This study was designed to investigate I)whether a protocol employing a gradual reduction in O-2 availability to submaximally contracting muscle results in relatively minor disturbances in intracellular homeostasis and 2) the interaction between tissue oxygenation and the proposed regulators of muscle respiration, metabolism, and force production. O-2 delivery to isolated submaximally contracting [isometric contractions at 3 Hz; similar to 50% of peak O-2 uptake (Vo(2))] in situ canine gastrocnemius (n = 6) was manipulated by decreasing arterial Pot (hypoxemia; H) or muscle blood flow (ischemia; I) during three separate periods in each muscle [control (C), H, or I; each separated by 45 min of rest]. O-2 delivery was reduced gradually in small steps every 3 min by H or I during two of the contraction periods (6 steps for a total of 21 min; O-2 delivery reduced by 67% by the end of 21 min), whereas C was at normal O-2 delivery for a 15-min period. Muscle Vo, was maintained at control levels for the first two O-2 delivery reduction steps for the Il and I conditions and then fell proportionally with O-2 delivery to similar to 35% of the initial value by the end of the al-min contraction period. Muscle force development generally fell in parallel with Vo(2). There were no significant changes from the values obtained during C contractions in intracellular concentrations of ATP, phosphocreatine, NH3, calculated free ADP, lactate, and redox state ratios as the O-2 delivery was reduced, even with the severe decline in Vo(2) and developed force. These results demonstrated that when O-2 availabilty was reduced gradually to contracting skeletal muscle, 1) developed force (ATP utilization) was reduced through a tight coupling with aerobic ATP supply, such that there was little additional disruption of intracellular homeostasis, and 2) there was an apparent dissociation of some of the proposed regulators of cell respiration and force development from the control of these processes.
|Number of pages||9|
|Journal||Journal of Applied Physiology|
|Publication status||Published - Apr 1996|