Muscle fatigue may be described as a decreased ability to repeat or sustain a muscle contraction. A number of cellular mechanisms are thought to contribute to this decline in muscle performance, including mechanisms related both to increases in oxygen utilization and decreases in oxygen delivery. However, the relative contribution of these factors remains unclear.
When the force of a muscle group in an intact individual exceeds approximately 50% of maximum, the circulation begins to collapse due to extravascular compression, markedly decreasing perfusion of the working muscle. Oxyhemoglobin in that relatively static blood can decrease rapidly during the first 10 seconds, corresponding with a significantly decreased contractile capacity. If the contraction is submaximal, the pressor response then causes an increase in mean arterial pressure (MAP), which may restore perfusion and help sustain the muscle contraction.
With the submaximal contraction of long duration, fatigue occurs relatively slowly, and complete recovery from fatigue may take hours to days. However, with maximal muscle contractions, the decrease in perfusion is more dramatic. Extravascular compression is such that resultant increases in MAP are insufficient to restore tissue perfusion, and fatigue typically occurs rapidly, with large decreases in maximal force within the first few seconds. This type of fatigue typically recovers very rapidly as well, with the considerable restoration of forces occurring within the first several seconds of recovery.
Mechanisms not directly related to intracellular changes have been found to affect muscle fatigue. For instance, neural changes altering the ability to recruit muscle fibers, perhaps in response to hypoxia or acidosis, appear to play a significant role. However, much muscle research is performed on isolated muscle, and it is generally agreed that a substantial component of muscle fatigue relates to decreased tissue O2 tension and takes place within the contractile mechanism of the muscle itself.
Hemoglobin is essentially fully saturated with oxygen while breathing normal atmospheric with a relatively insignificant amount of O2 carried in solution in the plasma. When breathing normobaric air, arterial PO2 (partial pressure of oxygen) is approximately 13.3 kPa, and tissue O2 tension is approximately 7.3kPa. At this PO2, the oxygen-carrying capacity of blood is relatively stable at 20ml/dL, with almost all oxygen carried as oxyhemoglobin. Hyperbaric oxygenation (HBO2) can produce substantial increases in plasma oxygen partial pressures and tissue oxygen tension, as well as the increased oxygen-carrying capacity of the blood.
Hyperbaric oxygenation has been touted, by some as a means for enhancing muscle performance and athletic performance. For this reason, it is being used by some as an ergogenic aid in an attempt to improve athletic performance or to promote recovery from exercise-induced muscle damage or fatigue. Many claims are based on studies that rely on anecdotal evidence or studies with limited study design.
Stewart et. Al gathers a total of 55 healthy volunteers for a study and asked them to refrain from exercise for at least 48 hours prior to any data-collection session. Exposure to hyperbaric oxygen in the experimental group significantly increased the maximal initial force of contraction for both initial grips (Max-I p<0.001) and recovery grip (Max-R p><0.001). Total effort was greater with hyperbaric oxygenation for both initial grip (TE-I p><0.01) and recovery grip (TE-R p><0.001). Exposure to HBo2 decreased the time it took for the force to drop to 50 percent of initial force for both initial grip (50%-I p><0.01) and recovery grip (50%-R p><0.01). However, as the initial HBo2 force was so much higher, force remained higher with HBo2 throughout the entire effort. Minimal grip at the end of each contraction tended to be higher with HBo2 but just failed to achieve significance (p>0.05). There was no difference in the recovery parameter calculated as the maximal recovery grip as a percentage of the initial grip, though again it tended to be higher with HBo2 (p>0.08).
No significant differences were seen in the control subjects between Weeks 1 and 2 for any parameters, thus reducing the possibility of a significant learning effect or fatigue effect. The hyperbaric curves were higher, for both initial and recovery grip, than the corresponding curves for normobaric air.
According to this study, short, sustained exposure to hyperbaric oxygen can enhance the ability of forearm muscles to produce force during maximal, sustained contractions, producing 25- 30% higher maximal contractions both initially and after a brief period of recovery, and increased total force production of 13-24% during a one-minute effort. Therefore, force to 50% of the initial grip is more rapid with HBOT.
Stewart J, Gosine D, Kaleel M, Kurtev A. 2011. Hyperbaric oxygen and muscle performance in maximal sustained muscle contraction. UHM 2011, Vol. 38, No. 6.
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