Bioenergetics of contracting skeletal muscle after partial reduction of blood flow

Abstract

Hogan, Michael C., L. Bruce Gladden, Bruno Grassi, Creed M. Stary, and Michele Samaja. Bioenergetics of contracting skeletal muscle after partial reduction of blood flow. J. Appl. Physiol. 84(6): 1882-1888, 1998.-The purpose of this study was to examine the bioenergetics and regulation of O 2 uptake (V O 2 ) and force production in contracting muscle when blood flow was moderately reduced during a steadystate contractile period. Canine gastrocnemius muscle (n ϭ 5) was isolated, and 3-min stimulation periods of isometric, tetanic contractions were elicited sequentially at rates of 0.25, 0.33, and 0.5 contractions/s (Hz) immediately followed by a reduction of blood flow [ischemic (I) condition] to 46 Ϯ 3% of the value obtained at 0.5 Hz with normal blood flow. The V O 2 of the contracting muscle was significantly (P Ͻ 0.05) reduced during the I condition [6.5 Ϯ 0.8 (SE) ml · 100 g Ϫ1 · min Ϫ1 ] compared with the same stimulation frequency with normal flow (11.2 Ϯ 1.5 ml · 100 g Ϫ1 · min Ϫ1 ), as was the tension-time index (79 Ϯ 12 vs. 123 Ϯ 22 N·g Ϫ1 · min Ϫ1 , respectively). The ratio of V O 2 to tension-time index remained constant throughout all contraction periods. Muscle phosphocreatine concentration, ATP concentration, and lactate efflux were not significantly different during the I condition compared with the 0.5-Hz condition with normal blood flow. However, at comparable rates of V O 2 and tension-time index, muscle phosphocreatine concentration and ATP concentration were significantly less during the I condition compared with normal-flow conditions. These results demonstrate that, in this highly oxidative muscle, the normal balance of O 2 supply to force output was maintained during moderate ischemia by downregulation of force production. In addition, 1) the minimal disruption in intracellular homeostasis after the initiation of ischemia was likely a result of steady-state metabolic conditions having already been activated, and 2) the difference in intracellular conditions at comparable rates of V O 2 and tension-time index between the normal flow and I condition may have been due to altered intracellular O 2 tension. oxygen uptake; exercise; adenosine 5Ј-triphosphate; lactate; lactic acid; mitochondrial respiration; phosphocreatine; glycolysis IN MOST CONDITIONS of steady-state muscle contractile activity, ATP production related to the O 2 uptake (V O 2 ) of the contracting muscle is tightly coupled to the rate of ATP demand so that steady-state energy expenditure is maintained with minimal change in intracellular ATP concentration ([ATP]; e.g., see Ref. 12). When the supply of O 2 (and oxidative substrate) to the mitochondria is sufficient, increases in myofibril ATPase activity with higher energy demands result in changes in the concentration of several signals [phosphocreatine (PCr), ADP, P i , etc.] that are thought to regulate mitochondrial respiration (4,5,18,20,22) in a manner that causes oxidative phosphorylation to increase proportionally with ATPase activity. However, when the supply of O 2 to ...

The influence of circulatory difference on muscle oxygenation and fatigue during intermittent static dorsiflexion

“…Thus, the Hb tot was always smaller in the leg up during the exercise, and the HbO 2 volume would also be smaller in leg up during the exercise. Hogan et al (1998) suggested that when stimulating the canine gastrocnemius muscle at a constant rate with a partial reduction of blood flow, the force generation would decrease according to the intracellular O 2 tension. Therefore, the steeper rise in iEMG, observed during FREE with the leg up, may be assumed to reflect the increased motor unit recruitment and/or discharge rate to counteract the decreased force generation capacity of the muscle caused by the reduction of blood flow.…”

What triggers the aerobic dive limit? Patterns of muscle oxygen depletion during dives of emperor penguins

“…The muscle O 2 consumption of the diving emperor penguin is only approximately one-fifth that of canine gastrocnemius stimulated at 0.25Hz (Fig.9) (Hogan et al, 1998), less than onetenth the pectoralis-supracoracoideus muscle O 2 consumption calculated from emperor penguins swimming maximally in a flume (160ml O 2 kg -1 musclemin -1 ) (Kooyman and Ponganis, 1994;Ponganis et al, 1997a) and far less than maximal O 2 consumption of human quadriceps femoris muscle (520ml O 2 kg -1 musclemin -1 ) (Richardson et al, 1995b). Although muscle ischemia may contribute to decreased muscle O 2 consumption (see example in Fig.9) (Duran and Renkin, 1974;Hogan et al, 1998;, we hypothesize that biomechanical efficiency and hydrodynamics are primarily responsible for this low muscle O 2 consumption during diving of the emperor penguin.…”

“…Even in dives longer than the Weddell seal ADL, including a dive of 27min, Mb was typically still 40-60% saturated (Guyton et al, 1995). In contrast, saturation values in long type B dives often declined to below 10% (Fig.8) (Scholander et al, 1942) and canine gastrocnemius muscle stimulated at different rates (Hogan et al, 1998).…”

“…The last bar represents canine muscle O 2 consumption during stimulation with muscle blood flow reduced to 46% (Hogan et al, 1998). Error bars for emperor penguin data are ±s.d.…”

Effect of type 2 diabetes on the dynamic response characteristics of leg vascular conductance during exercise

“…Impeding Vo 2 after the onset of exercise exaggerates the fall in muscle PCr and pH, increase in P i and loss of force production. [48][49][50][51] Therefore, it is likely that the slowing of the hyperaemic response (phase 2) contributes directly to the abnormal metabolic responses in contracting muscle and the loss of exercise tolerance in type 2 diabetes. 1-4, 6, 46 …”