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1.
AbstractTo determine whether developmental nicotine exposure (DNE) alters the ventilatory and metabolic response to hyperthermia in neonatal rats (postnatal age 2–4 days), pregnant dams were exposed to nicotine (6 mg kg−1 of nicotine tartrate daily) or saline with an osmotic mini‐pump implanted subdermally on day 5 of gestation. Rat pups (a total of 72 controls and 72 DNE pups) were studied under thermoneutral conditions (chamber temperature 33°C) and during moderate thermal stress (37.5°C). In all pups, core temperature was similar to chamber temperature, with no treatment effects. The rates of pulmonary ventilation (V˙I), O2 consumption (V˙O2) and CO2 production (V˙CO2) did not change with hyperthermia in either control or DNE pups. However, V˙I was lower in DNE pups at both chamber temperatures, whereas the duration of spontaneous apnoeas was longer in DNE pups than in controls at 33°C. The V˙I/V˙O2ratio increased at 37.5°C in control pups, although it did not change in DNE pups. To simulate severe thermal stress, additional pups were studied at 33°C and 43°C. V˙I increased with heating in control pups but not in DNE pups. As heat stress continued, gasping was evoked in both groups, with no effect of DNE on the gasping pattern. Over a 20 min recovery period at 33°C, V˙I returned to baseline in control pups but remained depressed in DNE pups. In addition to altering baseline V˙I and apnoea duration, DNE is associated with subtle but significant alterations in the ventilatory response to hyperthermia in neonatal rats.

Abbreviations

DNE
developmental nicotine exposure
P
postnatal day
RER
respiratory exchange ratio
Tchamber
chamber temperature
Tcore
core temperature
V˙I
pulmonary ventilation rate
V˙O2
oxygen consumption rate
V˙CO2
carbon dioxide production rate
VT
tidal volume
  相似文献   

2.

Key points

  • Severe acute hypoxia reduces sprint performance.
  • Muscle V˙O2 during sprint exercise in normoxia is not limited by O2 delivery, O2 offloading from haemoglobin or structure‐dependent diffusion constraints in the skeletal muscle of young healthy men.
  • A large functional reserve in muscle O2 diffusing capacity exists and remains available at exhaustion during exercise in normoxia; this functional reserve is recruited during exercise in hypoxia.
  • During whole‐body incremental exercise to exhaustion in severe hypoxia, leg V˙O2 is primarily dependent on convective O2 delivery and less limited by diffusion constraints than previously thought.
  • The kinetics of O2 offloading from haemoglobin does not limit V˙O2 peak in hypoxia.
  • Our results indicate that the limitation to V˙O2 during short sprints resides in mechanisms regulating mitochondrial respiration.

Abstract

To determine the contribution of convective and diffusive limitations to V˙O2 peak during exercise in humans, oxygen transport and haemodynamics were measured in 11 men (22 ± 2 years) during incremental (IE) and 30 s all‐out cycling sprints (Wingate test, WgT), in normoxia (Nx, PIO2: 143 mmHg) and hypoxia (Hyp, PIO2: 73 mmHg). Carboxyhaemoglobin (COHb) was increased to 6–7% before both WgTs to left‐shift the oxyhaemoglobin dissociation curve. Leg V˙O2 was measured by the Fick method and leg blood flow (BF) with thermodilution, and muscle O2 diffusing capacity (DMO2) was calculated. In the WgT mean power output, leg BF, leg O2 delivery and leg V˙O2 were 7, 5, 28 and 23% lower in Hyp than Nx (P < 0.05); however, peak WgT DMO2 was higher in Hyp (51.5 ± 9.7) than Nx (20.5 ± 3.0 ml min−1 mmHg−1, P < 0.05). Despite a similar PaO2 (33.3 ± 2.4 and 34.1 ± 3.3 mmHg), mean capillary PO2 (16.7 ± 1.2 and 17.1 ± 1.6 mmHg), and peak perfusion during IE and WgT in Hyp, DMO2 and leg V˙O2 were 12 and 14% higher, respectively, during WgT than IE in Hyp (both P < 0.05). DMO2 was insensitive to COHb (COHb: 0.7 vs. 7%, in IE Hyp and WgT Hyp). At exhaustion, the Y equilibration index was well above 1.0 in both conditions, reflecting greater convective than diffusive limitation to the O2 transfer in both Nx and Hyp. In conclusion, muscle V˙O2 during sprint exercise is not limited by O2 delivery, O2 offloading from haemoglobin or structure‐dependent diffusion constraints in the skeletal muscle. These findings reveal a remarkable functional reserve in muscle O2 diffusing capacity.

Abbreviations

a‐vO2diff
arteriovenous oxygen concentration difference
BF
blood flow
CaO2
arterial content of oxygen
CO
carbon monoxide
COHb
carboxyhaemoglobin
DLO2
lung O2 diffusing capacity
DMO2
muscle O2 diffusing capacity
DO2
O2 diffusing capacity
ECG
electrocardiogram
FIO2
inspired oxygen fraction
FV
femoral vein
HRmax
maximal heart rate
HRpeak
peak heart rate during Wingate
Hyp
hypoxia
LBF
leg blood flow
Nx
normoxia
SO2
haemoglobin saturation with O2
ODC
oxyhaemoglobin dissociation curve
P50
partial oxygen pressure at 50% SO2
PaO2
arterial oxygen pressure
PCO2
carbon dioxide pressure
PO2
oxygen pressure
PO2 cap
capillary O2 pressure
PO2 mit
mitochondrial O2 pressure
P FV O2
femoral vein PO2
PIO2
inspiratory O2 pressure
V˙CO2
carbon dioxide production
V˙CO2 peak
peak carbon dioxide production
V˙ Epeak
peak pulmonary ventilation
V˙O2
oxygen consumption
V˙O2 max
maximal oxygen consumption
V˙O2 peak
peak oxygen uptake
Wpeak‐i
instantaneous peak power output
Wmean‐10
mean power output during the first 10 s of the sprint exercise
Wmean‐30
mean power output during the whole sprint exercise
WgT
isokinetic 30 s Wingate test
  相似文献   

3.

Key points

  • The concept of symmorphosis predicts that the capacity of each step of the oxygen cascade is attuned to the task demanded of it during aerobic exercise at maximal rates of oxygen consumption (V˙O2 max ) such that no single process is limiting or in excess at V˙O2 max .
  • The present study challenges the applicability of this concept to humans by revealing clear, albeit very different, limitations and excesses in oxygen supply and consumption among untrained and endurance‐trained humans.
  • Among untrained individuals, V˙O2 max is limited by the capacity of the mitochondria to consume oxygen, despite an excess of oxygen supply, whereas, among trained individuals, V˙O2 max is limited by the supply of oxygen to the mitochondria, despite an excess of mitochondrial respiratory capacity.

Abstract

The concept of symmorphosis postulates a matching of structural capacity to functional demand within a defined physiological system, regardless of endurance exercise training status. Whether this concept applies to oxygen (O2) supply and demand during maximal skeletal muscle O2 consumption (V˙O2 max ) in humans is unclear. Therefore, in vitro skeletal muscle mitochondrial V˙O2 max (Mito V˙O2 max , mitochondrial respiration of fibres biopsied from vastus lateralis) was compared with in vivo skeletal muscle V˙O2 max during single leg knee extensor exercise (KE V˙O2 max , direct Fick by femoral arterial and venous blood samples and Doppler ultrasound blood flow measurements) and whole‐body V˙O2 max during cycling (Body V˙O2 max , indirect calorimetry) in 10 endurance exercise‐trained and 10 untrained young males. In untrained subjects, during KE exercise, maximal O2 supply (KE Q˙O2max) exceeded (462 ± 37 ml kg−1 min−1, P < 0.05) and KE V˙O2 max matched (340 ± 22 ml kg−1 min−1, P > 0.05) Mito V˙O2 max (364 ± 16 ml kg−1 min−1). Conversely, in trained subjects, both KE Q˙O2max (557 ± 35 ml kg−1 min−1) and KE V˙O2 max (458 ± 24 ml kg−1 min−1) fell far short of Mito V˙O2 max (743 ± 35 ml kg−1 min−1, P < 0.05). Although Mito V˙O2 max was related to KE V˙O2 max (r = 0.69, P < 0.05) and Body V˙O2 max (r = 0.91, P < 0.05) in untrained subjects, these variables were entirely unrelated in trained subjects. Therefore, in untrained subjects, V˙O2 max is limited by mitochondrial O2 demand, with evidence of adequate O2 supply, whereas, in trained subjects, an exercise training‐induced mitochondrial reserve results in skeletal muscle V˙O2 max being markedly limited by O2 supply. Taken together, these in vivo and in vitro measures reveal clearly differing limitations and excesses at V˙O2 max in untrained and trained humans and challenge the concept of symmorphosis as it applies to O2 supply and demand in humans.  相似文献   

4.

Key points

  • Patent foramen ovale (PFO) is present in ∼35% of the general population.
  • The respiratory system participates in thermoregulation via evaporative and convective heat loss so blood flow that bypasses the respiratory system, e.g. through a PFO, may not participate in respiratory system cooling.
  • We found that subjects with a PFO (PFO+) had a ∼0.4°C higher oesophageal temperature (T oesoph) than subjects without a PFO (PFO−) during pre‐exercise and exercise.
  • T oesoph in PFO+ subjects was associated with the estimated size of the PFO whereby subjects with a large PFO had a greater T oesoph than PFO− subjects and subjects with a small PFO.
  • During high intensity exercise breathing cold and dry air, PFO+ subjects achieved a higher T oesoph than PFO– subjects.
  • Absence of respiratory system cooling of shunted blood partially explains the differences in T oesoph between PFO+ and PFO– subjects; other differences in thermoregulatory responses that impact core temperature also likely exist.

Abstract

Respiratory system cooling occurs via convective and evaporative heat loss, so right‐to‐left shunted blood flow through a patent foramen ovale (PFO) would not be cooled. Accordingly, we hypothesized that PFO+ subjects would have a higher core temperature than PFO– subjects due, in part, to absence of respiratory system cooling of the shunted blood and that this effect would be dependent upon the estimated PFO size and inspired air temperature. Subjects were screened for the presence and size of a PFO using saline contrast echocardiography. Thirty well‐matched males (15 PFO−, 8 large PFO+, 7 small PFO+) completed cycle ergometer exercise trials on three separate days. During Trial 1, subjects completed a V˙O2 max test. For Trials 2 and 3, randomized, subjects completed four 2.5 min stages at 25, 50, 75 and 90% of the maximum workload achieved during Trial 1, breathing either ambient air (20.6 ± 1.0°C) or cold air (1.9 ± 3.5°C). PFO+ subjects had a higher oesophageal temperature (T oesoph) (P < 0.05) than PFO− subjects on Trial 1. During exercise breathing cold and dry air, PFO+ subjects achieved a higher T oesoph than PFO− subjects (P < 0.05). Subjects with a large PFO, but not those with a small PFO, had a higher T oesoph than PFO− subjects (P < 0.05) during Trial 1 and increased T oesoph breathing cold and dry air. These data suggest that the presence and size of a PFO are associated with T oesoph in healthy humans but this is explained only partially by absence of respiratory system cooling of shunted blood.

Abbreviations

DLCO
lung diffusion capacity for carbon monoxide
FEF25–75
forced mid‐expiratory flow
FEV1
forced expiratory volume in 1 s
FVC
forced vital capacity
HR
heart rate
PFO
patent foramen ovale
PFO+
subjects with a PFO
PFO−
subjects without a PFO
Q˙C
cardiac output
RER
respiratory exchange ratio
RPEleg discomfort
rate of perceived exertion for legs
RPE dyspnoea
rate of perceived exertion for lungs
SaO2
arterial saturation of oxygen
SpO2
peripheral arterial oxygen saturation
Tair
ambient air temperature
Tcore
core temperature
Toesoph
oesophageal temperature
Texp
expired air temperature
Tinsp
inspired air temperature
TLC
total lung capacity
V˙CO2
carbon dioxide elimination
V˙E
minute ventilation
V˙E/V˙O2
ventilatory equivalent of oxygen
V˙O2
oxygen uptake
Vt
tidal volume
  相似文献   

5.

Key points

  • At the end of an incremental exercise to exhaustion a large functional reserve remains in the muscles to generate power, even at levels far above the power output at which task failure occurs, regardless of the inspiratory O2 pressure during the incremental exercise.
  • Exhaustion (task failure) is not due to lactate accumulation and the associated muscle acidification; neither the aerobic energy pathways nor the glycolysis are blocked at exhaustion.
  • Muscle lactate accumulation may actually facilitate early recovery after exhaustive exercise even under ischaemic conditions.
  • Although the maximal rate of ATP provision is markedly reduced at task failure, the resynthesis capacity remaining exceeds the rate of ATP consumption, indicating that task failure during an incremental exercise to exhaustion depends more on central than peripheral mechanisms.

Abstract

To determine the mechanisms causing task failure during incremental exercise to exhaustion (IE), sprint performance (10 s all‐out isokinetic) and muscle metabolites were measured before (control) and immediately after IE in normoxia (PIO2: 143 mmHg) and hypoxia (PIO2: 73 mmHg) in 22 men (22 ± 3 years). After IE, subjects recovered for either 10 or 60 s, with open circulation or bilateral leg occlusion (300 mmHg) in random order. This was followed by a 10 s sprint with open circulation. Post‐IE peak power output (W peak) was higher than the power output reached at exhaustion during IE (P < 0.05). After 10 and 60 s recovery in normoxia, W peak was reduced by 38 ± 9 and 22 ± 10% without occlusion, and 61 ± 8 and 47 ± 10% with occlusion (P < 0.05). Following 10 s occlusion, W peak was 20% higher in hypoxia than normoxia (P < 0.05), despite similar muscle lactate accumulation ([La]) and phosphocreatine and ATP reduction. Sprint performance and anaerobic ATP resynthesis were greater after 60 s compared with 10 s occlusions, despite the higher [La] and [H+] after 60 s compared with 10 s occlusion recovery (P < 0.05). The mean rate of ATP turnover during the 60 s occlusion was 0.180 ± 0.133 mmol (kg wet wt)−1 s−1, i.e. equivalent to 32% of leg peak O2 uptake (the energy expended by the ion pumps). A greater degree of recovery is achieved, however, without occlusion. In conclusion, during incremental exercise task failure is not due to metabolite accumulation or lack of energy resources. Anaerobic metabolism, despite the accumulation of lactate and H+, facilitates early recovery even in anoxia. This points to central mechanisms as the principal determinants of task failure both in normoxia and hypoxia, with lower peripheral contribution in hypoxia.

Abbreviations

Cr
creatine
d.w.
dry weight
FIO2
inspired oxygen fraction
HR
heart rate
HRpeak
peak heart rate
Hyp
hypoxia
IE
incremental exercise to exhaustion
La
lactate
Mb
myoglobin
Nx
normoxia
PCr
phosphocreatine
P ETC O2
end‐tidal CO2 pressure
P ET O2
end‐tidal O2 pressure
PIO2
partial pressure of inspired O2
RER
respiratory exchange ratio
SpO2
haemoglobin oxygen saturation measured by pulse‐oximetry
TOI
tissue oxygenation index
V˙CO2
CO2 production
V˙CO2 peak
peak CO2 production
V˙E
minute ventilation
V˙O2
O2 consumption
V˙O2 max
maximal O2 uptake
V˙O2 peak
peak O2 uptake
WBIE
whole‐body incremental exercise
Wpeak‐i
instantaneous peak power output
Wpeak‐1
peak power output using 1 s averages
Wmax
peak power output at exhaustion during the incremental exercise test
Wmean
mean power output during the 10 s sprints
w.w.
wet weight
  相似文献   

6.
The 6-minute walk test (6MWT) is a simple field test that is widely used in clinical settings to assess functional exercise capacity. However, studies with healthy subjects are scarce. We hypothesized that the 6MWT might be useful to assess exercise capacity in healthy subjects. The purpose of this study was to evaluate 6MWT intensity in middle-aged and older adults, as well as to develop a simple equation to predict oxygen uptake (V˙O2) from the 6-min walk distance (6MWD). Eighty-six participants, 40 men and 46 women, 40-74 years of age and with a mean body mass index of 28±6 kg/m2, performed the 6MWT according to American Thoracic Society guidelines. Physiological responses were evaluated during the 6MWT using a K4b2 Cosmed telemetry gas analyzer. On a different occasion, the subjects performed ramp protocol cardiopulmonary exercise testing (CPET) on a treadmill. Peak V˙O2 in the 6MWT corresponded to 78±13% of the peak V˙O2 during CPET, and the maximum heart rate corresponded to 80±23% of that obtained in CPET. Peak V˙O2 in CPET was adequately predicted by the 6MWD by a linear regression equation: V˙O2 mL·min-1·kg-1 = -2.863 + (0.0563×6MWDm) (R2=0.76). The 6MWT represents a moderate-to-high intensity activity in middle-aged and older adults and proved to be useful for predicting cardiorespiratory fitness in the present study. Our results suggest that the 6MWT may also be useful in asymptomatic individuals, and its use in walk-based conditioning programs should be encouraged.  相似文献   

7.
The main purpose of this study was to investigate the level of agreement between the gas exchange threshold (GET) and heart rate variability threshold (HRVT) during maximal cardiopulmonary exercise testing (CPET) using three different exercise modalities. A further aim was to establish whether there was a 1:1 relationship between the percentage heart rate reserve (%HRR) and percentage oxygen uptake reserve (%V˙O2 R) at intensities corresponding to GET and HRVT. Sixteen apparently healthy men 17 to 28 years of age performed three maximal CPETs (cycling, walking, and running). Mean heart rate and V˙O2 at GET and HRVT were 16 bpm (P<0.001) and 5.2 mL·kg-1·min-1 (P=0.001) higher in running than cycling, but no significant differences were observed between running and walking, or cycling and walking (P>0.05). There was a strong relationship between GET and HRVT, with R2 ranging from 0.69 to 0.90. A 1:1 relationship between %HRR and %V˙O2 R was not observed at GET and HRVT. The %HRR was higher during cycling (GET mean difference=7%; HRVT mean difference=11%; both P<0.001), walking (GET mean difference=13%; HRVT mean difference=13%; both P<0.001), or running (GET mean difference=11%; HRVT mean difference=10%; both P<0.001). Therefore, using HRVT to prescribe aerobic exercise intensity appears to be valid. However, to assume a 1:1 relationship between %HRR and %V˙O2 R at HRVT would probably result in overestimation of the energy expenditure during the bout of exercise.  相似文献   

8.
This study aimed to verify the association between the contribution of energy systems during an incremental exercise test (IET), pacing, and performance during a 10-km running time trial. Thirteen male recreational runners completed an incremental exercise test on a treadmill to determine the respiratory compensation point (RCP), maximal oxygen uptake (V˙O2max), peak treadmill speed (PTS), and energy systems contribution; and a 10-km running time trial (T10-km) to determine endurance performance. The fractions of the aerobic (WAER) and glycolytic (WGLYCOL) contributions were calculated for each stage based on the oxygen uptake and the oxygen energy equivalents derived by blood lactate accumulation, respectively. Total metabolic demand (WTOTAL) was the sum of these two energy systems. Endurance performance during the T10-km was moderately correlated with RCP, V˙O2maxand PTS (P<@0.05), and moderate-to-highly correlated with WAER, WGLYCOL, and WTOTAL (P<0.05). In addition, WAER, WGLYCOL, and WTOTAL were also significantly correlated with running speed in the middle (P<0.01) and final (P<0.01) sections of the T10-km. These findings suggest that the assessment of energy contribution during IET is potentially useful as an alternative variable in the evaluation of endurance runners, especially because of its relationship with specific parts of a long-distance race.  相似文献   

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17.

Key points

  • Aerobic exercise, such as running, enhances adult hippocampal neurogenesis (AHN) in rodents.
  • Little is known about the effects of high‐intensity interval training (HIT) or of purely anaerobic resistance training on AHN.
  • Here, compared with a sedentary lifestyle, we report a very modest effect of HIT and no effect of resistance training on AHN in adult male rats.
  • We found the most AHN in rats that were selectively bred for an innately high response to aerobic exercise that also run voluntarily and increase maximal running capacity.
  • Our results confirm that sustained aerobic exercise is key in improving AHN.

Abstract

Aerobic exercise, such as running, has positive effects on brain structure and function, such as adult hippocampal neurogenesis (AHN) and learning. Whether high‐intensity interval training (HIT), referring to alternating short bouts of very intense anaerobic exercise with recovery periods, or anaerobic resistance training (RT) has similar effects on AHN is unclear. In addition, individual genetic variation in the overall response to physical exercise is likely to play a part in the effects of exercise on AHN but is less well studied. Recently, we developed polygenic rat models that gain differentially for running capacity in response to aerobic treadmill training. Here, we subjected these low‐response trainer (LRT) and high‐response trainer (HRT) adult male rats to various forms of physical exercise for 6–8 weeks and examined the effects on AHN. Compared with sedentary animals, the highest number of doublecortin‐positive hippocampal cells was observed in HRT rats that ran voluntarily on a running wheel, whereas HIT on the treadmill had a smaller, statistically non‐significant effect on AHN. Adult hippocampal neurogenesis was elevated in both LRT and HRT rats that underwent endurance training on a treadmill compared with those that performed RT by climbing a vertical ladder with weights, despite their significant gain in strength. Furthermore, RT had no effect on proliferation (Ki67), maturation (doublecortin) or survival (bromodeoxyuridine) of new adult‐born hippocampal neurons in adult male Sprague–Dawley rats. Our results suggest that physical exercise promotes AHN most effectively if the exercise is aerobic and sustained, especially when accompanied by a heightened genetic predisposition for response to physical exercise.

Abbreviations

AHN
adult hippocampal neurogenesis
BDNF
brain‐derived neurotrophic factor
BrdU
bromodeoxyuridine
HIT
high‐intensity interval training
HRT
high‐response trainer
LRT
low‐response trainer
RW
running wheel
Sed
sedentary
TBS
Tris‐buffered saline
V˙O2max
maximal oxygen uptake
  相似文献   

18.
19.
This study aimed to analyze the agreement between measurements of unloaded oxygen uptake and peak oxygen uptake based on equations proposed by Wasserman and on real measurements directly obtained with the ergospirometry system. We performed an incremental cardiopulmonary exercise test (CPET), which was applied to two groups of sedentary male subjects: one apparently healthy group (HG, n=12) and the other had stable coronary artery disease (n=16). The mean age in the HG was 47±4 years and that in the coronary artery disease group (CG) was 57±8 years. Both groups performed CPET on a cycle ergometer with a ramp-type protocol at an intensity that was calculated according to the Wasserman equation. In the HG, there was no significant difference between measurements predicted by the formula and real measurements obtained in CPET in the unloaded condition. However, at peak effort, a significant difference was observed between oxygen uptake (V˙O2)peak(predicted)and V˙O2peak(real)(nonparametric Wilcoxon test). In the CG, there was a significant difference of 116.26 mL/min between the predicted values by the formula and the real values obtained in the unloaded condition. A significant difference in peak effort was found, where V˙O2peak(real)was 40% lower than V˙O2peak(predicted)(nonparametric Wilcoxon test). There was no agreement between the real and predicted measurements as analyzed by Lin’s coefficient or the Bland and Altman model. The Wasserman formula does not appear to be appropriate for prediction of functional capacity of volunteers. Therefore, this formula cannot precisely predict the increase in power in incremental CPET on a cycle ergometer.  相似文献   

20.
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