More on Inroad, Muscle Fatigue
07/31/1423:05
Doug,
“The inroad theory is just that...a theory.”
Honestly, I am not sure we can call the concept of inroad a theory, perhaps a hypothesis. As you know in science, "theory" is a strong word and requires much supporting experimental evidence. I am not knocking you for this. I really can't remember who's brain-child the concept of "inroad" can be attributed, probably either Ken, Darden, or Arthur. I know it is in the SuperSlow manual and logically makes sense. However, it is not compatible with the experimental evidence. Briefly, the concept of inroad is based upon a momentary decrease in strength - such that (as I remember) training with 80% of one's 1 RM would lead to a 20% inroad. As I stated before, this concept is too simplistic and not indicative of what is occurring physiologically at the cellular level when you apply a stimulus and cut the sucker open to see what happened.
“The inroad theory is just that...a theory.”
Honestly, I am not sure we can call the concept of inroad a theory, perhaps a hypothesis. As you know in science, "theory" is a strong word and requires much supporting experimental evidence. I am not knocking you for this. I really can't remember who's brain-child the concept of "inroad" can be attributed, probably either Ken, Darden, or Arthur. I know it is in the SuperSlow manual and logically makes sense. However, it is not compatible with the experimental evidence. Briefly, the concept of inroad is based upon a momentary decrease in strength - such that (as I remember) training with 80% of one's 1 RM would lead to a 20% inroad. As I stated before, this concept is too simplistic and not indicative of what is occurring physiologically at the cellular level when you apply a stimulus and cut the sucker open to see what happened.
Doug,
“The inroad theory is just that...a theory.”
Honestly, I am not sure we can call the concept of inroad a theory, perhaps a hypothesis. As you know in science, "theory" is a strong word and requires much supporting experimental evidence. I am not knocking you for this. I really can't remember who's brain-child the concept of "inroad" can be attributed, probably either Ken, Darden, or Arthur. I know it is in the SuperSlow manual and logically makes sense. However, it is not compatible with the experimental evidence. Briefly, the concept of inroad is based upon a momentary decrease in strength - such that (as I remember) training with 80% of one's 1 RM would lead to a 20% inroad. As I stated before, this concept is too simplistic and not indicative of what is occurring physiologically at the cellular level when you apply a stimulus and cut the sucker open to see what happened.
If a muscle is stimulated statically to a 100% inroad (complete momentary loss of force production), yet muscle force production recovers completely within a few hours, is that indicative of a growth stimulus? On the other hand if high tension / low repetition eccentric contractions are administered and force production is greatly decreased and does not return to pre stimulation levels for 14 days accompanied by damage to much of the contractile and activation machinery, is that more indicative of a growth stimulus? My bet would be on the latter. Please see the references I listed, as this is exactly what occurred in the studies. I'm not trying to say that fatigue is not an important factor in initiating a growth stimulus. I think it is and there is research to support this. However, I think it has more to do with the effects of fatigue on the metabolic and mechanical properties of the muscle being worked. The concept of inroad sorely needs to be changed in light of newer evidence.
“However, my statement that hyperventilation blows off carbon dioxide that results in alkalinizing of the blood that offsets lactic acidosis IS NOT a guess or theory. Hyperventilation does raise blood pH and can be done consciously to raise blood pH or can occur unconsciously in response to lowering of blood pH. This mechanism is one of the major reasons you breath faster when you exert yourself, and it is why a diabetic in ketoacidosis is found to hyperventilate, or why a septic patient in lactic acidosis will be found to hyperventilate.”
Yes, I agree. This was drilled into our heads in both undergraduate and graduate school in exercise physiology. Although, I am not sure these examples have much in common with healthy subjects during low duration / high intensity resistance training. Newer evidence shows that H+ accumulation due to lactate breakdown has little effect on muscle fatigue. There are too many studies to list, but here are a few:
Journal of Physiology (2001), 536.3, pp. 657-665
Role of phosphate and calcium stores in muscle fatigue
D. G. Allen and H. Westerblad
"Failure of SR Ca2+ release has been shown to be a major contributor to muscle fatigue. Increasing evidence supports the hypothesis that precipitation of CaPi in the SR contributes to the failure of SR Ca2+ release. We suggest that this mechanism may be important in high intensity activities which lead to fatigue in > 1-2 min but other mechanisms are probably more important in lower intensity activities which cause fatigue in > 1 h."
News Physiol Sci 17: 17-21, 2002
Muscle Fatigue: Lactic Acid or Inorganic Phosphate the Major Cause?
Håkan Westerblad, David G. Allen and Jan Lännergren
"Intracellular acidosis due mainly to lactic acid accumulation has been regarded as the most impor-
tant cause of skeletal muscle fatigue. Recent studies on mammalian muscle, however, show little
direct effect of acidosis on muscle function at physiological temperatures. Instead, inorganic
phosphate, which increases during fatigue due to breakdown of creatine phosphate, appears
to be a major cause of muscle fatigue."
Physiol Rev. 2008 Jan;88(1):287-332.
Skeletal muscle fatigue: cellular mechanisms.
Allen DG, Lamb GD, Westerblad H.
"Repeated, intense use of muscles leads to a decline in performance known as muscle fatigue. Many muscle properties change during fatigue including the action potential, extracellular and intracellular ions, and many intracellular metabolites. A range of mechanisms have been identified that contribute to the decline of performance. The traditional explanation, accumulation of intracellular lactate and hydrogen ions causing impaired function of the contractile proteins, is probably of limited importance in mammals. Alternative explanations that will be considered are the effects of ionic changes on the action potential, failure of SR Ca2+ release by various mechanisms, and the effects of reactive oxygen species."
See also:
J Pysiol 558.1 (2004) pp 5-30
Lactate metabolism: a new paradigm for the third millennium
L.B. Gladden
Take care,
Ryan
Ryan A. Hall
“The inroad theory is just that...a theory.”
Honestly, I am not sure we can call the concept of inroad a theory, perhaps a hypothesis. As you know in science, "theory" is a strong word and requires much supporting experimental evidence. I am not knocking you for this. I really can't remember who's brain-child the concept of "inroad" can be attributed, probably either Ken, Darden, or Arthur. I know it is in the SuperSlow manual and logically makes sense. However, it is not compatible with the experimental evidence. Briefly, the concept of inroad is based upon a momentary decrease in strength - such that (as I remember) training with 80% of one's 1 RM would lead to a 20% inroad. As I stated before, this concept is too simplistic and not indicative of what is occurring physiologically at the cellular level when you apply a stimulus and cut the sucker open to see what happened.
If a muscle is stimulated statically to a 100% inroad (complete momentary loss of force production), yet muscle force production recovers completely within a few hours, is that indicative of a growth stimulus? On the other hand if high tension / low repetition eccentric contractions are administered and force production is greatly decreased and does not return to pre stimulation levels for 14 days accompanied by damage to much of the contractile and activation machinery, is that more indicative of a growth stimulus? My bet would be on the latter. Please see the references I listed, as this is exactly what occurred in the studies. I'm not trying to say that fatigue is not an important factor in initiating a growth stimulus. I think it is and there is research to support this. However, I think it has more to do with the effects of fatigue on the metabolic and mechanical properties of the muscle being worked. The concept of inroad sorely needs to be changed in light of newer evidence.
“However, my statement that hyperventilation blows off carbon dioxide that results in alkalinizing of the blood that offsets lactic acidosis IS NOT a guess or theory. Hyperventilation does raise blood pH and can be done consciously to raise blood pH or can occur unconsciously in response to lowering of blood pH. This mechanism is one of the major reasons you breath faster when you exert yourself, and it is why a diabetic in ketoacidosis is found to hyperventilate, or why a septic patient in lactic acidosis will be found to hyperventilate.”
Yes, I agree. This was drilled into our heads in both undergraduate and graduate school in exercise physiology. Although, I am not sure these examples have much in common with healthy subjects during low duration / high intensity resistance training. Newer evidence shows that H+ accumulation due to lactate breakdown has little effect on muscle fatigue. There are too many studies to list, but here are a few:
Journal of Physiology (2001), 536.3, pp. 657-665
Role of phosphate and calcium stores in muscle fatigue
D. G. Allen and H. Westerblad
"Failure of SR Ca2+ release has been shown to be a major contributor to muscle fatigue. Increasing evidence supports the hypothesis that precipitation of CaPi in the SR contributes to the failure of SR Ca2+ release. We suggest that this mechanism may be important in high intensity activities which lead to fatigue in > 1-2 min but other mechanisms are probably more important in lower intensity activities which cause fatigue in > 1 h."
News Physiol Sci 17: 17-21, 2002
Muscle Fatigue: Lactic Acid or Inorganic Phosphate the Major Cause?
Håkan Westerblad, David G. Allen and Jan Lännergren
"Intracellular acidosis due mainly to lactic acid accumulation has been regarded as the most impor-
tant cause of skeletal muscle fatigue. Recent studies on mammalian muscle, however, show little
direct effect of acidosis on muscle function at physiological temperatures. Instead, inorganic
phosphate, which increases during fatigue due to breakdown of creatine phosphate, appears
to be a major cause of muscle fatigue."
Physiol Rev. 2008 Jan;88(1):287-332.
Skeletal muscle fatigue: cellular mechanisms.
Allen DG, Lamb GD, Westerblad H.
"Repeated, intense use of muscles leads to a decline in performance known as muscle fatigue. Many muscle properties change during fatigue including the action potential, extracellular and intracellular ions, and many intracellular metabolites. A range of mechanisms have been identified that contribute to the decline of performance. The traditional explanation, accumulation of intracellular lactate and hydrogen ions causing impaired function of the contractile proteins, is probably of limited importance in mammals. Alternative explanations that will be considered are the effects of ionic changes on the action potential, failure of SR Ca2+ release by various mechanisms, and the effects of reactive oxygen species."
See also:
J Pysiol 558.1 (2004) pp 5-30
Lactate metabolism: a new paradigm for the third millennium
L.B. Gladden
Take care,
Ryan
Ryan A. Hall
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