Convective oxygen transport and fatigue

Abstract

During exercise, fatigue is defined as a reversible reduction in force- or power-generating capacity and can be elicited by "central" and/or "peripheral" mechanisms. During skeletal muscle contractions, both aspects of fatigue may develop independent of alterations in convective O(2) delivery; however, reductions in O(2) supply exacerbate and increases attenuate the rate of accumulation. In this regard, peripheral fatigue development is mediated via the O(2)-dependent rate of accumulation of metabolic by-products (e.g., inorganic phosphate) and their interference with excitation-contraction coupling within the myocyte. In contrast, the development of O(2)-dependent central fatigue is elicited 1) by interference with the development of central command and/or 2) via inhibitory feedback on central motor drive secondary to the peripheral effects of low convective O(2) transport. Changes in convective O(2) delivery in the healthy human can result from modifications in arterial O(2) content, blood flow, or a combination of both, and they can be induced via heavy exercise even at sea level; these changes are exacerbated during acute and chronic exposure to altitude. This review focuses on the effects of changes in convective O(2) delivery on the development of central and peripheral fatigue.

The interactive effect of cooling and hypoxia on forearm fatigue development

“…This is predominantly due to co-activation of the agonist-antagonist pair (Oksa et al 1997) resulting in higher workload for the agonist muscle (Oksa et al 2002) thereby reducing aerobic-mechanical efficiency (McArdle et al, 1976). Furthermore, dynamic exercise in cold muscle is likely affected by reductions in muscle blood flow (Yanagisawa et al, 2007;Gregson et al, 2011), which may hinder oxygen delivery (Amann & Calbet, 2007) and diminish the removal metabolic by-products (Blomstrand et al 1984). …”

“…However, increases in muscle fatigue during prolonged exercise in hypoxia have been observed during both whole-body (Amann & Calbet 2007) and repeated contractions of isolated muscle groups (Fulco 1994;Katayama et al 2007;Perrey & Rupp 2009;Millet et al 2008;Christian et al 2014a). The rise in muscle fatigue during hypoxia can be largely attributed to a shift of the relative exercise intensity, higher muscle fibre recruitment, and thereby increased intramuscular metabolic disturbance (Edwards 1981;Fulco et al 1996;Amann et al 2006a;2006b;2007a;2007b;Fulco et al 1994, Katayama et al 2007Christian et al 2014a).…”

“…The rise in muscle fatigue during hypoxia can be largely attributed to a shift of the relative exercise intensity, higher muscle fibre recruitment, and thereby increased intramuscular metabolic disturbance (Edwards 1981;Fulco et al 1996;Amann et al 2006a;2006b;2007a;2007b;Fulco et al 1994, Katayama et al 2007Christian et al 2014a). Specifically, the increase in inorganic phosphate, reactive oxygen species and hydrogen ion production and their interference with the contractile proteins and sarcoplasmic Ca 2+ release mechanisms are thought to be a major factor behind the increase in muscle fatigue development Hogan et al 1999;Amann & Calbet 2007;Perrey & Rupp 2008). In hypoxia, evidence also suggests increased afferent feedback and decreased cerebral oxygenation can reduce voluntary drive to the muscle, exacerbating net fatigue Amann et al 2006a;2007b;Goodall et al 2010;Millet, 2008;.…”

Metabolic Mechanisms of Vocal Fatigue

“…Compartmentalization of specific causes has clouded understanding the mechanisms in and the site of fatigue (Brooks et al, 2005). To further complicate the matter, fatigue seems to vary with the nature of activity (task specificity), training and physiological status of an individual (aerobically trained versus untrained) and the environmental conditions (e.g., heat leads to quicker onset of fatigue), (Amann & Calbet, 2008;Enoka & Stuart, 1992).…”

“…According to the school of thought that emphasizes peripheral factors, in which fatigue is defined as a decrease in the ability of a skeletal muscle to generate force following sustained physical activity ( According to a complementary if not contrasting approach, the focus is instead on central mechanisms in fatigue. In this approach, fatigue is seen as a reduction in neural drive to the muscle, resulting in a decline in force production, independent of changes in the contractile machinery (Amann & Calbet, 2008;Enoka & Stuart, 1992). Central fatigue is attributed to the reduction in neural drive to motor neurons and an inhibition of motoneuron excitability -where a motor neuron is defined as a single motor neuron and all the muscle fibers it innervatessubsequent to afferent feedback from the muscle (Davis & Bailey, 1997;Gandevia, et al, 1995).…”