Well , I got quite a few emails concerning my crazy take on the Canadian skater and his respiratory situation.
The majority come all with our " educated" point, that respiration is never a limiting factor and that SpO2 never drops in sport in a healthy athlete. The Main "educated" answer is , that we never reach MMV in any activity in sport.
After over 25 years of discussion this it is time to say : well if that is so so be it.
. Nevertheless I got as of yet no e mail back on the question:
How did you measured the MMV ? So please help.?
For the people still in between the idea that it is never and our idea, that it can be a limiter here a short review .
Exercise-induced respiratory muscle fatigue: implications for performance
1. Lee M. Romer1 and
2. Michael I. Polkey2
+ Author Affiliations
1. 1Centre for Sports Medicine and Human Performance, Brunel University, Uxbridge; and 2Respiratory Muscle Laboratory, Royal Brompton Hospital, and National Heart and Lung Institute, London, United Kingdom
1. Address for reprint requests and other correspondence: L. M. Romer, Centre for Sports Medicine and Human Performance, Brunel Univ., Uxbridge UB8 3PH, United Kingdom (e-mail: email@example.com)
It is commonly held that the respiratory system has ample capacity relative to the demand for maximal O2 and CO2 transport in healthy humans exercising near sea level. However, this situation may not apply during heavy-intensity, sustained exercise where exercise may encroach on the capacity of the respiratory system. Nerve stimulation techniques have provided objective evidence that the diaphragm and abdominal muscles are susceptible to fatigue with heavy, sustained exercise. The fatigue appears to be due to elevated levels of respiratory muscle work combined with an increased competition for blood flow with limb locomotor muscles. When respiratory muscles are prefatigued using voluntary respiratory maneuvers, time to exhaustion during subsequent exercise is decreased. Partially unloading the respiratory muscles during heavy exercise using low-density gas mixtures or mechanical ventilation can prevent exercise-induced diaphragm fatigue and increase exercise time to exhaustion. Collectively, these findings suggest that respiratory muscle fatigue may be involved in limiting exercise tolerance or that other factors, including alterations in the sensation of dyspnea or mechanical load, may be important. The major consequence of respiratory muscle fatigue is an increased sympathetic vasoconstrictor outflow to working skeletal muscle through a respiratory muscle metaboreflex, thereby reducing limb blood flow and increasing the severity of exercise-induced locomotor muscle fatigue. An increase in limb locomotor muscle fatigue may play a pivotal role in determining exercise tolerance through a direct effect on muscle force output and a feedback effect on effort perception, causing reduced motor output to the working limb muscles. Att shows you even more.
And in case it just may be that teh inspriartory muscel ( diaphragm ) may be abel to get tried here from anotehr source:
J Physiol. 1997 Dec 1;505 ( Pt 2):539-48.
Contraction of the human diaphragm during rapid postural adjustments.
Hodges PW, Butler JE, McKenzie DK, Gandevia SC.
Prince of Wales Medical Research Institute, Sydney, Australia.
1. The response of the diaphragm to the postural perturbation produced by rapid flexion of the shoulder to a visual stimulus was evaluated in standing subjects. Gastric, oesophageal and transdiaphragmatic pressures were measured together with intramuscular and oesophageal recordings of electromyographic activity (EMG) in the diaphragm. To assess the mechanics of contraction of the diaphragm, dynamic changes in the length of the diaphragm were measured with ultrasonography. 2. With rapid flexion of the shoulder in response to a visual stimulus, EMG activity in the costal and crural diaphragm occurred about 20 ms prior to the onset of deltoid EMG. This anticipatory contraction occurred irrespective of the phase of respiration in which arm movement began. The onset of diaphragm EMG coincided with that of transversus abdominis. 3. Gastric and transdiaphragmatic pressures increased in association with the rapid arm flexion by 13.8 +/- 1.9 (mean +/- S.E.M.) and 13.5 +/- 1.8 cmH2O, respectively. The increases occurred 49 +/- 4 ms after the onset of diaphragm EMG, but preceded the onset of movement of the limb by 63 +/- 7 ms. 4. Ultrasonographic measurements revealed that the costal diaphragm shortened and then lengthened progressively during the increase in transdiaphragmatic pressure. 5. This study provides definitive evidence that the human diaphragm is involved in the control of postural stability during sudden voluntary movement of the limbs.Or here:
Postural and respiratory functions of the pelvic floor muscles.
Hodges PW, Sapsford R, Pengel LH.
Division of Physiotherapy, the University of Queensland, Brisbane, Queensland, Australia. firstname.lastname@example.org
Due to their contribution to modulation of intra-abdominal pressure (IAP) and stiffness of the sacroiliac joints, the pelvic floor muscles (PFM) have been argued to provide a contribution to control of the lumbar spine and pelvis. Furthermore, as IAP is modulated during respiration this is likely to be accompanied by changes in PFM activity.
In order to evaluate the postural and respiratory function of the PFM, recordings of anal and vaginal electromyographic activity (EMG) were made with surface electrodes during single and repetitive arm movements that challenge the stability of the spine. EMG recordings were also made during respiratory tasks: quiet breathing and breathing with increased dead-space to induce hypercapnoea.
EMG activity of the PFM was increased in advance of deltoid muscle activity as a component of the pre-programmed anticipatory postural activity. This activity was independent of the direction of arm movement. During repetitive movements, PFM EMG was tonic with phasic bursts at the frequency of arm movement. This activity was related to the peak acceleration of the arm, and therefore the amplitude of the reactive forces imposed on the spine. Respiratory activity was observed for the anal and vaginal EMG and was primarily expiratory. When subjects moved the arm repetitively while breathing, PFM EMG was primarily modulated in association with arm movement with little respiratory modulation.
This study provides evidence that the PFM contribute to both postural and respiratory functions.
And here one more about SpO2 and arterial desaturation. ( As well implcation on shift of the O2 diss curve and therefor the utilization of O2 ( bio availablity ) and whith MOXY is a great gadget to get this all together in a n easy way in the field. .
Arterial desaturation during exercise in man: implication for O2 uptake and work capacity.
- The Copenhagen Muscle Research Centre Department of Anaesthesia, Rigshospitalet, University of Copenhagen, Copenhagen, Denmark. email@example.com
Exercise-induced arterial hypoxaemia is defined as a reduction in the arterial O2 pressure (PaO2) by more than 1 kPa and/or a haemoglobin O2 saturation (SaO2) below 95%. With blood gas analyses ideally reported at the actual body temperature, desaturation is a consistent finding during maximal ergometer rowing. Arterial desaturation is most pronounced at the end of a maximal exercise bout, whereas the reduction in PaO2 is established from the onset of exercise. Exercise-induced arterial hypoxaemia is multifactorial. The ability to maintain a high alveolar O2 pressure (PAO2) is critical for blood oxygenation and this appears to be difficult in large individuals. A large lung capacity and, in turn, diffusion capacity seem to protect PaO2. A widening of the PAO2-PaO2 difference does indicate that a diffusion limitation, a ventilation-perfusion mismatch and/or a shunt influence the transport of O2 from alveoli to the pulmonary capillaries. An inspired O2 fraction of 0.30 reduces the widened PAO2-PaO2 difference by 75% and prevents a reduction of PaO2 and SaO2. With a marked increase in cardiac output, diffusion limitation combined with a fast transit time dominates the O2 transport problem. Furthermore, a postexercise reduction in pulmonary diffusion capacity suggests that the alveolo-capillary membrane is affected. An antioxidant attenuates oxidative burst by neutrophilic granulocytes, but it does not affect PaO2, SaO2 or O2 uptake (VO2), and the ventilatory response to maximal exercise also remains the same. It is proposed, though, that increased concentration of certain cytokines correlates to exercise-induced hypoxaemia as cytokines stimulate mast cells and basophilic granulocytes to degranulate histamine. The basophil count increases during maximal rowing. Equally, histamine release is associated with hypoxaemia and when the release of histamine is prevented, the reduction in PaO2 is attenuated. During maximal exercise, an extreme lactate spill-over to blood allows pH decrease to below 7.1 and according to the O2 dissociation curve this is critical for SaO2. When infusion of sodium bicarbonate maintains a stable blood buffer capacity, acidosis is attenuated and SaO2 increases from 89% to 95%. This enables exercise capacity to increase, an effect also seen when O2 supplementation to inspired air restores arterial oxygenation. In that case, exercise capacity increases less than can be explained by VO2 and CaO2. Furthermore, the change in muscle oxygenation during maximal exercise is not affected when hyperoxia and sodium bicarbonate attenuate desaturation. It is proposed that other organs benefit from enhanced O2 availability, and especially the brain appears to increase its oxygenation during maximal exercise with hyperoxia.
But that is it now on respiration.
If you believe respiration is never a limitation good for you.
If you think it could be in some cases a limitation good for you.
Remember it took the british Admirality only 250 years to accept the fact that Vit C may be helpfu if you stayedn many days on the sea.
. "classical " exercise physiology still has another 150 years time to possibly accept the fact, that Respiration can be a limiter.
. By the way, how long did it took the catholic church to accept Galileos point that the world is not the center of the universe. ???