Muscle Physiology and Feeding the Performance/Working Dog

Thanks kelticwarrior, if you understood heat build up, you wouldnt have made the original claim or still be trying to support it.Your original claim is contradicted in your opening paragraph with these words on the oxidative "it is a highly efficient way of releasing energy, compared to alternative fermentation processes such as anaerobic glycolysis."

 

Your confusing energy and heat generated in a process with heat build up and fatigue in a dog.Oxidative produces more energy than anaerobic glycolytic as a single process,but uses less energy and produces less toxicity which requires energy to process.Its a slower gradual process preventing energy loss as heat.Heat build up and fatigue are all about the heart output and mitochondrial function.When the mitochondria cannot function via aerobic means,heat will build up with an inability to dissipate it via the skin or respiratory system. If energy demands continue the blood pressure will start to fall,and the muscles and organs begin to fail.

First the supply to the skin is shut off disturbing heat regulation,then the muscles, ruining performance and the ability to regulate heat.Then the internal organs ruining ability to produce energy and process waste.Then the brain ruining the ability to think straight and multi task.Then finally the heart ruining the ability to keep alive and function.Which is why a dog will slow down, stop, and lie down to recover from the pain, inability to use the muscles, inability to think, and cardiac out put that is too low, depending on the severity of the heat build up and exhaustion from effort.

 

You're talking about heat shock which can cause what you call oxidative stress or its linked to oxidative stress. I don't think you will find many people that will allow their dog to run up to the point that the dog will experience this phenomena. If you're in a weight pull and the dog goes into heat shock I would recommend that he get picked up and the competition conceded because he won't be able to function properly and the pull will be over.

 

Thanks kelticwarrior,i covered heat and fatigue build up from mild discomfort to death,no matter what the performance,not only or simply heat shock.No ones talking about allowing their dog to go into shock but you.

The metabolic switch in the sled dog demonstrates their switching metabolism to utilize fat directly, aerobically and oxidatively.Conserving energy and its loss as heat allowing them to run cooler for longer.Making them essentially fatigue proof.

 

One should realize that the sled dogs are running in an extremely cold climate which helps a lot it keeping those types of dogs cool. The Sled dogs are also running at a low intensity of exercise on the oxidative system where as even though once a Bulldog switches over to the oxidative energy system, he can still can work at a very high intensity on this energy system which I believe is unique to these animals. The Bulldog will build up heat as he goes along with his work and will get hotter as he goes along the by product of accessing the oxidative system being heat. The oxidative system is the system where he is going to be doing most of his work throughout the greater duration of the weight pull so I believe the conditioner should make sure that dog is accustomed to the heat generated from the energy system and the initial hot spot the dog will experience when first switching onto the oxidative system. The bulldog has to be used to working on this system because its is going to have to kick in once the glycogen levels from the carbohydrates in the diet get depleted to the extent that he has to do the switch. The dogs will all get hot during work and they will get hotter and hotter to the point of failure if the pull goes on for a long duration. Just a point of note is that a truly game dog will continue pulling even though he has reached that point at the limits of his endurance and is in shock and dehydration, he will still go, its up to the handler to decide when to unhook the dog from the trolley or not.

You started talking about heat shock not I when you stated quote:-First the supply to the skin is shut off disturbing heat regulation,then the muscles, ruining performance and the ability to regulate heat.Then the internal organs ruining ability to produce energy and process waste.Then the brain ruining the ability to think straight and multi task.Then finally the heart ruining the ability to keep alive and function.Which is why a dog will slow down, stop, and lie down to recover from the pain, inability to use the muscles, inability to think, and cardiac out put that is too low, depending on the severity of the heat build up and exhaustion from effort.

 

Thanks kelticwarrior, that quote isnt explaining heat shock, its explaining fatigue and its effects on heat.

The key for the game dog is their type 2a fibers. They have a good resistance to fatigue,a high force output,a fast contraction speed,a high capacity to produce ATP by oxidative metabolic processes,a high oxidative capacity,a high glycolytic capacity,a high mitochondrial density,medium to large myoglobin content,large motor units, large motor neurons,long term anaerobic capacity,high stores of creatine phosphate and glycogen,medium tryglyceride stores, and a good capillary density and resistance to fatigue.

Both type 1 and type 2 fibers have oxidative and glycolytic mitochondria, and creatine phosphate, gycogen and trygliceride stores.When the dog first starts at what ever intensity, it will use the phosphogen system followed by the glycolytic and oxidative.The more demand for ATP the more reliance on the phosphogen and the glycolytic systems.Only the fast oxidative slow glycoltic can produce the energy for sustained effort at higher intensity for longer which is what the type 2a fibers are designed for.

The sled dog flips a metabolic switch to stop taxing the glycogen stores to run the muscles directly off fat as the primary fuel source,but they still use the glycolytic system.The game dog has a higher reliance on the glycolytic than the sled dog but both also rely on the aerobic system.The greyhound has a higher reliance on the phosphogen system ,fast anaerobic glycolytic and the anaerobic alactic than both the sled dog and the game dog.

When you get a heat spot its not caused by the oxidative but by the quick loss of energy as heat by the glycolytic system producing lactate and hidrogen ion build up and need for processing .The glycolytic is the first stage in the aerobic production of ATP from glucose via glycogen and lactate.Its followed by the krebs cycle and finally oxidative phosphorylation giving the max yield of ATP.The more you use ATP the more it needs to be produced and resynthesized and when the mitochondria fail in their ability to supply ATP aerobically, fatigue is the byproduct and the heat loss more rapid. Hydrogen ions build up ,ability to utilize oxygen decreases and more anaerobic metabolism is required to produce pyruvate and lactate from glucose and convert lactate back to glucose.

The ATP made from glucose is by conversion to pyruvate whih converts to lactate,the reverse process of converting lactate to glucose is a higher energy expensive process.As ATP demands increase beyond the mitochondrial ability to use and resynthesize it, anaerobic metabolism increases.The mitochondrial failure will effect the heart muscle cardiac output and the ability to maintain blood pressure, the only way the body can maintain it is to restrict the blood supply to the organs.

When the body is in fatigue and switches to more anaerobic metabolism with retricted blood supply,core heat rises and the ability to supply the skin and muscles effects heat control, oxygen delivery, and respiration causing intolerance to heat.If it cannot be dissipated via the skin and lungs the core temperature will rise further and the muscles will be forced to use more anaerobic metabolism to produce the ATP building more discomfort,more energy demand, and quicker loss of energy as heat.

The only way to lessen the need for the anaerobic,glycolytic and ATP ,is to lessen the demand by improving economy of motion improving glycogen and lactate efficiency and increasing the strength reserve.

All the fibers have to be trained and all have oxidative and glycolytic capacity, but they dont all respond the same to the same type of training.The energy systems that supply them also have to be trained and require different intensities, different recovery times, and different fuel sources to increase their efficiency.

The game dog needs both a high anaerobic capacity and a high aerobic capacity, but it needs the lowest level of anaerobic capacity relative to the aerobic capacity before ability to contract strongly or quickly is compromised. If the anaerobic capacity is to high the ability to utilize strength quickly will be improved but the ability to utilize the aerobic capacity and oxygen will be compromised and the lactate levels and hydrogen ions will be high.

In conditioning it is a necessity to raise the anaerobic capacity and utilize the anaerobic system from the phosphogen system to the lactate hydrogen (lactic acid) system to increase its efficiency and lessen the heat loss. But it must be lowered relative to the aerobic capacity before competition without compromising its efficiency.Which allows the dog to utilize and maintain the glycogen stores with out a high build up of hydrogen ions, oxygen use,energy loss,fatigue and discomfort, mitochondrial failure,and intolerance to heat.

 

Slim12,the science is all their for the game dog as much as we know for any dog.Its all about increasing the oxidative aerobic capacity of each fiber to increase its endurance, and increasing its glycolytic capacity increasing its strength speed and power.When each fiber has the highest percentage of each its at its peak.

When the game dog wrestles in and out of holds it will utilize both the glycolytic and oxidative to utilize the most efficient means to fuel contractions.The energy demands from the mouth to the limbs to the trunk will all be different.But the greater the strength and aerobic capacity the lesser the energy demands at all effort levels what ever the performance, and the greater the physiological efficiency.

Is it true in all cases that a game dog cant be fed like one and expected to perform like the others? a game dog surely must be fed like one if it ever hopes to emulate one in performance.The sled dog can sprint walk trot pull run for longer than any other breed,its just not as fast powerful or strong.The game dog is and will tax the anaerobic lactic system and glycolysis more than a sled dog.What the game dog needs is greater ability to utilize the aerobic system,at each effort level, and more efficiently use the glycolytic and phosphogen and anaerobic systems.The more it can fuel glycolysis aerobically the greater the energy produced and conserved.

You can find out the fibers in each muscles through a biopsy but you can have a rough measure what the fibers percentage is in a movement if you can find the one rep max and measure a percentage for reps.The higher the one rep max increase the less reliance on the anaerobic system and the more efficient glycolytic and aerobic metabolism.The strength, power, endurance, lactate levels, aerobic and anaerobic capacity can be measured,recorded and used to plan what work, when, how, and why.The more science you have to utilize the less need to be creative and the art used takes on a higher form and purpose.

 

These are two absolutely brilliant posts Tigerlines. thank you

 

Thanks kelticwarrior,no problem.

 

Slim12,weight pull.Carts sleds etc, its been used for centuries.Their where two rules to bull baiting,to pin or to pull it round the ring.The bull weighed 1000-2000lb.The dog had to be small enough to catch or break its fall.


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Assessment of alterations in triglyceride and glycogen concentrations in muscle tissue of Alaskan sled dogs during repetitive prolonged exercise.
McKenzie EC1, Hinchcliff KW, Valberg SJ, Williamson KK, Payton ME, Davis MS.

OBJECTIVE:To assess changes in muscle glycogen (MG) and triglyceride (MT) concentrations in aerobically conditioned sled dogs during prolonged exercise.
ANIMALS:54 Alaskan sled dogs fed a high-fat diet.
PROCEDURES:48 dogs ran 140-km distances on 4 consecutive days (cumulative distance, up to 560 km); 6 dogs remained as nonexercising control animals. Muscle biopsies were performed immediately after running 140, 420, or 560 km (6 dogs each) and subsequently after feeding and 7 hours of rest. Single muscle biopsies were performed during recovery at 28 hours in 7 dogs that completed 560 km and at 50 and 98 hours in 7 and 6 dogs that completed 510 km, respectively. Tissue samples were analyzed for MG and MT concentrations.
RESULTS:In control dogs, mean +/- SD MG and MT concentrations were 375 +/- 37 mmol/kg of dry weight (kgDW) and 25.9 +/- 10.3 mmol/kgDW, respectively. Compared with control values, MG concentration was lower after dogs completed 140 and 420 km (137 +/- 36 mmol/kgDW and 203 +/- 30 mmol/kgDW, respectively); MT concentration was lower after dogs completed 140, 420, and 560 km (7.4 +/- 5.4 mmol/kgDW; 9.6 +/- 6.9 mmol/kgDW, and 6.3 +/- 4.9 mmol/kgDW, respectively). Depletion rates during the first run exceeded rates during the final run. Replenishment rates during recovery periods were not different, regardless of distance; only MG concentration at 50 hours was significantly greater than the control value.
CONCLUSIONS AND CLINICAL RELEVANCE:Concentration of MG progressively increased in sled dogs undergoing prolonged exercise as a result of attenuated depletion.

Lipid metabolite responses to diet and training in sled dogs.
Reynolds AJ1, Fuhrer L, Dunlap HL, Finke MD, Kallfelz FA.

Two groups of Alaskan Huskies were fed either a high fat (HFD) or a high carbohydrate diet 4 wk before and during an 8-wk conditioning program. Aerobic bouts of exercise were performed before and after conditioning. Blood samples taken before and after each exercise test were analyzed for serum concentrations of free fatty acids (FFA), triglycerides (TG), vitamin E, glucose and serum lipase activity. The post-exercise FFA and TG values were greater in the HFD group both before and after training. There were no significant differences in plasma vitamin E or in serum lipase activity between diet groups. It is concluded that after an adequate period of adaptation, prolonged feeding of a HFD safely enhances the availability of local and peripheral lipid stores during exercise. Although the elevated levels of FFA and TG associated with HFD suggest enhanced potential for performance, further study of more prolonged and possibly more intense exercise is necessary to confirm this theory.

Factors affecting the rate of phosphocreatine resynthesis following intense exercise.
McMahon S1, Jenkins D.

Within the skeletal muscle cell at the onset of muscular contraction, phosphocreatine (PCr) represents the most immediate reserve for the rephosphorylation of adenosine triphosphate (ATP). As a result, its concentration can be reduced to less than 30% of resting levels during intense exercise. As a fall in the level of PCr appears to adversely affect muscle contraction, and therefore power output in a subsequent bout, maximising the rate of PCr resynthesis during a brief recovery period will be of benefit to an athlete involved in activities which demand intermittent exercise. Although this resynthesis process simply involves the rephosphorylation of creatine by aerobically produced ATP (with the release of protons), it has both a fast and slow component, each proceeding at a rate that is controlled by different components of the creatine kinase equilibrium. The initial fast phase appears to proceed at a rate independent of muscle pH. Instead, its rate appears to be controlled by adenosine diphosphate (ADP) levels; either directly through its free cytosolic concentration, or indirectly, through its effect on the free energy of ATP hydrolysis. Once this fast phase of recovery is complete, there is a secondary slower phase that appears almost certainly rate-dependent on the return of the muscle cell to homeostatic intracellular pH. Given the importance of oxidative phosphorylation in this resynthesis process, those individuals with an elevated aerobic power should be able to resynthesise PCr at a more rapid rate than their sedentary counterparts. However, results from studies that have used phosphorus nuclear magnetic resonance ((31)P-NMR) spectroscopy, have been somewhat inconsistent with respect to the relationship between aerobic power and PCr recovery following intense exercise. Because of the methodological constraints that appear to have limited a number of these studies, further research in this area is warranted.

Brain glycogen supercompensation following exhaustive exercise.
Matsui T1, Ishikawa T, Ito H, Okamoto M, Inoue K, Lee MC, Fujikawa T, Ichitani Y, Kawanaka K, Soya H.

Brain glycogen localized in astrocytes, a critical energy source for neurons, decreases during prolonged exhaustive exercise with hypoglycaemia. However, it is uncertain whether exhaustive exercise induces glycogen supercompensation in the brain as in skeletal muscle. To explore this question, we exercised adult male rats to exhaustion at moderate intensity (20 m min(-1)) by treadmill, and quantified glycogen levels in several brain loci and skeletal muscles using a high-power (10 kW) microwave irradiation method as a gold standard. Skeletal muscle glycogen was depleted by 82-90% with exhaustive exercise, and supercompensated by 43-46% at 24 h after exercise. Brain glycogen levels decreased by 50-64% with exhaustive exercise, and supercompensated by 29-63% (whole brain 46%, cortex 60%, hippocampus 33%, hypothalamus 29%, cerebellum 63% and brainstem 49%) at 6 h after exercise. The brain glycogen supercompensation rates after exercise positively correlated with their decrease rates during exercise. We also observed that cortical and hippocampal glycogen supercompensation were sustained until 24 h after exercise (long-lasting supercompensation), and their basal glycogen levels increased with 4 weeks of exercise training (60 min day(-1) at 20 m min(-1)). These results support the hypothesis that, like the effect in skeletal muscles, glycogen supercompensation also occurs in the brain following exhaustive exercise, and the extent of supercompensation is dependent on that of glycogen decrease during exercise across brain regions. However, supercompensation in the brain preceded that of skeletal muscles. Further, the long-lasting supercompensation of the cortex and hippocampus is probably a prerequisite for their training adaptation (increased basal levels), probably to meet the increased energy demands of the brain in exercising animals.

Effect of increased dietary protein and decreased dietary carbohydrate on performance and body composition in racing Greyhounds.
Hill RC1, Lewis DD, Scott KC, Omori M, Jackson M, Sundstrom DA, Jones GL, Speakman JR, Doyle CA, Butterwick RF.

OBJECTIVE:To determine effects of increased dietary protein and decreased dietary carbohydrate on hematologic variables, body composition, and racing performance in Greyhounds.
ANIMALS:8 adult Greyhounds.
PROCEDURE;dogs were fed a high-protein (HP; 37% metabolizable-energy [ME] protein, 33% ME fat, 30% ME carbohydrate) or moderate-protein (MP; 24% ME protein, 33% ME fat, 43% ME carbohydrate) extruded diet for 11 weeks. Dogs subsequently were fed the other diet for 11 weeks (crossover design). Dogs raced a distance of 500 m twice weekly. Rectal temperature, hematologic variables before and after racing, plasma volume, total body water, body weight, average weekly food intake, and race times were measured at the end of each diet period.
RESULTS:When dogs were fed the MP diet, compared with the HP diet, values (mean +/- SD) differed significantly for race time (32.43 +/- 0.48 vs 32.61 +/- 0.50 seconds), body weight (32.8 +/- 2.5 vs 32.2 +/- 2.9 kg), Hct before (56 +/- 4 vs 54 +/- 6%) and after (67 +/- 3 vs 64 +/- 8%) racing, and glucose (131 +/- 16 vs 151 +/- 27 mg/dl) and triglyceride (128 +/- 17 vs 104 +/- 28 mg/dl) concentrations after racing.
CONCLUSIONS AND CLINICAL RELEVANCE:Greyhounds were 0.18 seconds slower (equivalent to 0.08 m/s or 2.6 m) over a distance of 500 m when fed a diet with increased protein and decreased carbohydrate. Improved performance attributed to feeding meat to racing Greyhounds apparently is not attributable to increased dietary protein and decreased dietary carbohydrate.

Metabolic responses to exhaustive exercise in racing sled dogs fed diets containing medium, low, or zero carbohydrate.
Hammel EP, Kronfeld DS, Ganjam VK, Dunlap HL Jr.

Eighteen racing sled dogs were assigned to three diets containing protein, fat, and carbohydrate in proportions as follows: diet A, 39:61:0; diet B, 32:45:23; and diet C, 28:34:38 on an available energy basis. The dogs were studied through a 28-week training period and subjected to three special tests, the first after 12 weeks training, the second at 24 weeks, and the third 4 weeks later. Overnight fasting, resting blood samples were taken before exercise, then about 5 or 30 min after exercise in the first 2 tests, or 1,5...30 min after exercise in the third test. Negligible changes in the red cell indices or serum concentrations of total protein, sodium, and urea indicated that there were no major water shifts. Significant decrements were found in serum concentrations of albumin (3% of resting value), calcium (4%), magnesium (13%), and inorganic phosphorus (39%). Significant increments were found in serum concentrations of creatinine (50%) and activities of glutamic-pyruvic and glutamic-oxalacetic transaminases (31 and 52%, respectively). None of the above variables showed differences between diets, exercise bouts, or time after exercise. Significant decrements in plasma cholesterol (D, mg/100 ml) were linearly related to the initial concentration (I mg/100 ml); D - 0.161 I - 17 mg/100 ml. Hyperglycemic responses were exhibited by 14 dogs in the 3rd test, including five dogs on diet A. Resting plasma glucose concentrations, peak values after exercise, and removal rates were the same in dogs fed all three diets. Blood lactic acid concentrations were linearly related to plasma glance (two from each group) had significantly higher peak lactic/glucose ratios tthan the six "worst" dogs, but there was no significant difference between diets in other measures of glucose or lactic acid. Plasma concentrations of free fatty acids, acetoacetic acid and 3-OH-butyric acid reached a maximum 10 min after exercise. Peak values and mean increments of free fatty acids were highest in dogs fed diet A. Also, mean free fatty acid increment was significantly higher in the six best dogs than in the six worst. An enhanced ability to mobilize body fat should confer an advantage in a dog subjected to prolonged strenous exercise in which fatty acid oxidation accounts for most of the oxygen consumption

Effect of postexercise carbohydrate supplementation on muscle glycogen repletion in trained sled dogs.
Reynolds AJ1, Carey DP, Reinhart GA, Swenson RA, Kallfelz FA.

OBJECTIVE:To evaluate the effect of immediate postexercise carbohydrate supplementation on muscle glycogen (MG) repletion during the first 4 hours of recovery in sled dogs.
ANIMALS:24 Alaskan Huskies.
PROCEDURE: Dogs were assigned to 1 of 3 treatment groups, and a muscle biopsy specimen was obtained 1 hour before and immediately (group A) or 4 hours (groups B and C) after a 30-km run. Immediately after exercise, dogs in group A and group C were given water; dogs in group B were given a glucose polymer solution (1.5 g/kg of body weight) in water.
RESULTS:At 4 hours after exercise, MG concentration was significantly greater in group-B than in group-C dogs; the value in group-C dogs was not different from the value in group-A dogs immediately after exercise. Assuming similar rates of glycogen depletion between treatment groups, during the first 4 hours of recovery, group-B dogs replaced 49% of the glycogen used during exercise. Plasma glucose concentration was significantly greater in group-B than in group-A and group-C dogs at 100 minutes after exercise.
CONCLUSIONS:Immediate postexercise carbohydrate supplementation in sled dogs leads to increased glucose concentration, which in turn promotes more rapid rate of MG repletion in the first 4 hours of recovery than is observed in dogs not given supplements.
CLINICAL RELEVANCE:For dogs running in multiple heats on a single day or over several consecutive days, immediate postexercise carbohydrate supplementation may promote more rapid and complete recovery between bouts of exercise.

Effect of diet and training on muscle glycogen storage and utilization in sled dogs.
Reynolds AJ1, Fuhrer L, Dunlap HL, Finke M, Kallfelz FA.

Two groups of eight Alaskan huskies fed either a high-fat (HFD; 60% kcal from fat and 15% kcal from carbohydrate) or a high-carbohydrate diet (HCD; 60% kcal from carbohydrate and 15% kcal from fat) performed standard aerobic (1 h at 4 m/s on a 0% slope) and anaerobic (3 min at 6.7 m/s on a 10% slope) tests before and after training. Before and immediately after each exercise test, venous blood samples were collected and analyzed for lactate and pyruvate, and muscle biopsies were obtained under local anesthesia from the semitendinosus muscle and analyzed for total muscle glycogen (TMG) concentration. Training was associated with a significant increase in preexercise TMG in both diet groups; this effect was most marked in the HCD. There was no effect of diet or training on TMG utilization during the aerobic tests. The rate of TMG utilization during the anaerobic tests was between 20 and 40 times greater than that measured during the aerobic tests. The pre- to postexercise change in TMG was dependent on preexercise TMG in the HCD and HFD for both anaerobic tests (HCD: P < 0.01, r = 0.81; HFD: P < or = 0.03, r = 0.66). It is concluded that the increased glycogen storage associated with the HCD was more than offset by the more rapid rate of glycogen utilization in this group. HFD facilitated carbohydrate sparing during intense exercise and should thus be a better dietary strategy for endurance in sled dogs

Liver and muscle glycogen content after glucose infusion in dogs.
Brzezińska Z, Kobryń A.

The purpose of the present work was to determine the changes in the liver and muscle glycogen content during and after glucose infusion to elucidate tissue distribution of glucose in dogs. Glucose was infused intravenously during 2 hours in a dose of 1.7 mM . kg-1 . min-1. At designated time intervals venous blood samples were taken for determinations of glucose concentration, and the liver as well as muscle tissue samples were taken using a needle biopsy technique for determination of glycogen content. Liver glycogen content was increased significantly already at 30 th min of glucose infusion, and 60 min after termination of the infusion, it was by 53.1 +/- 0.58 and 174.3 +/- 48.3 mM glucosyl units per kg of wet liver higher than the initial value. Muscle glycogen content was also increasing progressively during the whole period of glucose infusion, and 1 h after termination of the infusion it was by 30.8 +/- 2.5 mM glucosyl units per kg of wet muscle above the initial value. It was calculated that 24.7 per cent of the glucose infused to dogs was stored as liver glycogen and 63.4 per cent as muscle glycogen.

Recovery of muscle glycogen concentrations in sled dogs during prolonged exercise.
McKenzie E1, Holbrook T, Williamson K, Royer C, Valberg S, Hinchcliff K, Jose-Cunilleras E, Nelson S, Willard M, Davis M.

PURPOSE:To determine the depletion of muscle glycogen during five consecutive days of endurance exercise in Alaskan sled dogs consuming a high-fat, low-carbohydrate diet.
METHODS:Forty-two fit Alaskan sled dogs were used in the study, of which six dogs served as nonexercising control animals. The remaining 36 dogs ran 160 km x d(-1) for up to 5 d while consuming a diet providing approximately 50% of calories as fat and 15% as carbohydrate. Muscle biopsies were performed on six randomly selected dogs before feeding and within 4 h after each 160-km run was completed. Muscle samples were prepared for analysis of glycogen content and myosin ATPase staining. Serum creatine kinase (CK) activity was measured once before exercise and after each 160-km run.
RESULTS:Thirty-three of 36 dogs completed the runs. Muscle glycogen concentration was highest in sedentary dogs (340 +/- 102 mmol x kg(-1) dry weight), declined to 73 +/- 16 after 160 km and subsequently increased to similar levels between 320 and 800 km (320 km: 177 +/- 34; 800 km: 213 +/- 44). Postexercise serum CK activity was significantly elevated throughout the study.
CONCLUSION:Skeletal muscle in Alaskan sled dogs has remarkable glyconeogenic ability as demonstrated by repletion to greater than 50% of resting muscle glycogen concentrations after the second of five consecutive 160-km runs even when fed a low-carbohydrate, high-fat diet. Whether this finding is attributable to rapid repletion of muscle glycogen during brief recovery periods versus progressive utilization of alternative substrates remains to be investigated.

Metabolic changes in skeletal muscle and blood of greyhounds during 800-m track sprint.
Dobson GP1, Parkhouse WS, Weber JM, Stuttard E, Harman J, Snow DH, Hochachka PW.

The aim of this study was to examine some metabolic properties and changes that occur in skeletal muscle and blood of greyhounds after an 800-m sprint. Three prime moving fast-twitch muscles were selected: biceps femoris (BF), gastrocnemius (G), and vastus lateralis (VL). The amount of glycogen utilized during the event was 42.57, 43.86, and 42.73 mumol glucosyl units/g wet wt, respectively. Expressed as a function of race time (48.3 +/- 0.7 s, n = 3), the mean rate of glycogen breakdown was 53.48 +/- 0.5 mumol.g wet wt-1.min-1 during the sprint. This is equivalent to an ATP turnover of 160 mumol.g wet wt-1.min-1, assuming 100% anaerobic conversion to lactate. This represents a conservative estimate, since greyhound muscle is heterogeneous and comprised of a large percentage of fast-twitch oxidative fibers (Armstrong et al., Am. J. Anat. 163: 87-98, 1982). The large decrease in muscle glycogen was accompanied by a 6- to 7-fold increase in muscle lactate from 3.48 +/- 0.13 to 25.42 +/- 3.54 (BF), 2.54 +/- 1.05 to 18.96 +/- 2.60 (G), and 4.57 +/- 0.44 to 30.09 +/- 1.94 mumol.g wet wt (VL), and a fall in muscle pH from 6.88 +/- 0.03 to 6.40 +/- 0.02 (BF), 6.92 +/- 0.02 to 6.56 +/- 0.02 (G), and 6.93 +/- 0.02 to 6.47 +/- 0.01 (VL). Cytosolic phosphorylation potential in BF decreased 10-fold from 11,360 +/- 680 to 1,184 +/- 347, and redox potential decreased 5-fold, indicating a marked reduction in the cytosol at this time.

Hematological and metabolic responses to training in racing sled dogs fed diets containing medium, low, or zero carbohydrate.
Kronfeld DS, Hammel EP, Ramberg CF Jr, Dunlap HL Jr.

In a 28 week study, 18 racing sled dogs were trained to maximal fitness in 12 weeks, sustained through a racing season of 12 weeks, followed by gradual of training of 4 weeks. The dogs were fed a predominantly cereal diet prior to the study; experimental diets containing more chicken and meat by products were introduced from the 2nd to the 4th week of training. On an energy basis, the diets contained protein, fat, and carbohydrate in the proportions of 39:61:0 (diet A), 32:45:23 (diet B), and 28:34:38 (diet C). Blood samples were taken at rest just before the start of training, at 6, 12,24 and 28 weeks; 33 variables were measured on most samples. The results were subjected to analysis of variance. No adverse effects were observed in dogs fed the extreme diet A. Significant relationships to training were shown by serum glutamic oxaloacetic transaminase, creatinine, packed cell volume, calcium, hemoglobin, and globulin. Serum cholesterol concentration increased with the introduction of the higher protein-fat diets; the high concentrations attenuated with time but rose again when training was abated. Dogs on diet A maintained higher serum concentrations of albumin, calcium, magnesium, and free fatty acids during the racing season than did dogs fed diets B or C. They also exhibited the greatest increases in red cell count, hemoglobin concentration, and packed cell volume during training. High values of red cell indices were not sustained through the racing season in dogs fed diet C. In addition to attributes already widely appreciated, viz. a higher energy density an digestibility, the carbohydrate-free, high-fat diet A appeared to confer advantages for prolonged strenuous running in terms of certain metabolic responses to training.

 

Thanks slim12,
Recovery for what is the question,the dog will recover in 3-6min(ATP CP in 2-3min the rest for the CNS).Its only one exercise,in contrast a human would have to do the same for at least 4 exercises.You will still be able to train the anaerobic and aerobic system in the same session,later or the next day but intense sprints jumps power or max strength that rely on CNS stimulation ATP PC stores and glycogen should be left for 48-72hrs.

The max may increase as work continues it depends on how much strength plays a part in it.

How often you find the max depends on why your building up to it.The general rule is once every 4 wks if you plan on using it to base work off say in a 3-4wk cycle.Or you could use the max effort method where you build up to a new 1 rep max effort once a week every week for 3-6wks(3wks recommended)using the same exercise.

I wouldnt advise you to utilize or implement any form of training you do not have full understanding of implication and application to the type of adaption you desire.

The best sources in the world of sports science training and planning from strength speed and power to ultra endurance are Yuri Verkhoshansky,Leonid Matveyev,Alexei Medvedyev,Anatoliy Bondarchuk,Vladimir Issurin,Tudor Bompa,Michael Yessis,Mell Siff,Jan Olbrecht,Randy wilber,Bobby McGee etc,which can only help with conditioning and its planning alongside the canine and animal sports science research.

 

Thanks slim12,

Whats stopping you getting intense sprinting out of the dog following the 6min recovery?

whats stopping you using a max rep converter?

Why is it an either or scenario with regards to sports science, dogmen, and a keep?

Does fat bill look after your hard earned money and dogs life, or do you?

 

Thanks slim12,
You didnt answer one of my questions.

If you dont want to utilize sports science, dont.

Your "eye" cant tell what flips the metabolic switch or when, or the maximum efficiency of strength, or the anaerobic capacity relative to the aerobic. So your "art" cant implement them for the dog to tell you what where when and how with conditioning and recovery.


If you have no experience of study and implementation of the science of those listed, your contradicting your earlier claim not to doubt or dispute science or to post on things you have no experience of.

Those i listed werent mentioned as conditioners requiring permission or in opposition to others,yours were.

A max rep converter doesnt need a rep max test,thats what its for.


The observed tells the "eye" through the scientific method creating the "art".Their is no great art without great science.Their is no art that trumps science.


Sports science looks nothing like world class architecture on paper,unless your "eye" is blind.Its proven to the "eye" at the highest level and under a microscope at the lowest.

 

THE BUGARIAN SYSTEM
Ivan Abadjiev is one of the most successful and prominent coaches in the history of Olympic weightlifting. He is the author of the famous Bulgarian training methodology that is currently widely followed by many elite lifters and coaches. • He was the first Bulgarian weightlifter to be awarded with the top national title of the Merited Master of Sports after he won a silver medal at the 1957 World Championship. • It was however coaching that brought Abadjiev to the level of unprecedented admiration of the weightlifting experts. Abadjiev coached the Bulgarian national team in 1969 -1989 and 1997 - 2000 and was able to bring it from a mediocre standing to the elite super power of Olympic weightlifting. • Abadjiev’s training system was based on high intensity sessions. Unlike the traditional Russian training methodology, Abadjiev’s sessions included mostly only classic Olympic lifts performed with lower repetitions but on maximum weights. Supporting lifts were limited predominately to squats. Abadjiev’s method contradicted major established views on training process and brought him as many followers as opponents. And, of course, it was proved to work at the time based on the medal track of Abadjiev’s students. • During his two decades of work with the national Team Bulgaria and with Team Turkey (in the late 1990s), Abadjiev prepared 12 Olympic champions, 13 silver Olympic medalists, 4 bronze Olympic medalists, 57 world champions, 64 European champion

• The physical ability of an athlete in all sports is viewed as an exhibition of three fundamental qualities: – Strength – Speed – Endurance • These qualities should not be viewed separately from one another • Instead they should be seen as an integrative system to be trained and developed simultaneously in a specific manner, according to the characteristics of the specific sport

• The keys to success of the Bulgarian Method is firmly rooted in scientific principles such as cell biology, molecular genetics, cell physiology, and other neuro-biological systems

The Four Key Scientific Principles of WHY IT WORKS:
• Actin Myosin Complex – Single Rep VS Multiple Reps
• Specific Adaptation to Imposed Demand - S.A.I.D.
• Jacob and Monod’s Gene Protein Response
• Hyden’s Theory of Protein Memory

The Russian Methodology – Multiple Reps • Called for a series of steps involving periodization, prep stage, interim stage and competition stage

The Bulgarian Method – Single Reps, Max • Has side-stepped the traditional weight training techniques employed involving multiple repetitions at “less-than- maximal ”workloads with a gradual build-up to higher weights • Was based on a single rep at the athletes
’
personal maximum • Before a maximum or PR (personal record) attempt is made, the skeletal muscle fibers are at maximal efficiency, i.e. protein levels, energy levels (ATP, glucose etc), ions (calcium etc) are at maximum output potential

• The Bulgarian Method contrasts with models based on repetition, in which the molecules (proteins, ATP etc.) are partially (or wholly!) used up • In this form of training, fibroblasts form around the skeletal muscle fibers, which use up invaluable ATP supplies • The muscle fibers themselves grow in mass, but are less efficient when the time arrives for PR attempts

• During single rep PR attempts, the speed of muscle contraction reaches very high levels which results in greater muscle mass • This is due in large part to an increase in the SR/actin-myosin complex ratio • This ratio is fundamental since the SR complex supplies the calcium essential for maximal contraction during later tries • During slower lifting or reduced-load lifting with repetition the SR/actin-myosin complex ratio actually decreases! • Another disadvantage of repetitive training with sub-maximal loads is the increased number of mitochondria produced in the muscle cell which actually depletes the muscle fiber of ATP • One might expect that the available ATP would increase as the number of mitochondria increase but this is not the case!

• Weight lifters who train with the Bulgarian single rep PR load system typically have a difficult time adjusting during the initial week of training • During the first week of weight training athletes will invariably suffer from the following symptoms: • Muscle soreness • Fatigue • Decline in performance • In the following week of training, weightlifters no longer experience the intense muscle soreness or fatigue • Many athletes have experienced an improvement in performance, • Able to lift higher maximum weights on prescribed days • Positive psychological change occurs, which made lifting seem easier


• The Bulgarian Method has been shown to heighten lifters’stress-limitation threshold – Does not occur in the traditional multiple-repetition methods at lower loads with gradual build-up • In other methods, athletes were urged to rest for 2-3 weeks to allow recovery from damaged muscle fibers • The fibers are not typically damaged but merely stretched -this is what causes the soreness (not fatigue) • And so our athletes were able to side-step the suggested recovery period and continued to train during the following week with excellent results • This does not mean that the Bulgarian Method does not allow for recovery periods and the rigorousness of training varies greatly on a weekly, monthly, and yearly basis – There are some months, in fact, when rigorous training takes place during only one week with three “lighter ”weeks

• Hans Selye, at McGill University, developed the concept of stress in living organisms and described the subsequent phenomenon of “adaptation to stress ” • In Selye’s experiments on rats, he noted that “stress ” was characterized by a syndrome consisting of a triad of symptoms: • Hypertrophy of the surrenal cortex • Atrophy of the lymphatic organs • Ulcers in the Gastro Intestinal tract • Divided the so-called “adaptation to stress ” into three stages • The alarm reaction • Resistance • Exhaustion

• Stress (stimulus) comes in many forms – Exercise / Physical Activity • Adaptation (response) to stress varies – Specific responsive biological adjustment to stress – Muscle, bone, heart, lung, vasculature, tendons, ligaments, joint cartilage, etc. • If stress is too great, or sufficient recovery time not allowed, then adaptation may be inhibited and there will be a decrement in capacity of physiological systems leading to exhaustion
• Adaptation is complete after limited time span – Continued stimulus no longer elicits adaptation

• In sports, stress is controlled and contained by the “Stress Limitation System ”
• During heavy exercise the Central Nervous System (CNS) becomes excited (also because of a marked increase in the production of adrenalin)
• If your brain and CNS become over-excited, it can run out of control and need some form of inhibition to keep it acting normal again

GABA (Amino Butyric Acid) • Is an inhibitory transmitter produced in the brain and the CNS that keeps the body from becoming increasingly restless during stress and also prevents seizures • GABA is the main player in the so-called
“Stress-Limitation System ” of the brain and the CNS • It is the main inhibitor in the brain, and helps in the production of endorphins that provide us with a sense of well-being • Prostaglandins also play a key role in the stress limitation system. • GABA is at its highest concentration in specific areas of the brain, including the hypothalamus, the hippocampus and the central brain area • Is present in up to 40% of all synapse

• We noted in our studies above that GABA plays an essential role in keeping the brain and CNS from becoming over-excited during exercise • One of the mechanisms involved is the suppression of Beta- receptors (located throughout the body), thus reducing the secretion of adrenalin which reaches high levels during exercise • Until the muscle cells are fully relaxed, these Beta receptors (which secrete adrenalin) will not be fully functional • Endorphins are involved in the suppression mechanism of the Beta receptors

• During heavy load lifting the stressors (including high adrenalin levels) are intensified which aid in the contractile process required for such lifts. • In this case the GABA system is even more important than it is for lesser-load lifts. • If stress exceeds a certain threshold, too much adrenalin (as well as other compounds) is produced which can lead to damage to the body over time . • The GABA system safeguards against stress-related diseases which are numerous: diabetes, heart disease and hypertension, GI ulcers and so on.

• The advantage of the Bulgarian method is that, over time, the body develops greater resistance to stress compared to multiple-rep methods at lighter loads • The scientific reason for this greater resistance is due to many factors, not least of which is an increase in the number and size of the GABA neuro-secretory cells in the brain and CNS • This structural and functional adaptation allows the brain to secrete greater and greater amounts of GABA as loads increase • Thus the Bulgarian method helps safeguard athletes against stress-related damage and disease over time • Other structural and functional changes also occur (the GABA system is very complex) but this presentation will not cover this in depth.

• The great French researchers Jacob and Monod were pioneers in genetic research and demonstrated the presence of gene activators and repressors • Following lifting, various metabolites build up and accumulate within the muscle fibers • When these waste products accumulate, gene repressors on the DNA are de-activated which allow transcription of DNA into specific mRNA molecules, that cause the nucleus in the cytoplasm to be “translated ”into proteins and enzymes that break down the metabolites

• When maximum loads are utilized, as in the Bulgarian method, a greater quantity of metabolites are accumulated in comparison to graduated repetitive lifting.
• The higher loads lead to a marked increase in the number of proteins produced (and the type of proteins produced are different.)
• The end-result is an anabolic effect with an increase in the amount of protein produced in the muscle fibers. As a result, the muscle cells get bigger which, in turn, enhances the contractile properties of the muscle fibers

• Another result of single rep maximal load lifts is a change in the Lysosomal System
• Lysosomes are specialized vacuoles in the cytoplasm that contain enzymes (proteins) that break down wastes deposited in the cell (in this case, muscle cells)
• The resulting enhancement of catabolic activity aids in faster and more efficient waste removal, and consequently speeds up muscle recovery

• When the loads are increased in weightlifting, the corresponding impulses passing through the neurons and the skeletal muscle fibers affect the proteins produced by both the neuronal mRNA and the muscle cell mRNA (the changes in mRNA are also due to changes in the DNA as well)
• The different impulses that result from the differing workloads lead to the translation of different proteins both in the neuron and in the innervated muscle fibers
• The cells develop a“memory ”of the proteins produced relative to the different impulses traveling along the nerve and muscle fiber

• During the first phase of weightlifting , after lifting, the muscle fibers lose their co-ordination and the muscle fibers experience impaired contractile functionality. • Much of this impairment Is caused by fatigue resulting from the exhaustion of ions, compounds and enzymes needed for contraction, These include, among others, ATP, calcium and adrenalin. • When lifting is below 95% PR, lifters are generally able to succeed with similar load lifting following recovery. • When the lifter attempts lifts beyond the 95% threshold (and especially beyond 97% when the stressors are much greater, initially, athletes are unable to lift similar loads and efficiency falls to about 80% of maximum.

• This should not discourage athletes to continue lifts at the same high load even if several tries are necessary to achieve results. • These lifts are vital because the stress adaption response at lifts above the 95 % and especially above the 97% level leads to the production of “specific proteins ”which are needed to succeed • By the second or third week, athletes will be able to lift maximal loads or even higher loads. • As training continues, the intervals between maximal load lifting is shortened due to the phenomenon of “protein memory ”as mentioned earlier.

Every sport requires different muscle fibers to develop.

Two Types of Muscle Growth
1. Sarcoplasmic Hypertrophy
• Most common among bodybuilders • Accomplished through higher reps (8-12) and lifting fairly heavy weights • Demands development of sarcoplasm, a fluid like substance within the cell – This form of development causes the muscles to appear bigger – This higher volume training does little for maximum strength, it does assist with ATP (energy) production and strength endurance • Many believe that this is non-functional muscle growing, however it still has a place when seeking to increase size and appearance of a muscle

2. Myofibrillar Hypertrophy
• Common among Olympic Weightlifters and those who lift with 85- 97% of their 1 rep max • Forms firm, solid muscles (Muscle Density) • The only way to get this muscle density is to lift in the lower rep ranges (1-5 rep ranges) • This form of growth produces increases in – Maximum strength – Eplosiveness – Causes the muscle to grow in size • It builds fully functional muscle by increasing the number of myosin/actin filaments (sarcomeres) within the cell