The impact of packaging system and temperature abuse on the shelf life characteristics of ground beef.

New ground beef packaging systems have warranted investigation of their spoilage and quality characteristics. Furthermore, analysis of ground beef spoilage in modified atmosphere packaging (MAP) and stored at abusive temperature is lacking. This research aimed to determine the effect of packaging systems and temperature abuse on the sensory and shelf-life characteristics of ground beef. Ground beef patties were packaged using polyvinyl chloride overwrap (OW), HI-OX MAP (80% O2, 20% CO2), LO-OX MAP (30% CO2, 70% N2), CO-MAP (0.4% CO, 30% CO2, 69.6% N2), or vacuum (VAC) prior to color, odor, biochemical, and microbial analyses over display. CO-MAP exhibited more desirable color and consumer acceptability throughout display. Lean discoloration and odor scores were lower for anaerobic packaging than aerobic packaging. Microbial results mirrored sensory preferences for anaerobic packaging. These results indicate anaerobic packaging extends shelf-life properties and desirable sensory attributes throughout display and temperature abuse.

Evaluation of the storage life of vacuum packaged Australian beef.

To establish the shelf-life of vacuum packaged Australian beef, 15 Strip-loins and 15 Cube-rolls for each Processor (A, B, and C) were evaluated at two week intervals (since wk 10 to 20). Steaks on the trays were placed in retail cabinets at 3 °C. Shelf-life evaluation was based on off-odor (only at week 10), microbial analysis, lipid oxidation, and color assessment by trained panelist and Hunter colorimeter. Panelists detected "slightly off-odor" in both primal cuts for Processors B and C (P<0.05). Processor A primal cut steaks displayed better color scores as well as CIE L*, a*, b*, Chroma and Hue values during storage and display period than steaks from the other processors. Also, primal cuts from Processor A showed lower microbial counts and TBARS values with respect to other processors during the trial. Processor A cuts showed improved shelf life attributes initially which helps to explain its slow shelf-life deterioration.

Cerebral blood flow during static exercise in humans.

Cerebral blood flow (CBF) was determined in humans at rest and during four consecutive unilateral static contractions of the knee extensors. Each contraction was maintained for 3 min 15 s with the subjects in a semisupine position. The contractions corresponded to 8, 16, 24, and 32% of the maximal voluntary contraction (MVC) and utilized alternate legs. CBF (measured by the 133Xe clearance technique) was expressed by a noncompartmental flow index (ISI). Heart rate and mean arterial pressure increased from resting values of 73 (55-80) beats/min and 88 (74-104) mmHg to 106 (86-138) beats/min and 124 (102-146) mmHg, respectively (P less than 0.0005), during the contraction at 32% MVC. Arterial PCO2 and central venous pressure did not change. Corrected to the average resting PCO2, CBF during control was 55 (35-73) ml.100 g-1.min-1 and remained constant during contractions. Cerebral vascular resistance increased from 1.5 (1.0-2.2) to 2.4 (1.4-3.0) mmHg. 100 g.min.ml-1 (P less than 0.025) at 32% of MVC. There was no difference in CBF between the two hemispheres at rest or during exercise. In contrast to dynamic leg exercise, static leg exercise is not associated with an increase in global CBF when measured by the 133Xe clearance technique.

Epidural anaesthesia and cardiovascular responses to static exercise in man.

1. In human subjects, sustained static contractions of the knee extensors were performed in one leg with the same absolute (10% of the initial maximal voluntary contraction) and relative (30% of the maximal voluntary contraction immediately prior to the static exercise) intensities before and during epidural anaesthesia. Epidural anaesthesia reduced strength to 62 +/- 8% of the control value and partially blocked sensory input from the working muscles. During contractions performed with the same relative force, the increases in mean arterial pressure and heart rate were greater during control contractions than during epidural anaesthesia. During contractions at the same absolute force, there was no significant difference in magnitude of cardiovascular responses between control contractions and contractions performed during epidural anaesthesia. 2. The metabolic role in the exercise pressor reflex was assessed by applying an arterial leg cuff 10 s before cessation of exercise and through the following 3 min of recovery. Although mean arterial pressure and heart rate decreased immediately after cessation of exercise, application of the arterial occlusion cuff resulted in higher post-exercise mean arterial pressure and heart rate values. Control and epidural mean arterial pressures during arterial occlusion were not significantly different. 3. The results of this study suggest that the reflex neural mechanism rather than the intended effort (central command) is important in determining the blood pressure and heart rate responses to static exercise in man. That is, when epidural anaesthesia diminishes sensory feedback and produces muscular weakness, central command does not determine the cardiovascular response. This conclusion, however, is opposite to that derived from experiments with partial neuromuscular blockade which demonstrated the importance of central command in determining the cardiovascular response to static exercise (Leonard, Mitchell, Mizuno, Rube, Saltin & Secher, 1985). Taken together, these two studies are complementary and support the concept that both central and reflex neural mechanisms play roles in regulating arterial blood pressure and heart rate during static exercise in man.

Autonomic blockade and cardiovascular responses to static exercise in partially curarized man.

1. The cardiovascular responses, heart rate and mean arterial pressure, were followed in seventeen human subjects who performed static handgrip contractions for 2 min at the same absolute force (15% of the initial maximal voluntary contraction strength) before and during partial curarization. In control contractions the rate of perceived exertion was 10 exertion units, 16 units in contractions with tubocurarine which could be maintained and 20 units in contractions that could not be maintained. Control contractions increased mean arterial pressure by 6 mmHg from 89 mmHg while heart rate was unchanged from the resting value of 68 beats min-1. With tubocurarine, larger increases in mean arterial pressure of 11 mmHg and for heart rate of 8 beats min-1 were obtained during maintained contractions, and 15 mmHg and 16 beats min-1, respectively, during non-maintained contractions. 2. Atropine increased resting heart rate and blood pressure with tubocurarine to 107 beats min-1 and 98 mmHg, respectively, in seven subjects. The blood pressure response to exercise with tubocurarine was unaffected by atropine, but the heart rate increase was reduced from 15 to 4 beats min-1. 3. Propranolol reduced resting heart rate with tubocurarine to 56 beats min-1 with no effect on blood pressure in seven subjects. The cardiovascular responses to exercise with tubocurarine were unaffected by propranolol. In contrast, phentolamine reduced resting blood pressure with tubocurarine to 80 mmHg without affecting heart rate in seven subjects. Exercise responses with tubocurarine were unaffected by phentolamine. Combinations of atropine and propranolol in fourteen subjects or atropine and phentolamine in five subjects showed similar results during exercise with tubocurarine as with the sole use of the agents used to block autonomic receptors. 4. The results suggest that when partial curarization induces a disproportion between the signal from central command and that from exercising muscles, the larger signal arising from central command determines the magnitude of the cardiovascular responses. The centrally generated heart rate response is in part caused by vagal withdrawal. However, the blood pressure response cannot be attenuated by the sole use of alpha- or beta-receptor adrenergic blockade or combinations of these with atropine. This suggests that there may be greater redundancy in the autonomic control of blood pressure than in the vagal control of heart rate associated with central command during static exercise in man.

Cardiovascular responses to brief static contractions in man with topical nervous blockade.

1. We tested the hypothesis that afferent nerves from working muscles are important in determining the heart rate and blood pressure responses to brief maximal static exercise. 2. In twenty human subjects, the heart rate and arterial blood pressure responses to a brief maximal voluntary handgrip were studied before and after axillary nerve anaesthesia or to maximal one-leg knee extension before and after epidural anaesthesia at L3-L4. Maximal knee extension could not be accomplished without performing a 'Valsalva-like' manoeuvre, but during handgrip it was possible to avoid the use of muscles other than those directly involved in the contraction. Heart rate and blood pressure were also monitored during a Valsalva manoeuvre of similar duration to the maximal voluntary contractions (4 s). 3. During handgrip with normal breathing, axillary nerve anaesthesia reduced the heart rate response but had no effect on the blood pressure response. 4. During a Valsalva manoeuvre, blood pressure increased but heart rate remained stable as long as expiratory pressure was maintained. During one-leg knee extension, epidural anaesthesia reduced the blood pressure response; however, the reduction in blood pressure was probably due to a reduction in the simultaneously performed 'Valsalva-like' manoeuvre. 5. The results of this study suggest that afferent input from the working muscles is of importance for the heart rate responses to brief static muscle contractions. That such influence may be important for the blood pressure response remains unproven.