Muscle fatigue and exhaustion during dynamic leg exercise in normoxia and hypobaric hypoxia

Abstract

Using an exercise device that integrates maximal voluntary static contraction (MVC) of knee extensor muscles with dynamic knee extension, we compared progressive muscle fatigue, i.e., rate of decline in force-generating capacity, in normoxia (758 Torr) and hypobaric hypoxia (464 Torr). Eight healthy men performed exhaustive constant work rate knee extension (21 +/- 3 W, 79 +/- 2 and 87 +/- 2% of 1-leg knee extension O2 peak uptake for normoxia and hypobaria, respectively) from knee angles of 90-150 degrees at a rate of 1 Hz. MVC (90 degrees knee angle) was performed before dynamic exercise and during < or = 5-s pauses every 2 min of dynamic exercise. MVC force was 578 +/- 29 N in normoxia and 569 +/- 29 N in hypobaria before exercise and fell, at exhaustion, to similar levels (265 +/- 10 and 284 +/- 20 N for normoxia and hypobaria, respectively; P > 0.05) that were higher (P < 0.01) than peak force of constant work rate knee extension (98 +/- 10 N, 18 +/- 3% of MVC). Time to exhaustion was 56% shorter for hypobaria than for normoxia (19 +/- 5 vs. 43 +/- 7 min, respectively; P < 0.01), and rate of right leg MVC fall was nearly twofold greater for hypobaria than for normoxia (mean slope = -22.3 vs. -11.9 N/min, respectively; P < 0.05). With increasing duration of dynamic exercise for normoxia and hypobaria, integrated electromyographic activity during MVC fell progressively with MVC force, implying attenuated maximal muscle excitation. Exhaustion, per se, was postulated to related more closely to impaired shortening velocity than to failure of force-generating capacity.

Cerebral perturbations during exercise in hypoxia

“…During MVC without fatigue, acute hypoxia has no effect on maximal EMG, in accordance with unchanged maximal voluntary strength (83). When comparing the evolution of maximal iEMG during MVC after submaximal contractions at the same absolute intensity, similar [after 3 sets of isometric leg extensions (54) and after 10 min of cycling (106)] or greater [after dynamic leg extensions to exhaustion (35)] reductions in MVC iEMG have been reported in hypoxia compared with normoxia. A greater reduction in MVC iEMG may reflect some alterations in central neural pathways, partly explaining the greater reduction in MVC observed under hypoxic conditions (35).…”

“…During intermittent submaximal contractions of the knee extensors, Fulco et al (35) and Katayama et al (54) showed that acute hypoxia (PI O 2 ϭ 464 Torr and FI O 2 ϭ 0.11, respectively) accelerates the increase in iEMG from the beginning to the end of exercise. This increase in iEMG is interpreted as an increase in motor command to recruit additional motor units and/or to increase motoneuron discharge rate to compensate for contractile failure in active muscle fibers.…”

The interactive effect of cooling and hypoxia on forearm fatigue development

“…It may also result from progressive cold penetration through the muscle tissue (Oksa et al 2002) gradually increasing the number of muscle fibres affected by slowed intramuscular energetics (Bergh, 1980;Faulkner et al 1990;De Ruiter & De Haan 2000;Allen et al 2008;Racinais & Oksa, 2010;Cahill et al 2011). Conversely, the mild effect of hypoxia on mechanical function (fatigue) has been widely attributed to increases in energetic metabolite interference with Ca 2+ handling and the contractile proteins (Edwards 1981;Fulco et al 1996;Fitts 1994;Haseler et al 1999;Hogan et al 1999;Amann & Calbet 2007;Perrey & Rupp 2009;Christian et al, 2014a).…”

“…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). 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).…”

“…Studies that have examined combined hypoxiccold stress have focused largely on thermogenesis, skin blood flow and thermal sensitivity (Robinson & Haymes 1991;Johnston et al 1996;Gautier et al 1987, Wood 1991Cipriano & Goldman 1975;Simmons et al 2010;, leaving fatigue development and human performance relatively unexamined (Tipton 2012). Given the potential for hypoxic-cold to severely compromise oxygen delivery to the active muscle -through simultaneous reductions in oxygen transport (muscle blood flow) and arterial oxygen content (hypoxemia) (Yanagisawa et al, 2007;Gregson et al, 2011;Amann & Calbet 2007) -as well as greatly increase metabolite production -through simultaneous rises in agonist-antagonist co-activation in the cold and type II recruitment in hypoxia (Edwards 1981;Fulco et al 1996;Oksa et al, 2002;Amann et al 2006a;2006b;2007a;2007b;Fulco et al 1994, Katayama et al 2007Christian et al 2014a) -we sought to investigate the independent and combined (interactive) effects of hypoxia and cold on forearm fatigue.…”