I like this first section of the explanation .
Don't feel stupid. None of us can have knowledge of everything. Even "experts" can differ in recommendations derived from the same data. Frank Day.
So here some of a small section on the discussion on respiratory ideas..
Based on the above forum discussion we may have a lot of "stupid" ????? Researchers below
Effects of different respiratory muscle training regimes on fatigue-related
variables during volitional hyperpnoea
Samuel Verges∗, Andrea S. Renggli, Dominic A. Notter, Christina M. Spengler
Exercise Physiology, Institute for Human Movement Sciences, ETH Zurich, and Institute of Physiology and Center for Integrative Human Physiology (ZIHP),
University of Zurich, Zurich, Switzerland
a r t i c l e i n f o
Accepted 7 September 2009
Respiratory muscle endurance training
Respiratory muscle fatigue
a b s t r a c t
We compared the effects of the most commonly used respiratory muscle (RM) training regimes: RM
endurance training (RMET; normocapnic hyperpnoea) and inspiratory resistive training (IMT), on RM
performance. Twenty-six healthy men were randomized into 3 groups performing 4 weeks of RMET, IMT
or sham-training. Lung function, RM strength and endurance were tested before and after training. RM
fatigue during intermittent hyperpnoea was assessed by twitch oesophageal (Poes,tw) and gastric pressures
with cervical and thoracic magnetic stimulation. Respiratory sensations (visual analogue scale, 0–10) and
blood lactate concentrations ([La]) were assessed during hyperpnoea.RMETincreased maximal voluntary
ventilation while IMT increased maximal inspiratory pressure. Both RMET and IMT increased vital capacity
and RM endurance, but only RMET improved the development of inspiratory muscle fatigue (from
−31% to −21% Poes,tw), perception of respiratory exertion (4.2±0.1 to 2.3±2.3 points) and [La] (1.8±0.4
to 1.3±0.3mmoll−1) during hyperpnoea. Whether these specific RMET-induced adaptations observed
during hyperpnoea would translate into greater improvements in exercise performance compared to IMT
remains to be investigated.
© 2009 Elsevier B.V. All rights reserved
The Biomedical Basis of Elite Performance
19-21 March 2012
Pulmonary system limitations to endurance exercise performance in humans
Internal Medicine, University of Utah, Salt Lake City, UT, USA
Accumulating evidence over the past 25 years depicts the healthy pulmonary system as a limiting factor of whole body endurance
exercise performance. This brief overview emphasizes three respiratory system-related mechanisms which impair O2 transport to the
locomotor musculature [arterial O2 content (CaO2) x leg blood flow (QL)], i.e. the key determinant of an individual’s aerobic capacity and
ability to resist fatigue. First, the respiratory system often fails to prevent arterial desaturation substantially below resting values and
thus compromises CaO2. Especially susceptible to this threat to convective O2 transport are well-trained endurance athletes characterized
by high metabolic and ventilatory demands and, likely due to anatomical and morphologic gender differences, active females. Second,
fatiguing respiratory muscle work (Wresp) associated with strenuous exercise elicits sympathetically-mediated vasoconstriction in limbmuscle
vasculature which compromises QL. This impact on limb O2 transport is independent of fitness level and affects all individuals,
however, only during sustained, high-intensity endurance exercise performed above ~85% VO2max. And third, excessive fluctuations in
intrathoracic pressures accompanying Wresp can limit cardiac output and therefore QL. Exposure to altitude exacerbates the respiratory
system limitations observed at sea level and further reduces CaO2 and substantially increases exercise-induced Wresp. Taken together,
the intact pulmonary system of healthy endurance athletes impairs locomotor muscle O2 transport during strenuous exercise by failing
to ensure optimal arterial oxygenation and compromising QL. This respiratory system-related impact exacerbates the exercise-induced
development of fatigue and compromises endurance performance.
Where applicable, the authors confirm that the experiments described here conform with The Physiological Society ethical requirements.
Fatiguing inspiratory muscle work causes reflex reduction
in resting leg blood flow in humans
A. William Sheel, P. Alexander Derchak, Barbara J. Morgan *,
David F. Pegelow, Anthony J. Jacques and Jerome A. Dempsey
Department of Population Health Sciences, John Rankin Laboratory of Pulmonary
Medicine and * Department of Surgery, University of Wisconsin-Madison, Madison,
(Received 20 April 2001; accepted after revision 12 July 2001)
1. We recently showed that fatigue of the inspiratory muscles via voluntary efforts caused a
time-dependent increase in limb muscle sympathetic nerve activity (MSNA) (St Croix et al.
2000). We now asked whether limb muscle vasoconstriction and reduction in limb blood flow
also accompany inspiratory muscle fatigue.
2. In six healthy human subjects at rest, we measured leg blood flow («QL) in the femoral artery
with Doppler ultrasound techniques and calculated limb vascular resistance (LVR) while
subjects performed two types of fatiguing inspiratory work to the point of task failure
(3–10 min). Subjects inspired primarily with their diaphragm through a resistor, generating
(i) 60 % maximal inspiratory mouth pressure (PM) and a prolonged duty cycle (TI/TTOT = 0.7);
and (ii) 60 % maximal PM and a TI/TTOT of 0.4. The first type of exercise caused prolonged
ischaemia of the diaphragm during each inspiration. The second type fatigued the diaphragm
with briefer periods of ischaemia using a shorter duty cycle and a higher frequency of
contraction. End-tidal PCO2 was maintained by increasing the inspired CO2 fraction (FI,CO2) as
needed. Both trials caused a 25–40 % reduction in diaphragm force production in response to
bilateral phrenic nerve stimulation.
3. «QL and LVR were unchanged during the first minute of the fatigue trials in most subjects;
however, «QL subsequently decreased (_30 %) and LVR increased (50–60 %) relative to control
in a time-dependent manner. This effect was present by 2 min in all subjects. During recovery,
the observed changes dissipated quickly (< 30 s). Mean arterial pressure (MAP; +4–13 mmHg)
and heart rate (+16–20 beats min_1) increased during fatiguing diaphragm contractions.
4. When central inspiratory motor output was increased for 2 min without diaphragm fatigue by
increasing either inspiratory force output (95 % of maximal inspiratory pressure (MIP)) or
inspiratory flow rate (5 w eupnoea), «QL, MAP and LVR were unchanged; although continuing
the high force output trials for 3 min did cause a relatively small but significant increase in
LVR and a reduction in «QL.
5. When the breathing pattern of the fatiguing trials was mimicked with no added resistance,
LVR was reduced and «QL increased significantly; these changes were attributed to the negative
feedback effects on MSNA from augmented tidal volume.
6. Voluntary increases in inspiratory effort, in the absence of diaphragm fatigue, had no effect
on «QL and LVR, whereas the two types of diaphragm-fatiguing trials elicited decreases in «QL
and increases in LVR. We attribute these changes to a metaboreflex originating in the
diaphragm. Diaphragm and forearm muscle fatigue showed very similar time-dependent