Weightlifting Forums

Free form thread about management of health conditions in weightlifting I guess.
There are a few topics/thoughts that have been stewing in my head for some time, so I thought I should get some word vomit out.

Scientific evidence preferred, anecdotal evidence welcome where there is an absence of appropriate scientific literature.

Polycystic Ovarian Syndrome (PCOS)
This is an opinion piece and not fuckin peer reviewed. Please dear god, satan and squidward do not take this to be scientific literature.

PCOS is a heterogeneous (coming from multiple sources) condition that has contributing factors from, and effects on these systems

• Reproductive
• Metabolic
• Neuroendocrine
• Genetic
• And more lol

PCOS is common in female athletes of all types (1), but IMO may be more relevant to strength and power sports as the increased secretion of insulin and/or androgens, depending on subtype, may contribute to greater anabolism (2).

What I've noticed anecdotally is that this is a 1.5 edged sword in weightlifting. Women with PCOS tend to be good at increasing strength/muscle mass but have a much harder time losing body fat (and also the reproductive/menstrual dysfunction can interfere with training). This seems to align with other anecdotal experiences from people I know. However, the athlete in this case was not hyperandrogenic so it may be different with elevated endogenous androgens.

There is also a behavioural/psychological component to PCOS and weightlifting. PCOS can bring with it various psychosocial stressors affecting mental health, which then affects its whole management. Women with PCOS may also be drawn to lifting weights as it's something they're more likely to be good at, progress in and ultimately stick to.

(Total conjecture) I suspect that the anabolism and endocrine differences brought on by PCOS make it easier to improve technique through gaining muscle mass more easily and the effects of androgens on neurology and motor learning.

My initial suspicions seem wrongish about lean PCOS (PCOS with BMI <25) and insulin resistance. It appears that insulin resistance is still present in lean PCOS, but to a lesser degree than overweight/obese PCOS (3).
Personally, I'm not convinced that lean PCOS is a subtype, at least not in the sense that other subtypes of PCOS have been proposed (e.g. diagnostic factors, genetics). I think that BMI in PCOS is related to PCOS but also other endocrinal/metabolic factors and of course behaviour.

Non-fertility management of PCOS has a few main components, ultimately boiling down to pharmacological and lifestyle management. (4)

• Pharmacological
• Psychosocial support for behaviour change and mental health stressors
• Dietary
• Exercise

I'm primarily addressing non-fertility management as fertility is not in my wheelhouse and I've not yet come across any PCOS-havers who wanted to get pregnant so I haven't looked into it in much depth.

The first line of pharmacology for PCOS is usually the combined oral contraceptive pill, which is very Marmite as to whether people respond well or poorly to it. The second line, if there is diagnosed clinical or biochemical hyperandrogenism, are anti-androgens.
The third line is generally blood glucose lowering/insulin sensitising drugs - Biguanides (e.g. metformin), myoinositol and d-chiro-inositols, GLP-1 agonists and so on.

Psychosocial support isn't necessarily just from psychiatrists, psychologists or counsellors but also from other people in their life to help them with behaviour change and adjusting to their diagnosis.

Dietary management seems to be, in short, "eat healthy and get to a lean(er) body composition". Probably highly individual based on individual and cultural factors, macronutrient distribution doesn't seem to play much of a role.

As far as training for PCOS goes, the recommendations are the same generic sportsmed gen-pop recommendations (Resistance training 2x/week, 150 min of moderate or 70 minutes of vigorous activity). I would add another one in that excessive exercise induced muscle damage may blunt insulin sensitivity (5), so it's probably wise for beginners or lifters coming back from a layoff to ease into the eccentric parts of the lifts and ease into volume training.


References (i mixed apa and vancouver. my forum, my rules)

• Hagmar, M., Berglund, B., Brismar, K., & Hirschberg, A. L. (2009). Hyperandrogenism may explain reproductive dysfunction in olympic athletes. Medicine and science in sports and exercise, 41(6), 1241–1248. https://doi.org/10.1249/MSS.0b013e318195a21a
• Rickenlund, A., Carlström, K., Ekblom, B., Brismar, T. B., von Schoultz, B., & Hirschberg, A. L. (2003). Hyperandrogenicity is an alternative mechanism underlying oligomenorrhea or amenorrhea in female athletes and may improve physical performance. Fertility and sterility, 79(4), 947–955. https://doi.org/10.1016/s0015-0282(02)04850-1
• Toosy, S., Sodi, R., & Pappachan, J. M. (2018). Lean polycystic ovary syndrome (PCOS): an evidence-based practical approach. Journal of diabetes and metabolic disorders, 17(2), 277–285. https://doi.org/10.1007/s40200-018-0371-5
• Teede, H. J., Misso, M. L., Costello, M. F., Dokras, A., Laven, J., Moran, L., Piltonen, T., Norman, R. J., & International PCOS Network (2018). Recommendations from the international evidence-based guideline for the assessment and management of polycystic ovary syndrome. Fertility and sterility, 110(3), 364–379. https://doi.org/10.1016/j.fertnstert.2018.05.004
• Tee, J. C., Bosch, A. N., & Lambert, M. I. (2007). Metabolic consequences of exercise-induced muscle damage. Sports medicine (Auckland, N.Z.), 37(10), 827–836. https://doi.org/10.2165/00007256-200737100-00001

COVID-19 - acute and long term
This will be a fun one, he says with dread and despair in his eyes. Again, opinion piece.

COVID-19, or SARS CoV-2 is a virus whose infection is often termed a respiratory syndrome. I'm not a fan of that labelling.
Whilst it is primarily spread through respiration, it appears to also affect the (1)

• Brain and other elements of the nervous system
• Heart
• Vascular system
• Kidneys
• Liver
• Gastrointestinal tract
• Endocrine system
• Skin

Which is a short way of saying fucking everything.

The immuno-inflammatory response to SARS CoV-2 in the short and long term suggests that long COVID may be caused by an increase in chronic/unnecessary inflammation (2, 3, 4) .

Like many before me, I see parallels between "long COVID" and myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) initially brought on by other viral/bacterial infections (5).


How it affects weightlifting
How this pertains to weightlifting is variable. Firstly, there should be some reasonable precautions (@2022 Worlds being a superspreader event).

Secondly, the symptoms appear to be variable but a weightlifter's presentation of Long COVID and a genpop presentation is probably going to be different. I think this is more likely to affect elite athletes who catch COVID (especially if they have had multiple infections) as they are more likely to unnecessarily train through post exertional symptom exacerbation (PESE) or not get enough rest, which tends to make those symptoms worse. Additionally, that will likely make chronic pain or increased risk of injury more likely due to increases in fatigue and lack of recovery.

As you would expect, there are decreases in VO2Max found in athletes, weeks after testing negative (6, 7). This seems fairly consistent across different people in my anecdotal experience, regardless of sport and behaviour.

How COVID/post COVID-positive symptoms affect strength and power appears to be somewhat dependent on the individual case. Though the football paper reports no loss in strength/power/sprint performance, I personally experienced significant post-COVID losses in strength/power after moderate symptoms (struggling to get out of bed, persistent cough with mucous, difficulty speaking due to laryngitis).

There are potential mechanisms, directly or indirectly mediated by SARS CoV-2, that result in decreased muscle strength in genpop (8). However, the indirect factor of malnutrition is probably less likely in athletes unless there are serious GI issues brought on by the disease. Inactivity can contribute, but IMO does not explain the magnitude of strength loss. I think that general fatigue and neurological impairments are the more likely contributors.

I estimate that my maximal strength initially dropped to about 65-70% (i.e. 65-70% previous 1RM would have been my 1RM on the day), however my I think my quick lift strength would have dropped to about 80%. Recovery between sessions was definitely prolonged, so training volume had to be reduced markedly. Either a few sets on piss weight, or eventually 1-2 sets on a "working" weight after 2-3 weeks.

Another person I know had the opposite - maximal strength almost completely unaffected, quick lifts were affected due to lack of coordination and speed characteristics (partially a skill issue, probably partially neurological). Definitely affected by fatigue and the fact that they were trying to push cardio too hard too soon.

There are some resources from Long COVID physio around exercise and other stuff which I highly recommend.


Myself as a case study

My weightlifting exercising (can't really call it training) for myself was just based on recovery parameters, trying not to do anything that would aggravate fatigue beyond baseline 24 hours post session and training on non-consecutive days.

First session was lifts on 50-60%/1-2 reps, a few sets, 3 or 4 exercises, ~3-5 min rest between each set.
I actually did 1 set of 3 reps on ~70% for front squats. That was egotistical and stupid, I was physically and mentally wiped for two days afterwards.
Did the same thing of classic lifts 50-60% for 1-2 reps and multiple sets another two times in the first week of the return, keeping strength exercises to 65% or less (3 reps, 3 sets), which was just about the right amount for recovery.

Second week, I progressed lifts as my recovery had allowed for, about 65-75% for 3 sets of 1-2 reps in quick lifts and 70%/3 x 3 for strength exercises.
Third week, about 70%/2-3 or 75-80%/1 for 3 sets, strength was returning so I could do about 80%/3 x 3. Again, on but not over the edge of recovery time.
Fourth week: 75-85%/1-2 x 3 sets for quick lifts, strength still at 80%/3 but up to 5 sets.
Fifth week: 75%/3 x 3 manageable (barely), 80%,85%,90%/1 was about what I could do. Strength wise, kept to 80%/3 x 5.
Sixth week: 80%/2 x 3 reasonable, 90%/1 x 2-3 manageable. Strength improved, 75%/5x5 or 85%/2x3 were manageable.

From there it was more just getting back into form, similar to coming back from a training after a layoff.
Cardiorespiratory fitness and tolerance of low intensity aerobic training or general physical activity took longer to come back (and truthfully, is still not where it was).

I've seen a lot of people push themselves too hard too soon, prolonging their illness and recovery. I suspect that some of the weird injuries or losses of form we've seen in athletes could be partially related to SARS CoV-2.

Luckily I've very briefly come across someone with ME/CFS. Whilst I don't fully understand his predicament, it helped me remember that exercise capability in the gym can be wildly different from what someone can recover from in a reasonable timeframe.
In his first session in the gym, he did a 30 second sit to stand and completed it reasonably well for someone who was sedentary. For the next two or three days, he was physically incapable of lifting/moving his legs to get out of bed.

Exercise progression for him then, was/is a very very slow process. e.g. 60%/5 x 3 to 60%/6 + 60%/5 x 2.
I'm not saying that athletes should necessarily progress that slowly, but I think ME/CFS and long COVID are very much an exercise in "hurry up and wait".


References

• Osuchowski, M. F., Winkler, M. S., Skirecki, T., Cajander, S., Shankar-Hari, M., Lachmann, G., Monneret, G., Venet, F., Bauer, M., Brunkhorst, F. M., Weis, S., Garcia-Salido, A., Kox, M., Cavaillon, J. M., Uhle, F., Weigand, M. A., Flohé, S. B., Wiersinga, W. J., Almansa, R., de la Fuente, A., … Rubio, I. (2021). The COVID-19 puzzle: deciphering pathophysiology and phenotypes of a new disease entity. The Lancet. Respiratory medicine, 9(6), 622–642. https://doi.org/10.1016/S2213-2600(21)00218-6
• Low, R. N., Low, R. J., & Akrami, A. (2023). A review of cytokine-based pathophysiology of Long COVID symptoms. Frontiers in medicine, 10, 1011936. https://doi.org/10.3389/fmed.2023.1011936
• Turner, S., Khan, M. A., Putrino, D., Woodcock, A., Kell, D. B., & Pretorius, E. (2023). Long COVID: pathophysiological factors and abnormalities of coagulation. Trends in endocrinology and metabolism: TEM, 34(6), 321–344. https://doi.org/10.1016/j.tem.2023.03.002
• Koc, H. C., Xiao, J., Liu, W., Li, Y., & Chen, G. (2022). Long COVID and its Management. International journal of biological sciences, 18(12), 4768–4780. https://doi.org/10.7150/ijbs.75056
• Komaroff, A. L., & Lipkin, W. I. (2023). ME/CFS and Long COVID share similar symptoms and biological abnormalities: road map to the literature. Frontiers in medicine, 10, 1187163. https://doi.org/10.3389/fmed.2023.1187163
• Wezenbeek, E., Denolf, S., Bourgois, J. G., Philippaerts, R. M., De Winne, B., Willems, T. M., Witvrouw, E., Verstockt, S., & Schuermans, J. (2023). Impact of (long) COVID on athletes' performance: a prospective study in elite football players. Annals of medicine, 55(1), 2198776. https://doi.org/10.1080/07853890.2023.2198776
• Vollrath, S., Bizjak, D. A., Zorn, J., Matits, L., Jerg, A., Munk, M., Schulz, S. V. W., Kirsten, J., Schellenberg, J., & Steinacker, J. M. (2022). Recovery of performance and persistent symptoms in athletes after COVID-19. PloS one, 17(12), e0277984. https://doi.org/10.1371/journal.pone.0277984
• Montes-Ibarra, M., Oliveira, C. L. P., Orsso, C. E., Landi, F., Marzetti, E., & Prado, C. M. (2022). The Impact of Long COVID-19 on Muscle Health. Clinics in geriatric medicine, 38(3), 545–557. https://doi.org/10.1016/j.cger.2022.03.004

Lateral hip pain

Lateral hip pain, or greater trochanteric pain syndrome (GTPS) is characterised by pain at the side of the hip near the greater trochanter, typically where the glute medius/minimus tendon attach. Conditions like gluteus medius/minimus tendinopathy, trochanteric bursitis fall under this umbrella term of GTPS.

It is more common in women and particularly women around 40-60 and above (1,2) possibly due to the hormonal changes that occur with menopause (3). Wider pelvic structure usually causes more loading of the lateral hip (4), so it's not unique to women.


Typical aggravating factors include

• Direct lateral compression of the greater trochanter or glute med/min tendons e.g. lying on the affected side
• Positional compression e.g. end range hip adduction or horizontal adduction, deep hip flexion
• Glute medius/minimus force or jerk (dF/dt) greater than what is tolerable e.g. standing on one leg, running, walking uphill.
• Usually feels worse in the morning, better later in the day.
• The combination of position causing compression + muscular force application can also be aggravating (e.g. deep, heavy squats)

Both intensity of force/jerk application and duration matter.
For example, lifting heavy weights can be fine for someone, but sitting in a chair for a long time can be aggravating.

Management includes general lifestyle management and exercise.
Potentially menopausal hormone therapy for menopausal/postmenopausal women, obviously subject to patient and medical doctor's discretion.

Lifestyle management will usually be activity modification where possible to reduce loading or increase movement, sometimes dietary or other intervention.

Exercise management in an isolated sense typically consists of gluteus medius resistance exercises at various loads.
In genpop the exercise doesn't need to have a strengthening effect in order to reduce pain, I'm not sure if that's true (not doubting, literally just don't know) for athletes.

Hip abduction, hip flexion and single leg weight bearing exercises are typically prescribed to genpop, trying to find the Goldilocks loading zone of not too much, not too little.

With respect to weightlifting, I would say that people with GTPS will have more pain and/or tightness getting deep into a squat, particularly at speed (i.e. squat snatches). This doesn't mean that athletes with GTPS shouldn't train deep heavy squats or squat snatches; but rather they should be dosed judiciously.

Less often (usually when already highly aggravated), it can affect

• The pull off the floor in the snatch or clean, typically the snatch.
• The front leg in the jerk, particularly if someone leans forward onto the front leg (and/or) laterally shifts their hips towards the affected side.

As a case study, I would say that the onset of GTPS with menopause (along with various life existing factors) has negatively affected one of my lifters' technique/training capacity as she has had a markedly reduced tolerance of squat loading, particularly squat snatches.

Where she used to be able to train some variation of snatch/clean and jerk/strength work including squats 3x/wk, she can currently only squat heavy once a week, on a different day to snatching heavy.

As always, you train what you can train rather than focusing on what you can't. So I'm having her do lots of high power snatches, high pulls and so on.
Snatch to parallel is definitely not currently tolerable with more than light weights.

As she's had a layoff, I've had her do high snatch (1/4 or 1/3 squat depth) triples on ~60% on week 1.
Week 2 doing power snatch + OHS @ 60%.
Week 3 a "relaxed" squat snatch at 60%, allowing the lower body squish to take up the loading more than the hip.
Then moving up to 65% (which is really a deload for the hip) and repeating.

Clean and jerks are able to be trained fairly normally with reduced loading, more due to lack of fitness due to life stuff/layoff.

Front squats once a week to maintain leg strength, just kinda whatever weight/sets/reps is heavy enough without being too aggravating as she's already strong in squats.

Strengthening/mobilising other areas of the kinetic chain to enable a reduction in hip strategies in lifting technique can also be useful (e.g. ankle/knee strength, oblique/rectus abdominis strength etc.

I've also had lateral hip pain as despite my maleness I have them childbearing hips, and managed it with a similar strategy.
Non positional slow strength > non positional fast strength or positional slow strength > positional fast strength.

1. Segal NA, Felson DT, Torner JC, et al. Greater trochanteric pain syndrome: epidemiology and associated factors. Arch Phys Med Rehabil. 2007;88(8):988-992. doi:10.1016/j.apmr.2007.04.014
2. Lievense A, Bierma-Zeinstra S, Schouten B, Bohnen A, Verhaar J, Koes B. Prognosis of trochanteric pain in primary care. Br J Gen Pract. 2005;55(512):199-204.
3. Frizziero A, Vittadini F, Gasparre G, Masiero S. Impact of oestrogen deficiency and aging on tendon: concise review. Muscles Ligaments Tendons J. 2014;4(3):324-328. Published 2014 Nov 17.
4. Fearon A, Stephens S, Cook J, et al. The relationship of femoral neck shaft angle and adiposity to greater trochanteric pain syndrome in women. A case control morphology and anthropometric study. Br J Sports Med. 2012;46(12):888-892. doi:10.1136/bjsports-2011-090744

Trendelenburg test useful here.

I had a masters lifter (F46y) who transitioned to sprinting but keep some WL skills in their training. Advent of sprint skill development (front side mechanics in particular eg B march/skip) and bend work brought on what was a minor pelvic control issue previously with just lifting skills.

I'd have to go back through my notes about how some of the leg dominance developed in split jerking might have hidden this issue in the beginning for her.