Effects of high-intensity interval training and resistance training on physiological parameters and performance of well-trained runners: A randomized controlled trial.

This study aimed to verify the effects of 4 weeks of high-intensity interval training (HIIT), heavy (HRT) and explosive (ERT) resistance training on aerobic, anaerobic and neuromuscular parameters and performance of well-trained runners. Twenty-six male athletes were divided into HIIT (n = 10), HRT (n = 7) and ERT (n = 9) groups. Maximal oxygen uptake (VO2max) and the corresponding velocity (vVO2max), anaerobic threshold (AT), running economy (RE), oxygen uptake kinetics, lower-body strength (1RM) and power (CMJ), and the 1500m and 5000m time-trial (TT) were determined. Improvements were observed in vVO2max (mean difference (Δ): 2.6%; effect size (ES): 0.63) with HIIT, while AT was incresead in ERT (Δ: 4.3%; ES: 0.73) and HRT (Δ: 6.9%; ES: 0.72) groups. The CMJ performance was increased in ERT (Δ: 13.8%; ES: 1.03), HRT (Δ: 6.9%; ES: 0.55) and HIIT (Δ: 5.4%; ES: 0.34), whereas 1RM increase in HRT (Δ: 38.1%; ES: 1.21) and ERT (Δ: 49.2%; ES: 0.96) groups. HIIT improved the 1500m (Δ: -2.3%; ES: -0.62) and both HRT (Δ: -1.6%; ES: -0.32) and ERT (Δ: -1.7%; ES: -0.31) the 5000m TT. Despite performance adaptations were dependent on the training characteristics, both RT and HIIT model constitute an alternative for training periodization.

Effect of recovery time on [Formula: see text]-ON kinetics in humans at the onset of moderate-intensity cycling exercise.

PURPOSE: τ of the primary phase of [Formula: see text] kinetics during square-wave, moderate-intensity exercise mirrors that of PCr splitting (τPCr). Pre-exercise [PCr] and the absolute variations of PCr (∆[PCr]) occurring during transient have been suggested to control τPCr and, in turn, to modulate [Formula: see text] kinetics. In addition, [Formula: see text] kinetics may be slower when exercise initiates from a raised metabolic level, i.e., from a less-favorable energetic state. We verified the hypothesis that: (i) pre-exercise [PCr], (ii) pre-exercise metabolic rate, or (iii) ∆[PCr] may affect the kinetics of muscular oxidative metabolism and, therefore, τ. METHODS: To this aim, seven active males (23.0 yy ± 2.3; 1.76 m ± 0.06, [Formula: see text]: 3.32 L min-1 ± 0.67) performed three repetitions of series consisting of six 6-min step exercise transitions of identical workload interspersed with different times of recovery: 30, 60, 90, 120, 300 s. RESULTS: Mono-exponential fitting was applied to breath-by-breath [Formula: see text], so that τ was determined. τ decays as a first-order exponential function of the time of recovery (τ = 109.5 × e(-t/14.0) + 18.9 r2 = 0.32) and linearly decreased as a function of the estimated pre-exercise [PCr] (τ = - 1.07 [PCr] + 44.9, r2 = 0.513, P < 0.01); it was unaffected by the estimated ∆[PCr]. CONCLUSIONS: Our results in vivo do not confirm the positive linear relationship between τ and pre-exercise [PCr] and ∆[PCr]. Instead, [Formula: see text] kinetics seems to be influenced by the pre-exercise metabolic rate and the altered intramuscular energetic state.

Aerobic capacity and [Formula: see text] kinetics adaptive responses to short-term high-intensity interval training and detraining in untrained females.

PURPOSE: This study investigated the physical fitness and oxygen uptake kinetics (τ[Formula: see text]) along with the O2 delivery and utilization (heart rate kinetics, τHR; deoxyhemoglobin/[Formula: see text] ratio, ∆[HHb]/[Formula: see text]) adaptations of untrained female participants responding to 4 weeks of high-intensity interval training (HIIT) and 2 weeks of detraining. METHODS: Participants were randomly assigned to HIIT (n = 11, 4 × 4 protocol) or nonexercising control (n = 9) groups. Exercising group engaged 4 weeks of treadmill HIIT followed by 2 weeks of detraining while maintaining daily activity level. Ramp-incremental (RI) tests and step-transitions to moderate-intensity exercise were performed. Aerobic capacity and performance (maximal oxygen uptake, [Formula: see text]; gas-exchange threshold, GET; power output, PO), body composition (skeletal muscle mass, SMM; body fat percentage, BF%), muscle oxygenation status (∆[HHb]), [Formula: see text], and HR kinetics were assessed. RESULTS: HIIT elicited improvements in aerobic capacity ([Formula: see text], + 0.17 ± 0.04 L/min; GET, + 0.18 ± 0.05 L/min, P < 0.01; PO-[Formula: see text], ± 23.36 ± 8.37 W; PO-GET, + 17.18 ± 3.07 W, P < 0.05), body composition (SMM, + 0.92 ± 0.17 kg; BF%, - 3.08% ± 0.58%, P < 0.001), and speed up the τ[Formula: see text] (- 8.04 ± 1.57 s, P < 0.001) significantly, extending to better ∆[HHb]/[Formula: see text] ratio (1.18 ± 0.08 to 1.05 ± 0.14). After a period of detraining, the adaptation in body composition and aerobic capacity, as well as the accelerated τ[Formula: see text] were maintained in the HIIT group, but the PO-[Formula: see text] and PO-GET declined below the post-training level (P < 0.05), whereas no changes were reported in controls (P > 0.05). Four weeks of HIIT induced widespread physiological adaptations in females, and the majority of improvements were preserved after 2 weeks of detraining except for power output corresponding to [Formula: see text] and GET.

Adaptations to 4 weeks of high-intensity interval training in healthy adults with different training backgrounds.

PURPOSE: This study investigated the physical fitness and oxygen uptake kinetics ([Formula: see text]) along with the exercise-onset O2 delivery (heart rate kinetics, τHR; changes in normalized deoxyhemoglobin/[Formula: see text] ratio, Δ[HHb]/[Formula: see text]) adaptations of individuals with different physical activity (PA) backgrounds responding to 4 weeks of high-intensity interval training (HIIT), and the possible effects of skeletal muscle mass (SMM) on training-induced adaptations. METHODS: Twenty subjects (10 high-PA level, HIIT-H; 10 moderate-PA level, HIIT-M) engaged in 4 weeks of treadmill HIIT. Ramp-incremental (RI) test and step-transitions to moderate-intensity exercise were performed. Cardiorespiratory fitness, body composition, muscle oxygenation status, VO2 and HR kinetics were assessed at baseline and post-training. RESULTS: HIIT improved fitness status for HIIT-H ([Formula: see text], + 0.26 ± 0.07 L/min; SMM, + 0.66 ± 0.70 kg; body fat, - 1.52 ± 1.93 kg; [Formula: see text], - 7.11 ± 1.05 s, p < 0.05) and HIIT-M ([Formula: see text], 0.24 ± 0.07 L/min, SMM, + 0.58 ± 0.61 kg; body fat, - 1.64 ± 1.37 kg; [Formula: see text], - 5.48 ± 1.05 s, p < 0.05) except for visceral fat area (p = 0.293) without between-group differences (p > 0.05). Oxygenated and deoxygenated hemoglobin amplitude during the RI test increased for both groups (p < 0.05) except for total hemoglobin (p = 0.179). The Δ[HHb]/[Formula: see text] overshoot was attenuated for both groups (p < 0.05) but only eliminated in HIIT-H (1.05 ± 0.14 to 0.92 ± 0.11), and no change was observed in τHR (p = 0.144). Linear mixed-effect models presented positive effects of SMM on absolute [Formula: see text] (p < 0.001) and ΔHHb (p = 0.034). CONCLUSION: Four weeks of HIIT promoted positive adaptations in physical fitness and [Formula: see text] kinetics, with the peripheral adaptations attributing to the observed improvements. The training effects are similar between groups suggesting that HIIT is effective for reaching higher physical fitness levels.

Different categories of VO2 kinetics in the 'extreme' exercise intensity domain.

The aim of this study was to classify potential sub-zones within the extreme exercise domain. Eight well-trained male cyclists participated in this study. The upper boundary of the severe exercise domain (Pupper-bound) was estimated by constant-work-rate tests. Then three further extreme-work-rate tests were performed in discrete regions within the extreme domain: extreme-1) at a work-rate greater than the Pupper-bound providing an 80-110-s time to task failure; extreme-2) a 30-s maximal sprint; and extreme-3) a 4-s maximal sprint. Different functions were used to describe the behaviour of the V˙O2 kinetics over time. V˙O2 on-kinetics during extreme-1 exercise was best described by a single-exponential model (R2 ≥ 0.97; SEE ≤ 0.10; p < 0.001), and recovery V˙O2 decreased immediately after the termination of exercise. In contrast, V˙O2 on-kinetics during extreme-2 exercise was best fitted by a linear function (R2 ≥ 0.96; SEE ≤ 0.16; p < 0.001), and V˙O2 responses continued to increase during the first 10-20 s of recovery. During the extreme-3 exercise, V˙O2 could not be modelled due to inadequate data, and there was an M-shape recovery V˙O2 response with an exponential decay at the end. The V˙O2 response to exercise across the extreme exercise domain has distinct features and must therefore be characterised with different fitting strategies in order to describe the responses accurately.

A Methodological Checklist for Studies of Pleasure and Enjoyment Responses to High-Intensity Interval Training: Part II. Intensity, Timing of Assessments, Data Modeling, and Interpretation.

Recent studies have concluded that high-intensity interval training should be seen as a "viable alternative" to, and may be more enjoyable than, moderate-intensity continuous exercise. If true, these claims have the potential to revolutionize the science and practice of exercise, establishing high-intensity interval training as not only a physiologically effective exercise modality but also a potentially sustainable one. However, these claims stand in contrast to voluminous evidence according to which high levels of exercise intensity are typically experienced as less pleasant than moderate levels. To help researchers, peer reviewers, editors, and critical readers appreciate possible reasons for the apparently conflicting results, we present a checklist that identifies crucial methodological elements in studies investigating the effects of high-intensity interval training on affect and enjoyment. This second installment covers how "high-intensity" and "moderate-intensity" experimental conditions are defined, the timing of assessments of affect, the modeling of affective responses, and data interpretation.

Validity of anaerobic threshold measured in resistance exercise.

[Purpose] Intensity for resistance exercise is estimated based on the maximum muscle strength. Exercise prescription without evaluating the biological response has a challenge. This study aimed to confirm whether anaerobic threshold measured using cardiopulmonary exercise test in resistance exercise is appropriate or not. [Participants and Methods] Resistance exercise adopted for the study was right-leg knee extension. The participants were 10 healthy young males. We investigated whether the oxygen uptake kinetics achieved a steady state within 3 min during the constant-load test with knee extension at 80% anaerobic threshold using cardiopulmonary exercise test with knee extension. If oxygen uptake kinetics achieved a steady state within 3 min, the exercise intensity measured using cardiopulmonary exercise test was considered appropriate. [Results] Anaerobic threshold was measured using the conventional approach in all participants. The steady state of oxygen uptake kinetics could be achieved within 3 min. In the constant-load test with knee extension at 80% anaerobic threshold, the oxygen uptake kinetics achieved a steady state within 3 min. [Conclusion] Based on the findings, the anaerobic threshold obtained using cardiopulmonary exercise test with resistance exercise was judged as appropriate. The results of this study contribute to the accurate setting of exercise load for resistance exercise and condition setting for the evaluation of skeletal muscle function.

The role of vascular function on exercise capacity in health and disease.

Three sentinel parameters of aerobic performance are the maximal oxygen uptake ( V̇O2max ), critical power (CP) and speed of the V̇O2 kinetics following exercise onset. Of these, the latter is, perhaps, the cardinal test of integrated function along the O2 transport pathway from lungs to skeletal muscle mitochondria. Fast V̇O2 kinetics demands that the cardiovascular system distributes exercise-induced blood flow elevations among and within those vascular beds subserving the contracting muscle(s). Ideally, this process must occur at least as rapidly as mitochondrial metabolism elevates V̇O2 . Chronic disease and ageing create an O2 delivery (i.e. blood flow × arterial [O2 ], Q̇O2 ) dependency that slows V̇O2 kinetics, decreasing CP and V̇O2max , increasing the O2 deficit and sowing the seeds of exercise intolerance. Exercise training, in contrast, does the opposite. Within the context of these three parameters (see Graphical Abstract), this brief review examines the training-induced plasticity of key elements in the O2 transport pathway. It asks how structural and functional vascular adaptations accelerate and redistribute muscle Q̇O2 and thus defend microvascular O2 partial pressures and capillary blood-myocyte O2 diffusion across a ∼100-fold range of muscle V̇O2 values. Recent discoveries, especially in the muscle microcirculation and Q̇O2 -to- V̇O2 heterogeneity, are integrated with the O2 transport pathway to appreciate how local and systemic vascular control helps defend V̇O2 kinetics and determine CP and V̇O2max in health and how vascular dysfunction in disease predicates exercise intolerance. Finally, the latest evidence that nitrate supplementation improves vascular and therefore aerobic function in health and disease is presented.

Priming the cardiodynamic phase of pulmonary oxygen uptake through voluntary modulations of the respiratory pump at the onset of exercise.

NEW FINDINGS: What is the central question of this study? The initial increase in oxygen uptake ( V̇O2 ) at exercise onset results from pulmonary perfusion changes secondary to an increased venous return. Breathing mechanics contribute to venous return through abdominal and intrathoracic pressures variation. Can voluntary breathing techniques (abdominal or rib cage breathing) increase venous return and improve V̇O2 at exercise onset? What is the main finding and its importance? Abdominal and rib cage breathing increase venous return and V̇O2 at exercise onset. This mechanism could be clinically relevant in patients with impaired cardiac function limiting oxygen transport. ABSTRACT: We examined how different breathing patterns can modulate venous return and alveolar gas transfer during exercise transients in humans. Ten healthy men transitioned from rest to moderate cycling while breathing spontaneously (SP) or with voluntary increases in abdominal (AB) or intrathoracic (RC) pressure swings. We used double body plethysmography to determine blood displacements between the trunk and the extremities (Vbs ). From continuous signals of airflow and O2 fraction, we calculated breath-by-breath oxygen uptake at the mouth and used optoelectronic plethysmography to correct for lung O2 store changes and calculate alveolar O2 transfer ( V̇O2A ). Oesophageal (Poes ) and gastric (Pga ) pressures were monitored using balloon-tipped catheters. Cardiac stroke volume was measured using impedance cardiography. During the cardiodynamic phase (Φ1) of V̇O2A -on kinetics (20 s following exercise onset), AB and RC increased total alveolar oxygen transfer compared to SP (227 ± 32, P = 0.019 vs. 235 ± 27, P = 0.001 vs. 206 ± 20 ml, mean ± SD). Pga and Poes swings increased with AB (by 24.4 ± 9.6 cmH2 O, P < 0.001) and RC (by 14.5 ± 5.7 cmH2 O, P < 0.001), respectively. AB yielded a greater increase in intra-breath Vbs swings compared with RC and SP (+0.30 ± 0.14 vs. +0.16 ± 0.11, P < 0.001 vs. +0.10 ± 0.05 ml, P = 0.006) and increased the sum of stroke volumes compared to SP (4.47 ± 1.28 vs. 3.89 ± 0.96 litres, P = 0.053), while RC produced significant central blood translocation from the extremities compared with SP (by 493 ± 311 ml, P < 0.001). Our findings indicate that combining exercise onset with AB or RC increases venous return, thus increasing mass oxygen transport above metabolic consumption during Φ1 and limiting the oxygen deficit incurred.

Cocoa-flavanols enhance moderate-intensity pulmonary [Formula: see text] kinetics but not exercise tolerance in sedentary middle-aged adults.

INTRODUCTION: Cocoa flavanols (CF) may exert health benefits through their potent vasodilatory effects, which are perpetuated by elevations in nitric oxide (NO) bioavailability. These vasodilatory effects may contribute to improved delivery of blood and oxygen (O2) to exercising muscle. PURPOSE: Therefore, the objective of this study was to examine how CF supplementation impacts pulmonary O2 uptake ([Formula: see text]) kinetics and exercise tolerance in sedentary middle-aged adults. METHODS: We employed a double-blind cross-over, placebo-controlled design whereby 17 participants (11 male, 6 female; mean ± SD, 45 ± 6 years) randomly received either 7 days of daily CF (400 mg) or placebo (PL) supplementation. On day 7, participants completed a series of 'step' moderate- and severe-intensity exercise tests for the determination of [Formula: see text] kinetics. RESULTS: During moderate-intensity exercise, the time constant of the phase II [Formula: see text] kinetics ([Formula: see text]) was decreased by 15% in CF as compared to PL (mean ± SD; PL 40 ± 12 s vs. CF 34 ± 9 s, P = 0.019), with no differences in the amplitude of [Formula: see text] (A[Formula: see text]; PL 0.77 ± 0.32 l min-1 vs. CF 0.79 ± 0.34 l min-1, P = 0.263). However, during severe-intensity exercise, [Formula: see text], the amplitude of the slow component ([Formula: see text]) and exercise tolerance (PL 435 ± 58 s vs. CF 424 ± 47 s, P = 0.480) were unchanged between conditions. CONCLUSION: Our data show that acute CF supplementation enhanced [Formula: see text] kinetics during moderate-, but not severe-intensity exercise in middle-aged participants. These novel effects of CFs, in this demographic, may contribute to improved tolerance of moderate-activity physical activities, which appear commonly present in daily life. TRIAL REGISTRATION: Registered under ClinicalTrials.gov Identifier no. NCT04370353, 30/04/20 retrospectively registered.

A clinical evaluation of VO2 kinetics in kidney transplant recipients.

PURPOSE: Aerobic exercise capacity is reduced in patients with chronic kidney disease, partly due to alterations at the muscular and microvascular level. This study evaluated oxygen uptake (VO2) kinetics as indicator of muscular oxidative metabolism in a population of Kidney Transplant Recipients (KTRs). METHODS: Two groups of KTRs enrolled 3 (n = 21) and 12 months (n = 14) after transplantation and a control group of healthy young adults (n = 16) underwent cardiopulmonary exercise testing on cycle-ergometer. The protocol consisted in two subsequent constant, moderate-load exercise phases with a final incremental test until exhaustion. RESULTS: The time constant of VO2 kinetics was slower in KTRs at 3 and 12 months after transplantation compared to controls (50.4 ± 13.1 s and 43.8 ± 11.6 s vs 28.9 ± 8.4 s, respectively; P < 0.01). Peak VO2 was lower in KTRs evaluated 3 months after transplantation compared to patients evaluated after 1 year (21.3 ± 4.3 and 26.4 ± 8.0 mL/kg/min; P = 0.04). Blood haemoglobin (Hb) concentration was higher in KTRs evaluated at 12 months (12.8 ± 1.7 vs 14.6 ± 1.7 g/dL; P < 0.01). Among KTRs, τ showed a moderate negative correlation with Peak VO2 (ρ = - 0.52) and Oxygen uptake efficiency slope (OUES) (r = - 0.57) while no significant correlation with Hb and peak heart rate. CONCLUSIONS: KTRs show slower VO2 kinetics compared to healthy controls. Hb and peak VO2 seem to improve during the first year after transplantation. VO2 kinetics were significantly associated with indices of cardiorespiratory fitness, but less with central determinants of aerobic capacity, thus suggesting a potential usefulness of adding this index of muscular oxidative metabolism to functional evaluation in KTRs.

Physiological responses and cycle characteristics during double-poling versus diagonal-stride roller-skiing in junior cross-country skiers.

PURPOSE: This study aimed to compare physiological factors and cycle characteristics during cross-country (XC) roller-skiing at matched inclines and speeds using the double-poling (DP) and diagonal-stride (DS) sub-techniques in junior female and male XC skiers. METHODS: Twenty-three well-trained junior XC skiers (11 women, 12 men; age 18.2 ± 1.2 yr.) completed two treadmill roller-skiing tests in a randomized order using either DP or DS. The exercise protocols were identical and included a 5 min warm-up, 4 × 5 min submaximal stages, and an incremental test to exhaustion, all performed at a 5° incline. RESULTS: No significant three-way interactions were observed between sex, submaximal exercise intensity, and sub-technique. For the pooled sample, higher values were observed for DP versus DS during submaximal exercise for the mean oxygen uptake kinetics response time (33%), energy cost (18%), heart rate (HR) (9%), blood lactate concentration (5.1 versus 2.1 mmol·L-1), rating of perceived exertion (12%), and cycle rate (25%), while cycle length was lower (19%) (all P < 0.001). During the time-to-exhaustion (TTE) test, peak oxygen uptake ([Formula: see text]O2peak), peak HR, and peak oxygen pulse were 8%, 2%, and 6% lower, respectively, for DP than DS, with a 29% shorter TTE during DP (pooled data, all P < 0.001). CONCLUSION: In well-trained junior XC skiers, DP was found to exert a greater physiological load than DS during uphill XC roller-skiing at submaximal intensities. During the TTE test, both female and male athletes were able to ski for longer and reached markedly higher [Formula: see text]O2peak values when using DS compared to DP.

Association between pulmonary oxygen uptake on-kinetics and acute cardiovascular responses to resistance exercise in patients with coronary artery disease: a preliminary study.

[Purpose] This study aimed to examine whether pulmonary oxygen uptake on-kinetics at the onset of moderate-intensity exercise can predict acute cardiovascular responses to resistance exercise. [Participants and Methods] The association between pulmonary oxygen uptake on-kinetics and acute cardiovascular responses to a single resistance exercise session was investigated in seven patients with low-risk coronary artery disease who underwent revascularization through percutaneous coronary intervention. The participants performed a cardiopulmonary exercise test on a cycle ergometer and a single resistance exercise session at 30% of maximum voluntary contraction on a bilateral leg-extension machine 1 week after surgery. We measured the ventilatory anaerobic threshold and pulmonary oxygen uptake on-kinetics during the cardiopulmonary exercise test; left ventricular ejection fraction at rest; and heart rate, systolic blood pressure, and rate pressure product during the single resistance exercise session. [Results] Pulmonary oxygen uptake on-kinetics showed a positive association with the amount of increase in systolic blood pressure and rate pressure product during the single resistance exercise session, but had no association with the amount of increase in heart rate. Ventilatory anaerobic threshold and left ventricular ejection fraction were not associated with these parameters. [Conclusion] These data suggested that pulmonary oxygen uptake on-kinetics can be a useful evaluation index for predicting acute systolic blood pressure and rate pressure product responses to low-intensity resistance exercise 1 week after percutaneous coronary intervention in patients with low-risk coronary artery disease.

August Krogh's theory of muscle microvascular control and oxygen delivery: a paradigm shift based on new data.

August Krogh twice won the prestigious international Steegen Prize, for nitrogen metabolism (1906) and overturning the concept of active transport of gases across the pulmonary epithelium (1910). Despite this, at the beginning of 1920, the consummate experimentalist was relatively unknown worldwide and even among his own University of Copenhagen faculty. But, in early 1919, he had submitted three papers to Dr Langley, then editor of The Journal of Physiology in England. These papers coalesced anatomical observations of skeletal muscle capillary numbers with O2 diffusion theory to propose a novel active role for capillaries that explained the prodigious increase in blood-muscle O2 flux from rest to exercise. Despite his own appraisal of the first two papers as "rather dull" to his friend, the eminent Cambridge respiratory physiologist, Joseph Barcroft, Krogh believed that the third one, dealing with O2 supply and capillary regulation, was"interesting". These papers, which won Krogh an unopposed Nobel Prize for Physiology or Medicine in 1920, form the foundation for this review. They single-handedly transformed the role of capillaries from passive conduit and exchange vessels, functioning at the mercy of their upstream arterioles, into independent contractile units that were predominantly closed at rest and opened actively during muscle contractions in a process he termed 'capillary recruitment'. Herein we examine Krogh's findings and some of the experimental difficulties he faced. In particular, the boundary conditions selected for his model (e.g. heavily anaesthetized animals, negligible intramyocyte O2 partial pressure, binary open-closed capillary function) have not withstood the test of time. Subsequently, we update the reader with intervening discoveries that underpin our current understanding of muscle microcirculatory control and place a retrospectroscope on Krogh's discoveries. The perspective is presented that the imprimatur of the Nobel Prize, in this instance, may have led scientists to discount compelling evidence. Much as he and Marie Krogh demonstrated that active transport of gases across the blood-gas barrier was unnecessary in the lung, capillaries in skeletal muscle do not open and close spontaneously or actively, nor is this necessary to account for the increase in blood-muscle O2 flux during exercise. Thus, a contemporary model of capillary function features most muscle capillaries supporting blood flow at rest, and, rather than capillaries actively vasodilating from rest to exercise, increased blood-myocyte O2 flux occurs predominantly via elevating red blood cell and plasma flux in already flowing capillaries. Krogh is lauded for his brilliance as an experimentalist and for raising scientific questions that led to fertile avenues of investigation, including the study of microvascular function.

5 km front crawl in pool and open water swimming: breath-by-breath energy expenditure and kinematic analysis.

PURPOSE: Breath-by-breath energy expenditure during open water swimming has not yet been explored in an ecological environment. This study aimed to investigate and compare energetics and kinematics of 5 km swimming, in both swimming pool and open water conditions. METHODS: Through four independent studies, oxygen uptake ([Formula: see text]2) kinetics, heart rate (HR), blood lactate concentration ([La-]) and glucose level (BGL), metabolic power ([Formula: see text]), energy cost (C) and kinematics were assessed during 5 km front crawl trials in a swimming pool and open water conditions. A total of 38 competitive open water swimmers aged 16-27 years volunteered for this four part investigation: Study A (pool, ten females, 11 males), Study B (pool, four females, six males), Study C (pool case study, one female) and Study D (open water, three females, four males). RESULTS: In the swimming pool, swimmers started with an above average swimming speed (v), losing efficiency along the 5 km, despite apparent homeostasis for [La-], BGL, [Formula: see text]2, [Formula: see text] and C. In open water, swimmers started the 5 km with a below average v, increasing the stroke rate (SR) in the last 1000 m. In open water, [Formula: see text]2 kinetics parameters, HR, [La-], BGL, respiratory exchange ratio and C were affected by the v and SR fluctuations along the 5 km. CONCLUSIONS: Small fluctuations were observed for energetic variables in both conditions, but changes in C were lower in swimming pool than in open water. Coaches should adjust the training plan accordingly to the specificity of open water swimming.

[Formula: see text] kinetics and energy contribution in simulated maximal performance during short and middle distance-trials in swimming.

PURPOSE: This study aims to analyze swimmers' oxygen uptake kinetics ([Formula: see text]K) and bioenergetic profiles in 50, 100, and 200 m simulated swimming events and determine which physiological variables relate with performance. METHODS: Twenty-eight well-trained swimmers completed an incremental test for maximal oxygen uptake (Peak-[Formula: see text]) and maximal aerobic velocity (MAV) assessment. Maximal trials (MT) of 50, 100, and 200-m in front crawl swimming were performed for [Formula: see text]K and bioenergetic profile. [Formula: see text]K parameters were calculated through monoexponential modeling and by a new growth rate method. The recovery phase was used along with the blood lactate concentration for bioenergetics profiling. RESULTS: Peak-[Formula: see text] (57.47 ± 5.7 ml kg-1 min-1 for male and 53.53 ± 4.21 ml kg-1 min-1 for female) did not differ from [Formula: see text]peak attained at the 200-MT for female and at the 100 and 200-MT for male. From the 50-MT to 100-MT and to the 200-MT the [Formula: see text]K presented slower time constants (8.6 ± 2.3 s, 11.5 ± 2.4 s and 16.7 ± 5.5 s, respectively), the aerobic contribution increased (~ 34%, 54% and 71%, respectively) and the anaerobic decreased (~ 66%, 46% and 29%, respectively), presenting a cross-over in the 100-MT. Both energy systems, MAV, Peak-[Formula: see text], and [Formula: see text] peak of the MT's were correlated with swimming performance. DISCUSSION: The aerobic energy contribution is an important factor for performance in 50, 100, and 200-m, regardless of the time taken to adjust the absolute oxidative response, when considering the effect on a mixed-group regarding sex. [Formula: see text]K speeding could be explained by a faster initial pacing strategy used in the shorter distances, that contributed for a more rapid increase of the oxidative contribution to the energy turnover.

Effects of heavy-intensity priming exercise on pulmonary oxygen uptake kinetics and muscle oxygenation in heart failure with preserved ejection fraction.

Exercise intolerance is a hallmark feature in heart failure with preserved ejection fraction (HFpEF). Prior heavy exercise ("priming exercise") speeds pulmonary oxygen uptake (V̇o2p) kinetics in older adults through increased muscle oxygen delivery and/or alterations in mitochondrial metabolic activity. We tested the hypothesis that priming exercise would speed V̇o2p on-kinetics in patients with HFpEF because of acute improvements in muscle oxygen delivery. Seven patients with HFpEF performed three bouts of two exercise transitions: MOD1, rest to 4-min moderate-intensity cycling and MOD2, MOD1 preceded by heavy-intensity cycling. V̇o2p, heart rate (HR), total peripheral resistance (TPR), and vastus lateralis tissue oxygenation index (TOI; near-infrared spectroscopy) were measured, interpolated, time-aligned, and averaged. V̇o2p and HR were monoexponentially curve-fitted. TPR and TOI levels were analyzed as repeated measures between pretransition baseline, minimum value, and steady state. Significance was P < 0.05. Time constant (τ; tau) V̇o2p (MOD1 49 ± 16 s) was significantly faster after priming (41 ± 14 s; P = 0.002), and the effective HR τ was slower following priming (41 ± 27 vs. 51 ± 32 s; P = 0.025). TPR in both conditions decreased from baseline to minimum TPR ( P < 0.001), increased from minimum to steady state ( P = 0.041) but remained below baseline throughout ( P = 0.001). Priming increased baseline ( P = 0.003) and minimum TOI ( P = 0.002) and decreased the TOI muscle deoxygenation overshoot ( P = 0.041). Priming may speed the slow V̇o2p on-kinetics in HFpEF and increase muscle oxygen delivery (TOI) at the onset of and throughout exercise. Microvascular muscle oxygen delivery may limit exercise tolerance in HFpEF.

Hyperoxia speeds pulmonary oxygen uptake kinetics and increases critical power during supine cycling.

NEW FINDINGS: What is the central question of this study? Critical power is a fundamental parameter defining high-intensity exercise tolerance and is related to the phase II time constant of pulmonary oxygen uptake kinetics ( τV̇O2 ). To test whether this relationship is causal, we assessed the impact of hyperoxia on τV̇O2 and critical power during supine cycle exercise. What is the main finding and its importance? The results demonstrate that hyperoxia increased muscle oxygenation, reduced τV̇O2 (i.e. sped up the oxygen uptake kinetics) and, subsequently, increased critical power when compared with normoxia. These results therefore suggest that τV̇O2 is a determinant of the upper limit for steady-state exercise, i.e. critical power. ABSTRACT: The present study determined the impact of hyperoxia on the phase II time constant of pulmonary oxygen uptake kinetics ( τV̇O2 ) and critical power (CP) during supine cycle exercise. Eight healthy men completed an incremental test to determine maximal oxygen uptake and the gas exchange threshold. Eight separate visits followed, whereby CP, τV̇O2 and absolute concentrations of oxyhaemoglobin ([HbO2 ]; via near-infrared spectroscopy) were determined via four constant-power tests to exhaustion, each repeated once in normoxia and once in hyperoxia (fraction of inspired O2  = 0.5). A 6 min bout of moderate-intensity exercise (70% of gas exchange threshold) was also undertaken before each severe-intensity bout, in both conditions. Critical power was greater (hyperoxia, 148 ± 29 W versus normoxia, 134 ± 27 W; P = 0.006) and the τV̇O2 reduced (hyperoxia, 33 ± 12 s versus normoxia, 52 ± 22 s, P = 0.007) during severe exercise in hyperoxia when compared with normoxia. Furthermore, [HbO2 ] was enhanced in hyperoxia compared with normoxia (hyperoxia, 67 ± 10 µm versus normoxia, 63 ± 11 µm; P = 0.020). The τV̇O2 was significantly related to CP in hyperoxia (R2  = 0.89, P < 0.001), but no relationship was observed in normoxia (r = 0.07, P = 0.68). Muscle oxygenation was increased, τV̇O2 reduced and CP increased in hyperoxia compared with normoxia, suggesting that τV̇O2 is an independent determinant of CP. The finding that τV̇O2 was related to CP in hyperoxia but not normoxia also supports this notion.

Dynamics of pleasure-displeasure at the limit of exercise tolerance: conceptualizing the sense of exertional physical fatigue as an affective response.

The search for variables involved in the regulation and termination of exercise performance has led to integrative models that attribute a central role to the brain and utilize an array of psychological terms (e.g. sensation, perception, discomfort, tolerance). We propose that theorizing about exercise regulation would benefit from establishing cross-disciplinary bridges to research fields, such as affective psychology and neuroscience, in which changes along the dimension of pleasure-displeasure are considered the main channel via which homeostatic perturbations enter consciousness and dictate corrective action (slowing down or stopping). We hypothesized that ratings of pleasure-displeasure would respond to the severity of homeostatic perturbation and would be related to time to exhaustion during exercise performed at an unsustainable intensity. In a within-subjects experiment (N=15, 13 men and 2 women, age 23.4±2.2 years; maximal oxygen uptake 46.0±8.0 ml kg-1 min-1), we compared the slope of ratings of pleasure-displeasure (acquired every 1 min) during cycling exercise at a power output 10% above critical power until volitional termination under glycogen-loaded and glycogen-depleted conditions. As hypothesized, ratings of pleasure-displeasure declined more steeply under glycogen depletion (P=0.009, d=0.70) and correlated closely with time to exhaustion under both glycogen-loaded (r=0.85; P<0.001) and glycogen-depleted conditions (r=0.83; P<0.001). We conclude that in exercise, as in other domains, changes in pleasure-displeasure may be the main channel via which homeostatic perturbations enter consciousness. This proposal may have important implications for conceptualizing and identifying the neurobiological mechanisms of the sense of exertional physical fatigue.