Comparative NMR and NIRS analysis of oxygen-dependent metabolism in exercising finger flexor muscles

Abstract

Muscle contraction requires the physiology to adapt rapidly to meet the surge in energy demand. To investigate the shift in metabolic control, especially between oxygen and metabolism, researchers often depend on near-infrared spectroscopy (NIRS) to measure noninvasively the tissue O Because NIRS detects the overlapping myoglobin (Mb) and hemoglobin (Hb) signals in muscle, interpreting the data as an index of cellular or vascular O requires deconvoluting the relative contribution. Currently, many in the NIRS field ascribe the signal to Hb. In contrast, H NMR has only detected the Mb signal in contracting muscle, and comparative NIRS and NMR experiments indicate a predominant Mb contribution. The present study has examined the question of the NIRS signal origin by measuring simultaneously theH NMR, P NMR, and NIRS signals in finger flexor muscles during the transition from rest to contraction, recovery, ischemia, and reperfusion. The experiment results confirm a predominant Mb contribution to the NIRS signal from muscle. Given the NMR and NIRS corroborated changes in the intracellular O, the analysis shows that at the onset of muscle contraction, O declines immediately and reaches new steady states as contraction intensity rises. Moreover, lactate formation increases even under quite aerobic condition.

Do we have to consider acidosis induced by exercise as deleterious in sickle cell disease?

“…It is now largely and commonly accepted that muscular exercise is associated with a significant intramuscular acidosis, even in aerobic conditions (Bendahan, Chatel, & Jue, ; Brooks, ). A variety of cellular processes can be activated in order to handle proton accumulation and the potential adverse effects (Juel, ).…”

“…It is now largely and commonly accepted that muscular exercise is associated with a significant intramuscular acidosis, even in aerobic conditions (Bendahan, Chatel, & Jue, 2017;Brooks, 2018).…”

The tortuous path of lactate shuttle discovery: From cinders and boards to the lab and ICU

“…The lactate/pyruvate (L/P) approximates 10, with net lactate production and release from resting muscle of healthy individuals occurring when arterial partial pressure of oxygen (PO 2 ) approximates 100 Torr and intramuscular PO 2 approximates 40 Torr, well above the critical mitochondrial PO 2 for maximal mitochondrial respiration (1–2 Torr). 195 , 196 , 197 During exercise at about 65% of maximal oxygen consumption (VO 2 max), lactate production and net lactate release from working muscle beds rise and the L/P rises more than an order of magnitude (to approximately 500). 57 However, the intramuscular PO 2 remains at 3–4 Torr, well above the critical mitochondrial O 2 level.…”

Quantitative Assessment of Blood Lactate in Shock: Measure of Hypoxia or Beneficial Energy Source

“…This argument is based on a variety of measurements that indicate that the tissue pO 2 is greater than the 1 mm Hg threshold required for optimal mitochondrial oxidative metabolism [ 9 ]. These measurements include the spectroscopic measurement of the NAD + /NADH ratio [ 45 ] and measurement of myoglobin saturation using either proton NMR [ 46 , 47 ] or flash-frozen samples [ 48 – 50 ]. It is important to recognize that, as shown in Figure 2 , muscle cellular pO 2 is highly heterogeneous, with the anoxic tissue localized to a region in the center of the cell at the venous end.…”