The results of the present study showed that the TF to induce muscle cramp after DHR decreased with the ingestion of spring water but increased with ingestion of OS-1 during DHR. This supported the hypothesis that post-exercise muscle cramp susceptibility would be increased by ingestion of spring water, but decreased by ingestinon of ORS during exercise.
In comparison to the previous study [16] in which no fluid intake was allowed during DHR, the increases in HR (159.1 ± 3.0 bpm vs 140.3 ± 17.9 bpm), RPE (13.2 ± 2.0 vs 11.6 ± 2.2), thermal sensation (5.9 ± 0.9 vs 5.2 ± 0.6), and tympanic temperature (38.7 ± 0.6ºC vs 37.5 ± 0.3ºC) were smaller in the present study. However, the total amount of loss of body mass by sweat in the present study (1,258 ± 267 g) was similar to that of the previous study (1,304 ± 300 g) [16]. It appears that the fluid intake during DHR reduced the increase in core temperature, which lowered HR and RPE. As shown in Table 1, no significant changes in Hct and Hb from baseline to immediately after DHR were observed for both conditions. Interestingly, plasma volume was greater for the OS-1 than the spring water condition from the baseline to immediately post-exercise, suggesting that water absorption was greater for the OS-1 condition. Serum osmolality and sodium concentration slightly decreased for the spring water condition, suggesting that sodium concentration in the blood was more diluted after the spring water than OS-1 ingestion. However, it is important to note that serum sodium concentration at immediately post-DHR did not reach the level of hyponatremia (< 135 mmol/L), even for the spring water condition.
TF has been used to assess muscle cramp susceptibility in the previous studies for the abductor halluces muscle [18, 19, 23] or the plantar flexors [14]. For example, Behringer et al. [14] showed that neuromuscular electrical stimulation performed twice a week for 6 weeks reduced the number of spontaneous calf cramps by 78%, and this was accompanied by an increase in the cramp threshold frequency from 15.5 ± 8.5 Hz to 21.7 ± 12.4 Hz. It should be noted that TF measures do not provide cramping intensity and duration, or pain associate with the muscle cramp, and it is not necessarily clear whether a change in TF reflects a change in muscle cramp sussceptability. Minetto et al. [18] were the first to use TF to examine muscle cramp, and demonstrated good inter-session (ICC = 0.82–0.92) and inter-day (ICC = 0.85) relliability. In the present study, the baseline TF measured in a week apart was the same (25.8 ± 0.6 Hz). Since TF was not assessed during exercise, the muscle cramp susceptibility during the exercise is not known in the present study. Although the present study showed that no muscle cramp occurred during DHR, the decrease in TF at immediately post-DHR is likely to indicate increased muscle cramp susceptibility during the exercise. The average magnitude of decrease in TF in the present study for the spring water condition was around 4 Hz (Fig. 2). This finding was in line with the study by Miller et al. [23] who reported that a decreased threshold frequency to induce muscle cramp by 4 Hz indicated an increase in muscle cramp susceptibility. Thus, the decrease (4 Hz) is considered to be physiologically significant, and a change in TF was likely to indicate a change in muscle cramp susceptibility.
In regards to the relationship between dehydration (serum sodium concentration) and muscle cramp, Schwellnus et al. [24] reported that serum sodium concentration immediately after a 56-km road race was significantly lower for the cramping group (139.8 ± 3.1 mmol/L) than the non-cramping group (142.3 ± 2.1 mmol/L). Sulzer et al. [25] found a significant difference in serum sodium concentration after Ironman triathlons between the cramping (140 ± 2 mmol/L) and non-cramping (143 ± 3 mmol/L) groups, but they did not consider that this was clinically significant. In contrast, Hoffman and Stuempfle [4] showed no difference in serum sodium concentration at the finish of a 161-km ultramarathon among those with muscle cramping, near cramping and no cramping in the last stage of the race. Using the TF to assess muscle cramp, Miller et al. [17] did not find changes in TF of electrically induced muscle cramp after 3% dehydration, in which an increase in serum sodium concentration from baseline (138.6 ± 0.2 mmol/L) to post-dehydration (145.1 ± 0.5 mmol/L) was found. Braulick et al. [26] reported an increase in serum sodium concentration in 3–5% dehydrated condition (149.5 ± 1.8 mmol/L) in comparison to euhydrated condition (141.9 ± 3.1 mmol/L), and found no difference in TF between the conditions. In the present study, the differences in serum sodium and chloride concentrations between the conditions were small at immediately after and 65 min post-DHR (Table 1), but TF was largely different between the conditions (Fig. 2). Additionally, no significant correlations were evident between the magnitude of change in TF and the magnitude of changes in serum sodium or chloride concentration. These suggest that muscle cramp susceptibility is not determined by serum sodium and chloride concentrations alone.
The limitation of the present study was that no control group (no fluid ingestion) was included to compare with other conditions. However, our previous study [16] showed that TF did not change significantly at immediately after DHR from the baseline without fluid intake during exercise. Thus, it seems likely that no significant change in TF would have been observed, if a control group (no fluid ingestion during exercise) had been included. In the previous study [16], TF increased after OS-1 intake by 3.7 Hz at 30 min and 5.4 Hz at 60 min, respectively. In the present study, TF increased by 6.5 ± 4.9 (immediately post-DHR) to 13.6 ± 6.0 Hz (65 min post-DHR) for the OS-1 condition (Fig. 2). It seems possible that the increases in TF after OS-1 ingestion suggest a decrease in muscle cramp susceptibility. It is important to note that OS-1 contains glucose (18,000 mg/L), and serum electrolyte concentrations were not largely different from the baseline values and between conditions as shown in Table 1. Thus, it might be that the increase in TF was more due to glucose than electrolytes. Unfortunately, glucose concentration in the blood was not measured in the present study. It is necessary to add the same amount of glucose to spring water to examine the effects of glucose on muscle cramp in a future study.
Behringer et al. [27] reported that orally administered transient receptor potential vanilloid 1 (TRPV1) and ankyrin 1 (TRPA1) activators decreased muscle cramp susceptibility. It is possible that sodium in OS-1 stimulated TRP receptors in the gastrointestinal tract. It is interesting to investigate how spring water or OS-1 intake affects oropharyngeal reflex, muscle spindles, Golgi tendon organs and alpha motor neurons, and how a small change in electrolyte concentrations in the extracellular fluid surrounding muscle fibres could affect muscle cramp susceptibility. It is also necessary to include female participants, athletes, and other age groups to confirm the present study findings. The goal of fluid intake during exercise is to prevent excessive dehydration and changes in electrolyte balance [28]. Evans et al. [29] stated that the addition of sodium to a rehydration solution is beneficial for maintenance of fluid balance due to its effect on extracellular fluid osmolality and volume. Thus, to prevent EAMC, ingesting OS-1 appears to be effective, but further research is warranted to investigate how OS-1 works to reduce the susceptibility. In the present study, no muscle cramp assessment was performed during exercise, and no voluntary muscle cramp was observed. It would be interesting to observe whether muscle cramp does not occur during exercise, when OS-1 or other ORS is ingested during exercise.
It ws concluded that spring water intake during exercise in the heat increased muscle cramp susceptibility after the exercise (downhill running), and ingestion of OS-1 decreased the muscle cramp susceptibility. These were in line with the findings of our previous study [16] showing that spring water intake after dehydration made muscles more susceptible to muscle cramp, but when OS-1 was consumed, the muscle cramp susceptibility was reduced. It should be investigated further as to what and how much electrolytes should be contained in the beverage, and whether commercially available sport drinks that contain some electrolytes are as effective as OS-1 to reduce muscle cramp susceptiblilty.