Purpose
To analyze if live high–train low (LHTL) effectiveness is improved when daily training is guided by heart rate variability (HRV).
Methods
Twenty-four elite Nordic skiers took part in a 15-day ...LHTL study and were randomized into a HRV-guided training hypoxic group (H-HRV,
n
= 9, sleeping in normobaric hypoxia, FiO
2
= 15.0%) and two predefined training groups sleeping either in hypoxia (H,
n
= 9, FiO
2
= 15.0%) or normoxia (N,
n
= 6). HRV and training loads (TL) were recorded daily. Prior (Pre), one (Post-1), and 21 days (Post-21) following LHTL, athletes performed a 10-km roller-ski test, and a treadmill test for determination of
V
˙
O
2max
was performed at Pre and Post-1.
Results
Some HRV parameters measured in supine position were different between H-HRV and H: low and high (HF) frequency power in absolute (ms
2
) (16.0 ± 35.1 vs. 137.0 ± 54.9%,
p
= 0.05) and normalized units (− 3.8 ± 10.1 vs. 53.0 ± 19.5%,
p
= 0.02), HF(nu) (6.3 ± 6.8 vs. − 13.7 ± 8.0%,
p
= 0.03) as well as heart rate (3.7 ± 6.3 vs. 12.3 ± 4.1%,
p
= 0.008). At Post-1,
V
˙
O
2max
was improved in H-HRV and H (3.8 ± 3.1%;
p
= 0.02 vs. 3.0 ± 4.4%;
p
= 0.08) but not in N (0.9 ± 5.1%;
p
= 0.7). Only H-HRV improved the roller-ski performance at Post-21 (− 2.7 ± 3.6%,
p
= 0.05).
Conclusion
The daily individualization of TL reduced the decrease in autonomic nervous system parasympathetic activity commonly associated with LHTL. The improved performance and oxygen consumption in the two LHTL groups confirm the effectiveness of LHTL even in elite endurance athletes.
Introduction:
The determination of the optimal occlusion level is a key parameter in blood flow restriction (BFR). This study aimed to compare the effects of elastic (BStrong) vs. nylon (Hokanson) ...BFR cuffs on blood flow in the lower and upper limbs.
Methods:
Eleven healthy participants undertook several BFR sessions with 2 different cuffs of similar width on their lower and upper limbs at different pressures 200, 250, 300, 350, and 400 mmHg for BStrong and 0, 40, and 60% of the arterial occlusion pressure (AOP) for Hokanson. Doppler ultrasound recorded blood flows through the brachial and femoral artery at rest.
Results:
With BStrong, only 350 and 400 mmHg pressures were significantly different from resting values (0% AOP). With Hokanson, both 40% and 60% of the AOP were significantly different from resting values (
p
< 0.05).
Discussion:
While both cuffs elicited BFR, they failed to accurately modulate blood flow. Hokanson is appropriate for research settings while BStrong appears to be a convenient tool for practitioners due to its safety (i.e., the impossibility of completely occluding arteries) and the possibility of exercising freely detached from the pump.
This study investigates the effects of normobaric hypoxia on repeated sprint exercise (RSE) with different balance between oxidative (phosphocreatine and oxidative pathway) and glycolytic ...contributions. Therefore, performance and psychophysiological responses were compared during RSE to exhaustion with the same exercise-to-rest ratio (1:2) but different sprint durations (5, 10, or 20 s) either in normoxic (RSN) or hypoxic (RSH; F io2 = 0.13) conditions.
On separate visits, 10 active participants completed in random order three cycling RSN (5:10; 10:20 and 20:40) and three similar RSH sessions to exhaustion. Vastus lateralis muscle oxygenation was recorded by near-infrared spectroscopy. Blood lactate concentration, limb and breathing discomfort, and ratings of perceived exertion were measured.
Total sprint number was smaller in hypoxia than in normoxia for 5:10 (20.8 ± 8.6 vs 14.7 ± 3.4; P = 0.014) and 10:20 (13.7 ± 6.3 vs 8.8 ± 2.5; P = 0.018) but not 20:40 (5.6 ± 1.9 vs 5.6 ± 2.5). The fatigue index was larger in hypoxia only for 5:10 (-43.5%, P < 0.001). Irrespective of condition, blood lactate concentration increased with the sprint duration with higher values for 20:40 than 5:10 (13.1 ± 2.7 vs 11.5 ± 2.2 mmoL·L -1 ; P = 0.027). Limb and breathing discomfort and ratings of perceived exertion did not differ in all RSE. Muscle oxygenation was mainly impacted by sprint duration (i.e., main effect of sprint duration on HHb min, tHb max, ΔHHb, and ΔtHb) but not by hypoxia. The normoxia-to-hypoxia percentage decrease for total sprint number for 5:10 was correlated with the highest power output over 5 s ( R2 = 0.55; P = 0.013) and 10 s ( R2 = 0.53; P = 0.016).
Hypoxia impairs repeated sprint ability when the oxidative but not the glycolytic contribution is substantial. The oxidative-glycolytic balance, influenced partly by sprint duration, is key during repeated sprint in hypoxia.
Aims
The body responds to exercise training by profound adaptations throughout the cardiorespiratory and muscular systems, which may result in improvements in maximal oxygen consumption (VO2peak) and ...mitochondrial capacity. By convenience, mitochondrial respiration is often measured at supra‐physiological oxygen levels, an approach that ignores any potential regulatory role of mitochondrial affinity for oxygen (p50mito) at physiological oxygen levels.
Methods
In this study, we examined the p50mito of mitochondria isolated from the Vastus lateralis and Triceps brachii in 12 healthy volunteers before and after a training intervention with seven sessions of sprint interval training using both leg cycling and arm cranking. The changes in p50mito were compared to changes in whole‐body VO2peak.
Results
We here show that p50mito is similar in isolated mitochondria from the Vastus (40 ± 3.8 Pa) compared to Triceps (39 ± 3.3) but decreases (mitochondrial oxygen affinity increases) after seven sessions of sprint interval training (to 26 ± 2.2 Pa in Vastus and 22 ± 2.7 Pa in Triceps, both P < .01). The change in VO2peak modelled from changes in p50mito was correlated to actual measured changes in VO2peak (R2 = .41, P = .002).
Conclusion
Together with mitochondrial respiratory capacity, p50mito is a critical factor when measuring mitochondrial function, it can decrease with sprint interval training and should be considered in the integrative analysis of the oxygen cascade from lung to mitochondria.
Purpose
This study aimed to determine the effects of hypoxia and/or blood flow restriction (BFR) on an arm-cycling repeated sprint ability test (aRSA) and its impact on elbow flexor neuromuscular ...function.
Methods
Fourteen volunteers performed an aRSA (10 s sprint/20 s recovery) to exhaustion in four randomized conditions: normoxia (NOR), normoxia plus BFR (N
BFR
), hypoxia (FiO
2
= 0.13, HYP) and hypoxia plus BFR (H
BFR
). Maximal voluntary contraction (MVC), resting twitch force (Db10), and electromyographic responses from the elbow flexors biceps brachii (BB) to electrical and transcranial magnetic stimulation were obtained to assess neuromuscular function. Main effects of hypoxia, BFR, and interaction were analyzed on delta values from pre- to post-exercise.
Results
BFR and hypoxia decreased the number of sprints during aRSA with no significant cumulative effect (NOR 16 ± 8; N
BFR
12 ± 4; HYP 10 ± 3 and H
BFR
8 ± 3;
P
< 0.01). MVC decrease from pre- to post-exercise was comparable whatever the condition.
M
-wave amplitude (− 9.4 ± 1.9% vs. + 0.8 ± 2.0%,
P
< 0.01) and Db10 force (− 41.8 ± 4.7% vs. − 27.9 ± 4.5%,
P
< 0.01) were more altered after aRSA with BFR compared to without BFR. The exercise-induced increase in corticospinal excitability was significantly lower in hypoxic vs. normoxic conditions (e.g., BB motor evoked potential at 75% of MVC: − 2.4 ± 4.2% vs. + 16.0 ± 5.9%, respectively,
P
= 0.03).
Conclusion
BFR and hypoxia led to comparable aRSA performance impairments but with distinct fatigue etiology. BFR impaired the muscle excitation–contraction coupling whereas hypoxia predominantly affected corticospinal excitability indicating incapacity of the corticospinal pathway to adapt to fatigue as in normoxia.
To elucidate the mechanisms underlying the differences in adaptation of arm and leg muscles to sprint training, over a period of 11 days 16 untrained men performed six sessions of 4-6 × 30-s all-out ...sprints (SIT) with the legs and arms, separately, with a 1-h interval of recovery. Limb-specific VO
peak, sprint performance (two 30-s Wingate tests with 4-min recovery), muscle efficiency and time-trial performance (TT, 5-min all-out) were assessed and biopsies from the
and
taken before and after training. VO
peak and Wmax increased 3-11% after training, with a more pronounced change in the arms (
< 0.05). Gross efficiency improved for the arms (+8.8%,
< 0.05), but not the legs (-0.6%). Wingate peak and mean power outputs improved similarly for the arms and legs, as did TT performance. After training, VO
during the two Wingate tests was increased by 52 and 6% for the arms and legs, respectively (
< 0.001). In the case of the arms, VO
was higher during the first than second Wingate test (64 vs. 44%,
< 0.05). During the TT, relative exercise intensity, HR, VO
, VCO
, V
, and V
were all lower during arm-cranking than leg-pedaling, and oxidation of fat was minimal, remaining so after training. Despite the higher relative intensity, fat oxidation was 70% greater during leg-pedaling (
= 0.017). The aerobic energy contribution in the legs was larger than for the arms during the Wingate tests, although VO
for the arms was enhanced more by training, reducing the O
deficit after SIT. The levels of muscle glycogen, as well as the myosin heavy chain composition were unchanged in both cases, while the activities of 3-hydroxyacyl-CoA-dehydrogenase and citrate synthase were elevated only in the legs and capillarization enhanced in both limbs. Multiple regression analysis demonstrated that the variables that predict TT performance differ for the arms and legs. The primary mechanism of adaptation to SIT by both the arms and legs is enhancement of aerobic energy production. However, with their higher proportion of fast muscle fibers, the arms exhibit greater plasticity.
During supramaximal exercise, exacerbated at exhaustion and in hypoxia, the circulatory system is challenged to facilitate oxygen delivery to working tissues through cerebral autoregulation which ...influences fatigue development and muscle performance. The aim of the study was to evaluate the effects of different levels of normobaric hypoxia on the changes in peripheral and cerebral oxygenation and performance during repeated sprints to exhaustion. Eleven recreationally active participants (six men and five women; 26.7 ± 4.2 years, 68.0 ± 14.0 kg, 172 ± 12 cm, 14.1 ± 4.7% body fat) completed three randomized testing visits in conditions of simulated altitude near sea-level (~380 m, F
O
20.9%), ~2000 m (F
O
16.5 ± 0.4%), and ~3800 m (F
O
13.3 ± 0.4%). Each session began with a 12-min warm-up followed by two 10-s sprints and the repeated cycling sprint (10-s sprint: 20-s recovery) test to exhaustion. Measurements included power output, vastus lateralis, and prefrontal deoxygenation near-infrared spectroscopy, delta (Δ) corresponds to the difference between maximal and minimal values, oxygen uptake, femoral artery blood flow (Doppler ultrasound), hemodynamic variables (transthoracic impedance), blood lactate concentration, and rating of perceived exertion. Performance (total work, kJ; -27.1 ± 25.8% at 2000 m,
< 0.01 and -49.4 ± 19.3% at 3800 m,
< 0.001) and pulse oxygen saturation (-7.5 ± 6.0%,
< 0.05 and -18.4 ± 5.3%,
< 0.001, respectively) decreased with hypoxia, when compared to 400 m. Muscle Δ hemoglobin difference (Hbdiff) and Δ tissue saturation index (TSI) were lower (
< 0.01) at 3800 m than at 2000 and 400 m, and lower Δ deoxyhemoglobin resulted at 3800 m compared with 2000 m. There were reduced changes in peripheral ΔHbdiff, ΔTSI, Δ total hemoglobin (tHb) and greater changes in cerebral (ΔHbdiff, ΔtHb) oxygenation throughout the test to exhaustion (
< 0.05). Changes in cerebral deoxygenation were greater at 3800 m than at 2000 and 400 m (
< 0.01). This study confirms that performance in hypoxia is limited by continually decreasing oxygen saturation, even though exercise can be sustained despite maximal peripheral deoxygenation. There may be a cerebral autoregulation of increased perfusion accounting for the decreased arterial oxygen content and allowing for task continuation, as shown by the continued cerebral deoxygenation.
•Interstitial lung water accumulation at altitude might precede high-altitude pulmonary oedema development.•We studied independent effects of hypobaria on interstitial lung water accumulation ...following hypoxic exercise in prematurely born adults.•Short, moderate-intensity exercise provokes a significant increase in the interstitial lung water accumulation after 8 h of exposure to terrestrial but not simulated altitude.
We aimed to gauge the interstitial lung water accumulation following moderate-intensity exercise under normobaric and hypobaric hypoxic conditions in a group of preterm born but otherwise healthy young adults.
Sixteen pre-term-born individuals (age = 21±2yrs.; gestational age = 29±3wk.; birth weight = 1160±273 g) underwent two 8 -h hypoxic/altitude exposures in a cross-over manner: 1) Normobaric hypoxic exposure (NH; FIO2 = 0.142±0.001; PIO2 = 90.6±0.9 mmHg) 2) Hypobaric hypoxic exposure (HH; terrestrial high-altitude 3840 m; PIO2 = 90.2±0.5 mmHg). Interstitial lung water was assessed via quantification of B-Lines (using lung ultrasound) before (normoxia) and after 4-h and 8-h of respective exposures. At each time point, B-Lines were quantified before (Pre) and immediately after (Post) a 6-min moderate-intensity exercise.
The baseline B-lines count were comparable between both conditions (P = 0.191). A higher B-lines count was noted at Pre-H4 in HH versus NH (P = 0.0420). At Post-H8 B-lines score was significantly higher in HH (4.6 ± 1.6) than in NH (3.1 ± 1.4; P = 0.0073). Furthermore, at this time point, a significantly higher number of individuals with B-line scores ≥5 was observed in HH (n = 7) than in NH (n = 3; P = 0.0420).
These findings suggest that short moderate-intensity exercise provokes a significant increase in the interstitial lung water accumulation after 8 h of exposure to terrestrial but not simulated altitude (≈3840 m) in prematurely born adults. Further work is needed to elucidate the exact mechanisms of (moderate-intensity) exercise-induced interstitial lung water accumulation in this population and directly compare the obtained data to full-term born adults.
Key points
High altitude‐induced hypoxia in humans evokes a pattern of breathing known as periodic breathing (PB), in which the regular oscillations corresponding to rhythmic expiration and ...inspiration are modulated by slow periodic oscillations.
The phase coherence between instantaneous heart rate and respiration is shown to increase significantly at the frequency of periodic breathing during acute and sustained normobaric and hypobaric hypoxia.
It is also shown that polymorphism in specific genes, NOTCH4 and CAT, is significantly correlated with this coherence, and thus with the incidence of PB.
Differences in phase shifts between blood flow signals and respiratory and PB oscillations clearly demonstrate contrasting origins of the mechanisms underlying normal respiration and PB.
These novel findings provide a better understanding of both the genetic and the physiological mechanisms responsible for respiratory control during hypoxia at altitude, by linking genetic factors with cardiovascular dynamics, as evaluated by phase coherence.
Periodic breathing (PB) occurs in most humans at high altitudes and is characterised by low‐frequency periodic alternation between hyperventilation and apnoea. In hypoxia‐induced PB the dynamics and coherence between heart rate and respiration and their relationship to underlying genetic factors is still poorly understood. The aim of this study was to investigate, through novel usage of time–frequency analysis methods, the dynamics of hypoxia‐induced PB in healthy individuals genotyped for a selection of antioxidative and neurodevelopmental genes. Breathing, ECG and microvascular blood flow were simultaneously monitored for 30 min in 22 healthy males. The same measurements were repeated under normoxic and hypoxic (normobaric (NH) and hypobaric (HH)) conditions, at real and simulated altitudes of up to 3800 m. Wavelet phase coherence and phase difference around the frequency of breathing (approximately 0.3 Hz) and around the frequency of PB (approximately 0.06 Hz) were evaluated. Subjects were genotyped for common functional polymorphisms in antioxidative and neurodevelopmental genes. During hypoxia, PB resulted in increased cardiorespiratory coherence at the PB frequency. This coherence was significantly higher in subjects with NOTCH4 polymorphism, and significantly lower in those with CAT polymorphism (HH only). Study of the phase shifts clearly indicates that the physiological mechanism of PB is different from that of the normal respiratory cycle. The results illustrate the power of time‐evolving oscillatory analysis content in obtaining important insight into high altitude physiology. In particular, it provides further evidence for a genetic predisposition to PB and may partly explain the heterogeneity in the hypoxic response.
Key points
High altitude‐induced hypoxia in humans evokes a pattern of breathing known as periodic breathing (PB), in which the regular oscillations corresponding to rhythmic expiration and inspiration are modulated by slow periodic oscillations.
The phase coherence between instantaneous heart rate and respiration is shown to increase significantly at the frequency of periodic breathing during acute and sustained normobaric and hypobaric hypoxia.
It is also shown that polymorphism in specific genes, NOTCH4 and CAT, is significantly correlated with this coherence, and thus with the incidence of PB.
Differences in phase shifts between blood flow signals and respiratory and PB oscillations clearly demonstrate contrasting origins of the mechanisms underlying normal respiration and PB.
These novel findings provide a better understanding of both the genetic and the physiological mechanisms responsible for respiratory control during hypoxia at altitude, by linking genetic factors with cardiovascular dynamics, as evaluated by phase coherence.
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