Even in pandemic times, science marches on and progress is made. Or not. Here is the news — and my views — on sports medical and societal aspects of heat stroke, carbon monoxide for athletes, and exercise-associated muscle cramping.
On Saturday, September 5, 2020, a 41-year-old woman hiking in a heat wave died from heat stroke in Malibu Creek State Park when, according to the National Weather Service, the temperature was >110°F. That same day, also in California, a 20-year-old man hiking in Joshua Tree National Park died from heat stroke as the temperature spiked to 120°F. His death came just 16 d after another man was found dead near his sedan (stuck in deep sand) on Black Eagle Mine Road in the Joshua Tree National Park. That park covers >1200 square miles of the rugged Colorado and Mojave deserts. Black Eagle Mine Road, an unmaintained dirt road strewn with rocks and boulders, runs just 16 or so miles, past abandoned jade and gold mines, to end at the once-famous but now-closed Kaiser Steel iron mine. In the summer heat and the wrong car, it can be a dead-end road in more ways than one. In the summer of 2011, a young man and woman, tourists from Europe, were found dead from heat stroke on that remote road. Their bodies were about a mile apart and 5 miles away from their stranded rental car. They walked for help, but did not make it.
In the summer of 2020, during our killing pandemic, when we added COVID-19 to our troubling concerns about the health risks of youth football, exertional heat stroke (EHS) continued to plague us. EHS should never be fatal in football, yet in the summer of 2020, it continued to kill kids.
Among high school football deaths in the summer of 2020, at least two and maybe four were from EHS. All four were large linemen (weights known in 3: 250, 270, 300 lb). Two collapsed in football practices in mid-August, one in northeast Arkansas, one in west Texas. One, aged 16 years, died 5 d after collapse, soon after an urgent liver transplant. The other, aged 18 years, died 11 d after collapse, in a Houston hospital. The official cause of death for both was EHS. In two other boys who died (one in late August, one in early September), the cause of death has not yet been issued, but EHS seems plausible. One boy, aged 17 years, in Pennsylvania, collapsed as practice ended for the day (after complaining of a leg cramp) and was pronounced dead soon after arriving in a hospital. The other boy, aged 16 years, in South Carolina, made it home after football practice ended, but soon was found unresponsive in the shower. He died later that night in a hospital. We await the “official” causes of death. A fifth high school boy, aged 16 years, in Mississippi, collapsed in football practice (in mid-June 2020), and died soon after. His cause of death is still unknown as I write this, but the coroner does not suspect EHS.
But here we are, the year 2020, and EHS is still killing our kids in football. It is shameful. As I covered in 2019, the coaches are the culprits, as they push high school and college football players to collapse in workouts of irrational intensity (1). My view agrees with that in a comprehensive new study, the article on it subtitled: “Excess in conditioning kills” (2). Something should be done— and soon — about the reckless endangerment of kids by football coaches.
Carbon monoxide (CO) can be a mimic and a silent killer. In 2018, I covered the sports medicine aspects of CO poisoning, including in ice hockey players (and coaches) and mountain climbers, and in recreational boaters and mud boggers (3). Tennis player, Vitas Gerulaitis, died from CO poisoning as he napped in a cottage room above a faulty pool heater in the basement below. Fatal CO poisoning has occurred when children ride under canopies in the back of pickup trucks, or when keyless car owners forget to turn off their car when they park it in a garage attached to their home. CO poisoning kills an average of more than 400 Americans a year.
So I was surprised by a new article in our literature on exposure to low-dose CO as a way to increase hemoglobin mass (Hbmass) and V˙O2max (4). Researchers noted that CO, produced in low levels endogenously, is a signal that alters some physiologic functions, perhaps to our benefit. They hypothesized that a chronic fall in oxygen transport by inhaling CO could mimic some adaptations of altitude training. For 3 wk, 11 healthy, trained men inhaled a CO bolus five times a day to increase carboxyhemoglobin levels by about 5% over the entire day. Another 11 subjects got a placebo. In the CO group, erythropoietin (Epo) and erythropoiesis increased, and Hbmass increased nearly 5%, similar to an altitude exposure of 2500 m. The small overall increase in V˙O2max was not significant, but the individual increases in V˙O2max did correlate with those in Hbmass. The researchers concluded that chronic exposure to low-dose CO has a “positive effect” on performance. They caution that they may have opened a “Pandora's box,” but they imply that some athletes may already be using CO as a “new kind of blood manipulation” (4).
Woe is me. Here we go again. Even in the past 2 years, elite runners and cyclists continue to be caught blood-doping by injecting small doses of recombinant erythropoietin (rEpo), and now they can study a new way to boost their Epo levels: inhaling a poison gas. In 2013, I covered the many deaths of elite cyclists and other athletes from overdosing on rEpo (5). Let us hope we never see athletes die from foolishly inhaling CO to “boost” their performance.
Exercise-associated muscle cramping (EAMC) occurred again in the United States Open tennis tournament in September 2020. Dominic Thiem won the championship in a comeback over Alexander Zverev that had both players battling EAMC near the end of the fifth-set tiebreaker that capped a 4-h match. A trainer massaged Thiem's cramping right thigh during a changeover. EAMC is a tradition in this tennis tournament in the heat of New York City. I covered the widespread EAMC during the 2018 U.S. Open (6).
The two main hypotheses for EAMC are: 1) loss of salt and water in sweat (notably in “salty sweaters”), along with muscle fatigue; and 2) altered neuromuscular control, when muscle fatigue increases spinal reflex “excitatory” drive to the muscle as it decreases “inhibitory” drive from the Golgi tendon organ. In field studies, we and others tied EAMC in football and tennis to the first hypothesis, that is, loss of salt and water in sweat. Another research group, using a laboratory model of cramping (shocking the big toe until it cramps), argued for the second hypothesis. Pickle juice seemed to work fast to alleviate big-toe cramping, and this led to the commercial “cramp-buster” cocktail, “Hotshot,” that had its 15 min of fame. I argued that the unique laboratory model of big-toe cramping may be solid, but does not apply to EAMC in summer football or tennis (7).
I recently covered three articles that gave some support to our “salty sweater” hypothesis for EAMC (8). Now there are four more. A 25-year-old man who was a “salty sweater” because of cystic fibrosis and suffered EAMC underwent heat acclimation that cut the salt in his sweat and cured his EAMC (9). A 17-year-old football lineman with cystic fibrosis had disabling EAMC during two seasons of high school football. After a sharp increase in salt in his diet and sports drinks, he completed a football season with almost no EAMC and is considering college football (10). And a review of EAMC by a group that keys on tennis favors our “salty sweater” hypothesis to explain EAMC in tennis (11).
Best of all, a lead researcher in the “altered neuromuscular control” camp is finally inching our way. He is first author of a new study of sweat characteristics in 350 NCAA athletes (in 11 sports) with or without a history of EAMC. Although only minimal differences in sweat characteristics were found in those with versus without EAMC in most sports (only nine tennis players in the study), in the largest group (by far) of 110 football players, those with EAMC were “salty sweaters,” that is, had significantly higher sweat rates and sweat salt content than those without EAMC. Hence this sentence in their conclusion (12): “Fluid and electrolyte replacement may help American footballers.” Halleluyah!
The author declares no conflict of interest and does not have any financial disclosures.
1. Eichner ER. Fatal exertional heat stroke in football: the coaches are the culprits. Curr. Sports Med. Rep
. 2019; 18:251–2.
2. Boden BP, Fine KM, Spencer TA, et al. Nontraumatic exertional fatalities in football players, part 2: Excess in conditioning kills. Orthop. J. Sports Med
. 2020; 8:232596712094349. doi:10.1177/2325967120943491.
3. Eichner ER. Accidental carbon monoxide poisoning in sports and other settings. Curr. Sports Med. Rep
. 2018; 17:78–9.
4. Schmidt WFJ, Hoffmeister T, Haupt S, et al. Chronic exposure to low dose carbon monoxide alters hemoglobin mass and VO2max. Med. Sci. Sports Exerc
. 2020; 52:1879–87.
5. Eichner ER. Dying to win: memories of doping and duping. Curr. Sports Med. Rep
. 2013; 12:2–3.
6. Eichner ER. Muscle cramping in the heat. Curr. Sports Med. Rep
. 2018; 17:356–7.
7. Eichner ER. Fighting muscle cramps with two spices and one hot fruit. Curr. Sports Med. Rep
. 2016; 15:304–5.
8. Eichner ER. News and views on heating, sweating, and cramping in sports. Curr. Sports Med. Rep
. 2020; 19:165–6.
9. Willmott AGB, Holliss R, Saynor Z, et al. Heat acclimation improves sweat gland function and lowers sweat sodium concentration in an adult with cystic fibrosis. J. Cyst. Fibros
. 2020. doi:10.1016/j.jcf.2020.07.013.
10. Wise P, Lafferty L, Phillips SF. A case of persistent muscle cramps in an American football player with cystic fibrosis. Cureus
. 2020; 12:e8621. doi:10.7759/cureus.8621.
11. Troyer W, Render A, Jayanthi N. Exercise-associated muscle cramps in the tennis player. Curr. Rev. Musculoskelet. Med
. 2020; 13:612–21.
12. Miller KC, McDermott BP, Yeargin SW. Sweat characteristics of cramp-prone and cramp-resistant athletes. Int. J. Sport Nutr. Exerc. Metab
. 2020; 30:218–28.