Inverted exercise Flashcards
(16 cards)
VO₂ max is the key limiter of exercise and is limited predominantly by the ability of the cardiorespiratory system; Hill’s subjects, even during severe exercise, never showed signs of cyanosis, predicting oxygen content of the blood never significantly decreases during exercise, therefore the pulmonary system doesn’t significantly limit exercise capacity.
Hill et al (1923-24)
Early conclusion about exercise limitation
20 healthy male volunteers divided into trained (mean VO₂ max 56.5 ml·kg⁻¹·min⁻¹) and highly trained (mean VO₂ max 70.1 ml·kg⁻¹·min⁻¹) groups performed incremental cycle tests in normoxia and hyperoxia (26% O₂).
(Order randomised and subejcts naive)
Hyperoxia significnatly increased mean SaO2 during maximal exercise in both groups but only increased VO2 max in the highly trained group.
Suggests that gas exchange may limit VO2 max in highly trained athletes with reductions in SaO2 at sea level.
Limitations: subjects had to breathe throw a low resistance valve for testing, not quite the same as just breathing normally
Powers et al (1989)
Pulmonary limitation in athletes
Review of 15–20 double‐blind, placebo‐controlled blood‐doping studies showing reinfusion of 900–1,350 mL blood elevates O₂‐carrying capacity and increases VO₂ max by 4–9% in treated subjects, with no change in sham‐treated controls.
Likely to be biased though towards highly trained individuals taking part in blood doping to improve performance in endurance events. These individausl do have capacity to increase theri VO2 max if oxygen saturation of the blood increases.
Gledhill et al (1982)
Effects of blood doping
Study of COPD patients showing ~30% identify muscle effort/fatigue as their limiting factor during exercise; responses vary widely and are difficult to predict from resting measures, reflecting defective interactions between metabolic demand, breathing control, and V/Q matching.
Smith et al (1991)
Exercise limitation in disease
Used electrocardiography in trained vs. untrained subjects to show trained individuals have lower HR at fixed submaximal workloads, implying higher stroke volume and that cardiac output limits VO₂ max.
Electrocardiography only rcdently developed at the time
Christensen (1930)
Demonstrated that isolated small‐muscle exercise achieves higher oxygen uptake than whole‐body exercise, highlighting that muscle O₂ utilization capacity can exceed cardiac delivery during whole‐body activity.
Limitations: during small-muscle group exericse, systemic blood flow is disproportionately diverted to the active region, bypassing the usual distribution challenges seen in whole-body activity; no functional outcome (fatigue, endurance, performance) was tested
Saltin et al (1985)
Evidence for CO being a limiting factor
Examined the effects of one-legged cycle training on the increase in VO2 max in a trained leg, a control leg, and a 2-legged bicycling.
It was found that the trained leg had a 23% increase in VO2 max, compared with a 7% increase in VO2 max in the control leg, suggesting that peripheral adaptations occurred in the trained skeletal muscle.
The study was correct in demonstrating the occurrence of local muscle adaptations but incorrect in assuming tehse are the dominant factor limiting VO2 max because you can’t extrapolate limb-specific VO2 max improvements to whole-body capacity.
Saltin et al (1976)
Role of local muscle adaptations
15 pigs split into 3 groups with 3 diffrent protocols (see image).
Pericardiectomy led to a 10% increase in LV and diastolic dimension, ~33% increase in EDV and 18% increase in LV mass.
This was associated with a 29% increase in maximal CO, and a 31% increase in VO2 max.
Suggests that in a healthy individual, the pericardium limits the heart from stretching to max size, thsu limitng max CO that could be generated according to Starling’s law.
Hammond et al (1992)
Relationship between heart size and VO2 max
Skeletal muscle biopsies in chronic heart failure patients revealed muscle atrophy and reduced aerobic enzyme activity, linking reduced skeletal muscle oxidative capacity to exercise intolerance.
Sullivan et al (1990)
Exercise limitation in heart failure
Showed reduced citrate synthase activity in leg muscles of heart failure patients correlates with higher femoral venous lactate during exercise, indicating impaired aerobic metabolism contributes to early fatigue.
Sullivan et al (1995)
Exercise limitation in heart failure
16 healthy males received recombinant human erythropoietin (rHuEpo) or placebo; rHuEpo group saw VO₂ max increase by ~9% at 4 weeks and ~8% at 11 weeks, and time-to-exhaustion at 80% VO₂ max improved by ~54%, demonstrating EPO’s impact on endurance performance.
However, when tested at the same relative intensity, TTE was 27% lower at week 11 than before treatment.
Lactate concentrations were lower during submaximal efforts post treatment suggesting improved metabolic efficiency
Shows that EPO substantially improves endurance capacity especially submaximal performance, beyond what is rpedicted from VO2 max increases alone.
TTE is subjective and other factors can influence when sujects “give up”.
Not double-blinded; small sample size; not tested in elite athletes (the group that usually would use Epo doping)
Thomsen et al (2007)
Effect of exogenous EPO
Double-blind study to assess the effects of autologous erythrocyte reinfusion on thermoregulation and blood volume during exercise in the heat.
In unacclimated men, reinfusion of 600 mL of a NaCl-glucose-phosphate solution containing 50% haematocrit led to an 11% increase in erythrocyte volume and VO₂max, without increasing total blood volume due to a compensatory reduction in plasma volume.
While polycythaemia did not significantly alter key plasma parameters or fluid shifts during exercise, it tended to reduce heat storage, suggesting improved thermoregulatory efficiency.
Sawka et al (1987)
Improving thermoregulation
Adjusted haematocrit in 8 males via withdrawal/reinfusion to 5 target values; VO₂ max and TTE at submaximal workload increased up to 50–55% Hct, then declined at higher levels, demonstrating an inverted-U relationship between Hct and performance.
Schlumpf et al (2010)
Optimal haematocrit
Isolated muscle model
The greatest resistance to oxygen diffusion occurs between the RBC surface and the sarcolemma; the PO2 drops sharply, making this region the rate-limiting step in oxygen delivery
As VO2 increases, PO2 inside the cell drops below 5 torr which is lower than myoglobin’s P50
Low PO2 maintains a strong diffusion gradient and increases the fraction of myoglobin that gives up oxygen to mitochondria
Such findings may not be applicabel to whole-body exercise in intact human systems
Honig et al (1992)
Oxygen diffusion limitations
Mitochondrial respiratory capacity measured in vitro ~5.8 mL O2mL-1 mitochondria min-1 exceeds the maximal in vivo O2 delivery ~4-5 mL O2 ml-1 mitochondria min-1 demonstrating that under normal whole-body exercise the limit is set by O2 delivery, not mitochondrial capacity.
Harvested skeletal muscle from running dogs and/or human biopsies and isolated mitochondria by differential centrifugation.
Using a Clark-type oxygen electrode at 37ºC, they measured ADP-stimulated respiration with saturating substrates and found max O2 flux rates on the order of 5-6 mL O2 per mL of mitochondrial volume per min
The same animals (or a matched cohort) performed graded treadmill running to exhaustion while pulmonary (humans) or direct limb (dogs) O2 consumption was recorded. These ranged around 3.5-4.5mL O2 per mL muscle mitochondria per minute once they had been normalised whole-body VO2 max back to mitochondrial volume in the working muscle (which had been assessed by electron microscopy). The mitochondria’s ability to consume O2 is greater than what is permitted by delivery of O2 to the mitochondria via the cardiorespiratory system so mitochondrial metabolism does not normally limit exercise capacity
Taylor, Wiebel and Hoppeler (1991)
Mitochondria in exercise limitation
Age-related decreases in exercise efficiency and an increase in the O2 cost of exercise are reversed with exercise training.
Exercise efficiency improves to a greater degree in the elederly than in the young.
O2 consumption was adjusted for weight not for fat-free mass, which may have allowed a more accurate comparison between older and younger subjects of varying weight and body composition; direct measurement of stroke volume or cardiac output, as well as biochemical or muscle biopsy data, would be helpful to delineate the relative contribution of central vs peripheral factors; didn’t have data from subjects aged 30 to 65 so don’t know when the changes occur
Woo et al 2006
Changes to exercising with age
