Participants ingested either 0.35 g/kg body mass of (R)-3-hydroxybutyl (R)-3-hydroxybutyrate KE or a flavor-matched PL 30 min before exercise in a randomized, triple-blind, crossover manner. Exercise involved a 15-min warm-up followed by the 20-min TT on a cycle ergometer. The only feedback provided was time elapsed. Preexercise venous [ß-hydroxybutyrate] was higher after KE versus PL (2.0 ± 0.6 vs. 0.2 ± 0.1 mM, p < .0001). Mean TT power output was 2.4% (0.6% to 4.1%; mean [95% confidence interval]) lower after KE versus PL (255 ± 54 vs. 261 ± 54 W, p < .01; dz = 0.60). The mechanistic basis for the impaired TT performance after KE ingestion under the present study conditions remains to be determined.

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].

High-Intensity Interval vs. Moderate-Intensity Continuous Training in Parkinson's Disease: A Randomized Trial.

Exercise training is recommended to improve quality of life in those living with Parkinson's Disease (PD); however, the optimal prescription to improve cardiorespiratory fitness and disease-related motor symptoms remains unknown. Twenty-nine participants with PD were randomly allocated to either 10-weeks of high-intensity interval training (HIIT) (n=15; 6 female) or moderate-intensity continuous training (MICT) (n=14; 5 female). The primary outcome was the change in maximal oxygen consumption (VO2peak). Secondary outcomes included changes in the Unified Parkinson's Disease Rating Scale (UPDRS) Part III motor score, Parkinson's Disease Fatigue Scale (PFS-16), resting and exercise cardiovascular measures, gait, balance, and knee extensor strength and fatigability. Exercise training increased VO2peak (main effect of time, P<0.01), with a clinically-meaningful difference in the change following HIIT vs. MICT (∆3.7±3.7 vs. 1.7±3.2 ml∙kg-1∙min-1, P=0.099). The UPDRS motor score improved over time (P<0.001) but without any differences between HIIT vs. MICT (∆-9.7±1.3 vs. -8.4±1.4, P=0.51). Self-reported subjective fatigue (PFS-16) decreased over time (P<0.01) but was similar between HIIT and MICT groups (P=0.6). Gait, balance, blood pressure, and heart rate were unchanged with training (all P>0.09). Knee extensor strength increased over time (P=0.03) but did not differ between HIIT vs. MICT (∆8.2±5.9 vs. 11.7±6.2 Nm, P=0.69). HIIT alone increased muscular endurance of the knee extensors during an isotonic task to failure (P=0.04). In participants with PD, HIIT and MICT both increased VO2peak and led to improvements in motor symptoms and perceived fatigue; HIIT may offer the potential for larger changes in VO2peak and reduced knee extensor fatigability.

Peak Cardiac Output Determined Using Inert Gas Rebreathing: A Comparison of Two Exercise Protocols.

PURPOSE: This study aimed to compare Q˙peak elicited by a constant load protocol ( Q˙CL ) and an incremental step protocol ( Q˙step ). METHODS: A noninferiority randomized crossover trial was used to compare Q˙peak between protocols using a noninferiority margin of 0.5 L·min -1 . Participants ( n = 34 (19 female, 15 male); 25 ± 5 yr) performed two baseline V̇O 2peak tests to determine peak heart rate (HR peak ) and peak work rate ( Wpeak ). Participants then performed the Q˙CL and Q˙step protocols each on two separate occasions with the order of the four visits randomized. Q˙peak was measured using IGR (Innocor; COSMED, Rome, Italy). The Q˙CL protocol involved a V̇O 2peak test followed 10 min later by cycling at 90% Wpeak , with IGR initiated after 2 min. Q˙step involved an incremental step test with IGR initiated when the participant's HR reached 5 bpm below their HR peak . The first Q˙CL and Q˙step tests were compared for noninferiority, and the second series of tests was used to measure repeatability (typical error (TE)). RESULTS: The Q˙CL protocol was noninferior to Q˙step ( Q˙CL = 17.1 ± 3.2, Q˙step = 16.8 ± 3.1 L·min -1 ; 95% confidence intervals, -0.16 to 0.72 L·min -1 ). The baseline V̇O 2peak (3.13 ± 0.83 L·min -1 ) was achieved during Q˙CL (3.12 ± 0.72, P = 0.87) and Q˙step (3.12 ± 0.80, P = 0.82). The TE values for Q˙peak were 6.6% and 8.3% for Q˙CL and Q˙step , respectively. CONCLUSIONS: The Q˙CL protocol was noninferior to Q˙step and may be more convenient because of the reduced time commitment to perform the measurement.

Effect of Acute Ketone Monoester Ingestion on Cardiorespiratory Responses to Exercise and the Influence of Blood Acidosis.

PURPOSE: This study aimed to examine the effect of KE ingestion on exercise cardiac output ( Q˙ ) and the influence of blood acidosis. We hypothesized that KE versus placebo ingestion would increase Q ˙, and coingestion of the pH buffer bicarbonate would mitigate this effect. METHODS: In a randomized, double-blind, crossover manner, 15 endurance-trained adults (peak oxygen uptake (V̇O 2peak ), 60 ± 9 mL·kg -1 ·min -1 ) ingested either 0.2 g·kg -1 sodium bicarbonate or a salt placebo 60 min before exercise, and 0.6 g·kg -1 KE or a ketone-free placebo 30 min before exercise. Supplementation yielded three experimental conditions: basal ketone bodies and neutral pH (CON), hyperketonemia and blood acidosis (KE), and hyperketonemia and neutral pH (KE + BIC). Exercise involved 30 min of cycling at ventilatory threshold intensity, followed by determinations of V̇O 2peak and peak Q ˙. RESULTS: Blood [ß-hydroxybutyrate], a ketone body, was higher in KE (3.5 ± 0.1 mM) and KE + BIC (4.4 ± 0.2) versus CON (0.1 ± 0.0, P < 0.0001). Blood pH was lower in KE versus CON (7.30 ± 0.01 vs 7.34 ± 0.01, P < 0.001) and KE + BIC (7.35 ± 0.01, P < 0.001). Q ˙ during submaximal exercise was not different between conditions (CON: 18.2 ± 3.6, KE: 17.7 ± 3.7, KE + BIC: 18.1 ± 3.5 L·min -1 ; P = 0.4). HR was higher in KE (153 ± 9 bpm) and KE + BIC (154 ± 9) versus CON (150 ± 9, P < 0.02). V̇O 2peak ( P = 0.2) and peak Q ˙ ( P = 0.3) were not different between conditions, but peak workload was lower in KE (359 ± 61 W) and KE + BIC (363 ± 63) versus CON (375 ± 64, P < 0.02). CONCLUSIONS: KE ingestion did not increase Q ˙ during submaximal exercise despite a modest elevation of HR. This response occurred independent of blood acidosis and was associated with a lower workload at V̇O 2peak .

Menstrual cycle hormones and oral contraceptives: a multimethod systems physiology-based review of their impact on key aspects of female physiology.

Hormonal changes around ovulation divide the menstrual cycle (MC) into the follicular and luteal phases. In addition, oral contraceptives (OCs) have active (higher hormone) and placebo phases. Although there are some MC-based effects on various physiological outcomes, we found these differences relatively subtle and difficult to attribute to specific hormones, as estrogen and progesterone fluctuate rather than operating in a complete on/off pattern as observed in cellular or preclinical models often used to substantiate human data. A broad review reveals that the differences between the follicular and luteal phases and between OC active and placebo phases are not associated with marked differences in exercise performance and appear unlikely to influence muscular hypertrophy in response to resistance exercise training. A systematic review and meta-analysis of substrate oxidation between MC phases revealed no difference between phases in the relative carbohydrate and fat oxidation at rest and during acute aerobic exercise. Vascular differences between MC phases are also relatively small or nonexistent. Although OCs can vary in composition and androgenicity, we acknowledge that much more work remains to be done in this area; however, based on what little evidence is currently available, we do not find compelling support for the notion that OC use significantly influences exercise performance, substrate oxidation, or hypertrophy. It is important to note that the study of females requires better methodological control in many areas. Previous studies lacking such rigor have contributed to premature or incorrect conclusions regarding the effects of the MC and systemic hormones on outcomes. While we acknowledge that the evidence in certain research areas is limited, the consensus view is that the impact of the MC and OC use on various aspects of physiology is small or nonexistent.

Dietary Intake of Young Male Ice Hockey Players 10-13 Years of Age during a Week-Long Hockey Camp.

This study recorded the dietary intakes of young male ice hockey players (10-13 year (yr)) for 3 consecutive days while participating in a 5-day summer hockey camp. Players were categorized as older children (OC, n = 10; 10.7 ± 0.2 yr; 37.1 ± 1.5 kg; 147.9 ± 2.1 cm) and young adolescents (YA, n = 10; 12.9 ± 0.1 yr; 45.2 ± 1.5 kg; 157.0 ± 2.4 cm). Players consumed their usual daily intakes. Parents recorded food intake in the mornings and evenings, while the researchers recorded food intake at camp. Energy intake was higher in both groups when compared to data for age-matched young Canadian (CDN) males (OC, 2967 ± 211 vs. 2000 kcal/day; YA, 2773 ± 91 vs. 2250 kcal/day). Carbohydrate (CHO) (OC, 11.2 ± 0.8 vs. YO, 8.9 ± 0.5 g/kg body mass/day) and protein (OC, 3.2 ± 0.3; YO, 2.4 ± 0.1 g/kg/day) intakes were higher than reported for young CDN males (CHO, 3.6 and protein, 1.0 g/kg/day) and were within the Acceptable Macronutrient Distribution Range (AMDR; CHO, 56 ± 2.3; 57.4 ± 0.8%; protein, 16.1 ± 1.0; 15.7 ± 0.7%). Fat intake was also within the AMDR in both groups (OC, 29.8 ± 1.6%; YA, 28.3 ± 1.0%). Micronutrient intake was adequate except for Vitamin D intakes that were below the recommended 15 ug/day at 6.3 ± 0.7 (OC) and 5.0 ± 1.5 ug/day (YA). In summary, energy and macronutrient intakes of the OC (10-11 yr) and YA (12-13 yr) players were high and well above the age matched CDN norms. The older children had higher energy intakes/kg body mass than the young adolescents. Higher energy intakes allowed for micronutrients intakes to be met in these young active males, except for vitamin D intake.

Increased cardiorespiratory stress during submaximal cycling after ketone monoester ingestion in endurance-trained adults.

There is growing interest in the effect of exogenous ketone body supplementation on exercise responses and performance. The limited studies to date have yielded equivocal data, likely due in part to differences in dosing strategy, increase in blood ketones, and participant training status. Using a randomized, double-blind, counterbalanced design, we examined the effect of ingesting a ketone monoester (KE) supplement (600 mg/kg body mass) or flavour-matched placebo in endurance-trained adults (n = 10 males, n = 9 females; V̇O2peak = 57 ± 8 mL/kg/min). Participants performed a 30-min cycling bout at ventilatory threshold intensity (71 ± 3% V̇O2peak), followed 15 min later by a 3 kJ/kg body mass time-trial. KE versus placebo ingestion increased plasma ß-hydroxybutyrate concentration before exercise (3.9 ± 1.0 vs 0.2 ± 0.3 mM, p < 0.0001, dz = 3.4), ventilation (77 ± 17 vs 71 ± 15 L/min, p < 0.0001, dz = 1.3) and heart rate (155 ± 11 vs 150 ± 11 beats/min, p < 0.001, dz = 1.2) during exercise, and rating of perceived exertion at the end of exercise (15.4 ± 1.6 vs 14.5 ± 1.2, p < 0.01, dz = 0.85). Plasma ß-hydroxybutyrate concentration remained higher after KE vs placebo ingestion before the time-trial (3.5 ± 1.0 vs 0.3 ± 0.2 mM, p < 0.0001, dz = 3.1), but performance was not different (KE: 16:25 ± 2:50 vs placebo: 16:06 ± 2:40 min:s, p = 0.20; dz = 0.31). We conclude that acute ingestion of a relatively large KE bolus dose increased markers of cardiorespiratory stress during submaximal exercise in endurance-trained participants. Novelty: Limited studies have yielded equivocal data regarding exercise responses after acute ketone body supplementation. Using a randomized, double-blind, placebo-controlled, counterbalanced design, we found that ingestion of a large bolus dose of a commercial ketone monoester supplement increased markers of cardiorespiratory stress during cycling at ventilatory threshold intensity in endurance-trained adults.

Performance Effects of Carbohydrate Ingestion Between Bouts of Intense Aerobic Interval Exercise.

PURPOSE: This study tested whether CHO intake during a 2-h rest between exercise bouts improved performance in the subsequent bout. METHODS: In a randomized, single-blinded, crossover design, 10 recreationally-active participants (23 ± 4 yr, 70.8 ± 6.6 kg, VO2peak:47.0 ± 5.4 mL O2·min-1·kg body mass-1) arrived at the lab post-prandial and completed 2 exercise bouts separated by 2-h rest. Bouts included 5 x 4-min intervals at ~80% VO2peak separated by 2-min at ~40% VO2peak and ended with an endurance trial (ET) to voluntary exhaustion at ~90% VO2peak. During intervals 1 and 4 in each bout expired gases were collected and O2 deficit was estimated. Immediately following bout-1, either a CHO (1.2 g CHO·kg body mass-1) or placebo (PL) solution was consumed. RESULTS: ET duration decreased in bout-2 vs. 1 in both conditions (P<0.01) but was ~35% longer in bout-2 with CHO vs. PL (Interaction, P=0.03; post-hoc, P=0.03). VO2 increased during interval 4 vs. 1 in both bouts (P<0.01) but was unaffected by CHO (P≥0.58). O2 deficit was unaffected by CHO (P=0.93), bout or interval (P≥0.15). Perceived exertion was higher in bout-2 vs. 1 (P<0.001) and reduced in intervals 2 and 4 in CHO (P≤0.01). CONCLUSIONS: When rest between training sessions is 2 hours, athletes may improve subsequent performance by consuming CHO during recovery. Supported by NSERC, Canada.

Mild dehydration impaired intermittent sprint performance and thermoregulation in females.

The effects of mild dehydration during ice hockey are well-studied in males but not females. In a randomized, crossover design, 11 female varsity hockey players drank no fluid (1.7% ± 0.3% body mass loss) or water to maintain hydration during simulated-hockey exercise. Core temperature (P < 0.01) and perceived fatigue (P = 0.02) were higher and sprint power lower (P < 0.01) when mildly dehydrated. Thus, mild dehydration may impair hockey performance and thermoregulation while increasing perceived fatigue in females. Novelty Female stop-and-go sport athletes may benefit their in-game sprint performance and thermoregulation by following personalized in-game hydration to prevent becoming mildly dehydrated.

Impairment of Thermoregulation and Performance via Mild Dehydration in Ice Hockey Goaltenders.

During play, ice hockey goaltenders routinely dehydrate through sweating and lose ≥2% body mass, which may impair thermoregulation and performance. PURPOSE: This randomized, crossover study examined the effects of mild dehydration on goaltender on-ice thermoregulation, heart rate, fatigue, and performance. METHODS: Eleven goaltenders played a 70-minute scrimmage followed by a shootout and drills to analyze reaction time and movements. On ice, they either consumed no fluid (NF) and lost 2.4% (0.3%) body mass or maintained body mass with water (WAT) or a carbohydrate-electrolyte solution (CES). Save percentage, rating of perceived exertion, heart rate, and core temperature were recorded throughout, and a postskate questionnaire assessed perceived fatigue. RESULTS: Relative to NF, intake of both fluids decreased heart rate (interaction: P = .03), core temperature (peak NF = 39.0°C [0.1°C], WAT = 38.6°C [0.1°C], and CES = 38.5°C [0.1°C]; P = .005), and rating of perceived exertion in the scrimmage (post hoc: P < .04), as well as increasing save percentage in the final 10 minutes of scrimmage (NF = 75.8% [1.9%], WAT = 81.7% [2.3%], and CES = 81.3% [2.3%], post hoc: P < .04). In drills, movement speed (post hoc: P < .05) and reaction time (post hoc: P < .04) were slower in the NF versus both fluid conditions. Intake of either fluid similarly reduced postskate questionnaire scores (condition: P < .0001). Only CES significantly reduced rating of perceived exertion in drills (post hoc: P < .05) and increased peak movement power versus NF (post hoc: P = .02). Shootout save percentage was similar between conditions (P = .37). CONCLUSIONS: Mild dehydration increased physiological strain and fatigue and decreased ice hockey goaltender performance versus maintaining hydration. Also, maintaining hydration with a CES versus WAT may further reduce perceived fatigue and positively affect movements.

No effect of beetroot juice supplementation on exercise economy and performance in recreationally active females despite increased torque production.

This study investigated the effects of acute and chronic beetroot juice (BRJ) supplementation on submaximal exercise oxygen uptake (VO2 ), time trial (TT) performance, and contractile properties of the plantar flexors in females. Study 1: Using a double blind, randomized, crossover design, 12 recreationally active females using hormonal contraceptives supplemented acutely (2.5 h) and chronically (8 days) with 280 mL BRJ/d (~26 mmoles nitrate [ NO3- ]) or a NO3- -free placebo (PLA). On days 1 and 8, participants cycled for 10 min at 50% and 70% VO2peak and completed a 4 kJ/kg body mass TT. Plasma [ NO3- ] and nitrite ([NO2- ]) increased significantly following BRJ supplementation versus PLA. There was no effect of BRJ supplementation on VO2 at 50% or 70% VO2peak , or TT performance. Study 2: 12 recreationally active females (n = 7 from Study 1) using hormonal contraceptives participated in a baseline visit and were supplemented acutely (2.5 h) and chronically (8 days) with 280 mL BRJ/d. Maximum voluntary strength (MVC) of the plantar flexors was assessed and a torque-frequency curve performed. BRJ had no effect on MVC, voluntary activation, peak twitch torque, time to peak torque, or half relaxation time. Following both acute (46.6 ± 4.9% of 100 Hz torque) and chronic (47.2 ± 4.4%) supplementation, 10 Hz torque was significantly greater compared to baseline (32.9 ± 2.6%). In summary, BRJ may not be an effective ergogenic aid in recreationally active females as it did not reduce submaximal exercise VO2 or improve aerobic TT performance despite increasing low frequency torque production.