Initial fall in skeletal muscle force development during ischemia is related to oxygen availability

Abstract

We examined the hypothesis that the initial decline (first 1-2 min) in force development that occurs in working muscle when blood flow is halted is caused by O2 availability and not another factor related to blood flow. This was tested by reducing O2 delivery (muscle blood flow X arterial O2 content) to working muscle by either stopping blood flow [ischemia (I)] or maintaining blood flow with low arterial O2 content [hypoxemia (H)]. If initial decline in force development were similar between these two methods of reducing O2 delivery, it would suggest O2 availability as the common pathway. Isolated dog gastrocnemius muscle was stimulated at approximately 60-70% of maximal O2 uptake (1 isometric tetanic contraction every 2 s) until steady-state conditions of muscle blood flow and developed force were attained (approximately 3 min). Two conditions were then sequentially imposed on the working muscle: I, induced by shutting off pump controlling arterial perfusion of the muscle and clamping venous outflow, and H, induced by perfusing the muscle with deoxygenated blood (collected before testing while animal breathed N2) at steady-state blood flow level. Rates of the fall in force production in 17 matched conditions of H and I (approximately 40 s for each condition) were compared in 6 muscles tested. The blood perfusing the muscle during H had arterial PO2 = 8 +/- 1 (SE) Torr, arterial PCO2 = 37 +/- 1 Torr, and arterial pH = 7.39 +/- 0.03. The rate of decline in developed force was not significantly different (P = 0.46) between the 17 matched conditions of H (0.66 +/- 0.10 g force.g mass-1.s-1) and I (0.79 +/- 0.15 g force.g mass-1.s-1). These findings suggest that the initial fall in developed force in working skeletal muscle that occurs with ischemia is related to O2 availability.

Blood flow response in individuals with incomplete spinal cord injuries

“…Muscle fatigue is multifactoral, 8 but impaired oxygen delivery has been shown to contribute to increased rates of fatigue. 38 Consistent with this suggestion are studies that have suggested that long term SCI patients have increased fatiging that is not explained by reduced oxidative enzymes. 39,40 In summary, this study is one of the ®rst to examine incomplete SCI, who make up as much as 55% of all SCI patients.…”

Electrically stimulated resistance training in SCI individuals increases muscle fatigue resistance but not femoral artery size or blood flow

“…12 A delayed or reduced blood flow response at the onset of exercise appears to alter oxidative metabolism in healthy individuals 14,15 and this may exacerbate fatigue. 16 However, increasing blood flow prior to electrical stimulation had no effect on muscle fatigue of the quadriceps muscle group in individuals with SCI. 12 Therefore, it appears from these investigations that the increased muscle fatigue in individuals with SCI is not due to limitations in blood flow.…”

Ischemia causes muscle fatigue

“…Among them, impairment of excitation-contraction coupling and alteration of contractile properties by changes in concentrations of metabolic product [2] are commonly studied and potentially important mechanisms. Reduced blood flow [4,9] or decreased muscle oxygenation [20) has also been associated with fatigue. In canine gastrocnemius muscle, Hogan and colleagues [19] demonstrated a 30'Yo reduction in force with a 67%) reduction in arterial oxygenation, while no change in other intracellular metabolic processes was noted.…”