Glycogen metabolism in sheep and cattle shapes meat quality outcomes

Why glycogen metabolism became the focus#

Glycogen is the body's stored form of carbohydrate, a branched chain of glucose units built around a small protein core. Liver and muscle hold most of an animal's supply. In muscle, glycogen is not primarily under nutritional control in the way liver glycogen is; it responds more to stress and the energy demands placed on the tissue, a point the paper draws from earlier work by Harriss (1992).

The commercial reason for caring about glycogen is straightforward. At slaughter, muscle cells keep converting glycogen to lactic acid for a period afterward, and the paper describes this process as largely complete within 48 hours under refrigeration, or within 24 hours if carcasses receive electrical stimulation. If there is enough glycogen on board, the resulting acid build-up pushes the ultimate pH, referred to throughout as pHu, down to around 5.5. Too little glycogen and the pHu stays high, producing the dark-firm-dry condition that the paper says causes real financial losses for the sheep and cattle industries, citing Warriss (1990) and Fabiansson and colleagues (1989).

The authors note that most previous research used pHu itself as a stand-in measure for glycogen status, which they argue is a poor approach because pHu barely moves until glycogen has been heavily run down. Their aim was to look at glycogen directly, in live sheep and cattle, and to build a practical model for sampling muscle both on the farm and again at the abattoir.

Muscle types and why fibre composition matters#

Skeletal muscle is not uniform tissue. The paper describes three broad fibre types: type I, slow acting with low glycogen; type IIa, fast acting but also strongly aerobic, holding high glycogen and resynthesising it quickly, and least affected by stress; and type IIb, with lower glycogen reserves, slower resynthesis, and the greatest vulnerability to stress-induced depletion. These differences trace back to each fibre type's mix of enzymes controlling glycogen breakdown and rebuilding, summarised in the paper from Saltin and Gollnick (1983).

Because muscles are blends of these fibre types, the choice of sampling site matters. The paper identifies the m. semimembranosis and m. longissimus dorsi as tending toward type IIa, while the m. semitendinosis leans more to type IIb, drawing on Monin (1981) and Conlee and colleagues (1978). The semimembranosis and semitendinosis were used as the main biopsy sites in the experimental work described.

Cuts built from more type IIa fibre tend to be the higher quality ones, while a greater share of type IIb fibre is linked to toughness. This fibre-level detail explains why different muscles in the same carcase can behave quite differently under identical pre-slaughter conditions, a theme that recurs throughout the paper's experimental results.

How the experiments were designed#

The central sheep trial used 12 month old merino wethers fed a pelleted diet combining hay, barley and lupin in a 20:53:26 ratio, with four groups offered different multiples of maintenance intake, and eight sheep assigned to each treatment. An additional factor layered regular exercise onto the nutrition comparison, so that each nutrition level was also split between exercised and sedentary animals, again with eight sheep per treatment. The exercise group trotted for one hour at 8 to 9 km/h, three times a week for six weeks.

Muscle samples came from biopsies taken in the sheep shed and then again within 10 minutes of slaughter at the abattoir, allowing a direct before-and-after comparison. Sheep were transported for 60 minutes and slaughtered within two hours of arrival, a detail that matters because it shows even a short, apparently mild pre-slaughter sequence was enough to produce measurable glycogen loss.

Parallel work in cattle examined steers finished on a feedlot ration against steers grazing dry pasture in December in south west Western Australia, and also compared steers fed the same ration either in individual pens at a research station or in a commercial feedlot. A further cattle experiment compared glycogen in steers grazing dry summer pasture, sampled by biopsy on farm, with levels found immediately after slaughter following a 24 hour fast on farm, 18 hours of lairage and four hours of transport.

What the glycogen and pHu figures showed#

The nutrition trial in sheep produced a consistent pattern linking higher feed intake to higher muscle glycogen, with the same pattern appearing in both muscle types sampled and at both the on-farm and abattoir time points. The paper states that adequate glycogen for a normal pHu is in the order of 40 to 50 mmol glucose per kg muscle, and that a well fed, unstressed feedlot steer's longissimus dorsi would typically sit around 100 mmol glucose per kg, meaning more than half of that reserve would need to be lost before pHu started to rise.

Residual glycogen, the amount left in meat some 48 hours after slaughter once the post-mortem acid-producing process has largely finished, also tracked nutrition closely. The paper treats this residual pool as a buffer: once it falls below roughly 10 to 20 mmol glucose per kg, a pHu above 5.7 becomes likely. Consistent with this, pHu in the semimembranosis and longissimus dorsi barely moved with nutrition, but the semitendinosis, which inherently carries less glycogen, was markedly more sensitive to feed intake.

On the cattle side, steers grazing dry pasture carried dramatically lower muscle glycogen than those on a feedlot ration, and there was a further, smaller but still significant drop in glycogen comparing a commercial feedlot setting against individually penned animals. Regular exercise in the sheep trial raised both glycogen and residual glycogen, with the biggest gains in the semimembranosis and longissimus dorsi, the more aerobic, type IIa-dominant muscles, and smaller gains in the semitendinosis.

Losses between the farm and the abattoir#

One of the more striking findings concerns glycogen lost purely through ordinary handling between farm and slaughter, separate from anything to do with diet. In the sheep trial, glycogen fell by about 30 mmol glucose per kg, representing a 30 to 40% drop depending on muscle type, despite only one hour of transport and roughly half an hour to two hours of lairage. The paper notes this loss is not explained by post-mortem glycogen breakdown, since glycogen levels are known not to change within 30 minutes of death, citing Tarrant and McVeigh (1979).

A similar pattern appeared in the steers grazing dry pasture: a drop of around 20 mmol glucose per kg muscle, again amounting to 30 to 40% depending on muscle type, following a 24 hour fast on farm, 18 hours of lairage and four hours of transport. Combined with already low pasture-driven glycogen, this placed the semimembranosis and longissimus dorsi right at the 40 mmol glucose per kg threshold the paper associates with a rising pHu, and left the semitendinosis almost certain to show an elevated pHu.

The authors describe these contributing factors as additive, meaning modest nutritional shortfalls combine with modest handling losses to tip a carcase over the threshold into dark-firm-dry territory, even where no single factor looks severe on its own.

Stress, mixing and the limits of what pHu can tell us#

Much of the established literature on dark-firm-dry meat comes from Northern Hemisphere work with bulls, summarised in the paper through Tarrant (1989) and Warriss (1990). Mixing unfamiliar bulls triggers agonistic behaviour, including butting, pushing, mounting and chin-resting, which heavily depletes glycogen; fitting overhead electrical grids to stop mounting reduced the incidence of dark-firm-dry beef, which the paper takes as evidence that physical stress, rather than mixing itself, was the operative cause. Growth promotant implants that increase steers' aggressive behaviour were flagged as a possible added risk when unfamiliar animals are mixed, as were heifers in oestrus because of similar mounting behaviour.

Transport alone caused only small increases in pHu unless animals were physically floored, in which case dark-firm-dry beef was almost guaranteed. The study by Bray and colleagues (1989) is cited as a clear demonstration of additive stress: undernutrition, shearing or swimming on their own produced no significant change in pHu, but combining them produced a dramatic effect. Restraint stress in an unfamiliar setting, and overnight penning followed by 27 hours of lairage without food, were both shown elsewhere to deplete glycogen and raise pHu modestly.

Exercise itself is more complicated than a simple stress story suggests. Low intensity exercise such as a slow to brisk walk did not deplete glycogen in the paper's own work, and even a gallop might not cause a net loss because rapid resynthesis from lactate can occur during recovery. Sustained medium to high intensity work, trotting through to cantering, was the pattern reliably linked to glycogen depletion. This nuance matters for anyone trying to translate the dark-firm-dry literature into handling advice: not all movement before slaughter is equally risky, and the paper is explicit that pHu itself is too blunt a measure to capture these more subtle effects.

Repletion rates and the unanswered questions#

A recurring problem the paper raises is how slowly ruminants rebuild muscle glycogen once it has been lost, with published repletion times in the order of 3 to 11 days according to Warriss (1990) and Warriss and colleagues (1984). The authors suggest this slow rate may partly reflect how those studies were done, since Northern Hemisphere work commonly used tethered animals that were rarely exercised, a management system the paper links to slower adaptation for glycogen synthesis.

Harman and Pethick (1994), cited within this paper, found repletion rates markedly faster in exercised, trained sheep compared with the published tethered-animal data, suggesting Australian pasture and paddock-based systems might allow considerably quicker recovery, though the paper is careful to say actual rates under Australian conditions remain unknown. It notes that processors in Western Australia already favour 36 hours of lairage over 12 to 24 hours for cattle that have travelled around 10 hours, a practical judgement the paper says needs proper evidence behind it.

Glycogen is also floated as a possible integrated welfare indicator, since it reflects the balance between substrate supply and the hormonal signals of stress and energy demand across the whole production cycle, rather than a single acute hormone reading. We would treat that welfare application, and the broader on-farm management implications, as a promising direction rather than an established finding, since the paper itself repeatedly stresses that the underlying mechanisms and Australian repletion rates still need dedicated study. Readers following related work on muscle physiology may find it useful to compare this account with the discussion in the summary on nutrition, management and marbling outcomes in feedlot cattle, and with the broader account of what drives fat within cattle muscle, both held in the same RAAN Conference Proceedings collection alongside other papers from the Recent Advances in Animal Nutrition community.

Sources and further reading#

• Trove library search: find a library that holds the paper
• Meat & Livestock Australia: red meat industry research and marketing body
• Feedipedia animal feed database: an open-access database of animal feeds
• Australian Meat Processor Corporation: research for red meat processors

Questions#

— The Livestock Library team