If your pre-workout stretching doesn't seem to be doing much for you, give the following 10-minute warm-up routine a try.

(1) Increase your heart rate, so that the initial stages of your training session don't overtax your ticker

(2) Prepare your muscles for strenuous activity

(3) Wake up your nervous system - so that it's ready to control your muscles properly during a vigorous workout. This protocol will do all three, and it only takes 10 minutes:

* Wake up your leg muscles (1 minute): Walk in a relaxed fashion, alternating light, relaxed steps with long, exaggerated strides. On each extended stride, vigorously swing the opposite arm forward.

* Wake up your heart and leg muscles (4 minutes): As you jog unbelievably slowly, notice any tight spots in your body and focus on unkinking the tension.

* Wake up your nervous system (1 minute): Skip - in place or in a forward direction - while trying to lift your knees as high as possible.

* Wake up your heart (2 minutes): Run at the basic pace you'll utilize in your workout for one minute, and then jog very easily for one minute.

* Give your nervous system a green light (2 minutes): Hop lightly on both feet for about 20 seconds, and then hop lightly on your right foot for 15 seconds and your left for 15 seconds. Walk easily for 10 seconds, and then jump continuously - as high as possible on both feet - for 15 seconds. Walk for 10 seconds, and then try "hot-stove" jumping, getting your feet barely off the ground on each jump and trying to make as many contacts with the ground (with both feet) as you can in 20-25 seconds. Walk for 10 seconds or so.

* Run!

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Exercise terminology is supposed to help us figure out how to train, but that is certainly not the case with the term "Anaerobic Threshold" and "Aerobic Threshold." The Anaerobic Threshold does not occur at a point at which muscles plunge downward in a lack-of-oxygen spiral, and the Aerobic Threshold does not signal an underlying limit in the oxygen-delivery-and utilization system, as some coaches and experts implied.

When we exercise, it is possible to cross over many thresholds and transition points. For example, research carried out by the British scientist, R. McNeil Alexander, tells us that the movement speed of 2 meters per second represents an important boundary. At velocities of 2 meters per second or less (e.g., at all tempos of 13:24 per mile or slower), walking requires less energy than runnign, and so we almost always walk at such lethargic speeds.

If we want to move faster than 2 meters per secod, we invaribly jog or run, because running is more economical than walking at such tempos. Humans (and other animals) automatically adjust gait to minimize the energy cost of locomotion, and so we rarely see individuals jogging at 15-minute per mile tempo - or walking with 10-minute per mile alacrity.

Another important transition occurs at a walking speed of about 5 kilometers per hour (a tempo of around 19 minutes per mile). Exercise scientists have known for years that if one plucks an average person off the street and asks him/her to walk "normally" he/she will usually settle in at a pace of about 4.8 to 5 kilometers per hour. This is nothing new: The first truly human footprints, left in Kenya/Tanzanian mud two million years ago and preserved for study today, suggest that these first imprint-leavers were strolling through East Africa, following their cattle, at a rate of 5 kilometers per hour, too!

Why is 5 kilometers per hour such a popular walking speed? AT velocities above 5 kilometers per hour, the oxidation of carbohydrate by leg muscles increases dramatically, and as a result perceived effort rises significantly. At 5 kilometers per hour and below, carb-burning falls, fat breakdown ascends, and perceived effort moderates considerably. The human brain monitors carbohydrate oxidation during exercise quite carefully - and rather perversely cranks up perceived effort when carb-burning is on the upswing. In effect, the brain tries to keep exercisers from burning up their precious carbohydrate (glycogen) stores by making exertion which produces high rates of carbohydrate oxidation feel very difficult. This is a key reason why sustained runs at a high intensity such as vVO2max feels so incredibly hard. Nothing bad is really happening to your muscles at vVO2max - it's just that your brain doesn't like red-hot exertions, given it's constant worries over glcogen depots in your muscles. On the other hand, the brain is content at paces of ~5 kilometers per hour and below because carb-burning is minimal, and thus 5km/hour is a universal walking speed. If you walk faster than 5 km/hour, your brain sounds warning bells; to turn down these internal tocsins, you naturally return to 5 (incidentally, speeds below 5 carry with them the feeling that one will never arrive at a destination, and thus they are very lightly used).

Another transition point - this time running one - has often been called the "anaerobic threshold." In fact, you can't be a real runner until you have used the term anaerobic threshold in a sentence at least once. And - you can't be a truly hip runner until you have advised a running friend that the concept of an "anaerobic threshold " is hopelessly out of date.

If you are a regular reader of Running Research News, you will know that back in the dark, early days of exercise science, the phrase anaerobic threshold was minted to denote an exercise intensity at which there was a systematic rise in blood lactate. It was thought that this was the result of hypoxia )low oxygen) in the muscles, and thus the word "anaerobic" (without oxygen) seemed somewhat appropriate.

A lackadaisical anaerobic threshold (i.e., a case in which blood lactate began to pile up at a slow running speed) was viewed as a bad thing, and the remedy was usually thought to be high-mileage training, which was supposed to enhance the functioning of the cardiovascular system and improve the delivery of oxygen to the muscles (and the utilixation of oxygen once it got there). As you can see, this seemed to make sense: If anaerobic threshold occurred because of a lack of oxygen, then runners should do things which ensured that lots of oxygen would be flowing toward their muscles. What could be better for the heart and the oxygen-delivering capillaries than running tons of miles?

However, such conceptions ignored the simple and unavoidable facts that anaerobic threshold occurs at just 50 percent of max aerobic capacity in many untrained individuals and at 85 percent of max aerobic capacity in a large number of elite runners - in other word in situations in which oxygen is quite plentiful and the oxygen-delivery-and-utilization system has not been taxed to its limit. It's clear that the anaerobic threshold is not caused by a lack of oxygen in the muscles, and thus we shouldn't call the transition point an "anaerobic" threshold. The term "lactate threshold", without any implied mechanisms related to oxygen, is much better.

To learn more about Thresholds of Training (the full article can be read by purchasing Vol. 21 Issue 10 of Running Research News) and many more running related topics, simply click-on the Back Issues link, and select the volume and issues number, from the drop-down menu. A subscription to Running Research News is another way to receive valuable information about running. BUY NOW.

There's no doubt about it: High-intensity training sharpens your speed and improves your running economy. Unfortunately, conventional wisdom says that upbeat running also increases your risk of injury, overtraining, and "burn-out." Fast running also enhances the breakdown of carbohydrate - not fat - for fuel, and high-velocity workouts are of shorter duration than long, slow runs, leading to less calorie burning. For those reasons, speedy running isn't supposed to be as good as long, slow ambling at trimming excess corpulence from the body. Training

Those knocks on upscale training seem logical enough, but hold on! Recent research demonstrates that fast training is far better than inchmeal pacing at boosting blood levels of an important chemical called human growth hormone (GH). Produced by the pituitary gland, GH also helps break down fat and heightens body leanness. Since swift training sessions amplify GH levels, it may be time to bring on the speed!!

In recent growth-hormone research carried out at the University of Virginia, 16 healthy female runners gradually expanded their training mileage from five to 40 weekly miles over a 12-month time span. Nine of the woman ran six times per week and completed all of their training at or below their lactate threshold running speed (LTRS), the velocity above which large amounts of lactic acids begin to accumulate in the blood. Generally, LTRS corresponds with a heart rate of 80-88 percent of maximum and a running pace which is 10 to 15 seconds per mile slower than 10K race pace.

The seven other women also trained six times weekly, but three of their sessions were conducted at much higher speeds. In fact, up to one-half of their weekly mileage, not to exceed five miles per workout or 15 miles per week, was completed at above-LTRS velocities. Usually, the above-LTRS workouts consisted of intervals run on the track at a speed about half-way between LTRS and two-mile race pace. Although training speeds differed, total weekly mileage was the same for the two groups ("Endurance Training Amplifies the Pulsatile Release of Growth Hormone: Effects of Training Intensity," journal of Applied Physiology. Training

After one year of training, both groups improved maximal aerobic capacity (VO2max), but the improvements were significantly greater in the above-LTRS runners. The higher intensity trainees boosted their average VO2max from 44.2 to 50.1 ml/kg/min, a 13-percent advance which is comparable to lowering 10K times from 45:58 to only 41:16. Both groups of athletes also increased lean body mass, but the above-LTRS runners tended to achieve greater reductions in fat weight and percent body fat.

                                                     Pulses of Growth Hormone

The biggest difference between the groups, though, was in the growth hormone production. Above-LTRS trainers nearly doubled the average amount of growth hormone in their blood, and their "pulsatile" release of GH was also dramatically heightened (The pituitary gland releases growth hormone not continuously but in sudden "pulses," or surges, at various times of the day). Since muscles and bones are especially responsive to abrupt increases in GH levels, this improved pulsatility could greatly enhance bone and muscle repair.

Prior studies had suggested that endurance training might gradually diminish the amount of growth hormone released from the pituitary gland, but the Virginia research indicates that at-the-below-LTRS training maintains GH levels while above-threshold intensities might - because of heightened GH - recover more quickly from strenuous workouts and races, uses fuel more efficiently during exercise, and amplify body leanness.

Also, since growth hormone stimulates the formation of new bony tissue, master's runners who want to fend off age-related decline in bone mass might profit from an increased frequency of above LTRS sessions. Chunkier runners who train slowly tend to produce miserly amounts of growth hormone, so above LTRS exercise should help heavier harriers break down fat and become leaner. Although it's unrealistic to expect masters or overweight runners to spend huge amounts of time exercising at above-threshold intensities, the Virginia scientists suggest that a schedule of three times a week for 20-30 minutes at slightly above threshold should be enough to jump-start GH production.

However, it takes time for the above-threshold training to promote growth-hormone levels. In the Virginia research, which utilized subjects who were initially untrained, growth hormone levels didn't begin to increase dramatically until eight months of above-threshold running had been completed. It's possible that training above threshold for only six months of the year - and training easily for the other six months - might not spike blood concentrations of GH: Fairly regular "doses" of upscale running may be required.

                                                                Speed Kills?

The link between chronic above-threshold training and enhanced blood-GH levels suggests that experienced runners might want to revamp their "base" training and that novice joggers should consider adjusting their initial workouts. Runners doing base or beginning training often rely almost exclusively on slow, steady miles, but it may be far better to mix moderate quantities of above- LTRS intervals with the easier runs. Inclusion of speed into base training won't lead to surges in injury rates; in fact, it might lower the frequency of injuries because the augmented GH could do a better job of fortifying bones, muscles, tendons, and ligaments. Recent research in Holland confirms that early, up-tempo training actually tends to downgrade - not increase - average injury rates. In the Virginia study, above threshold runners were not injured more often than the slower trainees, even though as much as 38 percent of their weekly miles were completed at above-threshold intensities. Generally, scientific surveys have been able to link higher total mileage - but not faster training speeds - with a greater risk of injury. Speed seems to produce problems primarily when it is combined with unusually high mileages or when large amounts of speed are added to a training program too quickly. Even beginning runners are ready for reasonable doses of speed. Training

If you decide to increase your above-LTRS training, it makes sense to add the speed in amounts which your body can tolerate easily. One sensible rule is to tag on no more than an additional half-mile of above-threshold work each week. How fast should you run? An easy way to accrue more above-LTRS miles is simply to run at your current 10K-race speed, which is usually two to three percent faster than LTRS. For example, during a few of your easy runs, cruise along for a half-mile at 10K speed midway through the run and then scoot through another half-mile at 10K intensity near the end of the workout. Or, instead of doing a three-mile easy run, jog two miles easily and then complete two 400-meter intervals at 10K tempo, with 400 meters of easy running after each interval. Even neophyte runners can insert several fast 100-meter intervals inside their short, easy runs.

"Strides" - 20 to 30-seconds bursts at current one-mile race pace - represent another great way to add more above threshold running to a training program. Most runners can ultimately attach four to eight 150-meter strides to three or four of their usual weekly workouts without risking excess fatigue, injury, or mental burnout. Although the strides are short, stride mileage can add up surprisingly quickly: Just 10 strides - five on one day and five on another - add nearly a full mile of above threshold running to a weekly training schedule. In addition, an experienced runner who currently logs 40 miles per week, including 10 miles at above-threshold speed, can increase his/her percentage of above-threshold miles from 25 percent to 31 percent - comparable to the levels reached by the above-threshold trainers in the Virginia study - simply by adding a total of 22 150-meter strides to your usual training too abruptly; about five additional strides per week represent the maximal allowable increase.

Although intense running is claimed to increase the risk of "burnout" and overtraining, it's more likely that a gradually-increased quantity of above-LTRS sessions will boost your growth hormone production, bolster your speed, strengthen your muscles and connective tissues, optimize fat breakdown, and help you develop the ability to recover from tough training sessions and hard races more quickly. Training

About 65 percent of endurance runners suffer from significant injury each year (with injury defined as a physical problem which is serious enough to limit normal training). Common wisdom suggests that the function of the foot and ankle is linked in some way with this extremely high rate of injury. Specifically, it is believed that specific foot shapes, as well as poor foot and ankle function and strength, predispose runners to problems. "Low-arched" feet, for example, are thought to increase the risk of a running-related malady. Perhaps paradoxically, "high-arched" feet are also viewed with disrespect - they are believed to be injury-promoting, too. Almost universally, "weak ankles" are linked in runners' minds with a large catalog of impairments, including shin splints, Achilles-tendon flare-ups, and sore knees.

Gradually, a large segment of the running community has come to accept the idea that the wearing of orthotics devices while running can compensate for potential weaknesses and structural faults and reduce the risk of injury. Implicit in this acceptance is the belief that orthotics will magically restore normal function in the lower limbs during running. Tens of thousands of athletes run with orthotics in their shoes in the belief that this practice will decrease their chances of getting hurt.

Are all of these assumptions correct? Do specific foot configurations spike a runner's risk of injury? Can orthotics actually change the kinematics of the foot and ankle in just the right way, reducing the forces placed on vulnerable muscles and connective tissues during gait? Is it possible that orthotics might reduce the impact forces traveling up the legs during running - and thus thwart "overuse" injuries? Can orthotics compensate for "injury-prone", abnormally constructed feet and ankles and keep athletes with bad anatomical set-ups out of trouble?

To find the answers to these key questions, Mohsen Razeghi and Mark Edward Batt of the Centre for Sports Medicine at the University of Nottingham in the United Kingdom recently carried out an extensive review of the scientific literature concerning the cause of overuse injuries, as they related to biochemical abnormalities and the use of orthotics (1).

Their findings shatter many of the myths about injury, foot structure, and orthotic shoe inserts which have become very popular in the running community and shed much welcome light on the difficult-to-untangle relationships between foot type, orthodics, and running-related injury.

To learn more about Running Injuries, Foot Types, and Orthotics (the full article can be read by purchasing Vol.21 Issue 2 of Running Research News) and many more running related topics, simply enter "can foot type predict running injury?", in the Search-Archives" box to the right. A subscription to Running Research News is another way to receive valuable information about running. BUY NOW.

Let's face it: Most of us define the limits of endurance running performance in terms of the ability to transport and utilize oxygen.

We speak of expanding the heart as a result of endurance training-so that it can send more oxygen to the leg muscles. We talk about enriching capillary beds around muscle fibers-so that muscle cells can greedily devour more oxygen. We note that one goal of training is to build up higher concentrations of "aerobic enzymes" in our muscles- and higher densities of mitochondroa, the little structures which permit oxygen-dependent energy creation to proceed. And we orate about VO2max (the maximal-possible rate of oxygen consumption), vVO2max (the minimal running velocity which elicits VO2max), TlimvVO2max (the duration of time that vVO2max can actually be sustained), and even running economy (the oxygen "cost" of running at a specific speed), saying that these oxygen-related variables are critical predictors of running success.

This kind of thinking dates all the way back to 1923, when noted physiologists A.V. Hill and H. Lupton published a paper which contended that "hypoxia" (low oxygen levels) in muscles during strenuous exertion produced fatigue and therefore limited exercise performance (1). This "oxygen-limitation paradigm" for explaining fatigue and endurance performance seemed to be verified in later research. For example, a variety of studies completely in the 1970s suggested that VO2max was responsible for setting the upper limit for endurance performance (2, 3, & 4).

One small problem for the paradigm popped up when researchers noted that athletes with identical values for VO2max could have quite-different performances! These variations in competitive times were postulated to result from differences in economy between runners (5 & 6). Here's how that kind of situation might work: Let's say that VO2max is 70 ml.kg-1.min-1 for both Runner A and Runner B, but when A cruises along at 4:40 per mile pace he is using all 70 of those mls (per kilogram per minute), while at 4:40 Runner B is utilizing just 63 ml.kg-1.min-1 (he is more economical). You can see that B would win any race conducted at 4:40 tempo (the speed is easier for him-it is a smaller fraction of VO2max). The same could be said for any race involving a pace slower than 4:40 (it would be significantly easier for Runner B). At faster-than-4:40 velocity, A would immediately be above VO2max and would begin to really struggle, while B would still have "room to maneuver" before VO2max was actually attained. A would be a decent runner, but B would be taking home the cash prizes.

Of course, no one bothered to examine closely the performance differences which still existed between runners with the same running economy and VO2max values, but the bottom line was that it seemed fully possible to explain performance differences in terms of oxygen utilization, even in cases when there were no differences in VO2max between runners. If VO2max was not the performance determinant, then oxygen utilization (economy) would fill the bill. Ultimately, a "consensus" emerged that VO2max and running economy were the major variables which determined endurance racing ability (7 & 8). To find out more information about training, BUY NOW To start a subscription to Running Research News.

What has Soren Mavrogenis been doing lately?

That question has not exactly been rolling off athletes' lips, especially since Soren's latest published paper - "Pyeloureteral Junction Stenosis and Ureteral Valve Causing Hydronephrosis" (Scandinavian Journal of Urology and Nephrology, Vol.35(3), pp. 245-247, June 2001) - has nothing at all to do with athletics. But give the fellow a chance! In addition to his pyeloureteral pursuits, the Dane is currently carrying out extremely interesting research on the treatment of athletic injuries, and his findings may one day help you bounce back from an injury more quickly than expected and as a result set a new personal record or win an important competition. A physiotherapist with Denmark's Olympic Committee, Mavrogenis has effectively treated several hundred cases of recurrent inflammatory injuries with a novel dietary supplement (Reuters Health, April 27, 2001). Tested for the first time in 1996 on a group of rowers from Denmark's National Rowing Team, Soren's nostrum appears to have remarkable anti-inflammatory properties (research on the overall healing properties of the treatment will be published in a peer-reviewed journal shortly).

Of course, most routine athletic injuries are treated with icing, rest, physiotherapy, and the use of non-steroidal anti-inflammatory drugs (NSAIDS), and Soren does not sermonize against the use of either rest or ice. However, the innovative Dane does leave the NSAIDS on the shelf, instead relying on a combination of essential fatty acids, vitamins, and minerals to soothe inflammation and restore injured body parts. He has reportedly found success with a variety of ailments, including both "tennis elbow" and golf elbow."

Soren's supplement does contain fats, so you might be reasonably asking, "Don't golfers already eat enough fat?" That's a reasonable question, but the problem, of course, is that they usually eat the wrong fats (i.e., the ones which seem to be pro-rather than anti-inflammatory). Soren's nutritional supplement contains a rich lode of inflammation-fighting omega-3 fatty acids (from fish oil), some omega-6 fats (from borage oil), four vitamins (A, B6, C, and E), and also the minerals selenium and zinc. According to Mavrogenis, most patients respond positively to the treatment in just two to three weeks, although very serious cases may require several months. "The results of this research confirm our clinical observations and leave us with the clear impression that inflammatory injuries can be treated without the use of NSAIDS. I see this as a ......breakthrough in modern physiotherapy. For the first time, we are able to offer our patients a safe and reliable treatment for stress injuries with chronic inflammatory response. In fact, it is our experience that with this new treatment, as opposed to conventional treatment, athletes are able to train actively while receiving treatment," says Soren. "The bad cases require the use of intensive ultrasound and certain massage techniques in addition to the antioxidants and essential fatty acids, but in the milder cases the use of nutrients alone is adequate," notes Mavrogenis. Norwegian sports authorities have been carefully watching Soren's work (naturally, Norwegians do not want Danes to leave them behind). Since inflammatory injuries to shoulders, elbows, knees, and Achilles tendons account for one-fourth of all job-related absences in Norway, Soren's anti-inflammatory regimen is now being tested by NIMI (no need to mention that this is Norsk Idrettsmedisinsk Institut). one of Scandinavia's foremost treatment facilities for sports injuries. We'll report on NIMI's findings in a future issue of this newsletter.

But isn't this all a little far-fetched? How can a few fatty acids - plus several vitamins and minerals - foster fast healing in an elbow nearly wrecked by overuse on the tennis courts - or in a knee inflamed by hundreds of miles of endurance running? The story just sounds too good to be true.

But it may not be. Bear in mind that scientific research has actually been fairly kind to the idea that omega-3 fatty acids and anti-oxidants can help to control inflammatory injuries. To understand why this is, remember that exercise generates increased quantities of "oxygen free radicals" and increases lipid peroxidation (the oxidative attack on key fats found in cell membranes, including muscle-fiber membranes fall apart and produce leaky, non-functional muscle cells.

As a defense against this disastrous possibility, the human body produces a fairly potent anti-oxidant called superoxide dismutase; superoxide -dismanyus production speeds up when individuals embark on regular and at least moderately strenuous training programs. Evidence suggests, however, that the superoxide-dismantus system is prone to being overwhelmed. Prolonged submaximal exercise has been shown to result in elevated amounts of skeletal-muscle lipid-peroxidation byproducts, indicating significant damage to the muscles (Free Radicals and Tissue Damage Produced by Exercise," Biochem Biophys Res Commun, Vol. 107, pp. 1198-1205, 1982). Clearly, the superoxide-dismutase system lets a significant number of free radicals "through its net."

Before we continue, let's review our story: Exercise can greatly increase the production of cell-damage free radicals. The magnified rates of lipid peroxidation resulting from this oxygen radical production may cause muscle damage. The human body has its own anti-radical defense system, but it doesn't provide complete protection from injury. In addition, the damage produced in the muscles as a result of exercise can "snowball" over relatively short periods of time. For example, in one study researchers found more muscle damage three days after a strenuous workout than they had found one hour after exercise ceased ("Adaptive Response in Human Skeletal Muscle Subjected to Prolonged Eccentric Training, " International Journal of Sports Medicine, Volume 4, pp. 177-183, 1983). This was a bit surprising, since researchers believed significant muscle repair would have occurred during the three-day interim. In another investigation, exercise scientists found that intense exercise produced immediate muscle damage, but the damage actually became much worse 24 and 48 hours after the workout was over, even though no follow-up exercise had taken place ("Ultrastructural Changes after Concentric and Eccentric Contractions of Human Muscle," Journal of Neurol Science, Vol. 61, pp. 109-122, 1983). In other word, in a muscle traumatized by exertion, there is a post-exercise period lasting for up to three days or more in which muscle damage is actually accelerated, rather than minimized, even when no further exercise occurs.

To learn more about how to Fats, Vitamins, and Your Sore Achilles  (the full article can be read by purchasing Vol. 17 Issue 3 of Running Research News) and many more running related topics, simply click-on the Back Issues link, and select the volume and issues number, from the drop-down menu. A subscription to Running Research News is another way to receive valuable information about running. BUY NOW.

    What is the best possible workout for advancing your running velocity at lactate-threshold? Best Lactate-Threshold

    That is an important but "dangerous" question. After all, a single workout does not exist in a training vacuum, producing adaptations which occur totally uniquely, without any influence from the overall training plan in which the workout is deployed. In one set of circumstances, for example, a session of 3 X 1600 at 5-K race pace might help put a sharper edge on a runner's vVO2max. In a different context, the 3 X 1600 could push the same athlete "over the brink" into an over-trained state.

    Nonetheless, we know that certain sessions can produce unique effects on lactate-threshold speed, and that these effects are often specific to the runner involved in the training. For example, running for 60 minutes at a moderate pace (below lactate-threshold velocity) probably will have a significant, positive effect on lactate-threshold speed for the relatively inexperienced runner who has been logging about 10 to 15 miles of running per week. However, this same session would have no effect at all on lactate-threshold velocity for the experienced, 70-mile per week runner who has been engaged in lots of high-quality training. The latter individual would probably have to soar up to intensities of 90 to 95 percent of VO2max and beyond to get lactate-threshold speed moving in the right direction.

    As you can see, it is possible to give specific workouts the "thumbs-up" or "thumbs-down" sign when it comes to lactate-threshold improvement, and one of our tasks as runners is to identify the sessions which are likely to have the greatest impact on threshold and then position them properly in our training. Best Lactate-Threshold

    But how do we identify such sessions? Fortunately, that job has been made easier for us, thanks to recent work carried out by Carl Paton and Will Hopkins of the Centre for Sport and Exercise Science at the Waikato Institute of Technology and the Department of Sport and Recreation at the Auckland University of Technology in New Zealand (1). Paton and Hopkins have conducted an extensive literature search for scientific papers dealing with the effects of training on the performance and physiology of endurance athletes.

    This search used stringent criteria. For examplem Paton and Hopkins excluded studies which investigated the effects of training on performance in subjects who were merely recreationally active, instead of being involved in serious training. The New-Zealand duo also eliminated inquiries carried out with individuals who did not have the characteristics of serious endurance athletes ( for example, exercisers with low aerobic capacities, low training frequencies, etc.). The studies examined by Paton and Hopkins also had to be peer-reviewed and published in a respected scientific journal.

    In addition to looking for research which explored the link between training and improvement in lactate-threshold speed, Paton and Hopkins also searched for studies whick looked at the effects of training on general endurance performance, maximum power (measured during an incremental test), maximal oxygen consumption, exercise economy, and body mass. Included in the Paton-Hopkins diggings were studies which focused on moderate- and high-intensity interval training, tempo running, plyometrics, and resistance training.

    The study which produced the greatest increase in lactate threshold in runners was the research (often mentioned in the pages of Running Research News) carried out by Leena Paavolainen and Heikki Rusko in which experienced runners reduced their mileage from 70 to 45 miles per week, substituting( for this mileage) explosive training which includes progressive series of jumps, bounds, hops, and very fast running(2). The jumping-bounding-hopping-sprinting workouts designed by Paavolainen-Rusko team, carried out three times a week for nine weeks, yielded about a 6.8-percent increase in lactate threshold. Best Lactate-Threshold

    Almost as good for threshold were the workouts employed by Edmund Acevedo and Allan Goldfarb of the University of North Carolina at Greensboro in their study of seven well-trained male distance runners (3). These runners had an average age of 22, and they were actively involved in competitive racing; mean VO2max was 65.3 ml.kg-1.min-1. As the study began, the young runners were training six to seven days per week, averaging five to 12 miles of daily running. Weekly volume averaged 50 to 65 miles before and throughout the investigation. RRNEWS Subscription