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.
You can use a MOXY and a Spiro Tiger and test this out.
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.
That is exactly what you do with a Spiro Tiger , so no CO2 tank needed just simply a Spiro tiegr and you go.
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 effects on LVR and «QL. is consistent with the idea of a metaboreflex that increases sympathetic vasoconstrictor outflow. Furthermore, increased sympathetic outflow to, or vasoconstriction in, selected vascular beds has been elicited in anaesthetized
animals by electrical (Szulczyk et al. 1988; Offner et al. 1992) or chemical (Hussain et al. 1991) stimulation of phrenic afferent fibres.
We now asked whether respiratory muscle fatigue in humans would also have functional consequences in the form of vasoconstriction and reduced blood flow in the resting limb.
In addition, we addressed the cardiovascular consequences of augmented central respiratory motor output, per se, and determined to what extent the cardiovascular effects of inspiratory muscle fatigue paralleled those during fatigue of the forearm muscles. We believe these proposed reflexes from the respiratory
muscles may influence blood flow distribution during exercise (Harmset al. 1997, 1998; Wetter, 1999
COMPONENTS OF CELLULAR PROTON PRODUCTION, BUFFERING, AND REMOVAL
The cause of metabolic acidosis is not merely proton release, but an imbalance between the rate of proton release and the rate of proton buffering and removal. As previously shown from fundamental biochemistry, proton release occurs from glycolysis and ATP hydrolysis. However, there is not an immediate decrease in cellular pH due to the capacity and multiple components of cell proton buffering and removal (Table 5). The intracellular buffering system, which includes amino acids, proteins, Pi, HCO3−, creatine phosphate (CrP) hydrolysis, and lactate production, binds or consumes H+ to protect the cell against intracellular proton accumulation. Protons are also removed from the cytosol via mitochondrial transport, sarcolemmal transport (lactate−/H+ symporters, Na+/H+ exchangers), and a bicarbonate-dependent exchanger (HCO3−/Cl−) (Fig. 13). Such membrane exchange systems are crucial for the influence of the strong ion difference approach at understanding acid-base regulation during metabolic acidosis (5, 26). However, when the rate of H+ production exceeds the rate or the capacity to buffer or remove protons from skeletal muscle, metabolic acidosis ensues. It is important to note that lactate production acts as both a buffering system, by consuming H+, and a proton remover, by transporting H+ across the sarcolemma, to protect the cell against metabolic acidosis.
Once it is in the blood we have one great ability to get rid of H + .
Respiratory training / Spiro Tiger