Metabolic and sarcoplasmic reticulum Ca2+ cycling responses in human muscle 4 days following prolonged exercise

This study investigated the effects of prolonged exercise on muscle sarcoplasmic reticulum (SR) Ca2+ cycling properties and the metabolic responses with and without a session of exercise designed to reduce muscle glycogen reserves while on a normal carbohydrate (CHO) diet. Eight untrained males (VO2peak = 3.81 +/- 0.12 L/min, mean +/- SE) performed a standardized cycle-to-fatigue at 55% VO2peak while on a normal CHO diet (Norm CHO) and 4 days following prolonged exercise while on a normal CHO diet (Ex+Norm CHO). Compared to rest, exercise in Norm CHO to fatigue resulted in significant reductions (p < 0.05) in Ca2+ uptake (3.17 +/- 0.21 vs. 2.47 +/- 0.12 mu mol center dot(g protein)- (1 center dot)min(-1)), maximal Ca2+ ATPase activity (V-max, 152 +/- 12 vs. 119 +/- 9 mu mol center dot(g protein)(-1 center dot)min(-1)) and both phase 1 (15.1 +/- 0.98 vs. 13.1 +/- 0.28 mu mol center dot(g protein)(-1 center dot)min(-1)) and phase 2 (6.56 +/- 0.33 vs. 4.91 +/- 0.28 mu mol center dot(g protein)(-1 center dot)min(-1)) Ca2+ release in vastus lateralis muscle. No differences were observed between Norm CHO and Ex-Norm CHO in the response of these properties to exercise. Compared with Norm CHO, Ex+Norm CHO resulted in higher (p < 0.05) resting Ca2+ uptake (3.17 +/- 0.21 vs. 3.49 +/- 0.24 mu mol center dot(g protein)center dot min(-1) and higher ionophore ratio, defined as the ratio of V-max measured with and without the Ca(2+-)ionophore A23187, (2.3 +/- 0.3 vs. 4.4 +/- 0.3 mu mol center dot(g protein)center dot min(-1)) at fatigue. No differences were observed between conditions in the concentration of muscle glycogen, the high-energy phosphates (ATP and PCr), or metabolites (Pi, Cr, and lactate). Ex+Norm CHO also failed to modify the exercise-induced changes in CHO and fat oxidation. We conclude that prolonged exercise to fatigue performed 4 days following glycogen-depleting exercise while on a normal CHO diet elevates resting Ca2+ uptake and prevents increases in SR membrane permeability to Ca2+ as measured by the ionophore ratio.