Evidence that a central governor regulates exercise performance during acute hypoxia and hyperoxia

2001 ◽  
Vol 204 (18) ◽  
pp. 3225-3234 ◽  
Author(s):  
Timothy D. Noakes ◽  
Juha E. Peltonen ◽  
Heikki K. Rusko
Keyword(s):  
Skeletal Muscle ◽  
Exercise Performance ◽  
Chronic Hypoxia ◽  
Maximal Exercise ◽  
Cardiovascular Function ◽  
Arterial Oxygen ◽  
Peripheral Fatigue ◽  
Electromyographic Activity ◽  
Cardiorespiratory Function ◽  
Sensitive Organ

SUMMARY An enduring hypothesis in exercise physiology holds that a limiting cardiorespiratory function determines maximal exercise performance as a result of specific metabolic changes in the exercising skeletal muscle, so-called peripheral fatigue. The origins of this classical hypothesis can be traced to work undertaken by Nobel Laureate A. V. Hill and his colleagues in London between 1923 and 1925. According to their classical model, peripheral fatigue occurs only after the onset of heart fatigue or failure. Thus, correctly interpreted, the Hill hypothesis predicts that it is the heart, not the skeletal muscle, that is at risk of anaerobiosis or ischaemia during maximal exercise. To prevent myocardial damage during maximal exercise, Hill proposed the existence of a ‘governor’ in either the heart or brain to limit heart work when myocardial ischaemia developed. Cardiorespiratory function during maximal exercise at different altitudes or at different oxygen fractions of inspired air provides a definitive test for the presence of a governor and its function. If skeletal muscle anaerobiosis is the protected variable then, under conditions in which arterial oxygen content is reduced, maximal exercise should terminate with peak cardiovascular function to ensure maximum delivery of oxygen to the active muscle. In contrast, if the function of the heart or some other oxygen-sensitive organ is to be protected, then peak cardiovascular function will be higher during hyperoxia and reduced during hypoxia compared with normoxia. This paper reviews the evidence that peak cardiovascular function is reduced during maximal exercise in both acute and chronic hypoxia with no evidence for any primary alterations in myocardial function. Since peak skeletal muscle electromyographic activity is also reduced during hypoxia, these data support a model in which a central, neural governor constrains the cardiac output by regulating the mass of skeletal muscle that can be activated during maximal exercise in both acute and chronic hypoxia.

scholarly journals Skeletal muscle bioenergetics during all-out exercise: mechanistic insight into the oxygen uptake slow component and neuromuscular fatigue

2017 ◽  
Vol 122 (5) ◽  
pp. 1208-1217 ◽  
Author(s):  
Ryan M. Broxterman ◽  
Gwenael Layec ◽  
Thomas J. Hureau ◽  
Markus Amann ◽  
Russell S. Richardson
Keyword(s):  
Skeletal Muscle ◽  
Oxygen Uptake ◽  
Exercise Performance ◽  
Slow Component ◽  
Force Production ◽  
Atp Synthesis ◽  
Peripheral Fatigue ◽  
Synthesis Rate ◽  
Physiological Mechanisms ◽  
Exercise Induced

Although all-out exercise protocols are commonly used, the physiological mechanisms underlying all-out exercise performance are still unclear, and an in-depth assessment of skeletal muscle bioenergetics is lacking. Therefore, phosphorus magnetic resonance spectroscopy (31P-MRS) was utilized to assess skeletal muscle bioenergetics during a 5-min all-out intermittent isometric knee-extensor protocol in eight healthy men. Metabolic perturbation, adenosine triphosphate (ATP) synthesis rates, ATP cost of contraction, and mitochondrial capacity were determined from intramuscular concentrations of phosphocreatine (PCr), inorganic phosphate (Pi), diprotonated phosphate ([Formula: see text]), and pH. Peripheral fatigue was determined by exercise-induced alterations in potentiated quadriceps twitch force (Qtw) evoked by supramaximal electrical femoral nerve stimulation. The oxidative ATP synthesis rate (ATPOX) attained and then maintained peak values throughout the protocol, despite an ~63% decrease in quadriceps maximal force production. ThusATPOX normalized to force production (ATPOX gain) significantly increased throughout the exercise (1st min: 0.02 ± 0.01, 5th min: 0.04 ± 0.01 mM·min−1·N−1), as did the ATP cost of contraction (1st min: 0.048 ± 0.019, 5th min: 0.052 ± 0.015 mM·min−1·N−1). Additionally, the pre- to postexercise change in Qtw (−52 ± 26%) was significantly correlated with the exercise-induced change in intramuscular pH ( r = 0.75) and [Formula: see text] concentration ( r = 0.77). In conclusion, the all-out exercise protocol utilized in the present study elicited a “slow component-like” increase in intramuscular ATPOX gain as well as a progressive increase in the phosphate cost of contraction. Furthermore, the development of peripheral fatigue was closely related to the perturbation of specific fatigue-inducing intramuscular factors (i.e., pH and [Formula: see text] concentration). NEW & NOTEWORTHY The physiological mechanisms and skeletal muscle bioenergetics underlying all-out exercise performance are unclear. This study revealed an increase in oxidative ATP synthesis rate gain and the ATP cost of contraction during all-out exercise. Furthermore, peripheral fatigue was related to the perturbation in pH and deprotonated phosphate ion. These findings support the concept that the oxygen uptake slow component arises from within active skeletal muscle and that skeletal muscle force generating capacity is linked to the intramuscular metabolic milieu.

scholarly journals Effects of Acute Exposure to Thermal Stress on Cardiorespiratory Function, Skeletal Muscle Oxygenation, and Exercise Performance in Healthy Males

2021 ◽  
Vol 18 (14) ◽  
pp. 7404
Author(s):  
Won-Sang Jung ◽  
Sung-Woo Kim ◽  
Hun-Young Park ◽  
Jisu Kim ◽  
Kiwon Lim
Keyword(s):  
Skeletal Muscle ◽  
Thermal Stress ◽  
Body Temperature ◽  
Exercise Performance ◽  
Muscle Oxygenation ◽  
Environmental Condition ◽  
Oxygen Pulse ◽  
Cardiorespiratory Function ◽  
Skeletal Muscle Oxygenation ◽  
Lactate Levels

We investigated the effects of acute thermal stress (30 °C and 40 °C) and ordinary temperature (20 °C) on cardiorespiratory function, skeletal muscle oxygenation, and exercise performance in healthy men. Eleven healthy males (21.5 ± 2.3 years) performed a graded exercise test (GXT) using a cycle ergometer in each environmental condition (20 °C, 30 °C, and 40 °C) in a random order with an interval of 1 week between each test. Before the test, they were allowed to rest for 30 min in a given environmental condition. All dependent variables (body temperature, cardiorespiratory function parameters, skeletal muscle oxygenation profiles, and exercise performance) were measured at rest and during GXT. GXT was started at 50 W and increased by 25 W every 2 min until subjects were exhausted. Body temperature increased proportionally at rest and at the end of exercise as thermal stress increased. There were no differences in the rating of perceived exertion, oxygen uptake, respiratory exchange ratio, and carbon dioxide excretion between environmental conditions. Heart rate (HR), minute ventilation (VE), and blood lactate levels were significantly higher at 30 °C and 40 °C than at 20 °C, and oxygen pulse was significantly lower at 40 °C than at 20 °C at various exercise loads. None of the skeletal muscle oxygenation profiles showed significant changes at rest or during exercise. Maximal oxygen uptake, peak power, and exercise time significantly decreased proportionally as thermal stress increased, and this decrease was most pronounced at 40 °C. Acute thermal stress induces a decrease in exercise performance via increased body temperature, HR, VE, and blood lactate levels and decreased oxygen pulse during load-homogenized exercise. This phenomenon was more prominent at 40 °C than at 30 °C and 20 °C.

Maximal Exercise Performance in Chronic Hypoxia and Acute Normoxia in High-Altitude Natives

1994 ◽  
Vol 87 (s1) ◽  
pp. 46-47
Author(s):  
R Favier ◽  
H Spielvogel ◽  
D Desplanches ◽  
G Ferretti ◽  
B Kayser ◽  
...  
Keyword(s):  
High Altitude ◽  
Exercise Performance ◽  
Chronic Hypoxia ◽  
Maximal Exercise ◽  
High Altitude Natives

Improvements in exercise performance with high-intensity interval training coincide with an increase in skeletal muscle mitochondrial content and function

2013 ◽  
Vol 115 (6) ◽  
pp. 785-793 ◽  
Author(s):  
Robert Acton Jacobs ◽  
Daniela Flück ◽  
Thomas Christian Bonne ◽  
Simon Bürgi ◽  
Peter Møller Christensen ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Exercise Capacity ◽  
Exercise Performance ◽  
High Intensity ◽  
Interval Training ◽  
Peripheral Fatigue ◽  
High Intensity Interval Training ◽  
Mitochondrial Content ◽  
Respiratory Capacity ◽  
High Intensity Interval

Six sessions of high-intensity interval training (HIT) are sufficient to improve exercise capacity. The mechanisms explaining such improvements are unclear. Accordingly, the aim of this study was to perform a comprehensive evaluation of physiologically relevant adaptations occurring after six sessions of HIT to determine the mechanisms explaining improvements in exercise performance. Sixteen untrained (43 ± 6 ml·kg−1·min−1) subjects completed six sessions of repeated ( 8 – 12 ) 60 s intervals of high-intensity cycling (100% peak power output elicited during incremental maximal exercise test) intermixed with 75 s of recovery cycling at a low intensity (30 W) over a 2-wk period. Potential training-induced alterations in skeletal muscle respiratory capacity, mitochondrial content, skeletal muscle oxygenation, cardiac capacity, blood volumes, and peripheral fatigue resistance were all assessed prior to and again following training. Maximal measures of oxygen uptake (V̇o2peak; ∼8%; P = 0.026) and cycling time to complete a set amount of work (∼5%; P = 0.008) improved. Skeletal muscle respiratory capacities increased, most likely as a result of an expansion of skeletal muscle mitochondria (∼20%, P = 0.026), as assessed by cytochrome c oxidase activity. Skeletal muscle deoxygenation also increased while maximal cardiac output, total hemoglobin, plasma volume, total blood volume, and relative measures of peripheral fatigue resistance were all unaltered with training. These results suggest that increases in mitochondrial content following six HIT sessions may facilitate improvements in respiratory capacity and oxygen extraction, and ultimately are responsible for the improvements in maximal whole body exercise capacity and endurance performance in previously untrained individuals.

Effects of Helium and 40% O2 on Graded Exercise With Self-Contained Breathing Apparatus

2003 ◽  
Vol 28 (6) ◽  
pp. 910-926 ◽  
Author(s):  
Neil D. Eves ◽  
Stewart R. Petersen ◽  
Richard L. Jones
Keyword(s):  
Exercise Performance ◽  
Maximal Exercise ◽  
Ventilatory Threshold ◽  
Arterial Oxygen ◽  
Peak Exercise ◽  
Helium Mixtures ◽  
Breathing Resistance ◽  
Breathing Apparatus ◽  
Graded Exercise ◽  
Ventilatory Limitation

Maximal exercise performance is decreased when breathing from a self-contained breathing apparatus (SCBA), owing to a ventilatory limitation imposed by the increased expiratory resistance. To test the hypothesis that decreasing the density of the breathing gas would improve maximal exercise performance, we studied 15 men during four graded exercise tests with the SCBA. Participants breathed a different gas mixture during each test: normoxia (NOX; 21% O2, 79% N2), hyperoxia (HOX; 40% O2, 60% N2), normoxic helium (HE-OX; 21% O2, 79% He), and hyperoxic helium (HE-HOX; 40% O2, 60% He). Compared to NOX, power output at the ventilatory threshold and at maximal exercise significantly increased with both hyperoxic mixtures. Minute ventilation was increased at peak exercise with both helium mixtures, and maximal aerobic power ([Formula: see text]) was significantly increased by 12.9 ± 5.6%, 10.2 ± 6.3%, and 21.8 ± 5.6% with HOX, HE-OX, and HE-HOX, respectively. At peak exercise, the expired breathing resistance imposed by the SCBA was significantly decreased with both helium mixtures, and perceived respiratory distress was lower with HE-HOX. The results show that HE-OX improved maximal exercise performance by minimizing the ventilation limitation. The performance-enhancing effect of HOX may be explained by increased arterial oxygen content. Moreover, HE-HOX appeared to combine the effects of helium and hyperoxia on [Formula: see text]Key words:[Formula: see text] breathing resistance, ventilatory limitation, heliox, firefighting

scholarly journals Skeletal muscle mass and exercise performance in stable ambulatory patients with heart failure

1997 ◽  
Vol 82 (1) ◽  
pp. 257-261 ◽  
Author(s):  
Chim C. Lang ◽  
Don B. Chomsky ◽  
Glenn Rayos ◽  
T. K. Yeoh ◽  
John R. Wilson
Keyword(s):  
Heart Failure ◽  
Skeletal Muscle ◽  
Muscle Mass ◽  
Exercise Performance ◽  
Skeletal Muscle Mass ◽  
Maximal Exercise ◽  
Skeletal Muscle Atrophy ◽  
Patients With Heart Failure ◽  
Ambulatory Patients ◽  
Maximal Exercise Capacity

Lang, Chim C., Don B. Chomsky, Glenn Rayos, T. K. Yeoh, and John R. Wilson. Skeletal muscle mass and exercise performance in stable ambulatory patients with heart failure. J. Appl. Physiol. 82(1): 257–261, 1997.—The purpose of this study was to determine whether skeletal muscle atrophy limits the maximal exercise capacity of stable ambulatory patients with heart failure. Body composition and maximal exercise capacity were measured in 100 stable ambulatory patients with heart failure. Body composition was assessed by using dual-energy X-ray absorption. Peak exercise oxygen consumption (V˙o 2 peak) and the anaerobic threshold were measured by using a Naughton treadmill protocol and a Medical Graphics CardioO2 System.V˙o 2 peak averaged 13.4 ± 3.3 ml ⋅ min−1 ⋅ kg−1or 43 ± 12% of normal. Lean body mass averaged 52.9 ± 10.5 kg and leg lean mass 16.5 ± 3.6 kg. Leg lean mass correlated linearly with V˙o 2 peak( r= 0.68, P < 0.01), suggesting that exercise performance is influenced by skeletal muscle mass. However, lean body mass was comparable to levels noted in 1,584 normal control subjects, suggesting no decrease in muscle mass. Leg muscle mass was comparable to levels noted in 34 normal control subjects, further supporting this conclusion. These findings suggest that exercise intolerance in stable ambulatory patients with heart failure is not due to skeletal muscle atrophy.

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