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Posted: July 9, 2005

Science of Sport: Fighting Fiber Fall-Offs

By Owen Anderson, Ph. D. (Copyright © 2004-2005)

VO2max (maximal aerobic capacity) is a very poor predictor of performance among athletes of fairly similar ability levels. For example, if you measured the VO2max of all female runners in the world who can run the 10K in less than 35 minutes, you would find a weak correlation between the VO2max readings you obtained and actual 10-K performance times.

On the other hand, rises and falls in VO2max can play a strong role in determining your individual performance capacity. If you are fortunate enough to elevate your VO2max from 52 to 60 ml kg-1 min-1, for example, you can reasonably expect a major improvement in your 5-K, 10-K, and marathon times – as long as you have not slaughtered your running economy and terrorized your lactate threshold in the process.

Conversely, if your VO2max falls from 60 to 52 ml kg-1 min-1, trouble usually lies ahead! Unless you have enhanced your running economy enormously and/or lifted your lactate-threshold intensity to a much-higher percentage of VO2max, your performances will be sad things for you to bear.

And that’s where this little story starts. Drops in VO2max are considered to be a natural part of the ageing process for endurance athletes, and these declines can contribute to very disappointing performances as one gets older. Some studies have suggested that VO2max likes to decline by approximately 1 percent per year after an athlete reaches the age of 40. On average, a 1-percent decline in VO2max produces about a 1-percent loss of performance, which means that a serious 40-year-old runner might see his/her 10-K time plummet from 40 to 44 minutes by the time the half-century mark is reached. What is the best way to prevent such fall-offs?

To answer the query appropriately it is first important to remember that the traditional view of VO2max suggests that it is determined to a large extent in every endurance athlete by three key things: (A) The rate at which the heart delivers oxygenated blood to the muscles, (B) The amount of oxygen the blood can actually carry (if hemoglobin, the oxygen-carrying molecule in the blood, is low, for example, the blood can offer the muscles only miserly supplies of the life-giving gas), and (C) The rate at which muscles can extract oxygen from the blood as it passes by them and utilize it to furnish the energy needed for intense exercise.

I would argue that VO2max is also a function of a fourth – neuromuscular – factor. That is, the ability of the neuromuscular system to produce very high work outputs and sustain them for reasonable amounts of time without undue fatigue can also have a strong impact on VO2max.

In addition, VO2max is strongly influenced by body composition. As you are well aware, human beings (and even human athletes) tend to lose muscle and accumulate fat as they get older. Most peoples’ muscles reach their maximum size during their 25th year of life, grow smaller by about 10 percent between the ages of 25 and 50, and then shrink by 45 percent over the next three decades (1). The primary reason for this sinew slenderizing is that the total number of cells in any particular muscle stays fairly constant until the age of 30 but then begins to turn south. The fall-off in muscle-cell quantity is a slow process at first but increases dramatically after the age of about 50. For example, if one of your muscles consisted of 1000 cells (fibers) when you were 30, the muscle would probably still contain 900 to 950 fibers 20 years later, but the fiber count would plummet to just 500-550 by the time you became an octogenarian.

Muscle tissue has a high appetite for oxygen, so drops in sinew can cut VO2max down considerably. Fat, on the other hand, utilizes oxygen at low rates, so advances in corpulence do little to expand VO2max. This is especially true since VO2max is measured during intense exercise: Fat – unlike muscles – does not undergo a dramatic rise in metabolic rate during exertion, so if you let your muscles rot and make your adipose tissue robust, you will hardly be able to blow the socks off your neighborhood exercise physiologist when he/she determines your VO2max on the treadmill. When fat acts to increase body weight, it also plays with the denominator of the VO2max expression, which is stated as milliliters of oxygen utilized per kilogram of body weight per minute. Add on a couple of kilos of fat, and your VO2max will shrink, even if your heart, blood, and muscles have continued to play the oxygen game very well.

However, even among individuals who manage to perfectly maintain their body compositions, VO2max still gets smaller with senectitude (2). If we look at our “big-three” factors for VO2max (the heart, hemoglobin-hematocrit, and muscles), which one is most responsible for this sad state of affairs?

Hemoglobin concentration and hematocrit (indicators of the ability of the blood to carry oxygen) can fall with chronological decrepitude among male athletes. Hemoglobin levels are partially determined by circulating androgen concentrations, and male testicular outputs are generally on the downslope after the age of 40 has been attained. However, the drop-offs in hemoglobin are generally quite small (3). As a result, we can’t pin the blame on hemoglobin for the steady slide in VO2max.

On the other hand, it is certain that the typical athlete’s heart is handcuffed by the ravages of time. The stiffness of the heart increases with ageing, making it more difficult for the big thoracic pump to re-fill with blood after each blood-discharging beat. Stroke volume (the amount of red fluid pumped out of the heart to the body per beat) consequently falls, and maximal heart rate can decline as part of the ageing process. As a result, cardiac output (the rate at which blood can be pumped by the heart per minute) tends to diminish fairly steadily in our senior years.

What is not so certain is whether muscles lose their ability to extract oxygen from the blood as we become more-senior athletes. This is more than an esoteric question: If the muscles hold up well to Father Time, one might expect that training which forces the muscles into intense bouts of oxygen utilization might actually increase their oxygen-using capacities – and counteract the harsh things happening to the ticker.

Research in this area has been very interesting, with some studies showing no loss in oxygen-utilization ability by the muscles and others revealing significant drop-offs. Part of the problem here is that physical activity has an impact on muscles’ abilities to snare oxygen from the blood, and yet physical-activity levels have sometimes been ignored in the research. If individuals exercise less as they get older, their muscles’ handiness with oxygen will certainly decline, but that declivity may be primarily a function of the lack of activity, not an inherent problem with the muscles. In contrast, if athletes tend to exercise more (or more intensely) as they get older, the muscles’ oxidative capacity may not fall at all, and one might conclude that ageing has no effect on the muscles, even though it was actually the heightened activity which kept oxygen-utilization ability in line. Another methodological problem has been that individuals with a wide variety of ages have been studied in the various investigations, even though muscles might lose their prowess with oxygen at a different rate when athletes are in their 80s, compared with when they are whippersnapping fifty-year-olds.

How might we find out whether muscles lose their ability to use oxygen as they age? If we find that losses in oxygen-utilization rates are not so much age-related as training-related, how should we train in order to preserve as much O2 pizzazz as possible?

A traditional way to look at oxidative capacity in muscles is to biopsy muscle tissue from athletes of various ages and then to assay the tissue for key oxidative enzymes such as citrate synthase (CS), succinate dehydrogenase (SDH), and cytochrome-c oxidase (COX); these three are all mitochondrial enzymes which help muscle cells utilize oxygen to supply the chemical energy (in the form of a compound called ATP) needed for muscular contractions.

Many studies have shown that the activities of CS, SDH, and COX all decline as age increases, but – as mentioned – most of these studies have failed to control very precisely for the exercise habits of their subjects (4). However, it is worth noting that two of these investigations have uncovered an extremely fascinating fact: Declines in the activities of aerobic enzymes tend to be very muscle-specific.

For example, outstanding researcher Joe Houmard (you will probably recall his name from the great tapering research he has conducted with runners, which we have described in various issues of Running Research News) and his colleagues found that CS activity was reduced with ageing in the lateral gastrocnemius (calf) muscles – but not in the vastus lateralis (outer-quad) muscles – of their subjects (5). This is an interesting finding, because the gastrocnemius is recruited to a much greater extent than the vastus lateralis during human locomotion (walking and running) (6). As individuals become less active with age, the CS activity of the gastrocnemius should naturally fall, since the gastroc is used heavily during exertion. However, as individuals become less active, the CS activity of the vastus lateralis should not change very much in response to the reduced amount of training, since the vastus lateralis plays a more-minor role. If CS drops in potency in the vastus lateralis, it should be dropping as a result of ageing, not as a result of declining physical activity; if it doesn’t drop, it should mean that ageing doesn’t bother with the poor fellow (CS). The important message from Houmard is that it doesn’t drop! The CS plunge in the gastrocnemius may have been entirely caused by reductions in exercise.

A separate study found that the activity of CS in the butt and abdominal muscles of ageing sedentary individuals did not diminish as a function of ageing (7). Was this because the sedentary people did such a great job of exercising their abs and butts? Not likely: In fact, the butt and ab muscles are seldom recruited in a significant way by sedentary people (if you doubt this, think back to the last truly sedentary person you have seen). Therefore, changes in the butt-abs’ CS potency should be purely a function of ageing, not physical action (since butt-ab recruitment is at near-zero throughout the ageing process for truly sedentary folks). CS concentration and activity do not change in the buttocks and abs, so getting older does not seem to produce an erosion of aerobic enzyme activity (provided CS status reflects the puissance of aerobic enzymes generally).

In a great study, researchers compared older men (average age was about 58 years) with younger men (average age ~25); some of the men in each group were well-trained, while others were sedentary (8). Interestingly enough, no differences in CS or SDH were observed between the trained old and young men. As it turned out, both CS and SDH were diminished with age in the sedentary group, but this was true only in the Type-IIa (aerobic-fast-twitch) muscle fibers, not in the Type-1 (slow-twitch) and Type-IIb (anaerobic-fast-twitch) cells. One might reasonably conclude that the diminishments in CS and SDH observed in the sedentary subjects were the result of declining activity of the leg muscles over time. One might also decide that the lack of difference in CS and SDH between trained groups suggests that training can almost-perfectly preserve aerobic-enzyme activity, especially since we have seen that the effects of ageing per se can be modest (or nil). That being the case, selective training involving the IIa fibers might have kept everything equal between the old and young men.

What kind of workout would specifically activate your IIa fibers and would also ensure that your leg-muscle cells did not lose any of their capacity to utilize oxygen as you aged? Here is a gem of a muscular-oxidative-capacity-amplifying session:

(1) Warm up with easy running and dynamic-mobility exertions until you feel relaxed, loose, and ready to run fast.
(2) Run steadily for 10 minutes at approximately your 10-K pace (it is OK to use “feel” for this; you don’t have to focus tightly on splits over measured distances). Make this a free-flowing, smooth, intense run which causes blood and oxygen to begin cascading into your legs. Do not take a break before you begin step # 3.
(3) Move up a 50- to 60-meter, fairly steep (4 to 8 percent or so) hill as quickly as you can, and then jog back down to recover. The only hitch here is that you must move up the hill by hopping on one leg only, with quick, explosive hops. If ample fatigue greets you before you reach the top, simply shorten your hopping distance and keep on plugging.
(4) Once you have reached the bottom of the hill as a result of your jog-down recovery, hop explosively up the hill on the same leg you used for the first climb. Continue in this manner, hopping up the hill on the same leg and recovering by jogging down, until you have completed five total reps. Then, shift over to the other leg for five consecutive repetitions. Cool down with 2 miles of light jogging. Over time, you can increase the number of reps per leg to 10 to 12.

The rationale for this workout? Oxygen delivery to the leg muscles during normal, two-leg running is limited by the fact that the cardiovascular system must parcel blood out to both lower appendages in approximately equal amounts. During one-leg hopping, on the other hand, the c-system can devote almost all of its efforts to the leg which is doing the work, and the rate of oxygen use by that leg increases appreciably, compared to the rate at which the leg utilizes oxygen in the two-leg condition. As a result, the leg “learns” (develops the capacity) to use oxygen at higher rates; there is a greater stimulus for the leg muscles to heighten aerobic-enzyme concentrations, for example. Using the hill instead of flat ground is simply a means to spike the intensity of the effort, so that oxygen usage reaches true maximum (for that point in time). Performing all of the reps on one leg before advancing to the other is a way to make sure that oxygen utilization in each leg remains very high for its portion of the workout. It is nice to know that such hill exertions should also improve strength, fatigue-resistance, and lactate threshold.

The above is a stand-alone workout which is nice to include with the other high-quality sessions which you routinely conduct. Note, however, that you can actually perform one-leg hill hops once or twice a week, “folded” within many different types of sessions. As long as you carry out several consecutive reps with each leg, you should get some benefit. Note, too, that (as we have mentioned many times in these pages) high-intensity workouts in general have a much-stronger impact on muscular oxidative capacity, compared with longer running at more-temperate intensities.

Earlier in our story, I mentioned that muscles shrink as part of the ageing process; part of this shrinkage is caused by a dramatic decline in the number of muscle cells, while a reduction in individual muscle-cell size also contributes to the problem. What I didn’t mention is that the loss in muscle-cell numbers is caused to a large degree by the fact that “motor nerve cells” in the spinal cord begin to deteriorate at a steady rate as one gets older, especially after the age of 50. By means of their long arms, which spread outward from the spinal cord like the tentacles of an octopus, the motor nerve cells are normally in close contact with muscle cells. The motor nerves’ key function, of course, is to “tell” muscle fibers when to contract during physical activity, but the connection between motor nerves and their associated muscle cells is also necessary to keep the muscle fibers alive. As motor nerve cells die, the muscle cells to which they are attached also bite the dust.

Fortunately, there is a way to arrest this negative process – by working on the fiber-size part of the equation. Athletes who engage in regular, strenuous resistance training don’t necessarily halt the fiber-death process, but they can compensate for the massive fiber suicide by stopping and even reversing the tendency of their Type-II (fast-twitch) cells to grow smaller. Generally, fast-twitch cells shrink by about 25 to 30 percent between the ages of 20 and 80, but consistent, strenuous, strength training can actually make the Type-II cells bigger. In some athletes, this can lead to an actual advancement – instead of a loss – in total muscle tissue in the body. Type-I (slow-twitch) cells can also get into the act, increasing in size in response to strength training. As a fringe benefit, strength training in older individuals also increases the number of small blood vessels around muscles by up to 15 percent, which augments the oxygen-delivery side of VO2max.

Intense, consistent training in general also tends to advance slow-twitch dimensions. In one investigation, the cross-sectional areas of Type-I muscle cells advanced by 25 percent between the ages of 26 and 48 in athletes who continued to carry out high-quality workouts (9).

Since the overall process of muscle atrophy really picks up steam after the age of 50, strength training for athletes over the age of 50 is not just important – it is essential. Any endurance athlete over the age of 50 who is not hitting at least two strength-training sessions per week is truly missing the boat. These resistance workouts do more than upgrade economy and fatigue-resistance: By preserving or adding to muscle mass, they safeguard or augment VO2max and thus are a critical part of performance preservation. ©

References

(1) “Muscles Incredible Disappearing Act,” Running Research News, Vol. 9(6), p. 5, 1993
(2) “Skeletal Muscle Mass and the Reduction of VO2max in Trained Older Subjects,” Journal of Applied Physiology, Vol. 82, pp. 1411-1415, 1997
(3) Randy Eichner, personal communication
(4) “Is Skeletal Muscle Oxidative Capacity Decreased in Old Age?” Sports Medicine, Vol. 34(4), pp. 221-229, 2004
(5) “Fiber Type and Citrate Synthase Activity in the Human Gastrocnemius and Vastus Lateralis with Aging,” Journal of Applied Physiology, Vol. 85, pp. 1337-1341, 1998
(6) “Biomechanics of Walking and Running: Center of Mass Movements to Muscle Action,” Exercise & Sports Science Reviews, Vol. 26, pp. 253-285, 1998
(7) “The Effects of Aging on Enzyme Activities and Metabolite Concentrations in Skeletal Muscle from Sedentary Male and Female Subjects,” Experimental Gerontology, Vol. 35, pp. 95-104, 2000
(8) “Oxidative Capacity of Human Muscle Fiber Types: Effects of Age and Training Status,” Journal of Applied Physiology, Vol. 78, pp. 2033-2038, 1995
(9) “Secrets of the Preservers: How Some Runners Maintain Their Performances as They Age,” Running Research News, Vol. 9(6), pp. 1-4, 1993

To learn about Owen's running camp in Malibu, California this summer, please visit www.RRNews.com, scroll to the bottom of the page, and click on the running-camp "splash."

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