As summer approaches, it is time to cover old debates and new research on heating and sweating in sports and their roles in muscle cramping in athletes. Exertional heat stroke also is a continuing threat, alas, especially in football, but I covered it recently (1) and will not repeat it here. Recent research on the epidemiology of exertional heat illness (EHI) in 25 National Collegiate Athletic Association (NCAA) sports finds that EHI is still most common in football, and is characterized most often by “heat cramps,” followed by heat exhaustion and dehydration (2). Heat cramps, described as early as 1878 in men working in extreme heat in gold mines in Nevada, is the term still used today to describe the severe, spreading, sustained, sharply painful muscle contractions that can sideline athletes. In my opinion, a more precise term would be “sweat cramps.” Let the debate commence.
Not Just the Heat
“Heating up” during your sport, as an isolated factor, does not necessarily lead to heat cramps. Consider two recent studies. In one study, core temperature was tracked via an ingestible capsule in 40 elite male and female cyclists during the 2016 Union Cycliste Internationale Road World Championships in high heat in Qatar. Ten of the 40 reached a peak core temperature >104 F; the highest recorded was 106.7 F. Higher core temperatures were seen during time trials than the road race, consistent with the fact that body heat builds more from intensity than duration of exercise. In this study, no cyclist was treated for EHI, and cramping was not mentioned (3). In the other study, rectal temperature was tracked via a telemetric capsule in 14 elite male and female race walkers during four races. Despite only moderate-warm conditions, peak rectal temperatures >104 F were seen in all races; the highest recorded was 106.2 F. Yet the only EHI was muscle cramping in one athlete in one race (4).
The pearl here is that elite distance athletes can reach very high core temperatures during their races without developing EHI. High body heat alone does not necessarily cause muscle cramping in top athletes in action.
In field studies, we and others in football tied heat cramping to heavy, salty sweating. In NCAA football, we found that “crampers” lost more salt in sweat than position-matched noncrampers, and we concluded that large acute salt and water loss in sweat may be typical of players prone to heat cramping (5). Bergeron (6) found the same in tennis players. In National Football League (NFL) players, we found similar trends, and other researchers agreed that NFL players during preseason practice can be heavy, salty sweaters (7). In a study using forearm patches to gauge sweat sodium concentrations, 20% of 157 experienced runners in a marathon race were judged to be “salty sweaters,” and the authors speculated that they might benefit from more salt to offset high sweat salt losses (8).
I have argued that if up to 1 in 20 white adults is a heterozygote for cystic fibrosis (CF), in a marathon with 20,000 white runners, up to 1000 runners may be genetically programmed for salty sweating. Contrarian views have been voiced (9), but a fair reading of all the studies on this point suggests that at least some CF heterozygotes do have elevated sweat sodium levels (10–12). These athletes may be prone to heat or “sweat” cramping in marathons, football training, or tennis.
The Two Hypotheses
Not all cramps are alike. As I have covered, salty sweating does not cause writer's cramp, fiddler's cramp, or golfer's yips. Nor does it cause the “side-stitch” in a cross-country runner or the acute cramp in the torn hamstring of a racing hurdler. Nor does salty sweating cause the tetany of the hyperventilation syndrome, the ischemic-pain “cramp” of exertional sickling, or the acute cramp in the rapid “calf-fatiguing” cramp-research protocol (5).
A recent, informative review puts it vividly: “Two main causes for muscle cramps have been proposed. This suggests an either/or dichotomy, and this is how the literature is often presented, with loud voices expressing strongly held views on either side. It should be recognized though that the picture is not at all clear, and the evidence on both sides of the debate is weak. It is unlikely that a single mechanism can account for all cramps in all situations” (13).
The two main causes — or hypotheses — for exertional muscle cramping are: 1) loss of salt and water in sweat, along with muscle fatigue; and 2) “altered neuromuscular control” from muscle fatigue that increases spinal reflex “excitatory” drive to the affected muscle as it decreases “inhibitory” drive from the Golgi tendon organ. Both hypotheses, thus, invoke muscle fatigue.
Although the recent review questions both sides of this debate, it favors aspects of the “salty sweater” hypothesis. It gives heavy weight to the largely forgotten or dismissed large-scale studies of industrial workers — mainly miners, stokers, construction workers, and steel workers — in the 1920s and 1930s. It calls some of these studies: “extensive, meticulous, prescient.” It covers intervention studies showing that intravenous saline quickly reversed cramping, as well as prospective studies showing that saline drinks or salt tablets greatly reduced cramping in these industrial workers in the heat. I too have covered these studies and have reached the same conclusion (5). The review also notes new research that favors the “role of disturbances of water and salt balance” in exertional muscle cramps (13).
New Research: Salty Sweating Redux
One new study explored the role of dehydration in cramping. Nine young men (football and tennis players) with a history of exertional cramping were dehydrated, on three different days, by 1%, 2%, and 3% of body mass, via sweating in a sauna, to remove the effects of exercise and muscle fatigue on cramping. Each subject underwent a “cramp test” of maximal voluntary contraction of the hamstrings at maximally shortened position. The test evoked no cramping at zero and 1% dehydration, but three men cramped at 2% and six men cramped at 3% dehydration (P < 0.05). This supports the role of body water loss (via sweating) in exertional muscle cramping (14).
The other new study tested whether water ingestion after dehydration would increase and a sports drink would decrease muscle cramp susceptibility. Ten young men ran downhill in the heat until they lost 2% of their body mass. Ten minutes after running, they drank either water or a sports drink (with sodium, other electrolytes, and glucose) in a volume equal to the mass lost. Cramp susceptibility was gauged by a threshold frequency test of electrical stimulation to induce acute calf cramp. Cramp susceptibility did not change immediately after running, but increased 30 and 60 min after water intake. In contrast, cramp susceptibility decreased at the same intervals after the sports drink, which better maintained serum sodium levels (15). These results suggest that dehydration and loss of salt via “salty sweating” — and then drinking water — contribute to heat cramping. Call it “sweat cramping.”
As summer draws nigh, there is more reason than ever to consider “salty solutions” for heat cramping. Athletes prone to major cramping should eat healthful salt-rich foods and add extra salt to their sports drinks on-field. If a player heat cramps in a game and fails to respond to rest, stretching, massage, ice, and salt-rich drinks, you can often reverse it with 2 L of normal saline intravenously. A pitfall is that quaffing plain water in the face of major cramping poses the risk of dire hyponatremia. Use “saline solutions” for sweat cramping in athletes.
The author declares no conflict of interest and does not have any financial disclosures.
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