Muscle glycogen depletion during exercise at 9 degrees C and 21 degrees C

This study compared glycogen depletion in active skeletal muscle after light and moderate exercise in both cold and comfortable ambient conditions. Twelve male subjects (Ss) were divided into two groups equally matched for the submaximal exercise intensity corresponding to a blood lactate concentration of 4 mM (W4) during cycle exercise. On two separate days Ss rested for 30 min at ambient temperatures of either 9 degrees C or 21 degrees C, with the order of temperature exposure being counter-balanced among Ss. Following rest a tissue specimen was obtained from the m. vastus lateralis with the needle biopsy technique. Six Ss then exercised on a cycle ergometer for 30 min at 30% W4 (range = 50 - 65 W) while the remaining group exercised at 60% W4 (range = 85 - 120 W). Another biopsy was taken immediately after exercise and both samples were assayed for glycogen content. Identical procedures were repeated for the second environmental exposure. No significant glycogen depletion was observed in the Ss exercising at 30% W4 in 21 degrees C, but a 23% decrease (p = 0.04) was observed when the same exercise was performed at 9 degrees C. A 22% decrease (p = 0.002) in glycogen occurred in the 60% W4 group at 21 degrees C, which was not significantly different from that observed during the same exercise at 9 degrees C. The results suggest that muscle substrate utilization is increased during light exercise in a cold environment as compared to similar exercise at a comfortable temperature, probably due to shivering thermogenesis.(ABSTRACT TRUNCATED AT 250 WORDS)     

Cross-bridge kinetics modeled from myoplasmic [Ca2+] and LV pressure at 17 degrees C and after 37 degrees C and 17 degrees C ischemia

We modeled changes in contractile element kinetics derived from the cyclic relationship between myoplasmic [Ca(2+)], measured by indo 1 fluorescence, and left ventricular pressure (LVP). We estimated model rate constants of the Ca(2+) affinity for troponin C (TnC) on actin (A) filament (TnCA) and actin and myosin (M) cross-bridge (A x M) cycling in intact guinea pig hearts during baseline 37 degrees C perfusion and evaluated changes at 1) 20 min 17 degrees C pressure, 2) 30-min reperfusion (RP) after 30-min 37 degrees C global ischemia during 37 degrees C RP, and 3) 30-min RP after 240-min 17 degrees C global ischemia during 37 degrees C RP. At 17 degrees C perfusion versus 37 degrees C perfusion, the model predicted: A x M binding was less sensitive; A x M dissociation was slower; Ca(2+) was less likely to bind to TnCA with A x M present; and Ca(2+) and TnCA binding was less sensitive in the absence of A x M. Model results were consistent with a cold-induced fall in heart rate from 260 beats/min (37 degrees C) to 33 beats/min (17 degrees C), increased diastolic LVP, and increased phasic Ca(2+). On RP after 37 degrees C ischemia vs. 37 degrees C perfusion, the model predicted the following: A x M binding was less sensitive; A x M dissociation was slower; and Ca(2+) was less likely to bind to TnCA in the absence of A. M. Model results were consistent with reduced myofilament responsiveness to [Ca(2+)] and diastolic contracture on 37 degrees C RP. In contrast, after cold ischemia versus 37 degrees C perfusion, A x M association and dissociation rates, and Ca(2+) and TnCA association rates, returned to preischemic values, whereas the dissociation rate of Ca(2+) from A x M was ninefold faster. This cardiac muscle kinetic model predicted a better-restored relationship between Ca(2+) and cross-bridge function on RP after an eightfold longer period of 17 degrees C than 37 degrees C ischemia.     

Six degrees of separation

A web and print Focus on systems biology from Nature Publishing Group provides a practical introduction to a field that for all its promise still has many skeptics.     

Carvacrol and cinnamic acid inhibit microbial growth in fresh-cut melon and kiwifruit at 4 degrees and 8 degrees C

AIM: To establish whether or not carvacrol and cinnamic acid delay microbial spoilage of fresh-cut fruit. METHODS AND RESULTS: Dipping of fresh-cut kiwifruit in carvacrol solutions at 5-15 mM reduced total viable counts from 6.6 to < 2 log cfu g-1 for 21 d at 4 degrees C; however, undesirable colour and odour changes were also observed. Treatment with 1 mM of carvacrol or cinnamic acid reduced viable counts on kiwifruit by 4 and 1.5 log cfu g-1 for 5 d at 4 degrees C and 8 degrees C, respectively. Treatment of fresh-cut honeydew melon with 1 mM of carvacrol or cinnamic acid extended the lag phase of the microbial flora from less than 1 d in the untreated controls to 3 d at 8 degrees C and 5 d at 4 degrees C. Viable counts on the treated melon were 6 log cfu g-1 lower on Day 3 at 8 degrees C and 4 log cfu g-1 lower on Day 5 at 4 degrees C, compared with the untreated controls. IMPACT OF THE STUDY: Treatment with 1 mM of carvacrol or cinnamic acid delays spoilage of fresh-cut kiwifruit and honeydew melon at chill temperatures without adverse sensory consequences.